Printable list of al respiratory Medicine SAQs

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Question 1d - 2000, Paper 1

A 50 year old man is brought into the Emergency Department after acute flexion injury to the neck while surjing.  He is unable to move both arms or kgs and has a sensory level at C4·5.   He ls a heavy smoker with a history of chronic bronchitis.

(d) Five days later he is orally intubated and has a forced vital capacity of  200 mls.  His unstable cervical injury has been managed by tongs and traction. 
What will you do to facilitate weaning?
 

College Answer

(d) A VC of 200ml if correctly measured suggests weaning such a patient will be a major problem. The question does not explain whether the cervical injury is  complete or incomplete and stable or unstable. This is central to this management. If the lesion is complete at C4.5 in this mature man with some degree of chronic lung disease, he is going to be very difficult to wean from tracheostomy and will require some degree of mechanical support.

If the lesion is incomplete then with time some recovery may be expected and the aim in the short term would be to maintain spontaneous respiration, prevent nosocomial infection etc.

As in (c). considering surgical stabilisation and tracheostomy are essential. Percutaneous forceps technique of ·tracheostomy with the neck stabilised in the neutral position is not contraindicated.

General weaning principles should also have been applied {eg. optimise nutrition, treat sepsis, optimise breathing circuit and ventilator, treat abdo distension and lung pathology).

Discussion

Strategy for weaning

  • Minimise sedation
  • Maximise postural assistance to respiration: sit in a chair if possible
  • Adequate sleep and nutrition
  • Respiratory physiotherapy
  • Optimise cardiac function; aim for dry fluid balance
  • Optimise respiratory function; manage pulmonary infections aggressively
  • Prevent VAP with post-jejunal feeding, oral hygiene and possibly selective digestive tract decontamination. Cease the regular PPIs.
  • Consider tracheostomy
  • Consider NAVA

Plan B

  • Consider the neccesity for long term ventilation at home
  • discuss this possibility with the family

References

Question 2c - 2000, Paper 1

A 58 year old man is brought in by ambulance moribund with barely palpable pulse and a sinus tachycardia.


(c) A large pulmonary embolus is confirmed.  What management will you institute? 

College Answer

{c) At last a diagnosis. Management at this stage would depend on his clinical state  and include supportive measures (02, inotropes, ulcer prophylaxis) and specific (heparin, IVC filter). Dobutamine (lesser forms of haemodynamic disturbance) and noradrenaline (severe RV failure) are the only inotropic agents supported by evidence in this setting.-Adrenaline·may be the only ··

agent immediately available on the arrest trolley though.

NB. Excessive fluid may distend the RV and worsen the situation.

(i)       If resuscitated  adequately and haemodynamically  stable, IV  heparin would be the mainstay. Venous .duplex scans may help to gauge further  thrombus load. The history of DU and a large mobile DVT may be an indication for insertion of a caval filter but lysis appears contraindicated if the history is confirmed.

(ii)      If the patient is haemodynamically  unstable and on  large doses of vasopressor (preferably noradrenaline at this stage).embolectomy on bypass is indicated. Fibrinolysis is contraindicated by recent surgery and DU.

Discussion

A question like this would benefit from a systematic answer.

  • Attention to ABCs, with correction of immediately life threatening complications
  • Airway
    • intubation may be required to apply a controlled FiO2
  • Breathing
    • Increase FiO2 to correct hypoxia
  • Circulation
    • Fluid boluses to carefully increase right heart preload
    • pulmonary vasodilator and inotrope eg. milrinone, to increase forward flow though the pulmonary circulation
    • inhaled pulmonary vasodilators, eg nitric oxide or prostacycline
  • Anticoagulation/thrombolysis
    • thrombolysis likely to be absolutely contraindicated given the history of recent surgery
    • anticoagulation may be relatively contraindicated if there are evolving intracranial haemorrhagic events
  • Rescue therapy
    • Embolectomy
    • Clot lysis / clot retrieval by interventional radiology
    • VA ECMO if anticoagulation not contraindicated and other measures fail or are not available
  • Preventative therapy
    • long term anticoagulation
    • vena cava filter

References

Question 1a - 2000, Paper 2

A 44 year old man, with morbid obesity (175 cm tall and 210 kg) presents to the Emergency Department with respiratory failure.

He is obtunded with an arterial blood gas (ABG) showing 

  • pH 7.25
  • Pa C02 82 mmHg
  • PaO2 53 mm Hg

CXR reveals cardiomegaly and clear lung fields.

(a) Describe your management of this problem in the first 24 hours.

College Answer

Management  includes  history and  examination, investigations  (appropriate  and  interpreted)  and ongoing therapy (including triage, monitoring, pharmacology and non-pharmacological  inventions).

ABG confirms hypoxic and hypercapnic respiratory failure (on some unspecified level of supplemental  oxygen), with an acute on chronic respiratory acidosis (with a compensatory metabolic alkalosis [calculated HC03 of 36]).

Cardiomegaly could be due to an AP portable, semi-erect  film. but the cardiac enlargement should not be discounted(? cardiomyopathy,?? pericardial effusion). Obtundation should not be assumed to be due to the hypercapnia.

The goal  of overall  management  should  be to ensure  safety  of the patient  (attention  to  ABCs), support  the  patient (posture: upright or  on side, consider  non-invasive  ventilatory  support), and identify and treat any specific reversible causes.

History   and   examination should  suggest/exclude many  diagnoses  including: ischaemic  heart disease, cardiac failure  (left  and right  sided),  chronic  obstructive  lung disease,  venous thromboembolism,  respiratory  tract infection,  CNS  disorder  (stroke/haemorrhage), diabetes  (and      DKA/Hyperosmolar    Hyperoncotic    Non-ketotic    Coma) -·er   other   endocrine    -problem   (eg. hypothyroidism)  and  the potential  for drug  related  problems  (prescribed  or over  the counter  eg.codeine).

Simple investigations  should  be ordered  and  reviewed to assist  above  differential  diagnosis  and assist treatment (eg. blood glucose, electrolytes, full blood examination,  ECG) and to confirm suspicions.

Treatment  should  be directed  at  clinical  suspicions  (appropriate  antibiotics  [drugs  and  doses], heparin or equivalent [prevention or treatment], bronchodilators [including steroids] etc.). Discussion.of attempts  to prevent  intubation  should  be provided (difficulty  with  intubation,  and risks of  ventilation  higher). Non-invasive   ventilation  is  covered  in  short answers,  but  general principles should be mentioned.

Discussion

Sigh.

Management will consist of attention to the ABCs with simultaneous rapid focused physical examination, and brief history.

  • Airway
    • Assess the need for intubation
    • Assess the difficulty of intubation, and access relevant specialty staff to assist, as well as the equipment required
    • Maintain airway by basic adjuncts including oropharyngeal and nasopharyngeal airways
  • Breathing
    • Maintain normoxia by supplementing high flow oxygen
    • Progress to NIV as soon as it becomes avaliable, if airway reflexes are intact and there are no other contraindications
    • ventilator settings need to be adjusted to compensate for increase mass of the chest all, and increased upper airway resistance
    • Ideally, ventilation should remain non-invasive
  • Circulation
    • ECG
    • TTE to assess chamber volume and contractility, and to rule out pericardial effusion
    • Secure venous access
  • Specific management
    • history to determine aetiological cause of the hypercapnic hypoxic respiratory failure
    • consider drugs with potential to cause sedation
      • administer ny appropriate antidoes
    • consider sepsis and pneumonia as a cause of gas exchange defect
      • commence antibiotics
    • Correct cardiac failure with appropriate use of vasoactive drugs, afterload reduction and preload optimisation
    • Consider CTPA if allowed by CT scanner aperture, and V/Q scan if not.

References

Question 1b - 2000, Paper 2

A 44 year old man, with morbid obesity (175 cm tall and 210 kg) presents to the Emergency Department with respiratory failure. He is obtunded with an arterial blood gas (ABG) showing pH 7.25, Pa C02 82 mmHg and PaO2 53 mm Hg.

CXR reveals cardiomegaly and clear lung fields.

It is day 1. He is intubated  and  ventilated, and no  precipitant  was found  for his respiratory failure. CXR reveals an obscured left hemi-diaphragm and new infiltrates behind the heart.

(b) Outline your management

College Answer

Ongoing  management   now  relies  on  reversal  of  factors   resulting  in initial  requirement  for ventilation  (predominantly   fatigue   by  exclusion),   removal  of  factors   keeping  him  ventilator dependent,  and   consideration   of   techniques   to   prevent  and   treat   left   lower   lobe  collapse consolidation.

Reversal  of  initial  fatigue   will  occur  with  adequate   provision  of  rest  (including   sleep,  and minimization of imposed work of breathing  [eg. an adequate  sized ETI (probably at least 8 nun), the use of the smallest amount of work to trigger the ventilator (eg. flow triggering), and the use of adequate amounts of ventilatory support (eg. pressure support, or similar  mode)]. The patient will need to  be awake  as  much  as  possible  during  the  day  (using  appropriate  sedation  regimen  if necessary overnight).

Left lower lobe collapse  of some form  may be minimized  by the use of higher levels of PEEP, appropriate  posturing  (mcluding  semi-prone   and  prone). and  the  at  least  intermittent   use  of adequate tidal volumes (eg. sigh or  IMV  breath). The possibility  of nosocomial  pneumonia  and other  differential  diagnoses  (eg.  pulmonary  emboli)  needs  to  be  entertained, and  excluded  if appropriate.

Discussion

Supportive management

  • Nutrition, low carb and high fat.
  • Analgesia and sedation as required to maintain comfort rather than obtundation
  • Thromboprophylaxis
  • ulcer prophylaxis
  • appropriate ventilator settings to minimise work of breathing
  • increase PEEP to reinflate atelectatic left base
  • Posture 45 degrees, sitting up
  • When supine, rotation therapy (alternate between left and right recovery position)
  • Consider pneumonia and commence antibiotics if appropriate

References

Question 1c - 2000, Paper 2

A 44 year old man, with morbid obesity (175 cm tall and 210 kg) presents to the Emergency Department with respiratory failure. He is obtunded with an arterial blood gas (ABG) showing pH 7.25, Pa C02 82 mmHg and PaO2 53 mm Hg.

CXR reveals cardiomegaly and clear lung fields.

It is day and he has had a tracheostomy performed. He is on SIMV 12 breaths by 500 ml tidalvolume, with an FIO2 of 0.6 and his ABG is now pH 7.49, PaCO2 49 mm.Hg and Pa02 159.

(c) Describe your strategy for weaning.

College Answer

The principles of weaning are no different in this patient. He now has a reasonable PaO2 on 60%, and has an appropriate PaCO2 for his degree of metabolic alkalosis. General factors preventing weaning need to be excluded (cardiovascular function, metabolic state, nutrition, endocrine function (eg. thyroid), adequate sleep). Carbon dioxide production could be minimised by the use of lower CHO feeds if this is a clinical problem. Metabolic alkalosis could be reduced by the use of acetazolamide (with the risk of increasing ventilatory work required to maintain a given pH). Ventilatory strategies should be similar to (b) above, with more detailed plan including: attention to posture (sitting, lying on side), day/night cycling, minimising work of breathing during rest (triggering work, work to overcome resistance and compliance of lung and that imposed by chest wall and abdomen), and some periods of increased work (to assess ability to breath with no or 
minimal ventilatory support). Rest periods may require high levels of PEEP and pressure support (or equivalent) to counter imposed work. Pressures delivered may overestimate actual trans-pulmonary pressures. Depending on the difficulty of intubation, the patient will need to be kept for a period of time in the Intensive Care Unit after demonstrating ability to breath overnight for himself ( eg. 48 hours) or may stay until the team are happy for him to have the tracheostomy tube removed. Ongoing supportive care is required throughout to prevent Intensive Care Unit related problems (eg. pressure care, DVT prophylaxis, supportive psychological care, prevention of device related infections etc.).

Discussion

If one needed a good locally sourced article to discuss the best trategy for ventilator weaning in a patient with spinal cord injury, one could do much worse than this 2012 pearl scattered by the likes of  Oliver Flower and Sumesh Arora.

To summarise the strategy for weaning a high C-spine quad:

Mechanical ventilation strategy:

  • Large tidal volumes, over 10ml/kg (up to 15ml/kg!) - turns out that weaning is faster in high VT patients (Petersen et al, 1999 - the mean VT was 1.7L ). Intercostal muscles are initially atonic, but become spastic as time goes on, fixing the chest wall into a rigid bell. A high tidal volume may actually help fix the chest wall into a more productive shape. Arora and Flower also suggest the adding of extra dead space in the circuit, so the high-VT patient does not become hypocarbic and lose their respiratory drive.
  • Low or zero PEEP: provided the VT is high enough, and there is little atelectasis, you will not need a high PEEP, and it is to be avoided.
  • Resistance and endurance protocol (REP): A fond mention is made of the 2003 Gutierrez study, which used a clever weaning protocol to retrain the respiratory systems of seven high quad patients. A simplified version of the protocol would consist of three major training styles:
    • Inspiratory resistance training: patients breathe through a fixed inspiratory resistor applied at the mouth for 10 seconds, four times a day. Resistance is then progressively increased as tolerated.
    • Expiratory resistance training: breathing through an expiratory resistor.
    • Endurance training: gradually reducing ventilator support; then, gradually lengthening periods of off-ventilator breathing time.

Adjunctive measures:

  • Minimise sedation
  • Maximise postural assistance to respiration: sit in a chair if possible
  • Adequate sleep and nutrition
  • Respiratory physiotherapy
  • Optimise cardiac function; aim for dry fluid balance

Management of a difficult or failed wean:

References

El Solh, A. Aquilina, et al. "Noninvasive ventilation for prevention of post-extubation respiratory failure in obese patients." European Respiratory Journal28.3 (2006): 588-595.

Arora, Sumesh, et al. "Respiratory care of patients with cervical spinal cord injury: a review." Crit Care Resusc (2012): 14: 64-73

 

Peterson, W. P., et al. "The effect of tidal volumes on the time to wean persons with high tetraplegia from ventilators." Spinal Cord 37.4 (1999): 284-288.

Boles, Jean-Michel, et al. "Weaning from mechanical ventilation." European Respiratory Journal 29.5 (2007): 1033-1056.

Gutierrez, Charles J., Jeffrey Harrow, and Fred Haines. "Using an evidence-based protocol to guide rehabilitation and weaning of ventilator-dependent cervical spinal cord injury patients." Journal of rehabilitation research and development 40.5; SUPP/2 (2003): 99-110.

 

Question 3 - 2000, Paper 2

List the indications for and contraindications to the use of non-invasive ventilation in acute respiratory failure.

College Answer

Non-invasive ventilation usually encompasses face mask (full or nasal) CPAP with or without additional ventilatory support
Indications can be based on physiology or on specific aetiological cause:

1.  Desire to provide increased respiratory support without the need for endotracheal intUbation.
The respiratory support make take the form of:            ·
•  increased FI(closed circuit)
•  increased End Expiratory Pressure, or
• increased inspiratory pressure (as continuous positive airway pressure or additional inspiratory support in the form of pressure or volume assisted breaths)

2.   Desire  to. delay  or  prevent  the  complications  and  morbidity  associated  with  mechanical ventilatory support via an endotracheal tube.
The specific types of respiratory failure that may benefit from Non-Invasive Ventilation should be listed (ideally with some indication of the level of evidence in the published  literature to support the approach).

Conditions that may benefit include:
•  Hypercapnic respiratory failure:
- . acute  exacerbation   of  COPD,  post-extubation  acute  respiratory  failure,  respiratory failure in patients  with cystic fibrosis,  patients awaiting  lung-transplantation,  patients who are not candidates for intubation (eg. DNR?, terminal illness).

•  Hypoxaemic respiratory failure
- cardiogenic   pulmonary   oedema,   postoperative   respiratory   failure,   post-traumatic respiratory  failure,  respiratory  failure  in AIDS, patients  who  are  not  candidates  for intubation.

A list of contraindications should include those situations that make the potential disadvantages or complications  of  non invasive  ventilation  worse.  Differentiation  into  absolute  and  relative  is arbitrary.
•  lack of experience in technique (technical & mechanical problems), intubation required for other reasons including airway protection and sputum clearance, uncooperative patients (confused, comatose, reluctant), full stomach (risks of aspiration), local trauma (nose/face),
fractured base of skull, oesophageal surgery (risks of gastric/oesophageal insufflation)

Discussion

A model answer might benefit from point form:

Strong indications

  • Pulmonary oedema
  • Asthma
  • COPD
  • Lung infection in the neutropenic patient

Weak indications

  • weaning from invasive ventilation
  • prevention/avoidance of intubation

Contraindications

  • decreased level of consciousness
  • vomiting, high aspiration risk
  • facial trauma
  • hemodynamic instability, particularly poor preload states

References

Question 4 - 2000, Paper 2

What useful information can be gained from respiratory pressure-volume loops in the management of the ICU patient?

College Answer

The usefulness of the information depends on the awareness of the limitations of the technique.
PV loops require either steady state (super-syringe technique) or quasi-steady state techniques (slow constant flow) to minimise effects of flow characteristics on pressure. The use of non constant flow requires mathematical computerised correction of the curve.

Traditionally  curves  have  been  performed  from  zero  PEEP,  and  are  dependent  on  the  recent ventilatory history.

Assumptions have been made that the change in slope at the lower end of the inspiratory  curve
(lower inflection point) reflect recruitment of all/most/some of the collapsed and recruitable alveoli.

These assumptions are being questioned. This point/zone of inflection has been proposed to be used as a way of choosing a level of PEEP to allow recruitment or prevent derecruitment Despite some published literature seeming to support this approach, many limitations have been raised (eg. recent ventilatory history, variability due to underlying lung disease (primary versus secondary) presence of decreased compliance of abdominal or chest wall, greater  importance of expiratory component of curve,etc.).

The Upper Inflection Point has been proposed as a way of detecting overdistension of the lung. Many published studies have suggested that this is an oversimplification, as many areas of lung may already be overdistended (eg. CT studies) before the UIP is reached. Setting the ventilator to prevent "overdistension» is possible but may not be clinically relevant.
Inflection points/zones on the descending part of PV curve may eventually become useful to titrate levels of PEEP to prevent de-recruitment.

The shape of the dynamic PV curve (and its deviation from-expected) may allow some degree of estimation of the magnitude of the patient's (as opposed to mechanical) work of breathing, or the presence of airway obstruction.

Discussion

Interpretation of pressure-volume loops is dealt with elsewhere.

In summary, the following useful information can be derived from them:

  • graphical representation of lung compliance
  • estimation of lower inflection point
  • estimation of pressure required for complete alveolar recruitment
    • adjusting PEEP to this may pervent derecruitment
  • estimation of pressure which causes alveolar overdistension
    • adjusting plateau pressure to this may prevent VILI
  • estimation of the work of breathing
  • estimation of the degree of airway obstruction

Limitations of the loops are as follows:

  • Poor representation of heterogenous lung pathology
  • Inconsistent agreement among observers as to where the lower inflection point is

References

Frank Rittner, Martin Doring. Curves and loops in mechanical ventilation. not sure what year; published by Drager.

 

R Scott Harris, Pressure-Volume Curves of the Respiratory System Respir Care 2005;50(1):78–98. © 2005

Question 1b - 2001, Paper 1

A 72 year old woman (55kg), Mrs X, with a history of severe emphysema and chronic bronchitis is intubated in the Emergency Department (ED) because of drowsiness associated with hypercarbia after her initial arterial blood gas analysis revealed:

  • pH 7.219        
  • PC02 98mmHg     
  • PO2 48mmHg    
  • HC03 39mmol/l        
  • lactate 2.5 mmol/l

You are called to the ED to assess and admit this woman to ICU.

The history from her daughter reveals that Mrs X lives independently but is limited by severe breathlessness with exercise.  (b) Does this change your management?

College Answer

NO. The degree of incapacity is not inconsistent with the presentation and does not indicate a particularly good or poor prognosis. The management at this stage is intensive while resting the patient for 24hrs, treating the precipitant and awaiting an opportunity to start weaning.

Discussion

One is startled by the forceful "NO" form the college. Clearly, this examiner favours a gentle approach to the elderly COPD patient.

The question text does not mention the exact degree of exercise intolerance, which would be crucial in determining the prognosis. Mortality in the end-stage bed-bound or house-bound group increases significantly in the 12 months following extubation, so perhaps they shouldn't be intubated. That, of course, is a 1989 study, but still.... it sounds grim. And it continues to be grim in the modern era. A recent study from Thorax (Hajizadeh et al, 2015) retrospectively observed a cohort of 4791 end-stage oxygen dependent COPD patients who were itnubated, and foud that 23% died in the hospital, and 45% died in the subsequent 12 months, with 26.8% discharged to a nursing home within 30 days.

References

Menzies, R., William Gibbons, and Peter Goldberg. "Determinants of weaning and survival among patients with COPD who require mechanical ventilation for acute respiratory failure." CHEST Journal 95.2 (1989): 398-405.

Hajizadeh, Negin, Keith Goldfeld, and Kristina Crothers. "Audit, research and guideline update: What happens to patients with COPD with long-term oxygen treatment who receive mechanical ventilation for COPD exacerbation? A 1-year retrospective follow-up study." Thorax 70.3 (2015): 294.

Question 1c - 2001, Paper 1

A 72 year old woman (55kg), Mrs X, with a history of severe emphysema and chronic bronchitis is intubated in the Emergency Department (ED) because of drowsiness associated with hypercarbia after her initial arterial blood gas analysis revealed:

  • pH 7.219        
  • PC02 98mmHg     
  • PO2 48mmHg    
  • HC03 39mmol/l        
  • lactate 2.5 mmol/l

You are called to the ED to assess and admit this woman to ICU. The history from her daughter reveals that Mrs X lives independently but is limited by severe breathlessness with exercise. 

(c)What are the effects of her lung disease on her respiratory physiology and how will this effect your management?

College Answer

Although  usually  coexistent  these  problems  (emphysema/chronic  bronchitis)  have  theoretically different effects. Chronic bronchitis leads to increased airway resistance from mucosal oedema, secretions, bronchospasm, loss of elastic tissue supporting small airways leading to dynamic airway compression. Emphysema leads to loss of alveolar spaces and capillary bed. The end result is airflow limitation, prolonged expiration, hyperinflation (reducing diaphragm efficiency and increasing work of breathing), pulmonary hypertension, V/Q mismatch and tendency to degrees of hypoxia and hypercarbia. Chronic hypercarbia may lead to reliance on hypoxic drive and chronic hypoxia to cor pulmonale and polycythaemia. Skeletal muscle dysfunction may be prominent due to malnutrition, steroids, electrolyte abnormalities and reduced muscle blood flow.

These effect management by necessitating avoidance of gas trapping during ventilation (long exp time, bronchodilators etc), ensuring enteral nutrition and sputum clearance with physiotherapy, aiming to maintain the patient’s usual PCO2 and PO2 with a normal pH.

Discussion

A systematic approach is called for:

Emphysema

  • increased lung compliance
  • decreased gas exchange surface
  • increased dead space

Chronic bronchitis

  • increased airway reactivity
  • decreased airway diameter

COPD in general

  • hyperinflation, decreased diaphragm excursion
  • increased intrinsic PEEP

Consequences of chronic respiratory failure

  • chronic hypercapnea
  • decreased respiratory drive (reliance on hypoxic drive)
  • chronically increased work of breathing, thus cachexia and malnutrition

References

Question 1d - 2001, Paper 1

A 72 year old woman (55kg), Mrs X, with a history of severe emphysema and chronic bronchitis is intubated in the Emergency Department (ED) because of drowsiness associated with hypercarbia after her initial arterial blood gas analysis revealed:

  • pH 7.219        
  • PC02 98mmHg     
  • PO2 48mmHg    
  • HC03 39mmol/l        
  • lactate 2.5 mmol/l

You are called to the ED to assess and admit this woman to ICU. The history from her daughter reveals that Mrs X lives independently but is limited by severe breathlessness with exercise. 

At one week she remains ventilator dependent.

(d) What may interfere with her weaning and what may be done to facilitate weaning?

College Answer

A list may be best here:
-     breathing system; demand valve resistance, humidifier, turbulence
-     ETT; too small
-     Airway; untreated asthma, secretions
-     Lung interstitium; oedema, collapse, infection
-     Musculoskeletal; weakness, hyperinflation, kyphoscoliosis
-     Cardiovascular; low cardiac output state, ischaemia
-     CNS drive; dugs, stroke,

The aim is to minimise the external work of breathing against inefficient ventilators and tubing, consider a tracheostomy which allows staged separation from the ventilator and improve all aspects of the patients general condition including nutrition, K/PO4/Mg, lung function and cardiovascular status.

Discussion

A systematic approach is in order.

  • Airway:
    • increased work of breathing agaisnt ventilator tubing
  • Breathing:
    • Ongoing bronchospasm
    • ventilator-associated pneumonia
    • mechanical disadvantages of having a hyperinflated chest cavity and kyphosis
  • Circulation:
    • Cardiac failure, resulting in poor respiratory exercise tolerance and pulmonary oedema
  • Disability
    • Delirium, resulting in increased sedation requirements
    • Deconditioning of respiratory muscles
    • critical illness polyneuropathy
    • malnutrition resulting in weakness

In generic terms, this table lists the usual suspects:

Causes of Difficulty Weaning from Mechanical Ventilation

Respiratory load

Increased work of breathing

  • Inappropriate ventilator settings
  • Reduced compliance
  • Increased airway resistance
  • Dynamic hyperinflation
  • Endotracheal tube diameter
  • Increased airway secretions or sputum retention
Cardiac load
  • Heart failure
  • Increased cardiac workload (eg. increased metabolic demand)
  • Decreased oxygen-carrying capacity of blood, eg. anaemia or some sort of dyshaemoglobinaemia
Neurological causes
  • Depressed central drive, eg. due to drugs
  • Delirium, avolition
  • Peripheral neurological dysfunction, eg. ICU-acquired weakness
  • Pain, eg. due to a laparotomy wound
Musculoskeletal causes
  • Muscular problems (eg. steroid myopathy) or NMJ problems (eg, myasthenia)
  • Mechanical problems, eg. scolisosis-associated restrictive lung disease or a massive distended abdomen in ileus
  • Skeletal problems, eg. chest trauma, flail segments
Metabolic disturbances
  • Increased metabolic demand, eg. trauma, burns, sepsis
  • Extremes of nutrtion, eg. obesity or cachexia
  • Metabolic acidosis

References

Haas, Carl F., and Paul S. Loik. "Ventilator discontinuation protocols." Respiratory care 57.10 (2012): 1649-1662.McConville, John F., and John P. Kress. "Weaning patients from the ventilator." New England Journal of Medicine 367.23 (2012): 2233-2239COPLIN, WILLIAM M., et al. "Implications of extubation delay in brain-injured patients meeting standard weaning criteria." American Journal of Respiratory and Critical Care Medicine 161.5 (2000): 1530-1536.

Fernández, Jaime, et al. "Adaptive support ventilation: State of the art review." Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine 17.1 (2013): 16.

MacIntyre, Neil R., et al. "Management of patients requiring prolonged mechanical ventilation: report of a NAMDRC consensus conference." CHEST Journal 128.6 (2005): 3937-3954.

Girard, Timothy D., et al. "Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial." The Lancet 371.9607 (2008): 126-134.

Girard, Timothy D., and E. Wesley Ely. "Protocol-driven ventilator weaning: reviewing the evidence." Clinics in chest medicine 29.2 (2008): 241-252.

Funk, Georg-Christian, et al. "Incidence and outcome of weaning from mechanical ventilation according to new categories." European Respiratory Journal 35.1 (2010): 88-94.

Boles, Jean-Michel, et al. "Weaning from mechanical ventilation." European Respiratory Journal 29.5 (2007): 1033-1056.

Question 8 - 2001, Paper 1

Describe  the pathophysiology of  the Obstructive Sleep Apnoea Syndrome.        
What are  the potential long-term complications of this syndrome?

College Answer

(a)   Patency of the oropharyngeal airway is due to activity of paired sets of upper airway muscles.

The presence of respiratory activity in the muscles of the soft palate, pharyngeal walls and tongue prevents otherwise floppy strictures from being sucked into the airway. Obstruction during sleep may be due to a combination of factors:

1)         reduced  airways  size  -enlarged  tonsils/adenoids,  macroglossia  myxoedema,  acromegaly, malignancy. A large percentage of OSA patients have a structurally small airway.

2)         neuromuscular tone- reduced tone occurs in REM sleep, particularly in postural muscles of the pharynx, palate etc.

3)         neuromuscular coordination – the normal coordination of increased upper airway tone withinspiration is lost.

(b) Potential long-term complications include:

Cardiac- hypertension, nocturnal angina/arrhythmias

Pulmonary- respiratory failure, cor pulmonale

Neurological- headache, somnolence, dementia

Psychiatric – depression, personality changes

Other - impotence, polycythaemia, glaucoma

Discussion

Pathophysiology of sleep apnoea:

  • The oropharynx is a muscular tube which depends on muscle tone for patency.  
  • Three muscle groups are involved:
    • muscles influencing hyoid bone position (geniohyoid, sternohyoid)
    • the muscle of the tongue (genioglossus)
    • the muscles of the palate (tensor palatini, levator palatini)
  • During sleep there is a loss of background muscle tone.
    • This occurs mostly during REM sleep
    • Neuromuscular coordination is lost: the normal increase in upper airway tone with inspiration does not occur.
  • This is exacerbated by drugs, alcohol, bulbar stroke, myopathy, etc.
  • Several anatomical defects may coexist, which narrow the upper airway:
    • Acromegaly
    • Retrognathia
    • Macroglossia, eg. in Down syndrome
    • Fat infiltration of oropharyngeal tissues
    • Oedema (as a part of generalised oedema)
    • Upper airway infection, eg. tonsillitis
  • The combination of narrowed airway, reduced airway muscle tone and lost inspiratory coordination results in complete upper airway obstruction with inspiration.
  • The resulting apnoeic episodes have several pathological features:
    • Hypoxia
    • Hypercapnea
    • Extremely negative intrathoracic pressure
  • This has pathological consequences.
    • Hypertension
    • Pulmonary hypertension (due to chronic hypoxic vasoconstriction)
    • Right ventricular hypertrophy and right heart failure
    • Increased risk of myocardial infarction
    • Atrial fibrillation (3-4 fold higher odds)
    • Increased risk of stroke
    • Decreased seizure threshold (independently associated with epilepsy)
    • Diabetes (somehow, it is an independent risk factor)
    • Increased risk of post-operative reintubation

Consequences of sleep apnoea

  • Due to chronic REM sleep deprivation:
    • Daytime somnolence
    • Mood disturbances
    • Cognitive impairment
  • Due to chronic hypoxia:
    • Pulmonary hypertension (due to chronic hypoxic vasoconstriction)
    • Right ventricular hypertrophy and right heart failure`
    • Polycythaemia
  • Due to chronic hypercapnea:
    • Reset respiratory drive centre
  • Due to the influence of the above on cardiovascular function:
    • Hypertension
    • Increased risk of myocardial infarction
    • Atrial fibrillation (3-4 fold higher odds)
    • Increased risk of stroke (likely due to polycythaemia and hyperviscosity)
  • Associated with OSA, but not necessarily caused by it:
    • Decreased seizure threshold (independently associated with epilepsy)
    • Diabetes (somehow, it is an independent risk factor)
    • Increased risk of post-operative reintubation
    • Impotence

References

Malhotra, Atul, and David P. White. "Obstructive sleep apnoea." The lancet360.9328 (2002): 237-245.

SHEPARD Jr, J. O. H. N. "Cardiopulmonary consequences of obstructive sleep apnea." Mayo Clinic Proceedings. Vol. 65. No. 9. Elsevier, 1990.

Peter, J. H., et al. "Manifestations and consequences of obstructive sleep apnoea." European Respiratory Journal 8.9 (1995): 1572-1583.

Balachandran, Jay S., and Sanjay R. Patel. "Obstructive Sleep Apnea." Annals of internal medicine 161.9 (2014): ITC1-ITC1.

Jordan, Amy S., David G. McSharry, and Atul Malhotra. "Adult obstructive sleep apnoea." The Lancet 383.9918 (2014): 736-747.

Park, John G., M. D. KANNAN RAMAR, and ERIC J. OLs0N. "Updates on Definition, Consequences, and Management of Obstructive Sleep Apnea." (2011).

American Academy of Sleep Medicine. European Respiratory Society. Australasian Sleep Association. American Thoracic Society "Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research: the report of an American Academy of Sleep Medicine Task Force." Sleep. 1999;22:667-689

Fogel, R. B., A. Malhotra, and D. P. White. "Sleep· 2: pathophysiology of obstructive sleep apnoea/hypopnoea syndrome." Thorax 59.2 (2004): 159-163.

Young, Terry, James Skatrud, and Paul E. Peppard. "Risk factors for obstructive sleep apnea in adults." Jama 291.16 (2004): 2013-2016.

 

 

 

Question 1a - 2001, Paper 1

A 72 year old woman (55kg), Mrs X, with a history of severe emphysema and chronic bronchitis is intubated in the Emergency Department (ED) because of drowsiness associated with hypercarbia after her initial arterial blood gas analysis revealed:

  • pH 7.219        
  • PC02 98mmHg     
  • PO2 48mmHg    
  • HC03 39mmol/l        
  • lactate 2.5 mmol/l

You are called to the ED to assess and admit this woman to ICU.

(a) Outline your initial management including ventilator settings.

College Answer

This elderly lady with severe chronic lung disease is admitted with acute on chronic hypercarbia and drowsiness. She is intubated.

a)   Initial management should involve:

-     continued  resuscitation  (check  position  of  ETT,  establish  ventilation  to  rest  the  respiratory muscles, assess and restore the circulation with fluid bolus/inotrope etc)
-     mode of ventilation should be appropriate for her strength of respiration and in the first instance may involve sedation and either SIMV, CMV or PSV. The principle will be to allow a long expiratory time with TV 6-8mls/kg, rate 8-10 and PEEP no greater than the measured auto-PEEP. Auto-PEEP  greater  than  5  or  incomplete  expiration  should  be  treated  with  slower  rate  and increased bronchodilator.
-     diagnosis   of   precipitating   event   (acute   bronchitis,   pneumonia,   sputum   retention,   CCF, pneumothorax,  asthma,  sedation,  B-blocker,  aspiration,  hypokalaemia),  chronic  status,  other comorbidities. This requires talking to family, GP and specialist, examining from head to toe and getting a chest X-ray
-     complete medical history, allergies, medications etc
-     establishment of monitoring
-     contact with family/friends to gather information and establish lines of communication
-     continued  support  and  treatment  overnight  with  ventilation,  bronchodilators, antibiotics  (eg erythromycin, cefotaxime), steroids as indicated.

Discussion

This is another question about the management of an intubated COPD patient.

After doing an entire hundred-or-so CICM questions on respiratory failure, the constant appearance of COPD becomes rather tedious.

Oh well.

Management will consist of attention to the ABCs with simultanoues rapid focused physical examination, and brief history.

  • Airway
    • keep intubated for now;
    • assess for extubation at the earliest practical opportinuty, and extubate on to NIV
  • Breathing
    • PEEP to match AutoPEEP
    • titrate FiO2 to PaO2 55-65
    • Slow resp rate, decreased I:E ratio
    • bronchodilators (IV or nebulised)
  • Circulation
    • maintenance of adequate fluid volume
    • atention to co-existing heart failure
  • Supportive management
    • Nutrition (high fat, low carbohydrate)
    • Attention to pressure areas
    • sedation with short acting drugs eg. propofol, to minimise delirium
    • correction of electrolyte abnormalities
  • Specific management
    • history to determine aetiological cause of the COPD exacerbation
    • management of infective cause with antibiotics
    • management of bronchospasm with bronchodilators and steroids
    • family discussion regarding goals of care

References

Question 2 - 2001, Paper 2

 Briefly outline the role of non-invasive ventilation in the management of a 24 year old woman who presents with acute severe asthma.

College Answer

NIV includes CPAP, BiPAP and PAV. Non-invasive ventilation has been used with success in acute severe asthma but there are no RCTs to support its use. In theory it assists the patient by decreasing the inspiratory work, decreasing expiratory work and improving V/Q mismatch. The potential negative effects are numerous and include claustrophobia, agitation, gastric distension, dys-synchrony, increased expiratory work and hyperinflation.

Decreasing the pressure change that needs to be generated to initiate respiration in the presence of auto-peep may decrease inspiratory work. Expiratory work may be decreased by opposing dynamic airway compression and allowing more complete expiration with less gas-trapping and hyperinflation. Experimental work in induced asthma suggests that CPAP mainly acts to unload inspiratory muscles.

Since all these factors cannot be anticipated in an individual, the role of NIV is best found by testing the patient’s response to titrated therapy eg starting with 5 cm CPAP and titrating IPAP and EPAP.

There is of course no role in respiratory or cardiac arrest or in the patient who is unable to cooperate or protect the airway.

Discussion

Probably the best reference for this answer is the article by Teke et al (2015), which discusses the mechanisms in some detail. The SAQ asked to "briefly outline", rather than critically evaluate, the use of NIV in asthma. 

Role of NIV in asthma is basically to decrease respiratory workload (usually by by 30-70%)

(see also the chapter on Non-invasive mechanical ventilation)

Interestingly, the college answer makes the comment that the use of NIV may increase the expiratory workload. This would be the consequence of PEEP (or rather ePAP), seeing as it is workload during expiration when the bilevel pressure is at the lower level. By increasing airway pressure at the mask, the expiratory pressure gradient from alveoli to the mouth is decreased, which decreases expiratory flow.  Specifically, the peak tidal expiratory flow rate is reduced by this. On the other hand, end-expiratory flow rates are increased by PEEP (as the result of the abovementioned airway splinting and effects on dymanic compression). Generally, it appears that beyond a certain PEEP no further improvement in end-inspiratory flow is seen (because the airways are already maximally splinted open, and no further increases in pressure will produce any improvement in the degree of splintedness). However, as you keep cranking up the PEEP, the mouth-alveoli gradient will keep changing, and the peak expiratory flow will keep decreasing.  Thus, at low PEEPs the splinting mechanism is the dominant influence, and at high PEEPs the pressure gradient mechanism is dominant.  

From this it follows that the ideal level of PEEP is one which achieves the maximum expiratory flow rate. If the PEEP is high enough, the beneficial increase in end-expiratory flow rate is counteracted by the decrease in peak expiratory flow rate.   Shivaram et al (1987) determined that this is something asthmatics find uncomfortable at higher CPAP levels.  Ergo, for every asthmatic, at any given moment there is some optimal PEEP level at which the balance of these opposing influences achieves maximal expiratory flow, and this magic PEEP is indeed "best found by testing the patient’s response to titrated therapy".

References

Medoff, Benjamin D. "Invasive and noninvasive ventilation in patients with asthma." Respiratory care 53.6 (2008): 740-750.

Murase, K., et al. "Non-invasive ventilation in severe asthma attack, its possibilities and problems." Panminerva medica 53.2 (2011): 87-96.

Gupta, Dheeraj, et al. "A prospective randomized controlled trial on the efficacy of noninvasive ventilation in severe acute asthma." Respiratory care 55.5 (2010): 536-543.

Op't Holt, Timothy B. "Additional Evidence to Support the Use of Noninvasive Ventilation in Asthma Exacerbation." Respiratory care 58.2 (2013): 380-382.

Carson, Kristin V., Zafar A. Usmani, and Brian J. Smith. "Noninvasive ventilation in acute severe asthma: current evidence and future perspectives." Current opinion in pulmonary medicine 20.1 (2014): 118-123.

Teke, Turgut, Mehmet Yavsan, and Kürsat Uzun. "Noninvasive ventilation for severe acute asthmatic attacks." Journal of Academic Emergency Medicine 14.1 (2015): 30.

Shivaram, Urmila, et al. "Effects of continuous positive airway pressure in acute asthma." Respiration 52.3 (1987): 157-162.

Question 6 - 2001, Paper 2

What causes the oxygen haemoglobin dissociation curve to move to the right and what are the clinical implications of this change?

College Answer

Shift of the O2 – Hb dissociation curve to the right causes decreased affinity for O2 and release of O2 to the tissues. The O2 dissociation curve is shifted to the right by: –

•    increased temperature

•    increased CO2

•    increased 2 – 3 DPG

•    increased pH

•    rare abnormal haemoglobins

This is an important physiological effect responsible for the Bohr effect and allowing greater release of O2 to the tissues.

At present there is not enough data to support manipulation of the O2-Hb curve to improve O2 delivery. If arterial PO2 is critically low then O2 binding in the lungs may be impaired by a shift to the right. The end result is that a shift to the right may seriously impair tissue oxygenation.

Discussion

A right-shift of the oxyhemoglobin dissociation curve describes a decrease in the affinity of hemoglobin for oxygen; i.e. more and more oxygen is required to achieve the same level of haemoglobin saturation (eg. p50). The clinical implications of this become apparent when one is confronted by such severe hypoxia that any small change in oxygen delivery to the tissues may cause the organ systems to fail. In such circumstances, a small decrease in the oxygen-carrying capacity of the blood will result in diminished oxygen transport and thus systemic hypoxia.

Causes of a right shift include

  • Hyperthermia
  • high 2,3-DPG levels
  • Acidosis (eg. increased CO2)
  • dyshaemoglobinaemia

Now, you'll notice that the college answer has increased pH, i.e. alkalosis. This is incorrect, and the examiners clearly recognised that when they reviewed the Microsft Word document of the answer paper, helpfully highlighting the wrong answer in yellow. Unfortunately, that did not help, and their administrative staff published the uncorrected paper anyway. 

References

Question 11 - 2001, Paper 2

What is meant by the expression “patient – ventilator  dys-synchrony”?         

What are  the principles of managing this problem?

College Answer

Patient-ventilator dys-synchrony refers to the situation in which the patient fails to achieve comfortable respiration in synchrony with the ventilator in terms of timing of inspiration, adequate inspiratory flow for demand, timing of the switch to expiration and duration of inspiration.

Managing this problem may be addressed by –

•    treating patient respiratory problems eg sputum, irritable airways

•    checking ETT for kinking, secretion block, impinging on carina or between cords

•    choosing the appropriate ventilator

•    choosing the appropriate mode

•    selecting sensitivity not too low or high

•    choosing the appropriate ventilator rate

•    setting appropriate flow rate

•    sedating the patient to reduce agitation

•    taking over ventilation if fatigue is apparent

Discussion

Patient-ventilator dyssynchrony is discussed elsewhere. In essence, it is increased work of breathing and decreased patient comfort because of a mismatch between the ventilator gas delivery pattern and the patient's demands.

One can manage patient-ventilator dyssynchrony by

  • Making the mode patient-triggered
  • Improving trigger sensitivity to include patient efforts and exclude cardiac auto-triggering
  • Increasing flow rate if it is inadequate
  • Managing auto-PEEP
  • Increasing flow cycle-off to a higher value, terminating a breath early if the patient wants shorter breaths
  • Decreasing the flow cycle-off to a lower value if the patient requires longer breaths
  • Clearing the airway of sputum and secretions, and ensuring its patency
  • Increasing the sedation
  • Use of neuromuscular blockade

References

Question 12 - 2001, Paper 2

List  the  chest  physiotherapy  manoeuvres  that  you  prescribe  in  ICU  and  provide  the rationale for each.

College Answer

Chest physiotherapy encompasses many manoeuvres, which are used to aid sputum clearance, recruit  areas  of  collapse  and  prevent  the  effects  of  suppressed  cough,  disrupted  mucociliary clearance and reduced FRC. The evidence for much of these procedures is scant.

A list of manoeuvres may include:

•    Endotracheal suctioning

•    Nasopharyngeal suctioning

•    Bagging

•    Percussion

•    Assisted coughing

•    Recruitment manoeuvres

A simple rationale for each was expected.

Discussion

The role of physiotherapy in ICU is discussed more generally in Question 24 from the second paper of 2013.

This question, focusing on purely chest physiotherapy, is pulled stright out of Oh's Manual, Chapter 5.

In summary, the following techniques are discussed in that chapter:

  • Manual lung hyperinflation
    • Improves recruitment of atelectatic lung
    • Mobilises bronchial secretions
    • Improves lung compliance
  • Recruitment manoeuvres:
    • Transiently improve oxygenation
  • Suctioning:
    • Improves clearance of secretions
  • Inspiratory muscle training
    • May improve the chances of successful ventilator weaning
  • Chest shaking and vibration
    • Aid mucociliary clearance
  • Chest wall compression
    • Enhances expiratory manoeuvres and aids secretion clearance
  • Percussion
    • May mobilise secretions
  • Neurophysiological facilitation of respiration
    • Stimulates increased VT and cough
  • Positioning
    • May reduce the work of breathing
  • Gravity-assisted positioning
    • May enhance secretion clearance
  • Active cycle of breathing techniques (ACBT)
    • Breathing exercises to remove excess secretions

References

Oh's Manual (7th ed) Chapter 5 (pp.38)  Physiotherapy  in  intensive  care   by Fiona  H  Moffatt  and  Mandy  O  Jones

 

Stiller, Kathy. "Physiotherapy in intensive care: towards an evidence-based practice." CHEST Journal 118.6 (2000): 1801-1813.

Question 2 - 2002, Paper 1

The mortality in patients with ARDS has only shown a gradual decline over the last two decades.


(a)       What specific modalities of treatment have contributed to the improvement in mortality?

(b)       Discuss why the observed decline in mortality has not been greater in magnitude?

College Answer

The mortality in patients with ARDS has only shown a gradual decline over the last two decades.


(a)       What specific modalities of treatment have contributed to the improvement in mortality?

Many promising specific therapies have failed to demonstrate improved mortality when studied in more detail (eg. prone positioning, nitric oxide, exogenous surfactant, liquid ventilation, ECMO, infusion of PGE1, ketoconazole and N-acetylcysteine).   Most of these therapies are not routinely used, and are therefore unlikely to contribute to improved outcomes.

Specific therapies that have recently been demonstrated to potentially improve survival include the use of low tidal volume ventilation (ARDSnet, NEJM), in addition to recruitment and higher levels of PEEP (Amato, NEJM) and the use of steroids in late ARDS (Meduri JAMA).  These techniques are also relatively recent in acceptance/still being evaluated, and are not yet in widespread use.

A combination of factors not individually shown to be beneficial regarding mortality is more likely to have resulted in benefit. Most patients die a non-respiratory death, so general “supportive care” is more likely to have made an impact on survival.  

Specific approaches to be considered include:

  • Prevention: of pulmonary thromboembolism, gastrointestinal bleeding, nosocomial infections (pneumonia, line-related sepsis), complications of sedation and paralysis (better understanding of pharmacology).
  • Early diagnosis and treatment: of nosocomial infections, deficiencies in pituitary-adrenal access.
  • Early nutritional support: especially with regard to early enteral feeding.
  • Additional ventilatory strategies: including better synchrony of patient with ventilator, allowing lower levels of sedation/paralysis; semi-recumbent positioning etc.

(b)       Discuss why the observed decline in mortality has not been greater in magnitude?

A number of factors need to be considered,  in particular the large amount of background  noise making  accurate  assessment  of  improvements  near  impossible.    Indeed,  the  studies  that  have actually shown benefit may not be extrapolatable to the majority of the ARDS population seen in Intensive Care.

The mortality of ARDS is not usually due to respiratory disease per se, but instead to multiple organ dysfunction.    This  in turn  is due  to a multiplicity  of factors  (including  the  underlying  disease process  that  resulted  in  ARDS  [eg.  pancreatitis,  sepsis,  burns],  inflammatory  response  due  to ARDS, nosocomial infections.  No single specific therapy is likely to prevent the cascade of events that result in inflammation.   Insufficient studies have been performed to consistently demonstrate one technique has benefits, let alone which combinations of therapies may be useful.

ARDS  is  also  the  end  result  of  a  large  number  of  predisposing  insults.    The  outcomes  vary dramatically between subgroups (eg. trauma versus pneumonia).  More specific classification or stratification may allow more accurate comparisons.

As a result of better general supportive care, patients that would not previously been considered salvageable  could now be going on to develop  ARDS, and are more likely to have an adverse outcome.   It is probably impossible to accurately compare outcomes now with decades ago, given the inability to control for the many factors that influence outcome.

Discussion

The second part of this question closely resembles Question 28 from the first paper of 2006.

However, the first part is unique, and interesting.

Why indeed have the ARDS outcomes improved?

  • Improvement of old strategies
    • Low tidal volume ventilation
    • Open-lung ventilation
    • improved supportive care and surveillance of complications (eg. early nutrition)
  • Development of new strategies
    • Prone positioning
    • ECMO
    • inhaled pulmonary vasodilators

References

Question 11 - 2002, Paper 1

Outline the causes, consequences and management of intrinsic PEEP.

College Answer

Causes: consider increased expiratory resistance (prolonged expiratory time constant: eg. bronchospasm,  narrow/kinked  ETT,  inspissated  secretions,  exhalation  valves/HME/filters), increased minute ventilation (inadequate expiratory time).

Consequences:  consider increased intra-thoracic  volume (with increased pressures for a given Vt and  risks  of  barotrauma),   increased   intra-thoracic   pressure   (decreasing   venous   return,   and increasing inspiratory work to trigger the ventilator).

Management:   consider  treatment   of  reversible   factors  (bronchospasm,   secretions,  expiratory devices), prolongation of expiratory time (decrease respiratory rate, increase inspiratory flow) or decrease  tidal  volumes,  application  of  exogenous  PEEP  (to  50  –  85%  of  accurately  measured intrinsic PEEP) to decrease inspiratory triggering work and improve distribution of inspired gas.

Discussion

This question is identical to Question 4 from the first paper of 2006.

References

Question 15 - 2002, Paper 1

Outline the indications for high frequency oscillation in Intensive Care, and the mechanism of gas exchange when using high frequency oscillation.

College Answer

Indications: usually as part of experimental therapy or as part of a controlled clinical trial.  Potential rescue therapy for ARDS in Intensive Care Units who have suitable equipment available and are experienced in its use, where “open lung” ventilation strategy (adequate recruitment and avoidance of overdistension) is desirable.  In Paediatric Intensive Care as rescue therapy for severe respiratory failure.

Mechanism of gas exchange: normal bulk flow is much less important, as the tidal volumes used are much  smaller  than  anatomical  deadspace;  gas delivery  into  the system  (as bias flow)  will  stillprovide some gas exchange.   Other potential mechanisms described (many of which may work simultaneously) include Taylor dispersion (dispersion of molecules beyond the bulk flow front), augmented diffusion (gas mixing within alveolar units), coaxial flow patterns (net flow one way through centre of airway, other direction via periphery) and Pendelluft mixing (between lung units, mixing of gas due to impedance differences).

Discussion

This question is not entirely identical, but in its spirit very similar to Question 23 from the second paper of 2010.

References

Question 2 - 2002, Paper 2

Critically evaluate the significance of tidal volume in the management of patients undergoing mechanical  ventilation  in Intensive Care.

College Answer

There has been much interest in the use of low tidal volumes (eg. 6-9 mL/kg) in critically ill patients. The recent ARDSnet study confirmed a suspicion that the use of lower tidal volumes (6 vs 12 mL/kg) has significant benefits in those patients with Acute Lung Injury or ARDS (bilateral infiltrates and P/F ratio of < 300, within first 36 hours). Predicted body weight was used (calculated from height and sex). Many previous studies had not shown such a benefit (perhaps due to smaller differences in plateau pressures between groups ). In patients with “normal” lungs or those that do not meet entry criteria for the ARDSnet study, there is no evidence to suggest a benefit to the low tidal volume approach. On the contrary, the intermittent use of high tidal volumes (such as sighs or recruitment manoeuvres) has been shown to achieve short term benefits (improved P/F ratios, decreased shunt, open up collapsed areas) in patients with early ARDS or atelectasis. The global application of lower tidal volumes may well result in worse oxygen exchange unless counterbalanced with higher levels of PEEP (or intermittent recruitment manoeuvres).

Discussion

The ventilation strategies in ARDS are discussed elsewhere.

However, this question is not just about ARDS.

The key issues are:

  • Tidal volume factors into minute volume, and determines CO2 removal
  • Tidal volume also determines the degree of lung inflation and recruitment of atelectatic lung
  • Adequate tidal volumes are important in ensuring patient comfort and decreasing sedation requirements
  • Low tidal volume (6ml/kg) works well for ARDS patients, prevents volutrauma and improves survival; however its disadvantages are hypercapnea and need for higher levels of sedation.
  • As a ventilation strategy, there is no advantage to its use in patients whose lungs have a normal compliance
  • In fact in patients with normal lung compliance low tidal volumes may lead to atelectasis and deterioration of gas exchange

References

Question 11 - 2003, Paper 1

Outline  the  possible  effects  on  oxygenation  of  the  prone position  and  the  potential mechanisms  underlying these effects.

College Answer

The effects of prone positioning on oxygenation are best studied in ARDS patients.  Short lived improvements in oxygenation are common (eg. 70%) and sometimes dramatic.  Some patients have no effect, and others have a long lasting effect (persisting well after rolling supine again).  Potential mechanisms for improving oxygenation during proning include: an increase in end-expiratory lung volume (with better response to applied PEEP and tidal recruitment), better ventilation–perfusion matching (with more homogeneous distribution of ventilation, and less shunting), and regional changes in ventilation associated with alterations in chest-wall mechanics (allowing more of applied pressure to inflate the lungs).  Prolonged benefits may be seen if inflation of recruitable lung has resulted in more lung units being held open when returned to the baseline ventilatory settings (Vt and PEEP).

Discussion

Mechanisms for improved oxygenation during prone ventilation:

  • Improved V/Q matching: This is probably the most important contribution. In the ARDS patient the bases of lungs both receive the greatest amount of blood flow and the smallest amount of oxygenated gas (they are usually all collapsed). According to Tobin and Kelly  (1999), this is all because in the prone position the pleural pressure is less likely to exceed airway opening pressure and cause airway closure.
  • More homogeneous ventilation: Prone positioning reduces the difference between the dorsal and ventral pleural pressure, and the compliance of dorsal and ventral lung is therefore more homogeneous. As a consequence, there is no longer a situation where regions of lung have markedly different compliance, and this reduces ventilator-associated lung injury from alveolar overdistension. The benefits from this can be summarised as follows:
    • More uniform distribution of pleural pressure;
    • Thus, more uniform compliance;
    • Thus, more uniform distribution of plateau pressure;
    • Thus, less cyclical atelectasis and alveolar overdistension.
  • Less lung deformation: There is less compression of the lungs by the heart (which sits on the sternum in the prone position) and by the abdominal content. In general, the lungs fit better into the chest cavity. This improves compliance, as one does not have to use their ventilation pressure to push these organs out of the way.
  • Increased FRC: This ancient manuscript from 1977 reports that FRC in normal people increases by about 300-400ml when turned into the prone position.
  • Improved drainage of secretions: dorsoventral orientation of large airways apparently enhances the drainage of respiratory secretions and aspirated material. This data is extrapolated from physiotherapy patients which were not completely prone and very much awake, with no ARDS, but the fact remains.
  • Improved response to recruitment manoeuvres: Prone patients respond well to recruitment manoeuvres.  When compared to supine patients, prone patients seem to require less PEEP (8cm vs 14cm) to sustain the post-recruitment improvement in oxygenation.
  • Improved mechanics of the chest wall in obesity - in fact, if the literature is to be believed, the entire population of obese non-ARDS patients should spend most of their lives in the prone position because of how disastrously ineffective their V/Q matching is in the supine position.

References

Lai-Fook, STEPHEN J., and JOSEPH R. Rodarte. "Pleural pressure distribution and its relationship to lung volume and interstitial pressure." Journal of Applied Physiology 70.3 (1991): 967-978.

 

Tobin, A., and W. Kelly. "Prone ventilation-it's time." Anaesthesia and intensive care 27 (1999): 194-201.

 

Douglas, William W., et al. "Improved Oxygenation in Patients with Acute Respiratory Failure: The Prone Position 1–3." American Review of Respiratory Disease 115.4 (1977): 559-566.

Oczenski, Wolfgang, et al. "Recruitment maneuvers during prone positioning in patients with acute respiratory distress syndrome." Critical care medicine 33.1 (2005): 54-61.

 

Takahashi, Naoaki, et al. "Anatomic evaluation of postural bronchial drainage of the lung with special reference to patients with tracheal intubation: Which combination of postures provides the best simplification?." CHEST Journal 125.3 (2004): 935-944.

 

Mackenzie, Colin F. "Anatomy, physiology, and pathology of the prone position and postural drainage." Critical care medicine 29.5 (2001): 1084-1085.

 

Lamm, W. J., Michael M. Graham, and Richard K. Albert. "Mechanism by which the prone position improves oxygenation in acute lung injury." American journal of respiratory and critical care medicine 150.1 (1994): 184-193.

 

Lamm, W. J., Michael M. Graham, and Richard K. Albert. "Mechanism by which the prone position improves oxygenation in acute lung injury." American journal of respiratory and critical care medicine 150.1 (1994): 184-193.

Pelosi, Paolo, et al. "Effects of the prone position on respiratory mechanics and gas exchange during acute lung injury." American journal of respiratory and critical care medicine 157.2 (1998): 387-393.

Question 2 - 2003, Paper 2

Critically evaluate the role of hyperbaric oxygen therapy in the management of the critically ill patient.

College Answer

Critically evaluate implies evaluation (including risk/benefit assessment) is required rather than just providing a list of indications. Many indications are not supported by high levels of evidence. Recognised indications that may be relevant in the critically ill include: decompression sickness, arterial gas embolism, severe carbon monoxide poisoning, aggressive soft tissue infections (e.g. clostridial myonecrosis, necrotising fasciitis and Fournier’s gangrene), and crush injuries. Randomised studies in humans have been performed in carbon monoxide poisoning (with variable results; eg. Scheinkestel MJA 1999, and Weaver NEJM 2002) and crush injuries (with positive results).

Hyperbaric oxygen therapy is not without risks to the patient (including general risks associated with transport , and specific risks of ear and pulmonary barotrauma, and pulmonary and cerebral oxygen toxicity).  The delivery of hyperbaric oxygen to the critically ill also raises some significant logistic problems (including inter-hospital transport), but within centres with expertise these are minimised.  For most indications in the critically ill there is limited human data (eg. case series, retrospective controls etc.), and minimal animal data.

Discussion is required with the hyperbaric unit on a case-by-case basis, and other supportive/adjunctive therapy is essential in all conditions.

Discussion

There is a good NEJM article from 1996 which goes through the various applications of hyperbaric oxygen therapy. It also describes it as "a good treatment in search of a disease".

A systematic response would resemble the following:

Rationale

  • 100% FiO2 at 3 times the normal atmospheric pressure equates to a tissue oxygen tension ~ 400mmHg
  • This has been proposed as a treatment for conditions in which tissue oxygenation is for whatever reason reversibly and dangerously impaired.
  • Anaerobic bacteria are unable to reproduce at such a high oxygen tension, and HBOT may improve the effectivenes of antibiotics in such infections.

Indications

  • Carbon monoxide poisoning
  • Arterial gas embolism, eg. decompression sickness
  • Clostridial myonecrosis
  • Necrotising fasciitis
  • Refractory osteomyelitis
  • Compromised skin grafts/flaps
  • Severe burns
  • Catastrophic anaemia (life without haemoglobin is possible)
  • Compartment syndrome
  • Burns
  • Radiation necrosis

Contraindications

  • Untreated tension pneumothorax
  • Paraquat toxicity
  • Therapy with the following drugs:
    • Doxorubicin
    • Cisplatin
    • Disulfiram
    • Mafenide
    • Bleomycin

Adverse effects

  • Safe when limited 120 minutes
  • Myopia (revrsible)
  • Cataract formation
  • Rupture of the middle ear and cranial sinuses
  • Seizures
  • Claustrophobia
  • Pulmonary irritation and pulmonary oedema

Evidence

References

Shaw, Joshua J., et al. "Not Just Full of Hot Air: Hyperbaric Oxygen Therapy Increases Survival in Cases of Necrotizing Soft Tissue Infections." Surgical infections (2012).

 

Buckley, Nick A., et al. "Hyperbaric oxygen for carbon monoxide poisoning."Cochrane Database Syst Rev 4 (2011).

 

Stoekenbroek, R. M., et al. "Hyperbaric Oxygen for the Treatment of Diabetic Foot Ulcers: A Systematic Review." European Journal of Vascular and Endovascular Surgery 47.6 (2014): 647-655.

 

Eskes, Anne M., et al. "Hyperbaric oxygen therapy: solution for difficult to heal acute wounds? Systematic review." World journal of surgery 35.3 (2011): 535-542.

 

Tibbles, Patrick M., and John S. Edelsberg. "Hyperbaric-oxygen therapy." New England Journal of Medicine 334.25 (1996): 1642-1648.

 

Thom, Stephen R. "Hyperbaric oxygen–its mechanisms and efficacy." Plastic and reconstructive surgery 127.Suppl 1 (2011): 131S.

Question 11 - 2003, Paper 2

Outline the clinical manifestations, appropriate investigations and treatment of
“volutrauma”  in the critically ill patient

College Answer

Nomenclature used for defining ventilator induced lung damage are complex and continue to evolve.  “Volutrauma” should be considered as a potential complication of mechanical ventilation and may be manifest as extra-alveolar air, or acute (ventilator associated) lung injury.   A good answer would deal with both aspects.

Exacerbation of acute lung injury is detectable on analysis of BAL fluid, but is hard to differentiate from the inflammatory state associated with the initial lung injury, and its associated conditions. Treatment is the continuation of lung protective strategies (see below).

Extra-alveolar air results from alveolar rupture, and manifestations depend on where the gas  passes but include interstitial emphysema, mediastinal emphysema, pneumothorax, pneumoperitoneum, and subcutaneous emphysema.   Clinical signs may include haemodynamic and/or respiratory compromise in a ventilated patient (e.g. tension pneumothorax), in particular in a susceptible patient (e.g. obstructive airways disease, heterogeneous lung disease).   Manifestations may vary from a subtle deterioration to overwhelming collapse, or may just present with palpable (subcutaneous) emphysema.   Investigations should include radiographs to exclude the manifestations mentioned above, and to exclude differential diagnoses.  Treatment involves introduction of lung protective strategies to minimise further damage (in particular lower tidal volumes, lower ventilatory rates, lower mean airway pressures, and avoidance of auto-PEEP), drainage of collections of gas (e.g. urgent decompression of tension pneumothorax, and subsequent intercostal catheters, or even subcutaneous tubes). Double lumen tubes and/or differential lung ventilation is occasionally required.

Discussion

The idea of "volutrauma" is these days more refined; the term has narrowed in its definition to describe only the alveolar overdistension aspect of ventilator-associated lung injury. Question 10 from the first paper of 2012 gives a more thorough answer, which focuses on all aspects of VALI.

Overdistension of alveoli  leads to broken cell walls, and leaking pneumocyte contents is highly immunogenic. The ensuing inflammatory response not only creates more lung injury (by inflammation, so called "biotrauma") but contributes to the systemic inflammatory response sydnrome and mlti-organ system failure.

This process is worst when there is heterogenous lung disease: the healthy lung will suffer the side effects of whatever ventilator strategy is being used to improve gas exchange within the diseased lung. Thus, huge tidal volumes are not required to induce this sort of lung injury. The ultimate outcome of volutrauma may actually be pneumothorax and pneumomediastinum, as the alveoli rupture from overdistension.

Clinical manifestations

  • Worsening gas exchange
  • Increasing organ system failure due to cytokine release
  • worsening lactic acidosis
  • decreasing lung compliance
  • pneumothorax
  • pneumomediastinum
  • surgical emphysema

Appropriate investigations

  • CXR
  • Plateau pressure measurement by inspiratory hold

Treatment of volutrauma

  • Lung-protective ventilation
  • thoracocentesis for pneumothoraces
  • dual-lumen intubation to isolate the affected lung, with the potential to ventilate it independently and a different pressure.

References

Rocco PR, Dos Santos C, Pelosi P. Pathophysiology of ventilator-associated lung injury. Curr Opin Anaesthesiol. 2012 Apr;25(2):123-30

Question 2c - 2004, Paper 1

A 76-year-old woman with severe ischaemic heart disease being treated with aspirin, clopidogrel and metoprolol presents with severe abdominal and back pain, 6 hours after  being discharged home from a routine cardiac angiogram via the femoral route.

A large retroperitoneal  haematoma is diagnosed. After resuscitation, the bleeding is stopped by angiographic embolisation of a branch of the left internal iliac artery.
She  is  still  in  the  intensive care  unit  2  days  later  when  she  becomes suddenly dyspnoeic, hypoxaemic and hypotensive with a BP of 80 systolic. She stabilises and subsequent investigation reveals a moderate sized pulmonary embolism. 

Describe all the potential therapeutic strategies for her and describe in detail what your ongoing management would be in this case?

 

College Answer

c)        She stabilises and subsequent investigation reveals a moderate sized pulmonary embolism.
Describe all the potential therapeutic strategies for her and describe in detail what your ongoing management would be in this case?

Strategies can be classified as medical or surgical. Medical therapy, the mainstay of treatment includes resuscitation with fluids and vasoactive support, anticoagulation, usually heparin with thrombolysis in cases usually of associated hypotension. Surgical therapy includes thrombectomy
+/- RVAD, and the use of IVC filters to help prevent recurrence.  The benefits and risks of each individual modality should be stated.

In the above scenario, she has stabilised, so systemic anticoagulation with heparin is indicated (the iliac artery branch tear has been embolised, so is unlikely to rebleed) but thrombolysis is possibly too risky and unnecessary after 2 recent angiograms, With the high likelihood of the embolism coming from the pelvic veins and other clot still present, the judicious employment of a filter may be wise.

Discussion

c)        She stabilises and subsequent investigation reveals a moderate sized pulmonary embolism.
Describe all the potential therapeutic strategies for her and describe in detail what your ongoing management would be in this case?

  • Management of the embolism
    • Anticoagulation
      • if permitted by the presence or absence of bleeding
    • Thrombolysis
      • unless there are contraindications (and it sounds like it is not indicated, given that she has stabilised)
    • Surgical embolectomy or interventional radiology clot retrieval are options to consider
  • Prevention of further emboli
    • anticoagulation (as above)
    • determination of source (lower limb doppler ultrasound)
    • inferior vena cava filter
  • Management of cardiovascular instability and hypoxia
    • high FiO2
    • minimise PEEP to decrease RV afterload
    • Optimal fluid loading to ensure RV preload is satisfactory
    • Pulmonary vasodilators and inotropes to improve forward flow through pulmonary circulation

References

Question 2 - 2004, Paper 1

Critically evaluate the role of nitric oxide in the management of the critically ill patient.

College Answer

Nitric oxide has many potential benefits in the critically ill. In particular, selective delivery via the inhalational route allows local vasodilatation (potentially improving ventilation:perfusion matching, and reducing pulmonary arterial hypertension), as well as providing some immunomodulating effects (inhibiting neutrophil adhesion and platelet aggregation). Despite a number of prospective randomised trials (in acute lung injury and ARDS) demonstrating some short-term oxygenation benefits (up  to  72  hours), in  adult patients there have been  no improvements in  longer-term outcomes (such as weaning from ventilation or mortality). Similarly, physiological improvements in pulmonary hypertension in various clinical scenarios have been demonstrated (e.g. primary pulmonary hypertension, heart transplantation) but no longer-term benefits have been demonstrated. Use of NO requires complex equipment, including monitoring for NO and nitrogen dioxide concentrations. Administration of NO has not been without its own potential adverse effects: Methaemoglobinaemia, prolonged bleeding time, and reports of increased renal failure and nosocomial infections. (Adhikari N. JAMA 2004; 291:1629-31; Sokol J et al. Inhaled nitric oxide for acute hypoxemic respiratory failure in children and adults: A meta-analysis. Anesth Analg 2003;
97:989-98 & Sokol J et al. Inhaled nitric oxide for acute hypoxemic respiratory failure in children and adults (Cochrane Review). In: The Cochrane Library, Issue 1, 2004.)

Discussion

Nitric oxide is discussed elsewhere. It has fallen out of favour, but during 2004 it must have seemed like panacea. The pharmacology of nitric oxide is respectfully treated elsewhere.

Arguments for and against the use of nitric oxide:

  • NO is a potent pulmonary vasodilator
  • it improves ventilation-perfusion matching
  • it improves pulmonary pressures and oxygenation, but this effect is not sustained, nor is it associated with an improved outcome.
    • good Cochrane analysis demonstrated no benefit in mortality in ARDS
    • Oxygenation improves only for the first 24 hours of therapy.
  • It requires specialised equipment and its use is associated with complications eg. pulmonary haemorrhage, nitrogen dioxide toxicity and methaemoglobinaemia.
  • Thus, nitric oxide these days is seldom used.
  • In the manufacturers brochure, it is recommended for use only in the neonatal population.

Administration

  • via uniquely designed gas mixer
  • from its own tank
  • start at 5-10 ppm, go up to 160ppm as needed

Monitoring

  • Monitor PA pressures with PAC
  • monitor response with arterial oxygenation
  • regular CXR, watch for pulmonary haemorrhage
  • Monitor for toxicity, particularly methaemoglobin levels
  • Observe strict handling sfaeguards, including gas scavenging and ventilation precautions

References

Ikaria, the only company which produces this stuff in Australia, has an excellent product information pamphlet.

 

Question 13 - 2004, Paper 1

Outline your approach to the use of non-invasive ventilation in the critically ill patient.

College Answer

The discussion of the approach to the use of non-invasive ventilation should include various aspects including: indications (types of patients), contra-indications/precautions, and some discussion of the way it would be used. The use of CPAP alone (e.g. via face mask, or nasal mask) may be considered to be a form of non-invasive ventilatory support, but further discussion here is not required. There is good data to support its use in patients with exacerbations of chronic airways disease (improving symptoms, physiological endpoints, deceasing intubation rate, and even potentially decreasing hospital mortality). Less data supports its use in patients with acute asthma, pulmonary  oedema,  pneumonia,  other  causes  of  hypoxic  acute  respiratory  failure,  and  as  a technique  to  avoid  endotracheal  intubation  (where  considered  inappropriate),  or  to  facilitate weaning from invasive ventilation. Usual contraindications to the use of non-invasive ventilation include facial injury/trauma, cardiovascular instability, an inappropriate conscious state (e.g. an unconscious or uncooperative patient), an unprotected airway and excessive secretions. Non- invasive ventilation is usually delivered via a face mask (or nasal mask or helmet), using an inspiratory pressure above a level of CPAP. This inspiratory pressure may be time or flow cycled on and off. Usually the pressures (CPAP and inspiratory pressure) are started at a baseline which is well tolerated (e.g. 5 and 8), and are slowly titrated upward to achieve oxygenation, relief of dyspnoea (work of breathing) or tidal volume targets. Early improvements in oxygenation, respiratory rate and carbon dioxide/pH have been claimed to b predictors of success. An approach to weaning from the non-invasive supports should also be included.
At least one candidate misinterpreted this question to read “how you set up non-invasive ventilation”.
(Hore CT. Non-invasive positive pressure ventilation in patients with acute respiratory failure. Emerg Med (Fremantle). 2002 Sep;14(3):281-95. Lightowler JV, Wedzicha JA, Elliott MW, Ram FS. Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta- analysis. BMJ. 2003 Jan 25;326(7382):185 and Ram FSF, Picot J, Lightowler J, Wedzicha JA. Non- invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease (Cochrane Review). In: The Cochrane Library, Issue 1,
2004).

Discussion

A systematic answer should look like this:

Strong indications

  • Pulmonary oedema
  • Asthma
  • COPD
  • Lung infection in the neutropenic patient

Weak indications

  • weaning from invasive ventilation
  • prevention/avoidance of intubation

Contraindications

  • decreased level of consciousness
  • vomiting
  • facial trauma
  • hemodynamic instability, particularly poor preload states

Adjustment of NIV

  • Titrate IPAP and EPAP to work of breathing and tidal volume targets
  • Adjust inspiratory flow rate and expiratory cycle-off to increase or decrease the expiratory phase
  • Adjust delivery mechanism to suit patient needs (eg. nasal mask, full face mask or half face mask, or full helmet)

References

Hore, Craig T. "Non‐invasive positive pressure ventilation in patients with acute respiratory failure." Emergency Medicine 14.3 (2002): 281-295.

 

Lightowler, Josephine V., et al. "Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis." BMJ: British Medical Journal 326.7382 (2003): 185.

 

Ram, F. S., et al. "Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease." Cochrane Database Syst Rev 3.3 (2004).

 

 

Question 15 - 2004, Paper 1

Critically evaluate the role of the prone position in critically ill patients.

College Answer

The prone position has a number of obvious potential advantages to critically ill patients. These include enhancing the ability to rest and dress soft tissue injuries (including burns, skin grafts, plastic surgical flaps etc). The majority of ICU interest however relates to the potential ventilatory benefits associated with prone positioning: increased homogeneity of ventilation, improved ventilation:perfusion matching, increased Functional residual capacity, reduced atelectasis, and facilitation of drainage of secretions. Improved gas exchange is seen in approximately 2/3 of patients, and these improvements are persistent in some. A prospective randomised study confirmed these improvements in oxygenation in patients with Acute Lung Injury/ARDS, but was unable to demonstrate any short or long term mortality benefits. Many details are still under much discussion (e.g. which groups should be “proned”, when in their course, duration of time left prone, and for how many days to persist with prone positioning). Unfortunately, positioning patients prone is not without problems: expertise, manpower and time required for turning; potential for dislodgement of lines/tubes; problems with airway access; increased number of new pressure sores; increased new pressure sores in prone-related areas; increased intracranial pressure and decreased tolerance of enteral feeding. (Gattinoni L et al. N Engl J Med 2001; 345:568-73; Broccard AF. Chest 2003;
123:1334-6; Beuret P et al. Intensive Care Med 2002; 28 :564-69).

Discussion

Prone positioning is seldom seen during one's ICU practice as a junior, but one takes notice of it when it happens.

Rationale for prone ventilation

  • Improved V/Q matching
  • More homogeneous ventilation
    • More uniform distribution of pleural pressure;
    • Thus, more uniform compliance;
    • Thus, more uniform distribution of plateau pressure;
    • Thus, less cyclical atelectasis and alveolar overdistension.
  • Less compression of the lungs by the heart and by the abdominal content.
  • Increased FRC by about 300-400ml
  • Improved drainage of secretions
  • Improved response to recruitment manoeuvres: prone patients seem to require less PEEP (8cm vs 14cm) to sustain the post-recruitment improvement in oxygenation.
  • Improved mechanics of the chest wall in obesity

Limitations of prone ventilation

  • Limitations and contraindications by patient factors
    • Open abdomen, sternotomy, wounds or burns over the ventral body surface
    • Spinal or pelvic instability
    • Massive abdominal distension, eg. pancreatitis
  • Limitations of logistics:
    • difficulty of positioning and increased nursing workload
    • poor control of airway safety
      • In fact, poor control of all drains and tubes of any sort
      • There is a known risk of airway compromise
      • If the tube falls out, it is difficult to reintubate
    • poorer pressure area care
    • Difficult (impossible) central insertion while prone
    • Pressure prone areas include eyes, lips (frm the ETT), bridge of nose, shoulders, ulnar nerves at the elbow, breasts (particularly large ones and those that contain implants), pelvis (particularly interior superior iliac spines), penises and scrotums, and the knees.
  • Limitations of physiology
    • Poor NG feed tolerance
    • Facial oedema
    • Raised intraabdominal and intracranial pressure
  • Limitations of imagination
    • ECG electrode position will change, and so potentially "ECG changes" may appear
    • There is concern that some proportion of ARDS patients may not benefit from prone position, and so this manoeuvre may be a time-wasting exercise, delaying the decision to start ECMO. How large that proportion, remains debatable - in the literature one sees the figure of up to 50%, though these data are from Chatte et al (1997), pre-dating both PROSEVA and sane tidal volume ventilation. In the PROSEVA trial, only 0.8% of the proned patients transitioned to ECMO. The concern remains, i.e. it is possible that the clinician proning the patient has completely misread the situation and ECMO is inevitable.

Evidence in support of prone ventilation

Three studies (Gattinoni, Beuret and Guerin)  were available to the trainees at the time of writing Question 15 from the first  paper of 2004 and Question 11 from the first paper of 2003:

  • Gattinoni et al (2001): 304 patients, proned for only 7 hours a day, starting late in the course of ARDS; oxygenation improved but not survival.
  • Beuret (2002) 54 patients with coma (not ARDS), proned for only 4 hours a day- reduced incidence of VAP was observed, but the study wasn't looking at survival.
  • Guerin (2004): 791 patients proned for only 8 hours a day: no change in mortality

The college answer also quotes an optimistic review paper by Alain Broccard from 2003. Its overall tone was "don't write proning off just yet, the jury is still out".

More modern data in support of prone ventilation:

  • Sud et al (2010) meta-analysis (n=1,867): yes there was a survival benefit, but you had to have a P/F ratios worse than 100 to benefit. NNT for this group was 11.
  • PROSEVA (2013) multicentre RCT - 466 patients with severe ARDS, proned for at least 16 hours a day for 4-5 days on average (i.e. for ~ 70-75% of the time) - showed a significant improvement in 28-day and 90-day mortality (16% vs. 32% in the supine group).

References

Mancebo, Jordi, et al. "A multicenter trial of prolonged prone ventilation in severe acute respiratory distress syndrome." American journal of respiratory and critical care medicine 173.11 (2006): 1233-1239.

Gattinoni, Luciano, et al. "Effect of prone positioning on the survival of patients with acute respiratory failure." New England Journal of Medicine 345.8 (2001): 568-573.

Sud, Sachin, et al. "Prone ventilation reduces mortality in patients with acute respiratory failure and severe hypoxemia: systematic review and meta-analysis." Intensive care medicine 36.4 (2010): 585-599.

Beuret, Pascal, et al. "Prone position as prevention of lung injury in comatose patients: a prospective, randomized, controlled study." Intensive care medicine 28.5 (2002): 564-569.

Guerin, Claude, et al. "Effects of systematic prone positioning in hypoxemic acute respiratory failure: a randomized controlled trial." Jama 292.19 (2004): 2379-2387.

Broccard, Alain F. "Prone position in ARDS: are we looking at a half-empty or half-full glass?." CHEST Journal 123.5 (2003): 1334-1336.

Cho, Young-Jae, et al. "411: The Efficacy and Safety of Prone Positional Ventilation in Acute Respiratory Distress Syndrome." Critical Care Medicine41.12 (2013): A99.

Messerole, Erica, et al. "The pragmatics of prone positioning." American journal of respiratory and critical care medicine 165.10 (2002): 1359-1363.

Chatte, Gerard, et al. "Prone position in mechanically ventilated patients with severe acute respiratory failure." American journal of respiratory and critical care medicine155.2 (1997): 473-478.

Question 2b - 2004, Paper 1

A 76-year-old woman with severe ischaemic heart disease being treated with aspirin, clopidogrel and metoprolol presents with severe abdominal and back pain, 6 hours after  being discharged home from a routine cardiac angiogram via the femoral route.

A large retroperitoneal  haematoma is diagnosed. After resuscitation, the bleeding is stopped by angiographic embolisation of a branch of the left internal iliac artery.
She  is  still  in  the  intensive care  unit  2  days  later  when  she  becomes suddenly dyspnoeic, hypoxaemic and hypotensive with a BP of 80 systolic.

b)        What is your initial management?

College Answer

Most likely cause is a pulmonary embolism but cannot rule out other causes. Resuscitation, relevant investigations  and  therapy  go  hand  in  hand.  So,  ABC  Supplemental  oxygen,  fluid,  then  if inadequate response, consider appropriate vasoactive ie dobutamine/noradrenaline? Get an ECG, CXR, ABG. (D-Dimer of no use here due to large resolving haematoma) consider V/Q or more likely spiral CT scan to prove it.

Discussion

This is a question about the management of sudden onset hypoxia and hypotension in the ICU.

PE is high on your list of differentials.

However, the college is looking for a systematic approach.

  • Attention to ABCs, including immediate manageemnt of reversible factors, as well as a simultaneous focused physical examination and brief history
    • Airway:
      • ensure patency of the ETT and integrity of the ventilator circuit
    • Breathing:
      • examine for tension pneumothorax
      • ABG
      • CXR
    • Circulation
      • examine for features of acute heat failure
      • ECG
      • rapid bedside TTE to observe the volume and contractility of the chambers
  • Supportive management
    • high FiO2
    • fluid boluses
    • vasopressors and inotropes
  • Specific investigations
    • CTPA
    • formal TTE

References

Question 1 - 2004, Paper 2

List the causes and outline your management of a patient with methaemoglobinaemia.

College Answer

Methaemoglobin = altered state of haemoglobin where ferrous ions (Fe2+) of haem are oxidised to the ferric state (Fe3+), which are unable to bind oxygen. Usual level < 1.5%. Results in appearance of cyanosis despite normal arterial PaO2.

Causes of methaemoglobinaemia: congenital (eg. cytochrome b5 reductase deficiency, haemoglobin M disease), acquired (commonest cause overall; due to exposure to any of a number of toxins/drugs eg. aniline dyes, benzene derivatives, chloroquine, dapsone, plilocaine, metoclopramide, nitrites [including nitroglycerin and nitric oxide], sulphonamides).

Management: includes confirmation of diagnosis (co-oximetry ± specific assay), and history of exposures (including toxins and drugs). Congenital cases usually need no more than avoidance of precipitants. Acquired cases need cessation of exposure to precipitants, but in severe cases may require additional specific treatment. Methylene blue (1-2 mg/kg over 5 minutes, may need to be repeated) provides an artificial electron acceptor to facilitate reduction of MetHb via the NADPH-dependent pathway. Response to methylene blue cannot be followed by co-oximetry (detects methylene blue as MetHb).

Alternative agent (eg. ascorbic acid) may be given if methylene blue is contraindicated (eg. G6PD deficiency). Rarely, severe cases (eg. MetHb > 50%) may require exchange transfusion or hyperbaric oxygen.

Discussion

Methaemoglobin is what happens when the Fe2+ of iron is oxidised into Fe3+. The vast majority of the time it is drug-related. Question 29 from the second paper of 2012 presents a dapsone-related case. Very occasionally, some unlucky person is born with a congenital methaemoglobinaemia.  A list of causes of methaemoglobinaemia is offered below.

Physiological normality

  • Normal rate of autooxidation: 0.5-3% of total Hb per day

Direct Oxidants of Haemoglobin

  • Methylene blue
  • Nitrites
    • Sodium or potassium nitrite
    • Amyl nitrite
    • Nitric oxide
  • Nitrates
    • GTN
    • Nitroprusside
  • Antimalarial quinones
    • Pentaquine
    • Primaquine (maybe)
    • Chloroquine (big maybe)

Congential metabolic defects

  • Cytochome b5 deficiency
  • Cytochrome b5 reductase 3 deficiency
  • Haemoglobin M disease

Indirect Oxidants of Haemoglobin

  • Aromatic hydrocarbons
    • Aniline
    • Naphthalene
    • Nitrobenzene
  • Sulfonamides
    • Trimethoprim / sulfomethoxazole (Bactrim)
    • Dapsone
  • Random antibotics
    • Nitrofurantoin
  • Local anaesthetics
    • Benzocaine
    • Prilocaine

Management of methaemoglobinaemia consist of trying to reduce Fe3+ back to Fe2+.

Glucose infusion

  • Whichever reducing agent is used, glucose will be required for the generation of NADPH by the hexose monophosphate shunt.

Methylene blue

  • 1-2mg/kg over 5 minutes
  • By cycling through its two states (methylene blue and leucomethyene blue) this molecule burns through glucose to reduce Fe3+ to Fe2+ by donating electrons to the ferric iron.
  • This reaction requires G6PD.
  • In the absence of G6PD, haemolysis will develop;
  • thus, G6PD-deficient patients will require an alternative reducing agent.

Alternative reducing agents:

  • Ascorbic acid, 200mg/k: activity seems to rely on the presence of glutathione
  • N-acetylcysteine (well, it seems to work in vitro)

Blood transfusion

  • If one is unable to conver the affected haemoglobin, one needs to supplement with more fresh haemoglobin. An exchange transfusion is possible (i.e. replace all the red cells) if the causative agent has been convincingly cleared from the body; however this is an inelegant solution.

Supportive management

  • It is tiresome and ridiculous to write "supportive management" for all these "how would you manage" questions. Surely, the college does not believe that the candidates who fail to mention FASTHUG in writing would willfully withhold supportive management from their patients? No Mr Jones, I will not offer you nasogastric feeds, and you can sort out your own thromboprophylaxis. 

References

Wright, Robert O., William J. Lewander, and Alan D. Woolf. "Methemoglobinemia: etiology, pharmacology, and clinical management."Annals of emergency medicine 34.5 (1999): 646-656.

 

Modarai, B., et al. "Methylene blue: a treatment for severe methaemoglobinaemia secondary to misuse of amyl nitrite." Emergency Medicine Journal 19.3 (2002): 270-270.

 

Deeny, James, Eric T. Murdock, and John J. Rogan. "Familial Idiopathic Methaemoglobinaemia: Treatment with Ascorbic Acid." British medical journal1.4301 (1943): 721.

 

Ward, Kristina E., and Michelle W. McCarthy. "Dapsone-induced methemoglobinemia." Annals of Pharmacotherapy 32.5 (1998): 549-553.

 

Wright, Robert O., William J. Lewander, and Alan D. Woolf. "Methemoglobinemia: etiology, pharmacology, and clinical management."Annals of emergency medicine 34.5 (1999): 646-656.

Question 27 - 2005, Paper 1

Critically evaluate the role of open lung biopsy in the critically ill patient with a diffuse infiltrate on chest radiograph.

College Answer

There are a myriad of potential causes of a diffuse infiltrate. These include high pressure pulmonary oedema, low pressure pulmonary oedema, diffuse pneumonia, malignancy (eg. lung, haemopoetic), pulmonary haemorrhage or auto-immune/vasculitic. Most patients are able to be managed without invasive investigations.

Open lung biopsy is reserved for those situations where:

•    The cause is not apparent

•    The patient is not responding to management, or

•    There is a suspicion of another specific disease state which would require different management (eg. disseminated malignancy, alveolar haemorrhage, Bronchiolitis Obliterans Organising Pneumonia [BOOP] etc.), and

•    The diagnosis has not been able to be made on less invasive tests (eg. Broncho- Alveolar Lavage or even Video Assisted Thoracoscopic Surgery), or

•    Determination of prognosis is essential for management.

Open lung biopsy is associated with risks, especially in the critically ill patient, which include death, air-leak and even  a  sampling error (as  limited tissue removed).   These potential risks must be balanced against the information to be obtained.  The expectation is that, with further information some potentially harmful/expensive/un-necessary medications would be able to be stopped, and more specific management introduced (eg. high dose corticosteroids).

The biopsy needs to be taken from an area likely to be representative, not one with a high likelihood of non-specific fibrosis (eg. dependent segments of RML), and not too late in the disease process.(Patel 2004 Chest)

Discussion

So, you cannot arrive at a diagnosis of a diffuse interstitial infiltrate.

Lung biopsy is also asked about in Question 4 from the second paper of 2014; there the college answer is mroe comprehensive, as is the discussion.

In brief, lung biopsy is not without its risks, and is indicated only in specific situations.

Indications for lung biopsy

  • diagnosis of lung disease cannot be established by less invasive means (eg. BAL, bronchoscopic biopsy, HRCT)
  • the lung disease is not responding to the current management
  • Management for the differentials is substantially different and a tissue diagnosis will alter the course of management
  • The management suggested has significant side effects, and a biopsy may prevent such management
  • Prognosis will be influenced by tissue diagnosis, and may be grounds for a palliative course of management

Complications of lung biopsy

  • pneumothorax
  • bronchopleural fistula
  • haemothorax
  • major vessel damage
  • failure to establish a diagnosis due to poor sampling
  • death

The biopsy must be performed in several regions of the lung, and must yield specimens which offer a representative sample, without sampling any areas of irreversible fibrosis.

It cannot be performed in patients who cannot be ventilated on one lung for prolonged periods. Risks and contraindications of of thoracotomy apply.

References

 

UpToDate has a nice article about lung bippsy.

Bensard, Denis D., et al. "Comparison of video thoracoscopic lung biopsy to open lung biopsy in the diagnosis of interstitial lung disease." CHEST Journal103.3 (1993): 765-770.

 

Question 28 - 2005, Paper 2

A 65 year old woman with chronic airways disease presents with acute respiratory failure.

Outline  how  you  would  establish  the  precipitating cause  of  her acute  respiratory failure.

College Answer

History: consider

•    Duration of respiratory failure – is it acute deterioration on a normal functional background or acute on chronic?;

•    setting (in community or hospital); any trauma/surgery/anaesthesia/procedure related;

•    respiratory depressant drug use;

•    fever/sweats/cough/sputum production;

•    history of others developing respiratory infection or epidemics;

•    recent travel especially overseas;

•    history of DVT/PE, malignancy, cigarette smoking,

•    recent chest pain or symptoms of heart failure;

•    medication use related to potential anaphylaxis or upper airway oedema;

•    is there a septic or SIRS process generating a metabolic acidosis that this patient’s respiratory system cannot deal with?

Examination: consider

•    Level of consciousness

•    presence of stridor or wheeze

•    cyanosis indicative of oxygenation failure

•    barrel chested / pursed lips / nasal flaring indicating hyperinflation

•    tracheal deviation indicating severe collapse or PTX;

•    subcutaneous emphysema;

•    flap indicative of hypercapnia;

•    ?new heart murmur or other signs indicative of heart failure;

•    signs of non-respiratory sepsis (eg abdomen) or SIRS generating a severe metabolic acidosis;

•    focal limb oedema. Investigation: consider

•    ABG – assess oxygenation/ventilation/acid-base status (metabolic and respiratory)

•    Spirometry – obstructive or restrictive airflow pattern

•    Hb – is there polycythaemia due to chronic severe disease or severe anaemia contributing decreased O2 delivery?

•    ECG – is there RHF or myocardial ischaemia?

•    CXR – collapse / PTX / pneumonia / heart size / pulmonary oedema / hyperinflation /effusion / trauma / malignancy / airway compression.

•    Sophisticated investigations like thoracic CT are not necessarily appropriate in the acute setting unless suspecting a PE.

•    Possible use of V/Q scanning.

Discussion

This question is painfully broad.  It requires the candidate to think carefully about the diagnostic pathway in respiratory failure. A structured response is always better. This one has been derived from the excellent UpToDate topic, "Evaluation of the adult with dyspnea in the emergency department".

Causes of Respiratory Failure
Airway
  • Foreign body
  • Angioedema and anaphylaxis
  • Obstructive airway infections, eg. retropharyngeal abscess
  • Airway trauma
Breathing
  • Pulmonary embolism
  • Bronchospasm: COPD or asthma
  • Pneumothorax
  • Infection: pneumonia, pneumonitis, etc etc
  • ARDS from a pulmonary or non-pulmonary source
  • Pleural effusion for whatever reason
Circulation
  • Cardiogenic pulmonary oedema, due to...
    • Acute coronary syndrome
    • Heart failure, cardiomyopathy
    • Arrhythmia
    • Valve failure
    • Cardiac tamponade
Neurology
  • Neurogenic pulmonary oedema
  • Neuromuscular disease, with respiratory muscle weakness
  • Respiratory center injury, eg. stroke
  • Anxiety, hyperventilation
Endocrine and metabolic
  • Metabolic acidosis
  • Poisoning,  respiratory suppressants eg. opiates or respiratory stimulants eg. salicylates
  • Massive obesity
  • Hy
  • Neuromuscular disease, with respiratory muscle weakness
  • Respiratory center injury, eg. stroke
Haematological and oncological
  • Failure of oxygen-carrying capacity or oxygen delivery:
    • Anaemia
    • Dyshaemoglobinaemia
    • Carbon monoxide or cyanide toxicity
  • Malignancy, local (eg. bronchial carcinoma) or infiltrative (eg. lymphoma or lymphangitis carcinomatosis)
Infectious and immunological
  • Sepsis
  • Autoimmune SIRS or vasculitis
  • Graft vs host phenomena, eg. TRALI or engraftment syndrome

 

Investigations for Acute Respiratory Failure
History
  • General historical features
  • Past history
  • Chronology of the episode
  • Prior intubation
  • Severity of distress
  • Association of chest pain
  • History of trauma
  • Fevers, chills, rigors, night sweats
  • Cough, sputum, haemoptysis
  • Recent travel
  • Tobacco and drugs
Examination
  • Basic vital signs, including temperature and oximetry
  • Red flags:
    • Obtubdation
    • Fatigue
    • Cyanosis
  • Features of severe respiratory distress:
    • Retractions and the use of accessory muscles
    • Brief, fragmented speech
    • Inability to lie supine
    • Profound diaphoresis; dusky skin
    • Agitation or other altered mental status
  • Palpation, percussion, auscultation of the chest
Bloods
  • Full blood count (anaemia, WCC)
  • Inflammatory markers (infection, malignancy)
  • Urea creatinine and electrolytes (organ system function and acid-base balance)
  • ABG (gas exchange and acid-base balance)
Imaging
  • Chest Xray
  • ECG
  • Trans-thoracic echo (TTE)
  • CT of the chest, +/- pulmonary angiogram
Potentially relevant investigations
  • Spirometry
  • Cardiac biomarkers
  • Procalcitonin
  • Urinary pneumococcal and legionella antigens
  • Sputum culture
  • PJP PCR on sputum
  • Aspergillus galactomannan

References

Question 29 - 2005, Paper 2

A 65 year old woman with chronic airways disease presents with acute respiratory failure.

Outline how you would determine the severity of her underlying airways disease.

College Answer

History: consider – exercise tolerance; ADLs; home O2 use; home CPAP/NIV use; respiratory medication use and compliance; steroid use; need for heart failure medication; frequency of hospitalisations or previous mechanical ventilation.

Examination: consider – steroid skin; cachexia / nutritional assessment; plethora secondary to polycythaemia.

Investigations:  consider – previous ABGs (degree of hypoxaemia/hypercapnoea/metabolic compensation); Electrolytes: especially tCO2 indicative of bicarbonate compensation of chronic hypercapnoea; previous spirometry (FEV1/FVC - degree of emphysema/hyperexpansion/evidence of left or right heart failure); formal Pulmonary Function Tests (DLCO/flow-vol loops); ECG (?chronic right heart strain pattern); Hb (polycythaemia secondary to chronic hypoxaemia).

Discussion

This question asks about the assessment of the severity of COPD.

Historical features

  • exercise tolerance
  • breathlessness with everyday activities
  • presence of chronic cough
  • high volume of sputum, suggestive of bronchiectasis
  • haemoptysis, suggestive of malignancy
  • home O2 requirement
  • home CPAP requirement
  • pattern of bronchodilator use
  • pattern of steroid use
  • frequency of hospitalisations
  • previous mechanical ventilation
  • anorexia and weight loss

Examination

  • features of malnutrition
  • features of obesity (sedentary lifestyle)
  • features of chronic steroid use
  • central cyanosis
  • breathlessness at rest
  • hyperexpanded chest
  • degree of air entry
  • signs of right heart failure

Investigations

  • Bicarbonate levels
  • Hb (polycythaemia)
  • Spirometry, pre and post bronchodilator
  • Formal lung function tests
  • ABGs to determine degree of hypoxia and hypercapnea
  • TTE (pulmonary pressures)
  • High-resolution CT to assess the severity of emphysematous changes

References

Siafakas, N. M., et al. "Optimal assessment and management of chronic obstructive pulmonary disease (COPD)." European Respiratory Journal 8.8 (1995): 1398-1420.

Question 30 - 2005, Paper 2

A 65 year old woman with chronic airways disease presents with acute respiratory failure.

Outline  your principles of management of her mechanical  ventilation  during her stay in Intensive Care.

College Answer

Principles of management include:

•    NIV better than intubation (if possible).

•    Do no harm – if IPPV consider I:E ratio / RR / TV or insp. pressure settings / flow pattern of breath to avoid dynamic hyperinflation and barotrauma.

•    Supported spontaneous ventilation preferred to fully ventilated IPPV if possible.

•    High enough mechanical ventilatory support to avoid respiratory muscle fatigue balanced out to avoid generating respiratory skeletal atrophy.

•    Extubate sooner rather than later if safe to do so and be prepared to support with NIV post- extubation.

•    Assess cough, airway protection and sputum load when considering extubation or use of NIV.

•    Supplemental oxygen and PEEP to appropriate levels for adequate oxygenation (eg. PO2 55mmHg in some patients).

•    Ventilation to get CO2 to appropriate levels (may not necessarily mean normalising CO2 to 40; ?allow permissive hypercapnoea).

•    Discontinue futile therapies if prognosis hopeless and deemed ethically appropriate with understanding & agreement of patient or appropriate surrogate.

Discussion

Mechanical ventilation of the COPD patient is briefly discussed elsewhere.

In summary,

  • Avoid intubation; rely on NIV
  • Use NIV to manage hypercapnea and to improve work of breathing in the acute setting
  • If you have to intubate them, do so for the shortest possible period, and extubate them onto NIV as soon as is practical
  • Avoid high plateau pressures, to avoid pneumothorax from emphysematous bullae
  • Help sputum clearance by having regular breaks form NIV
  • Aim for a PaO2 around 55-65; avoid hyperoxia
  • use a short inspiratory rise time, match PEEP to auto-PEEP, increase the expiratory phase by increasing the expiratory flow trigger
  • Use bronchodilators; anticholinergics are probably better than beta-agonists
  • Use steroids
  • Commence antibiotics if there is an infectious trigger
  • Avoid futile treatment in severely exercise-limited patients

It has been pointed out that there are lots of different (reasonable-sounding) ways of answering a question which asks "how would you mechanically ventilate that". For example, it would be reasonable to discuss daily checks of ETT position, active circuit humidification, avoidance of ludicrously large tidal volumes or driving pressures, and so on. However, judging by the college answer, in a question like this these totally valid generic recommendations may not score marks.

One needs to read between the lines of the SAQ to score high marks (one of the qualities of a poorly written SAQ). Consider: the examiners gave you a woman with chronic airways disease, and asked you to discuss the management of her mechanical ventilation. The question really asks, "what are the principles of ventilating a COPD patient?" It is difficult to guess as to why the examiners designed this SAQ the way they did. Given how little additional information is available about the patient (she's female, 65 and her respiratory failure is acute), one can't exactly say that the rich detail of this complex clinical case vignette is necessary for the testing of candidates' higher analytic and synthesis skills. 

References

Siafakas, N. M., et al. "Optimal assessment and management of chronic obstructive pulmonary disease (COPD)." European Respiratory Journal 8.8 (1995): 1398-1420.

Question 3 - 2006, Paper 1

Describe the advantages  and disadvantages  of PaO2 (partial  pressure  of oxygen in the arterial  blood) and SpO2 (oxygen saturation  measured by a pulse oximeter) as indicators of arterial oxygenation.

College Answer

This question lends itself to an answer in table form. Such a table should include the following type of information:

PaO2

SpO2

Advantages

Allows calculation of P:Fratio and A-a gradient. Calculating SaO2 allows calculation of DO2/VO2/shunt fraction

Also a reliable indicator of

oxygenation particularly in the clinical relevant range

Accurate indicator of oxygenation, not influenced by position of Oxyhaemoglobin Dissociation Curve

Easy to use, non invasive,

reliable in most clinical situations both in ICU and on the wards

Measurement accurate evenin the presence of dyshaemoglobins.

Provides a continuous

measurement

Disadvantages

Invasive

Affected by peripheral

perfusion, arrhythmias, motion artefact

Prone to pre-analytic errors

– air bubbles, heparin contamination

Affected by

dyshemoglobins

Needs a blood gas analyser

Usually a time delay between sampling and result

Provides only intermittent

measurements

 

Discussion

An alternative tabulated answer would resemble the following:

PaO2

SpO2

Advantages

  • accurate impression of oxygenation
  • not confounded by dyshemoglobins
  • allows accurate calculation of hemoglobin saturation
  • real-time monitoring
  • Non-invasive
  • requires no special expertise

Disadvantages

  • Invasive
  • requires arterial access expertise
  • requires blood gas analyser
  • confounded by collection error, eg. bubbles in the syringe
  • Measurement delay exists
  • confused by dyshemoglobins
  • does not reflect level of oxygenation in hyperoxic patients
  • not a direct measurement of hemoglobin saturation - instead, uses a signal intensity and a look-up table derived from empirical data
  • no absolute method for calibration exists - only empirical data collected from hypoxic volunteers
  • unreliable in severely hypoxic patients
  • unreliable in poorly perfused patients
  • unreliable in arrhythmia
  • positional
  • unreliable in confused patients, confounded by mostion artifact

References

 

Hutton, P., and T. Clutton-Brock. "The benefits and pitfalls of pulse oximetry."BMJ: British Medical Journal 307.6902 (1993): 457.

Question 4 - 2006, Paper 1

Outline the causes, consequences and management of intrinsic PEEP.

College Answer

Causes: consider increased expiratory resistance (prolonged expiratory time constant: eg. bronchospasm, narrow/kinked ETT, inspissated secretions, exhalation valves/HME/filters), increased minute ventilation (inadequate expiratory time), prolonged inspiratory time.

Consequences: consider increased intra-thoracic lung volume (with increased pressures for a given tidal volume and risks of barotrauma), increased intra-thoracic pressure (decreasing venous return, and increasing inspiratory work to trigger the ventilator).

Management: consider treatment of reversible factors (bronchospasm, secretions, expiratory devices), prolongation of expiratory time (decrease respiratory rate, increase inspiratory flow, decrease in inspiratory time) or decrease tidal volumes, application of exogenous PEEP (to 50 –85% of accurately measured intrinsic PEEP) can be used to decrease inspiratory triggering work in spontaneously breathing patients, and possibly to improve distribution of inspired gas.

Discussion

Intrinsic PEEP seems to be a favourite college topic. There are numerous questions, all of which ultimately ask the same thing: what is intrinsic PEEP, and how does one detect it, and which ventilator settings does one twiddle with in order to defeat it?

So, here we go again.

Causes

  • Increased resistance to expiratory flow, due to:
    • Machine factors:
      • Blocked or faulty expiratory valve of the ventilator
      • kinked expiratory limb of the ventilator tubing
      • rain-out in the expiratory limb
      • clogged water-sodden HME
      • kinked ETT
      • ETT clogged with sputum
      • ETT being chewed on by the patient
    • Ventilator settings
      • Short expiratory time, eg. in very high respiratory rate
      • High I:E ratio
    • Patient factors
      • Bronchospasm
      • Increased respiratory rate

Consequences

  • CO2 retention
  • Increased work of breathing
  • increased intrathroracic pressure, thus
    • decreased venous return, hemodynamic instability
    • decreased lymphatic return
    • decreased organ perfusion, organ oedema and decreased organ function

Management

  • reverse reversible patient factors, eg. bronchospasm can be treated with bronchodilators
  • correct machine factors, eg. empty the water out of the tubes, cheange the HME, change the ventilator valve
  • Suction ETT, ensure patency
  • Increase expiratory time by decreasing respiratory rate and decreasing I:E ratio
  • Apply PEEP to counteract the increased work of breathing
  • Decrease tidal volume

References

Question 14 - 2006, Paper 1

A 40 year old woman requires a trial of inhaled nitric oxide for severe pulmonary hypertension with right ventricular failure following a mitral valve replacement.  She is intubated and ventilated.  Describe how you would provide this, including the safeguards that are required.

College Answer

Treatment should only be provided where forethought as to the key elements of safety and proper equipment are provided. Inhaled nitric oxide is still an investigational drug in Australia, and is not currently approved by TGA. Dose selection and titration should be done carefully observing effects by commencing at 5-10ppm and dialling up gradually increasing as necessary up to possibly 160 ppm. Monitoring of efficacy should be performed such as with PAP/PaO2 and/or Pulmonary Vascular Resistance (via pulmonary artery catheter or TOE).
Monitoring toxicity with NO2 and possibly methaemoglobin levels. Monitor also for risk of pulmonary haemorrhage.
Safe management of the cylinder is essential including knowledge of spill emergency procedure. Attention should be paid to waste gas evacuation, including at the least adequate air conditioning and possibly passive and active scavenging.

Discussion

The scope for the use of nitric oxide, and the number of people familiar with the practice, grows more and more slender with each passing day. Still it has applications in paediatric ICU, and there are still some staunch believers in its benefits. And one will note the vintage of the question (the drug has long since been approved, found good use, and subsequently has fallen out of favour).

A thorough (albeit amateurish) discussion of its various marvels can be found elsewhere.

Arguments for and against the use of nitric oxide:

  • NO is a potent pulmonary vasodilator
  • it improves ventilation-perfusion matching
  • it improves pulmonary pressures and oxygenation, but this effect is not sustained, nor is it associated with an improved outcome.
    • good Cochrane analysis demonstrated no benefit in mortality in ARDS
    • Oxygenation improves only for the first 24 hours of therapy.
  • It requires specialised equipment and its use is associated with complications eg. pulmonary haemorrhage, nitrogen dioxide toxicity and methaemoglobinaemia.
  • Thus, nitric oxide these days is seldom used.
  • In the manufacturers brochure, it is recommended for use only in the neonatal population.

Administration

  • via uniquely designed gas mixer
  • from its own tank
  • start at 5-10 ppm, go up to 160ppm as needed

Monitoring

  • Monitor PA pressures with PAC
  • monitor response with arterial oxygenation
  • regular CXR, watch for pulmonary haemorrhage
  • Monitor for toxicity, particularly methaemoglobin levels
  • Observe strict handling sfaeguards, including gas scavenging and ventilation precautions

References

Ikaria, the only company which produces this stuff in Australia, has an excellent product information pamphlet.

 

Afshari, Arash, et al. "Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) and acute lung injury in children and adults." Cochrane Database Syst Rev 7 (2010).

Question 21 - 2006, Paper 1

A 33 year old woman with severe multiple trauma to head, chest, liver and long bones has  been  in  your unit  for a  week  and  has  been  slowly recovering.    She  suddenly develops  acute  hypoxia  (PaO2  55 on  FiO2  of 0.8 + 10cm  PEEP)  and  hypotension (80/46) due to an acute pulmonary embolism.  Outline the key features of management, and your rationale for each.

College Answer

The key features of management and rationale should include:
•    Resuscitation: fluids, consideration of further monitoring/investigation, vasoactive support, and evaluation/adjustment of ventilation/FIO2 to increase PaO2.
•    Full  anti-coagulation unless  strong  contraindication still  exists  (eg.  worsening cerebral haemorrhages)
•    Consideration of thrombolytics based on haemodynamics [eg. echocardiography] (probably contraindicated unless peri-mortem!).
•    Consideration of surgical removal if thrombolysis contraindicated and haemodynamically unstable, but would need to tolerate anticoagulation and cardio-pulmonary bypass.
•    Consideration of vena caval filter for prevention of further emboli (depending on source of emboli, if unable to anticoagulate etc)
•    General supportive care

Discussion

This, given the haemodynamic instability, is a case of massive pulmonary embolism.

A question like this would benefit from a systematic answer.

  • Attention to ABCs, with correction of immediately life threatening complications
  • Airway
    • intubation may be required to apply a controlled FiO2
  • Breathing
    • Increase FiO2 to correct hypoxia
  • Circulation
    • Fluid boluses to increase right heart filling
    • pulmonary vasodilator and inotrope eg. milrinone, to increase forward flow though the pulmonary circulation
    • inhaled pulmonary vasodilators, eg nitric oxide or prostacycline
  • Anticoagulation/thrombolysis
    • thrombolysis likely to be absolutely contraindicated given the history of recent trauma
    • anticoagulation may be relatively contraindicated if there are evolving intracranial haemorrhagic events
  • Rescue therapy
    • Embolectomy
    • Clot lysis / clot retrieval by interventional radiology
    • VA ECMO if anticoagulation not contraindicated and other measures fail or are not available
  • Preventative therapy
    • long term anticoagulation
    • vena cava filter

References

Kucher, Nils, et al. "Massive pulmonary embolism." Circulation 113.4 (2006): 577-582.

 

Kucher, Nils, and Samuel Z. Goldhaber. "Management of massive pulmonary embolism." Circulation 112.2 (2005): e28-e32.

 

Question 28 - 2006, Paper 1

The mortality in patients  with ARDS has only shown a gradual decline over the last two decades.   Outline  why the observed decline in mortality has not been greater in magnitude.

College Answer

A number of factors need to be considered, in particular the large amount of background noise making accurate assessment of improvements near impossible.   Indeed, the studies that have actually shown benefit may not be extrapolatable to the majority of the ARDS population seen in Intensive Care.
The mortality of ARDS is not usually due to respiratory disease per se, but instead to multiple organ dysfunction.   This in turn is due to a multiplicity of factors (including the underlying disease process that resulted in  ARDS [eg. pancreatitis, sepsis, burns], inflammatory response due to ARDS, nosocomial infections.  No single specific therapy is likely to prevent the cascade of events that result in inflammation.  Insufficient studies have been performed to consistently demonstrate one technique has benefits, let alone which combinations of therapies may be useful.
ARDS is also the end result of a large number of predisposing insults.   The outcomes vary dramatically between subgroups (eg. trauma versus pneumonia).  More specific classification or stratification may allow more accurate comparisons.
As a result of better general supportive care, patients that would not previously been considered salvageable could now be going on to develop ARDS, and are more likely to have an adverse outcome.  Potential risk factors as they are discovered are continually being treated/corrected, decreasing the likelihood of less severe/complex cases developing ARDS. It is probably impossible to accurately compare outcomes now with decades ago, given the inability to control for the many factors that influence outcome.

Discussion

In comparison to more recent questions, this subtly hypothetical question calls upon the candidate to speculate about why the current state-of-the-art in ARDS management has failed to produce significant improvements.

This is explored in greater detail in the chapter on outcomes in adult ARDS.

Some points worth mentioning are:

  • Breakthroughs in ARDS management happen very infrequently.It would be unreasonable to expect major improvements in survival if there have been no major improvements in management.
  • Many widely-accepted therapies which were expected to improve mortality have failed to do so, but people kept using them anyway.
  • The trend towards improvement does not seem to be related with any specific breakthroughs in ventilation management
  • We expect an unrealistic improvement in mortality in a condition which is associated with such morbidity.
  • We are measuring mortality badly and inconsistently, especially when it comes to early studies.
  • ARDS patients die of multi-organ system failure rather than hypoxia, and MOSF management has not improved dramatically in recent history.
  • The ARDS patients today are sicker than they were 20 years ago.
  • There are fewer cases of  "mild" survivable ARDS due to aggressive early management of ARDS-associated conditions
  • Difficult to treat causes of ARDS (eg. sepsis and SIRS) have become more prevalent

That said, mortality in ARDS seems to have been declining steadily, at 1.1% per year (at least between 1994 and 2006).

References

Abel, S. J. C., et al. "Reduced mortality in association with the acute respiratory distress syndrome (ARDS)." Thorax 53.4 (1998): 292-294.

Zambon, Massimo, and Jean-Louis Vincent. "Mortality rates for patients with acute lung injury/ARDS have decreased over time." CHEST Journal 133.5 (2008): 1120-1127.

ARDS Definition Task Force. "Acute Respiratory Distress Syndrome." Jama307.23 (2012): 2526-2533.

De Campos, T. "Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network." N Engl J Med342.18 (2000): 1302-130g.

Villar, Jesús, et al. "A Clinical Classification of the Acute Respiratory Distress Syndrome for Predicting Outcome and Guiding Medical Therapy*." Critical care medicine 43.2 (2015): 346-353.

 

Erickson, Sara E., et al. "Recent trends in acute lung injury mortality: 1996-2005." Critical care medicine 37.5 (2009): 1574.

 

Zambon, Massimo, and Jean-Louis Vincent. "Mortality rates for patients with acute lung injury/ARDS have decreased over time." CHEST Journal 133.5 (2008): 1120-1127.

 

Milberg, John A., et al. "Improved survival of patients with acute respiratory distress syndrome (ARDS): 1983-1993." Jama 273.4 (1995): 306-309.

 

Stapleton, Renee D., et al. "Causes and timing of death in patients with ARDS." CHEST Journal 128.2 (2005): 525-532.

 

Ferring, Martine, and Jean Louis Vincent. "Is outcome from ARDS related to the severity of respiratory failure?." European Respiratory Journal 10.6 (1997): 1297-1300.

 

Pierrakos, Charalampos, and Jean-Louis Vincent. "The changing pattern of acute respiratory distress syndrome over time: a comparison of two periods." European Respiratory Journal 40.3 (2012): 589-595.

Villar, Jesús, Demet Sulemanji, and Robert M. Kacmarek. "The acute respiratory distress syndrome: incidence and mortality, has it changed?." Current opinion in critical care 20.1 (2014): 3-9.

Amato, Marcelo BP, et al. "Driving pressure and survival in the acute respiratory distress syndrome." New England Journal of Medicine 372.8 (2015): 747-755.

 

Question 2 - 2006, Paper 2

Outline the principles of management of a patient with life threatening haemoptysis.

College Answer

IMMEDIATE MEASURES

a) Protection of airway

b) ETT & Adequate ventilation, consider double lumen tube if site of bleeding known

c) Positioning of patient: Trendelenburg position may allow clearance of blood from airway or if the site of bleeding is known, rt or lt lateral position to keep the bleeding lung dependant

SEARCH FOR CAUSES –

Infections, Tumours, Mitral valve disease, Trauma, pulm vasc disorders, vasculitis, bleeding diatheses

INVESTIGATIONS

H/o and Clinical examination – upper and lower respiratory

CXR/CT Infection

Bleeding and coagulation profiles

Auto-antibody screen

Echo

SPECIFIC TREATMENT

1) Volume replacement

2) Bronchoscopy - ablation of lesions

3) arterial embolisation

4) Surgery

Discussion

  • Attention to the ABCS, with management of life-threatening problems simultaneous with a rapid focused examination and a brief history
  • Airway
    • Assess the safety of intubation
    • Prepare equipment required for a difficult intubation
    • Access skilled staff to assist
    • Intubate with a dual-lumen tube if it is obvious where the blood is coming from
  • Breathing/ventilation
    • High FiO2
    • High PEEP (as a means of putting pressure on the vessel which is bleeding)
    • Humidification, to prevent large dried clots from blocking the bronchi
    • CXR
    • ABG
  • Circulatory support
    • Support haemodynamic stability with fluids and inotropes
    • A lower systolic is appropriate, ~ 90mmHg
  • Supportive management
    • Sedate and ventilate with mandatory mode; paralysis prevents coughing and further injury to the site of haemoptysis
    • Correct coagulopathy
  • Specific management
    • Position the patient in a Trendelenberg position, or with the bleeding lung dependent.
    • Bronchoscopy to remove the larger clots, open airways, and potentially to manage the site of bleeding with cautery
    • Angioembolisation of the site of bleeding
    • Thoracotomy and surgical control of the bleeding

References

UpToDate has a nice summary of massive hemoptysis

 

Shigemura, Norihisa, et al. "Multidisciplinary management of life-threatening massive hemoptysis: a 10-year experience." The Annals of thoracic surgery87.3 (2009): 849-853.

 

Reechaipichitkul, Wipa, and Sirikan Latong. "Etiology and treatment outcomes of massive hemoptysis." (2005).

 

Question 7 - 2006, Paper 2

Examine this flow time curve generated from a mechanically ventilated patient.

What pathological process is revealed by this flow time trace?

b)  List 4 other features (both clinical and adjunctive tests) may support the diagnosis of this pathological process?

c)  List 2 therapeutic measures you will undertake on observing this phenomenon.

College Answer

What pathological process is revealed by this flow time trace?

- The trace reveals the commencement of inspiration before expiratory flow returns to zero, thus setting the scene for dynamic hyperinflation/ small airway obstruction. (Importantly, the trace does not reveal Auto-PEEP as that is a pressure measurement performed after an expiratory pause)

b)  List 4 other features (both clinical and adjunctive tests) may support the diagnosis of this pathological process?

  • Clinical: On auscultation, commencement of inspiration before end of expiration
  • Evidence of obstructive lung disease, the typical scenario in which this happens
  • Increased Auto PEEP
  • Increased Plateau pressure
  • Ventilator settings such as short exp time f) VEI > 20 ml /Kg

c)  List 2 therapeutic measures you will undertake on observing this phenomenon.

  •  Bronchodilators
  •  Increase exp time

Discussion

This is another in the long line of questions which ask the candiate to interrogate the flow/time waveform and make the diagnosis of airflow limitation.

Yes, yet again the flow curve fails to return to zero, demonstrating incomplete emptying and possibly gas trapping.

Again, 4 features of this are asked for. One could produce many more.

  • wheeze
  • prolonged expiratory phase
  • increased chest distension
  • decreased chest expansion
  • bilaterally decreased air entry
  • increased autoPEEP in the expiratory hold manoeuvre
  • increased peak airway pressures
  • increased plateau pressures
  • short expiratory time setting on the ventilator

Again, suggestions for management are asked for.

Apart from adjusting the ventilation (decreasing the I:E ratio and respiratory rate) one may consider using bronchodilators and steroids.

References

Milic-Emili, J. "Dynamic pulmonary hyperinflation and intrinsic PEEP: consequences and management in patients with chronic obstructive pulmonary disease.Recenti progressi in medicina 81.11 (1990): 733-737.

Question 27 - 2006, Paper 2

You are called urgently to the bedside of an endotracheally intubated and ventilated 45 year old man, day 7 in ICU with respiratory failure secondary to community acquired pneumonia  who has suddenly become impossible to ventilate. Outline your management of this emergency situation.

College Answer

Overview:       Is it machine, tubing or patient?

a)         Use 100% O2 with manual bag ventilation to exclude ventilator problem. If he ventilates, it’s a Ventilator problem.  Change/fix ventilator.

b)         Put a suction catheter down the endotracheal tube. If it passes easily, it is not a tube problem (kinked in mouth, bitten, blocked with blood/secretions from poor humidification). Ability to pass a suction catheter does not exclude a cuff prolapse or ball valve obstruction. If the catheter can’t be passed, quickly change it. If in doubt, consider a bronchoscopy

c)         If it is not the ventilator or the tube, it’s the patient! Look for causes (pneumothorax, bronchospasm) and treat appropriately.

Discussion

A lot of the college questions have this pattern of "Mr so-and-so is impossible to ventilate - what will you do?".

A structured stereotypical approach is expected.

  • Troubleshooting the circuit:
    • disconnect the patient from the ventilator, and manually bag the patient with 100% FiO2
    • If the lung compliance is good, the patient's ventilator or its tubing is the problem, and you can keep bagging the patient until the ventilator is changed.
    • if the bag ventilation is difficult, one must conclude that the patient is the problem.
  • Troubleshooting the patient:
      • Airway:
        • suction the patient, removing sputum plugs and clearing the ETT.
        • if the suction catheter cannot pass easily, the ETT may be blocked. Is there a cuff  herneation?
          • check whether the patient is chewing on it. Paralyse them if this is the case.
        • Auscultate the chest, ensuring the ETT is not in the right main bronchus
      • Breathing:
        • Auscultate the chest and perform a CXR looking for pneumothorax
        • Look for bronchospasm and features of anaphylaxis
        • The CXR will also reveal pleural effusions, hemothoraces and mucus-plugged atelectasis
        • Consider bronchoscopy to relieve the mechanical obstruction.

References

Jairo I. Santanilla "The Crashing Ventilated Patient"; Chapter 3 in Emergency Department Resuscitation of the Critically Ill, American College of Emergency Physicians, 2011.

Question 1 - 2007, Paper 1

List the contraindications for and complications of non invasive ventilation.

College Answer

Contraindications:
a)  Respiratory arrest
b)  Unprotected airway (coma, sedation)
c)  Inability to clear secretions
d)  Marked hemodynamic instability
e)  Oesophageal surgery or maxillofacial surgery pathology (eg ruptured
oesophagus)

Complications:

a)  Mask discomfort,  patient intolerance
·  b)  Facial or ocular abrasions, pressure necrosis

c)  Aspiration pneumonitis.
d)  Aerophagy and gastric distension
e)  Oronasal dryness
t)  Raised intracranial pressure
g)  Hypotension if hypovolemic

Discussion

Complications of non-invasive ventilation:

  • Mask intolerance, agitation and claustrophobia
  • Increased need for sedation
  • Delay of intubation
  • Aspiration
  • Poor clearance of secretions
  • Hypotension of hypovolemic patients
  • Facial pressure areas
  • Raised intracranial pressure
  • Aerophagy
  • Damage to facial, nasal and oesophageal surgical sites or traumatic injuries, leading to surgical emphysema, pneumothorax and pneumomediastinum

Contraindications of non-invasive ventilation

  • Decreased level of consciousness
  • Respiratory arrest
  • Vomiting
  • Hemodynamic instability
  • Poor clearance of secretions, eg. absent cough and gag
  • large sputum load and/or pneumonia
  • surgical or traumatic damage to the airways or oesophagus

References

Gay, Peter C. "Complications of noninvasive ventilation in acute care."Respiratory care 54.2 (2009): 246-258.

Question 21 - 2007, Paper 1

A 64 year old lady admitted with G~de V subarachnoid hemorrhage was pronounced brain dead based on a 4 vessel cerebral angiogram. Subsequent to the angiogram, the total respiratory rate was 15/min when the ventilator rate was set at 10/min.

What are the potential causes of the discrepancy between the set ventilator 
rate and the total respiratory rate? 

What steps will you take to distinguish the cause in this case? 

College Answer

What are the potential causes of the discrepancy between the set ventilator rate and the total respiratory rate? 

1) Auto-triggering of the. ventilator due to

- cardiogenic oscillations 
- High sensitivity settings 
- Circuit leaks 
- Water condensation in the circuit 

2) True spontaneous breath (although unlikely as there is a definitive test indicating brain death. 

b) What steps will you take to distinguish the cause in this case? 

1) Connect the patient to aT -piece circuit with a capnograph and look for 
spontaneous breathing movements and a C02 waveform.

Discussion

So, why is this braindead woman seemingly making spontaneous breathing efforts?

Note that the college does not rule out true spontaneous breaths.

  • Autotriggering:
    • Cardiac oscillation
    • Inappropriately sensitive trigger
    • Condensation pooling in the circuit
    • leaky circuit
  • Triggering by something other than the patient's brain:
    • Diaphragmatic "capture" of her pacemaker
    • External movements (eg. nursing care)

One excludes the embarrassing possibility of a breathing braindead patient by connecting her to a T-piece or by adjusting the trigger to a less sensitive setting.

References

Question 2 - 2007, Paper 2

What is your diagnostic approach to a 62 year old man in respiratory distress with UNILATERAL  wheeze?

College Answer

Monophonic wheeze suggests large airway – ETT malposition, foreign body, blood, secretions, tumour, compression by lymph nodes, aortic aneurysm

Polyphonic wheeze suggests smaller airway and multiple sites – aspiration, unilateral emphysema, contralateral pneumothorax, asthma in a pneumonectomised lung

Diagnostic approach

1.  History of depressed conscious state, trauma, previous lung disease

2.  Examination for tracheal position, contralateral signs, position ETT, clubbing, lymphadenopathy elsewhere

a.   Consider complications such as intrinsic PEEP, depressed venous return and hypotension, pneumothorax

3.  CXR for ETT position, contralateral disease, foreign body

4.  Bronchoscopy for luminal pathology such as blood clot, foreign body, tumour, compression

5.  CT chest if necessary

Discussion

The differential diagnosis of a unilateral wheeze really comes down to how many different ways of obstructing a main bronchus you can think of.

This question could benefit from a systematic answer.

Differential diagnosis of unilateral wheeze:

  • ETT malposition
  • foreign body
  • blood clot
  • Sputum secretions
  • Tumour
    • Bronchogenic carcinoma
    • Thymus carcinoma
    • Retrosternal goitre
  • compression by lymph nodes
  • compression by aortic aneurysm
  • traumatic dissection
  • Bronchial stenosis post infection
  • Bronchiectasis
  • Bronchial compression by enlarged left side of heart
  • Immediate management:
    • Attention to ABCs, with simultaneous focused examination and the retrieval of a detailed history.
    • Assess the need for urgent intubation;
      • or, assess the position of the existing ETT, ensuring it ventilates both lungs
    • Administer high FiO2
    • Collect an ABG and perfrom a CXR
  • Diagnostic strategies
    • CT of the chest to investigate lung parenchyma and find the cause of the obstruction
    • Bronchoscopy and biopsy of the lesion,
      • also permits aspiration/retriveal of the blood clot or foreign body, lavage of the lung for culture/cytology, and the potential stenting of the obstructed bronchus.
    • Alternatively, CT-guided biopsy

References

Question 12 - 2007, Paper 2

The figure below illustrates a  airway pressure waveform of a single breath during volume controlled ventilation, incorporating an end inspiratory pause and an auto-PEEP manoeuvre.

a)  What do the variables A, B, C & D indicate?

b)  What will determine the slope of the pressure curve between points Aand B?

c)  What are the factors which determine variable B?

d)  If the delivered tidal volume was 600 ml, what is the calculated static compliance?

e) List 2 adverse consequences of an increase in the value of variable D?  .

f) List the change(s) you would make to the ventilator settings to treat an increase in the value of variable D.

College Answer

a)  What do the variables A, B, C & D indicate?

A- PEEP, B- PIP, C- Plateau pressure, D- Auto PEEP

b)  What will determine the slope of the pressure curve between points Aand B?

Inspiratory flow pattern

Inspiratory flow rate

c)  What are the factors which determine variable B?

Resistance, compliance, tidal volume, PEEP, insp flow rate and flow pattern

d)  If the delivered tidal volume was 600 ml, what is the calculated static compliance?

30 ml/cm water  [TV/(Plateau-PEEP)]

e) List 2 adverse consequences of an increase in the value of variable D?  .

Decrease in cardiac output, barotrauma

f) List the change(s) you would make to the ventilator settings to treat an increase in the value of variable D.

Increase expiratory time

Decrease I:E ratio, decrease RR, reducing MV

Discussion

This question is identical to Question 17.3 from the first paper of 2010.

a) Variable B is the peak airway pressure. This variable is determined by the lung compliance, tidal volume, airway resistance and PEEP.

To some extent the flow patern also matters (the higher the inspiratory flow, the greater the contribution from airway resistance)

b) The calculation of compliance is not something we do every day, but people should probably be at least dimly aware of the equation which is involved. Compliance is pressure required per volume of lung distension; thus one can calculate it by dividing the tidal volume by the diference between the pleateau pressure and PEEP.

c) Variable D is the Auto-PEEP. This patient is gas-trapping.

In order to address this one, one can

  • minimise PEEP
  • decrease the I:E ratio to 1:4 or so
  • increase the inspiratory rise time
  • decrease the respiratory rate
  • decrease the tidal volume

References

Dubbert, Patricia M., et al. "Increasing ICU staff handwashing: effects of education and group feedback." Infection Control and Hospital Epidemiology(1990): 191-193.

 

Panhotra, B. R., A. K. Saxena, and Al-Ghamdi AM Al-Arabi. "The effect of a continuous educational program on handwashing compliance among healthcare workers in an intensive care unit." British Journal of Infection Control 5.3 (2004): 15-18.

 

Mayer, Joni A., et al. "Increasing handwashing in an intensive care unit."Infection Control (1986): 259-262.

 

Naikoba, Sarah, and Andrew Hayward. "The effectiveness of interventions aimed at increasing handwashing in healthcare workers-a systematic review." Journal of Hospital Infection 47.3 (2001): 173-180.

 

Kaplan, Lois M., and Maryanne McGuckin. "Increasing handwashing compliance with more accessible sinks." Infection Control (1986): 408-410.

 

WHO have this statement: A Guide to the Implementation of the WHO Multimodal Hand Hygiene Improvement Strategy (2009)

Question 17 - 2007, Paper 2

Outline the advantages  and limitations of the A-a gradient and PaO2/FiO2 ratio as indices of pulmonary oxygen transfer. (You may tabulate your answer)

College Answer

A-a gradient

PaO2/FiO2 ratio

Advantages

a) Bedside index,

b) easily calculated,

c) may allow the distinction between hypoventilation (normal gradient) and V/Q mismatch (raised gradient) as causes of hypoxemia

a) Bedside index


b) Easily calculated

c) Input variable in lung injury scores

Limitations

FiO2 dependent,
Age dependent

Varies with lung pathophysiology

a) Cannot distinguish
between hypoventilation and V/Q mismatch


b) P/F ratio unreliable unless FiO2 > 0.5 or PaO2 < 100


c) Not reliable in COPD because of V/Q mismatch


d) Barometric pressure dependent

Discussion

The tabulated college answer is comprehensive. Essentialy, the two indices differ slightly. Both assess the gradient of oxygen exchange. A-a gradient gives one some sort of impression of whether hypoventilation or diffusion are to blame for one's hypoxia. The PaO2/FiO2 ratio does not tell you anything about the diffusion, but is useful as a risk stratification tool for comparing the severities of hypoxic states. A-a gradient will change with age, and becomes confused by shunts. P/F ratio is also confused by shunts, and only works while the atmospheric pressure is normal (it breaks down at altitude and in hyperbaric oxygen chambers) A more detailed discussion of tension-based indices of oxygenation is carried out elsewhere. There, a table of indices is available, which closely resembles the college answer, and I reproduce it below to simplify revision.

Additionally, this whole thing seems heavily based on Chapter 18 from Oh's Manual ("Monitoring oxygenation") by Thomas J Morgan and Balasubramanian Venkatesh, where precisely this question is answered on pages 148-149.

Indices of Pulmonary Oxygen Transfer: Advantages and Limitations

Index

Calculation

Advantages

Disadvantages

A-a gradient

Alveolar gas equation

  • Simple
  • Minimally invasive
  • May distinguish alveolar hypoventilation from all other causes of hypoxia
  • Required by APACHE II, III and IV
  • The magnitude of the A-a gradient is highly dependent on FiO2, especially in the presence of a large shunt
  • Age dependent (increases with age)
  • Non-specific - influenced by numerous factors

PaO2/FiO2 ratio

Divison of alveolar tension by inspired O2 fraction

  • Simple
  • Minimally invasive
  • Required by APACHE IV
  • Used in severity stratification of ARDS
  • Cannot distinguish between alveolar hypoventilation and other causes of hypoxia
  • Makes no attempt to incorporate changes in PaCO2
  • Unreliable unless FiO2 > 0.5 or PaO2 < 100
  • Not reliable in COPD because of V/Q mismatch
  • Barometric pressure dependent
a/A ratio

Arterial pO2 divided by alveolar pO2.

  • Reasonably simple
  • Minimally invasive
  • May distinguish alveolar hypoventilation from all other causes of hypoxia
  • Independent of FiO2 changes
  • Age dependent (increases with age)
  • Non-specific - influenced by numerous factors
  • Oxygen tension based index;
Respiratory index

A-a gradient divided by the PaO2

  • Reasonably simple
  • Minimally invasive
  • May distinguish alveolar hypoventilation from all other causes of hypoxia
  • Independent of FiO2 changes
  • No addiitonal advantages over the a/A ratio
  • Not commonly used; difficult to relate findings to management decision criteria or compare them to published studies.
Estimated shunt fraction (Fshunt)

Shunt equation

(using a CaO2-CVO2difference of around 30-50ml/L)

  • Oxygen content rather than oxygen tension based index
  • Minimally invasive- does not require mixed venous sampling
  • Independent of FiO2 and PaCO2changes
  • Assigned CaO2-CVO2 difference can be completely incorrect in critical illness, completely invalidating the calculations.
Measured intrapulmonary shunt

Shunt equation

  • Gold standard of shunt assesment
  • Empiric measurement; accounts for unpredictable influences on shunt.
  • Maximally invasive (requires PA catheter)
  • Requires mixed venous sampling
  • Complex calculations involved

References

Hess, D., and C. Maxwell. "Which is the best index of oxygenation: P (Aa) o2, Pao2/Pao2, or Pao2/Fio2." Respir Care 30 (1985): 961-963.

 

Chapter 18 from Oh's Manual ("Monitoring oxygenation") by Thomas J Morgan and Balasubramanian Venkatesh (p. 148-149)

 

Cane, Roy D., et al. "Unreliability of oxygen tension-based indices in reflecting intrapulmonary shunting in critically ill patients." Critical care medicine 16.12 (1988): 1243-1245.

 

Wandrup, J. H. "Quantifying pulmonary oxygen transfer deficits in critically ill patients." Acta Anaesthesiologica Scandinavica 39.s107 (1995): 37-44.

 

Hahn, C. E. W. "Editorial I KISS and indices of pulmonary oxygen transfer."British journal of anaesthesia 86.4 (2001): 465-466.

 

Zander R, Mertzlufft F, eds. The Oxygen Status of Arterial Blood. Würzburg, Germany: Bonitas‐Bauer, 1991

 

Nirmalan, M., et al. "Effect of changes in arterial‐mixed venous oxygen content difference (C (a–v̄) O2) on indices of pulmonary oxygen transfer in a model ARDS lung†,††." British journal of anaesthesia 86.4 (2001): 477-485.

 

LAGHI, FRANCO, et al. "Respiratory index/pulmonary shunt relationship: Quantification of severity and prognosis in the post-traumatic adult respiratory distress syndrome." Critical care medicine 17.11 (1989): 1121-1128.

 

Zetterström, H. "Assessment of the efficiency of pulmonary oxygenation. The choice of oxygenation index." Acta anaesthesiologica scandinavica 32.7 (1988): 579-584.

 

Liliethal JL, Riley RL, Prommel DD, et al: "An experimental analysis in man of the oxygen pressure gradient from alveolar air to arterial blood" Am J Physiol 1946; 147:199-216

 

Gilbert, R., and J. F. Keighley. "The arterial-alveolar oxygen tension ratio. An index of gas exchange applicable to varying inspired oxygen concentrations."The American review of respiratory disease 109.1 (1974): 142.

 

Viale, JEAN-PAUL, et al. "Arterial-alveolar oxygen partial pressure ratio: a theoretical reappraisal." Critical care medicine 14.2 (1986): 153-154.

Question 4 - 2008, Paper 1

An anaesthetist from a provincial hospital appears on the video-link seeking advice.  He has a 20 year old man with suspected fat embolism syndrome following an isolated femoral fracture that was been repaired earlier that day. He has become increasingly hypoxic and difficult to ventilate, but transfer to a metropolitan centre has been delayed for 12 hours due to bad weather.

His arterial blood gases on SIMV mode of ventilation are as follows: FiO2  1.0, pH
7.21, PaO2  65 mm Hg (8.6kPa), PaCO2 72 mm Hg (9.3kPa), HCO3  28 mmol/L.  He 
has a four quadrant infiltrate on his Chest X-Ray.

Outline the advice that you would give to help your colleague manage this patient’s ventilation.

College Answer

General 
Confirm Diagnosis

- ARDS criteria: CXR, PF ratio, Etiology, no overload

•    exclude other etiologies - where is the ETT (not RMB), no pneumothorax, aspiration etc.
•    What ventilator is he using, are you familiar with it’s modes (such as pressure control, volume control)
•    Ventilatory strategy –pressure and volume limitation to minimise barotrauma)
•    PEEP increments to effect, ensuring Plateau Pressure < 30 cm H20
•    Heavy sedation and paralysis to minimize O2 consumption and CO2 generation to
GCS 3 and no spontaneous ventilation
•    Targets for ventilation SpO2 > 90-95 and PO2 > 60
- permissive hypercapnia as long as pH > 7.1
•    prone position probably not appropriate (if staff not experienced)

•    Fluids

- CVP only to ~PEEP+2 as maximum
- Consider frusemide if CVP PEEP +5
- Use inotrope to maintain MAP > 60 - suggest noradrenaline
- Transfuse only for Hb approaching 7

•    Reassure him and make yourself available for advice

NO, liquid ventilation, surfactant and tracheal gas insufflation – no role in this setting)

Discussion

This question is very similar to Question 13 from the first paper of 2011.

Initial ventilator strategy:

Additional ventilator manoeuvres to improve oxygenation:

Non-ventilator adjunctive therapies for ARDS:

Ventilator strategies to manage refractory hypoxia

  • Prone ventilation, for at least 16 hours a day (PROSEVA, 2013)
  • High frequency oscillatory ventilation may not improve mortality among all-comers (OSCAR, 2013) or it may actually increase mortality (OSCILLATE, 2013) but some authors feel that there were problems with methodology.

Non-ventilator adjuncts to manage refractory hypoxia

  • Nitric oxide was a cause for some excitement, but is no longer recommended.
  • Prostacyclin is still a cause for excitement, and is still vaguely recommended.
    • Neither agent improves mortality, but prostacyclin can improve oxygenation.
  • ECMO may improve survival (CESAR, 2009) but again there were problems with methodology.

References

Question 13.3 - 2008, Paper 1

List 4 clinical signs typically found on chest examination  that will fit with the findings on this chest X-Ray?

College Answer

Tachypnoea

Decreased chest expansion

Dull percussion note on R

Decreased VR

Absent breath sounds R. base / Whispering pectoriloquy above level of effusion

Apical impulse shift to left

Discussion

To the college answer, I would add that the percussion note will be "stony" dull, and that the "decreased chest expansion" they mention will be unilateral. As for the apex shifting to the left - I can see no evidence of that from the chest Xray; and yes that really is the CXR from the original paper (back when the college did not realise that it would be easier to just re-use the same pictures in every paper). One additional thing to consider is the sounds from the collapsed lung overlying the effusion: if the college expected to get whispering pectoriloquy, then bronchial breath sounds and creps would also be expected on auscultation there.

An excellent article from a bygone era when people actually listened to lungs (Sahebjami & Loudon, 1977) lists several characteristics. This was remixed with the college answer to give what is hopefully a more comprehensive list of clinical features

  • "A heavy or tight feeling" in the chest
  • "a gurgling sensation on changing posture"
  • Shortness of breath, tachypnoea
  • Pain (though this usually preceeds the effusion) - referred to the shoulder
  • Cough
  • "Stony" dullness to percussion
  • Absence of breath sounds
  • Absence of vocal fremitus (perhaps this is what the college referred to when they included "decreased VR" in their answer?)
  • Decreased chest expansion on the affected side
  • Bronchial breath sounds and creps above level of effusion
  • Whispering pectoriloquy above level of effusion
  • Features of mediastinal shift: displaced apex beat, trachea off midline

References

Sahebjami, Hamid, and Robert G. Loudon. "Pleural effusion: Pathophysiology and clinical features." Seminars in roentgenology. Vol. 12. No. 4. Elsevier, 1977.

Question 26.1 - 2008, Paper 2

A 64 year old man is admitted to ICU with a 5 day history of increasing shortness of breath, non-productive cough and acute respiratory failure.

Clinical examination reveals reduced breath sounds and inspiratory and expiratory wheeze  bilaterally. Chest  X-Ray  reveals  hyperinflated lung  fields.  The  following data are from pulmonary function  testing performed 3 months ago.

Variable                   Predicted        Pre- bronchodilator Post- bronchodilator

FEV1 (L/min)        3.15                   0.77                         0.85

FVC (L/min)          4.05                   3.00                         3.38

FEV1/FVC  %        70                      20                            25%

The  patient is intubated and  volume-controlled  ventilation instituted. The  settings are SIMV,  rate of  8,  TV  500  ml,  FIO2  1.0,  PEEP  0.  Three sets  of  ventilatory parameters are provided below.  Based on the information above, select from A, B or C, which pattern will be most  likely to fit with  his respiratory dysfunction and explain why.

A

B

C

Peak      pressure
(cm water)

65

65

35

Plateau 
pressure         (cm water)

20

63

33

b) The patient is intubated and volume-controlled ventilation instituted.  This is the patient’s flow-volume loop. What abnormality is illustrated by the flow pattern?

c)  This  is  the  patient’s  flow-time  respiratory  waveform.  What   abnormality  is illustrated by this trace?

d) List 3 changes  to the ventilator settings  you could do to correct the abnormality noted in c)?

College Answer

a) Answer:  A  (A  high  peak-plateau gradient  with  high  peaks  are consistent   with obstructive lung disease)

b) The patient is intubated and volume-controlled ventilation instituted.  This is the patient’s flow-volume loop. What abnormality is illustrated by the flow pattern?

Expiratory flow scooped out/Increased expiratory resistance

c)Incomplete emptying/potential for gas trapping

d) List 3 changes  to the ventilator settings  you could do to correct the abnormality noted in c)?

Decrease respiratory rate
Increase peak inspiratory flow
Decrease the I:E ratio (increase expiratory time//decrease inspiratory time)

Discussion

a) is straightforward. The patient with such an obstructive pattern of spirometry will generate a high peak airway pressure, but a reasonably normal plateau pressure (because beyond the obstructed air passages lies a relatively normal well-compliant lung parenchyma)

b) the flow-volume loop demonstrates a "scooped out" pattern. The return limb of the loop (helpfully labelled "expiration") demonstrates poor low flow, suggesting that in expiration the patient has trouble exhaling the gas. This is a feature of increased airway resistance.

c) The flow waveform (which are discussed elsewhere) demonstrates a failure of the flow to reach zero at the end of expiration, which suggests gas trapping.

d) In order to decrease gas trapping, one would decrease respiratory rate, decrease the I:E ratio, and decrease the peak inspiratory flow.

References

Question 26.2 - 2008, Paper 2

A 56 year old female with septic shock and multiple  organ failure is admitted to intensive  care.  She is endotracheally intubated and  ventilated. This is the patient’s pressure-volume loop. What abnormalities does the loop indicate?

College Answer

Reduced compliance / Increased resistance

Discussion

No better, more succinct answer is possible. Look at the inflection point- it is well above 20cm. This patient's lungs require a large amount of pressure before their compliance improves.

 Pressure-volume and flow-volume loops are discussed elsewhere.

References

Question 4 - 2009, paper 1

A 47 year old man has severe ARDS following a perioperative aspiration. He is endotracheally intubated and ventilated  in SIMV mode with PEEP 5 cm H2O and an FiO2  0.4 resulting in a PaO2  of 45 mm Hg (6 kPa). On the chest X-Ray, the endotracheal tube is properly positioned in the trachea. The only abnormality on the chest X-ray was bilateral diffuse alveolar infiltrates.

List the steps you could take to improve his oxygenation.  Include a brief comment on the rationale for each step.

College Answer

Basic Measures
°     Increase FiO2): Improve PAO2
°     Increase PEEP
°     surface area for gas exchange
°     Improvement of atelectasis
°     Redistribution of lung water

General Measures
°     Physio / suctioning
°     Sedation / Consider Paralysis: Decrease O2 requirements and CO2 production
°     Treat factors that increase metabolic demand, sepsis etc: Decrease O2 requirements and CO2 production
°     Optimise fluid balance: balance of interstitial overload and maximising cardiac output and DO2
°     Optimise Haemoglobin, optimal oxygen carriage / viscosity combination and minimise immune and volume effects of transfusion

Optimise Recruitment and FRC
°     Lung recruitment manoeuvre: Opening collapsed alveoli, increasing FRC and area available for gas exchange
°     Increase I:E Ratio towards 1:1: Increased FRC as above, recruitment, increase PAO2
°     Inverse ratio ventilation: Longer in inspiration with potential to gas trap and provide autoPEEP above set PEEP with subsequent increase FRC and area for gas exchange.
Positioning
°    Prone position: better VQ matching, improved mechanical advantage, less lung compression from abdominal and mediastinal contents

Optimise Flow to Ventilated  Alveoli
°    Inhaled Nitric oxide: inhaled dilator delivered only to ventilated alveoli
°    Prostacyclin: improved perfusion to ventilated alveoli

Last Resorts
°     Tracheal Gas insufflation and other measures to decrease circuit dead space: reduced dead space means lower CO2 with relative increase in partial pressure of O2
°     HFOV
°     ECMO, external membrane oxygenation and CO2 removal: lung rest and minimisation of VALI.

Discussion

This question is about the ventilation strategies in ARDS, which is a topic discussed elsewhere:

In summary:

Initial ventilator strategy:

Additional ventilator manoeuvres to improve oxygenation:

Non-ventilator adjunctive therapies for ARDS:

Ventilator strategies to manage refractory hypoxia

  • Prone ventilation, for at least 16 hours a day (PROSEVA, 2013)
  • High frequency oscillatory ventilation may not improve mortality among all-comers (OSCAR, 2013) or it may actually increase mortality (OSCILLATE, 2013) but some authors feel that there were problems with methodology.

Non-ventilator adjuncts to manage refractory hypoxia

  • Nitric oxide was a cause for some excitement, but is no longer recommended.
  • Prostacyclin is still a cause for excitement, and is still vaguely recommended.
    • Neither agent improves mortality, but prostacyclin can improve oxygenation.
  • ECMO may improve survival (CESAR, 2009) but again there were problems with methodology.

References

Question 15 - 2009, paper 1

A 60 year old patient  has been admitted to the ICU for 5 days with severe sepsis secondary to a perforated sigmoid colon. He had a sigmoid colectomy and washout of his peritoneum, and appropriate antibiotic therapy. His initial course was complicated  by severe septic shock that is now resolving and acute renal failure for which he is still receiving continuous  renal replacement therapy.  He is currently still ventilated  via an oral endotracheal tube, on SIMV with a rate of 16, TV of 700, PEEP of 5 and FiO2 of 0.45.

He is receiving a small dose of fentanyl and propofol, but is awake and co-operative although he has generalised weakness. His arterial blood gases are shown below:


pH            7.32

PaO2        85 mmHg         (11.3 Kpa)

PaCO2     45 mmHg             (6 Kpa)

HCO3      18 mmol/L

BE           -4.9 mmol/L

What criteria will you use to determine whether the patient  is ready to be extubated?

College Answer

Usually based upon combination of factors rather than a single number.

•    Has the process that required intubation resolved?
o Sepsis and shock
o Abdominal pain
o Intra-abdominal complications that require further intervention

•    Airway?
o Cuff leak
o Difficult airway at time of intubation

•    Respiratory?
o Rapid shallow breathing index (80-110??, on a spontaneous breathing mode)
o Secretions (volume/character)
o Vital capacity (>8-12ml/kg) measured with 0 PS.
o Minute ventilation (<10l/min)
o Adequate gas exchange
o Negative inspiratory force (< -20cm H2O)

•    Neurological?
o Awake and co-operative
o General muscle strength

•    Cardiovascular?
o Low/stable dose of vasopressors and inotropes
o Stable cardiac rhythm

•    Other factors
• Need for more procedures

Discussion

Again, this is a question regarding the standard criteria for extubation.

The Standard Criteria for Extubation

  • Resolution of the condition which had required the intubation and ventilation
  • Patient-triggered mode of ventilation
  • Adequate oxygenation
  • Low PEEP: 5-8 cmH2O
  • Hemodynamic stability
  • Good cough reflex on tracheal suctioning
  • Good gag reflex on oropharyngeal suctioning
  • Adequate muscle strength
  • Satisfactory vital capacity
  • Normal acid base status (pH >7.25)
  • Adequate neurological performance (oriented and obeying commands)

The Specific criteria for this patient

  • The severity of abdominal pain, and the extent to which it influences the patients ability to cough and take deep breaths.
  • Any further planned surgical procedures

References

I tend to throw these references out whenever the question clearly refers to standard extubation criteria.

Andrew D Bersen wrote chapter 27 of the Oh's Manual, which regards mechanical ventilation.

Table 27.3 on page 363 of the 6th edition of Ohs Manual is a nice list of the various indices meantioned above (eg. the rapid shallow breathing index).

On page 362, Bersen references this Chest article from 2001, where the evidence for extubation criteria is summarised. 

MacIntyre NR (chairman), Evidence-based guidelines for weaning and discontinuing ventilatory support: a collective task force facilitated by the American College of Chest Physicians; the American Association for Respiratory Care; and the American College of Critical Care Medicine. CHEST December 2001 vol. 120 no. 6 suppl 375S-396S.

Recommendations regarding which conditions favour extubation has been put forward in a 2007 practice guidelines statement by the AARC:
AARC GUIDELINE: REMOVAL OF THE ENDOTRACHEAL TUBE; RESPIRATORY CARE •JANUARY 2007 VOL 52 NO 1 

 

Question 26 - 2009, Paper 2

 A 78 year old woman ventilated  in intensive care suddenly develops surgical emphysema  over her chest, neck and face. Describe your management.

College Answer

Resuscitation if required. Is airway OK, is she being ventilated adequately, Is circulation intact?

Work out reason: Is it ventilator, tubing or patient. ie barotrauma, new tracheostomy or CVC, pneumothorax,

So, examine patients, get urgent CXR, insert chest drain if required, consider new ventilation strategy.

Discussion

The college answer leaves much to be desired.

This question would benefit from a systematic approach.

Thus, one would approach this patient by an immediate attention to the ABCs, whicle simultaneouesly performing a focused physical examination, and retrieving a focused history of recent events from attending nursing and medical staff.

  • Immediate management:
    • Increase FiO2 to 100%
    • Give a bolus of sedation and administer a neuromuscular junction blocker
    • Disconnect the patient from the ventilator and bag them manually to assess lung compliance
  • Airway:
    • Inspect ETT to ensure it has not slipped too far inside the patient, into the right main bronchus.
    • Confirm bilateral air entry by auscultation
  • Breathing:
    • Inspect palpate and auscultate the chest, looking for pneumothorax
    • CXR: inspect for pneumothorax, mediastinal gas and subdiaphragmatic gas
  • Circulation:
    • Assess hemodynamic stability and administer a rescue fluid blous as well as inotropes/vasopressors as appropriate, while working to diagnose and manage the cause of the problem.
    • Ask about recent procedures, particularly central line insertion, recent routine pressure area care rolls, naso/orogastric tube insertions and airway manipulation
  • Specific management
    • Insert unilateral or bilateral chest drains, as indicated by CXR
    • Consider dual-lumen intubation and lung isolation in the event of trachoebronchial tree disruption
      • urgent cardiothoracic surgical consultation if this is the case
      • urgent general or upper GI surgical consultation if oesophageal, gastric or intestinal perforation is thought to be the cause
    • Keep FiO2 high to aid in the resorption of surgical emphysema
    • Consider subcutaneous Penrose drains or infraclavicular incisions down to pectoralis fascia to assist in the clearance of surgical emphysema (if it is posing a threat to the patient's stability, and only after surgcal consultation)
    • Minimise positive pressure of ventilation if pneumothorax or bronchopleural fistula is implicated
 

References

Aghajanzadeh, Manouchehr, et al. "Classification and Management of Subcutaneous Emphysema: a 10-Year Experience." Indian Journal of Surgery(2013): 1-5.

ZIMMERMAN, JACK E., BURDETT S. DUNBAR, and HERMAN C. KLINGENMAIER. "Management of subcutaneous emphysema, pneumomediastinum, and pneumothorax during respirator therapy." Critical care medicine 3.2 (1975): 69-73.

Woehrlen Jr, Arthur E. "Subcutaneous emphysema." Anesthesia progress 32.4 (1985): 161.

Jairo I. Santanilla "The Crashing Ventilated Patient"; Chapter 3 in Emergency Department Resuscitation of the Critically Ill, American College of Emergency Physicians, 2011.

Question 27 - 2009, Paper 2

a)             Draw and label the pressure time curve for a patient  with normal lungs being ventilated  with constant flow volume controlled ventilation  with a respiratory rate of 20 an inspiratory to expiratory ratio of 1:2, PEEP 5 cm water.

b)         Using the same scale, and assuming the same ventilator settings, draw a representative pressure time curve for a patient  with acute severe asthma.

c)         Briefly, explain the basis for any changes that you have represented.

College Answer

Normal Pressure Time Curve should include the following:
Baseline pressure above zero equals PEEP
Peak Inspiratory pressure (PIP)
Plateau pressure should be included with the long inspiratory time (1second) from rate 20 and I:E 1:2 described in the question
Return of pressure to baseline PEEP
Time axis should have seconds, 1 second in inspiration, 2 in expiration 

Plateau Pressure of 15-20 cm H2O and PIP less than 30 cm H20 as patient described as having normal lungs.

Acute Severe Asthma :

Changes: Raised PIP with unchanged Plateau pressure, but accepting that PEEP and plateau pressure may be increased with successive breaths if illustrated (due to gas trapping / auto peep)

Basis: increase in inspiratory airflow resistance but not lung or chest wall compliance, unless significant gas trapping with ensuing AutoPEEP

Discussion

This college answer, together with the diagrams and explanations, is relatively thorough. Except for the fact that the college diagram needs some correction. The college mention nothing of an inspiratory pause, which is clearly present on their ventilator graphics. Without an inspiratory pause, they would not be able to illustrate the difference between plateau pressure and peak inspiratory pressure.

A more indepth discussion of ventilator pressure-time waveforms takes place elsewhere.

 

References

Question 3.3 - 2010, Paper 1

A previously fit 45 year old man was noted to be in respiratory distress 24 hours following maxillofacial surgery.

Clinical examination revealed the following:

•    Respiratory rate of 22/min
•    Decreased air entry left side
•    Crackles left base
•    HR-104/min, regular. JVP not raised. Apical impulse 5th left intercostal space anterior axillary line.

Investigations:

•    ECG – normal
•    Chest X-Ray – complete whiteout on the left side.

(a)        What is the likely cause of his respiratory distress?

College Answer

  • Left lung collapse from
    • Perioperative blood aspiration
    • Aspiration of gastric contents
    •  Sputum

Discussion

From the examination findings, it seems his patient in respiratory distress has some sort of left-sided lung pathology and a completely normal cardiovascular examination. The JVP is not raised , so probably this is not a heart-related thing. The usual apex beat is in the mid-clavicular line, so the apex beat is actually displaced - it has moved in the direction of the quiet lung. If the lung was quiet because of some sort of space-occupying process, the mediastinum would have shifted  away from the quiet lung (eg. if there was massive haemothorax or pleural effusion).

The maxillofacial surgery is a clue. They either inhaled some blood post-operatively, have a sputum plug, have aspirated, or are suffering post-operative atelectasis.

References

Question 17.3 - 2010, Paper 1

The figure below illustrates an airway pressure waveform of a single breath during volume controlled ventilation, incorporating an end inspiratory pause and an auto- PEEP manoeuvre.

X Axis – Time in seconds
Y axis – Airway pressure in cm water

(a)        What are the factors which determine variable B?

(b)        If the delivered tidal volume was 500 ml, what is the calculated compliance?

(c)        List the change(s) you would make to the ventilator settings to treat an increase in the value of variable D.

College Answer

(a)        What are the factors which determine variable B?

Resistance, compliance, tidal volume, PEEP, insp flow rate and flow pattern

(b)        If the delivered tidal volume was 500 ml, what is the calculated compliance?

25 ml/cm water   [TV/(Plateau-PEEP)]

(c)        List the change(s) you would make to the ventilator settings to treat an increase in the value of variable D.

Increase expiratory time
Decrease I:E ratio, decrease RR, reducing MV

Discussion

This is a question interrogating the candidate's familiarity with the pressure-time curve of the ventilator.

Local resources of questionable quality exist:

a) Variable B is the peak airway pressure. This variable is determined by the lung compliance, tidal volume, airway resistance and PEEP.

To some extent the flow patern also matters (the higher the inspiratory flow, the greater the contribution from airway resistance)

b) The calculation of compliance is not something we do every day, but people should probably be at least dimly aware of the equation which is involved. Compliance is pressure required per volume of lung distension; thus one can calculate it by dividing the tidal volume by the diference between the pleateau pressure and PEEP.

c) Variable D is the Auto-PEEP. This patient is gas-trapping.

In order to address this one, one can

  • minimise PEEP
  • decrease the I:E ratio to 1:4 or so
  • increase the inspiratory rise time
  • decrease the respiratory rate
  • decrease the tidal volume

References

Question 28 - 2010, Paper 1

   A 65 year old male with a past history of ischaemic heart disease is admitted to the ICU after a motorcycle  crash having sustained  long bone fractures  of the lower limbs. He has no head, chest or abdominal injuries. Prior to surgery, his GCS was 15 and SpO2 was 98% on 4l oxygen via Hudson mask with a normal chest X-Ray.


He required prolonged operative fixation of his fractures and that was complicated by significant blood loss. Intra-operatively, he also developed increasing oxygen requirement.  On arrival in ICU, his most recent arterial blood gas on an FiO2 of 0.7 shows a PaO2 55 mmHg.

28.1.   List the differential diagnoses for his respiratory failure.

28.2.   What  assessment  and  investigations  would  you  perform  to  help  establish  the diagnosis?

College Answer

28.1.   List the differential diagnoses for his respiratory failure.

•  Iatrogenic fluid volume overload due to blood product/resuscitation fluid
•  Atelectasis/Collapse/sputum  plugging
•  Unrecognised pulmonary contusions
•  Unrecognised pneumothorax – Mech vent, line insertion
•  Aspiration at time of MBA or at intubation
•  Endobronchial intubation
•  Transfusion related acute lung injury (TRALI)
•  Cardiogenic pulmonary oedema/myocardial event
•  Fat embolism syndrome
•  Anaphylaxis 
•   PE

28.2.   What  assessment  and  investigations  would  you  perform  to  help  establish  the diagnosis?

Clinical examination –          Ensure adequate tertiary survey Detailed respiratory examination Review fluid balance and urine output
Evidence of generalised allergic reaction
FBE – Hb, WCC, eosinophilia
Coags – ongoing coagulaopathy,
CXRay  –  infiltrates,  ETT  position,  hardware,  PTx,  pleural effusions
Cardiac enzymes – TnI
ECG – ischaemic changes, arrhythmia, R heart strain
Echo cardiogram – if suspect cardiogenic component, assess
LVF, or RVF for PE
CTPA – early for PE but possible if pt delayed in ED

Bronchoscopy -   if   evidence    of     localised collapse or unexplained infiltrates

Discussion

The list of differentials for post-operative hypoxia can be a long one.

Approached systematically, a list would resemble the following:

  • Vascular/embolic causes:
    • Fat embolism
    • Pulmonary thromboembolism
    • Pulmonary oedema due to MI
  • Infectious causes:
    • Aspiration pneumonia
  • Drug-associated causes:
    • Opiate-associated respiratory depression
  • Iatrogenic causes:
    • ETT maplosition
    • TRALI
    • Atelectasis
    • Resuscitation-associated fluid overload
  • Autoimmune causes
    • Anaphylaxis
  • Traumatic causes
    • Pneumothorax
    • Cardiac tamponade
    • Pulmonary contusions

Assessment and investigations would thus follow a systematic A-B-C algorithm:

  • Assess ETT position with auscultation
  • Examine for rash of anaphylaxis and petechii of fat embolism
  • Perfrom ECG and cardiac enzymes to exclude MI
  • Perform bedside TTE to rule out tamponade, and to grossly assess cardiac filling and contractility
  • Perform CXR to exclude pneumothorax, TRALI and aspiration
  • Perform CTPA for exclude PE

References

Sellery, G. R. "A review of the causes of postoperative hypoxia." Canadian Anaesthetists’ Society Journal 15.2 (1968): 142-151.

Question 10 - 2010, Paper 2

A  63  year  old  man  was  admitted  after  a  community  cardiac  arrest.  He  is currently day 5 post admission with uncertain neurological prognosis. He developed bilateral chest infiltrates yesterday and was started on Ampicillin/Clavulanic  acid for a presumed nosocomial pneumonia.   He has subsequently become progressively hypotensive requiring moderate dose noradrenaline,  He is pyrexial  39.2C, he is anuric on dialysis  and has an ALT495U/L (<40) and a blood glucose of 2.3 mmol/L (4 – 6).

a)  List the likely causes of the pulmonary infiltrate.

b)  List likely reasons for the raised ALT.

c)  The patient has a plasma lactate of 6.2 mmol/L. What are the likely causes of the raised lactate in this patient?

College Answer

a)  List the likely causes of the pulmonary infiltrate.

•    Cardiac Failure
•    Nosocomial /aspiration Pneumonia
•    Fluid overload secondary to renal failure
•    ARDS
•    Drug reaction (less likely)

b)  List likely reasons for the raised ALT.

•    Liver ischaemia at the time of the cardiac arrest
•    Ongoing liver ischaemia with possible venous hypertension secondary to cardiac failure
•    Septic hepatic dysfunction
•    Drug reaction

c)  The patient has a plasma lactate of 6.2 mmol/L. What are the likely causes of the raised lactate in this patient?

•    Lactate overproduction
Catecholamine infusion
Low cardiac output state with global hypoperfusion

Organ ischaemia (bowel or other organ ischaemia)

Sepsis with mitochondrial dysfunction

•    Decreased lactate catabolism
Liver failure
Renal Failure (especially lactate containing dialysate)

Discussion

a) is a question about the differential diagnosis of a bilateral lung infiltrate. The college did not specify that the candidate limit themselves to a certain number of differentials.

One's approach should be systematic:

  • Vascular:
    • Pulmonary oedema
    • Diffuse alveolar haemorrhage
  • Infectious
    • Pneumonia
  • Drug-related
    • Pneumonitis
  • Inflammatory
    • ARDS
  • Iatrogenic
    • Fluid overload
  • Autoimmune
    • Vasculitis
  • Traumatic
    • CPR-associated pulmonary contusions

A raised ALT is almost always of hepatic origin. However, small 
increases in ALT activity may occur in the following situations:

  • acute kidney injury
  • myocardial infarction
  • skeletal muscle damage

Thus, this is likely ischaemic hepatitis post cardiac arrest; other differential diagnoses of liver damage apply.

Causes of raised lactate are discussed in greater detail elsewhere.

In brief, they can be structured in the following way:

Increased production

  • Poor tissue perfusion due to shock
  • Poor tissue oxygenation due to hypoxia
  • Sepsis and "mitochondrial failure"
  • Catecholamine-associated glycogenolysis

Decreased clearance

  • Hepatic failure (necrosis)
  • Decreased hepatic blood flow due to shock

References

good monograph on ALT is available from the Association for Clinical Biochemistry and Laboratory Medicine (UK)

 

Question 23 - 2010, Paper 2

With regards to High Frequency Oscillatory Ventilation (HFOV),

a. What are the indications for HFOV in the ICU? 

b.    What  ventilation   principles   should  be  considered   when  using  a  high frequency oscillator?

c.    When  using  a high  frequency  oscillator,  what  parameters  determine  thePaO2?

d.    When using the high frequency oscillator, what parameters  determine thePaCO2?

e.     Briefly outline the mechanisms of gas transport during HFOV.

College Answer

a. What are the indications for HFOV in the ICU? 
•    Oxygenation failure:        Unable to maintain FiO2 < 0.6
•     Ventilation failure:           pH < 7.25 with Vt  > 6 mls/kg and Plateau pressure > 30 cm H2O

b.    What  ventilation   principles   should  be  considered   when  using  a  high frequency oscillator?

Target pH > 7.25 -7.35
Utilise the highest possible frequency to minimise the tidal volume and only decrease for CO2 control if delta P maximal.
Aim for saturations > 88% or PaO2  > 55 mm Hg to minimise the risk of oxygen
toxicity.

c.    When  using  a high  frequency  oscillator,  what  parameters  determine  the 
PaO2?

•    Mean airway pressure.
•    FiO2.

d.    When using the high frequency oscillator, what parameters  determine the 
PaCO2?

•    Amplitude of oscillations (∆ P).
•    Frequency of oscillations.
•    Inspiratory time
•    Cuff leak

e.     Briefly outline the mechanisms of gas transport during HFOV.

Gas transport during HFOV is thought to occur via

•    Bulk flow of gas in alveolar units close to proximal airways
•    Asymmetrical velocity profiles and Taylor dispersion.
•    In addition, asymmetrical filling of adjacent alveoli (termed pendelluft) due to differing emptying times, collateral ventilation through non-airway connections and cardiogenic mixing are other postulated mechanisms.

Discussion

This is a delicate question, as it is likely that it would not be asked in the post-OSCILLATE era.

Rather, one might expect something like "critically evaluate the use of HFOV in the management of respiratory failure".

But, anyway, let us proceed.

a. What are the indications for HFOV in the ICU?

This is an area now open for debate, and the correct answer may be "none".

However, I draw upon Google searches to suggest the following indications:

  • High FiO2 requirements (arbitrarily, 50% or 70% FiO2)
  • High PEEP requirements (arbitrarily, 14mmHg or 16mmHg- levels at which alveolar distension is maximal)
  • Poor lung compliance (plateau pressures over 30mHg)
  • Bronchopleural fistula

b.    What  ventilation   principles   should  be  considered   when  using  a  high frequency oscillator?

  • Minimise FiO2, aiming for sats of 88%
  • Tolerate high CO2 to minimise leak
  • Maximise frequency and minimise tidal volume
  • Tolerate a respiratory acidosis with a pH of 7.25-7.35

c.    When  using  a high  frequency  oscillator,  what  parameters  determine  the PaO2?

  • Mean airway pressure is the driving pressure which maintains open alveoli, and is the governing principle of oxygenation in HFOV.
    • Paw largely determines lung volume, which is why it is so important (lung volume being representative of the gas exchange surface)
  • FiO2 manipulates the O2 concentration gradient between the machine and the pulmonary circulation

d.    When using the high frequency oscillator, what parameters  determine the PaCO2?

  • Amplitude of oscillation (delta P) determines the nearest thing you have to "tidal volume".
  • Frequency of oscillations determines the brevity of the "expiratory" period, and thus the lower the frequency, the better the CO2 clearance
  • Cuff leak represents the amount of gas intentionally allows to exchange (one way) with the ouside environment, and thus represents an additional mechanism of CO2 clearance.
  • Inspiratory time is the time spent by the piston in forward motion; the lower the inspiratory time, the higher the "expiratory time" and thus the higher the CO2 clearance.

e.     Briefly outline the mechanisms of gas transport during HFOV.

The college lists a series of eponymous mechanisms, which are incomprehensible to the savage.

  • Bulk flow of gas in alveolar units close to proximal airways
  • Asymmetrical velocity profiles
  • Taylor dispersion
  • Pendelluft
  • Collateral ventilation through non-airway connections and cardiogenic mixing are other postulated mechanisms.

This topic is explored elsewhere:

Additionally, an excellent free article is available. The savvy candidate will recall that a detailed knowledge of these principles is probably not expected, as the oscillators in adult ICUs worldwide are gathering layers of dust.

References

The OSCAR trial didnt find any mortality benefit

Young, Duncan, et al. "High-frequency oscillation for acute respiratory distress syndrome." New England Journal of Medicine 368.9 (2013): 806-813.

The OSCIALLATE trial found INCREASED mortality:

Ferguson, Niall D., et al. "High-frequency oscillation in early acute respiratory distress syndrome." New England Journal of Medicine 368.9 (2013): 795-805.

HFOV is only mentioned on pages 360 and 1114 of Oh's manual.

LITFL have a lucid summary .

Additionally....

Ha, Duc V., and David Johnson. "High frequency oscillatory ventilation in the management of a high output bronchopleural fistula: a case report." Canadian Journal of Anesthesia 51.1 (2004): 78-83.

Stawicki, S. P., Munish Goyal, and Babak Sarani. "Analytic reviews: high-frequency oscillatory ventilation (HFOV) and airway pressure release ventilation (APRV): a practical guide." Journal of intensive care medicine 24.4 (2009): 215-229.

Ritacca, Frank V., and Thomas E. Stewart. "Clinical review: high-frequency oscillatory ventilation in adults–a review of the literature and practical applications." Critical Care 7.5 (2003): 385.

Pillow, J. Jane. "High-frequency oscillatory ventilation: mechanisms of gas exchange and lung mechanics." Critical care medicine 33.3 (2005): S135-S141.

Question 2 - 2010, Paper 2

A 36 year old female is brought into  your Emergency Department with acute shortness of breath. She is unable to provide any history due to her tachypnoea. She is sitting upright in bed grasping the bed sides. She has a respiratory rate of 30 breaths per minute, has a GCS of 15, is afebrile and has a BP of 90/60mmHg. She is using accessory muscles. On auscultation, she has widespread expiratory wheeze spread throughout both lung fields.

a)  In addition to acute severe asthma, what other differential diagnoses of her clinical presentation should be considered?

b)  Assuming     this   patient     has     acute   severe   asthma,      list    your     initial management steps at this stage.

c)  Despite optimal medical  management,  the patient tires. Briefly outline the role of BiPAP in acute severe asthma.

d)  BiPAP fails and the patient is successfully intubated. Following intubation, airway pressures rise and the chest becomes more silent. List other interventions may you consider.

College Answer

a)  In addition to acute severe asthma, what other differential diagnoses of her clinical presentation should be considered?

Differential diagnoses

•    anaphylaxis ( large % don’t have rash etc – just bronchospasm)
•    Acute exacerbation COPD
•    central foreign body
•    acute pulmonary oedema
•     Pneumothorax
•    Hysterical hyperventilation
•    acute Pulmonary embolus

b)  Assuming     this   patient     has     acute   severe   asthma,      list    your     initial management steps at this stage.

•    Resuscitation/ investigation and definitive management
•    Initial salbutamol nebulisation – continuously. Consider IV infusion
•    IV steroids - ? type and dose .
•    Replace K/Mg
•    Nebulised adrenalin if anaphylaxis still under consideration
•    IV access, bloods including mast cell tryptase cultures/  +/- procalcitonin
•    Portable CXR to exclude pnemothorax / localised consolidation and assess hyperinflation.

c)  Despite optimal medical  management,  the patient tires. Briefly outline the role of BiPAP in acute severe asthma.

Intrinisic PEEP increases the negative intrathoracic pressure the patient must generate to trigger a breath and hence increases WOB. Application of extrinsic PEEP minimises this difference and reduces WOB. IPAP reduces the WOB associated with resistance.

d)  BiPAP fails and the patient is successfully intubated. Following intubation, airway pressures rise and the chest becomes more silent. List other interventions may you consider.

•    Another CXR to check no PTX post PPV
•    Increasing salbutamol
•    Deepen sedation
•    Adding adrenalin/ aminophylline/ ketamine/ Mg ( no evidence) – doses required by candidate
•    Volatile anaesthesia
•    Paralysis- Train of four essential .
•    ? bronchoscopy
•    Measurement of iPEEP

Discussion

a)  In addition to acute severe asthma, what other differential diagnoses of her clinical presentation should be considered?

This is a question about the differential diagnosis of wheeze.

There can be a myriad answers.

UpToDate even has a page about this sort of thing.

  • Extrathoracic causes
    • Anaphylaxis
    • Vocal cord paralysis
    • Laryngeal stenosis
    • Goiter with thoracic inlet obstruction
    • Anxiety with hyperventilation
  • Intrathoracic central airway causes
    • Tracheal stenosis
    • Mediastinal tumours
    • Hyperdynamic airway collapse due to tracehomalacia
    • Mucus plugs
    • Thoracic aortic aneurysm
    • Foreign body inhalation
  • Intrathoracic lower airway causes
    • Bronchitis or bronchiolitis
    • COPD
    • Pulmonary oedema - "cardiac asthma"
    • Airway distortion due to mechanical causes, eg. bronchial mass, bronchiectasis, pneumothorax
    • Exposure to inhaled irritant or corrosive agent, and this includes the aspiration of gastric contents

b)  Assuming     this   patient     has     acute   severe   asthma,      list    your     initial management steps at this stage.

This answer lends itself well to a systematic approach

  • The management would include an immediate attention to the ABCs, with the focus on assessment of the immediate need for intubation and maintenance of normoxia, with simultaneous brief focused history and detailed respiratory examination.
  • Airway:
    • Attention to the airway and assessment of the difficulty of intubation
    • Attention to the patency of the airway and the need for immediate intubation
  • Breathing:
    • High flow humidified oxygen, via face mask or high-flow nasal prongs
    • Continous nebulised salbutamol
    • IV hydrocortisone (100mg)
    • Transition to BiPAP with IPAP and EPAP titrated to effort of breathing
    • Commencement of salbutamol infusion if continous nebs are not helpful in correcting the bronchospasm (as the air entry may be too poor)
    • Consideration of nebulised adrenaline
  • Circulation:
    • correction of hypovolemia, to help prevent the circulatory collapse due to dynamic hyperinflation
  • Electrolyte disturbance:
    • correction of hypokalemia caused by the salbutamol
    • attention to the lactic acidosis, due to salbutamol
    • Titration of magnesium levels to 1.0-1.5mmol/L, to prevent salbutamol-associated arrhythmias
  • Suportive investigations
    • ABG
    • CXR
    • ECG
    • Full set of bloods, including electrolytes and inflammatory markers
    • Viral PCR from nasal swabs to investigate for influenza A / B
    • Procalcitonin
    • Mast cell tryptase

b)  Assuming     this   patient     has     acute   severe   asthma,      list    your     initial management steps at this stage.

The usefulness of positive pressure ventilation in people with intrinsic PEPE is discussed elsewhere.

In summary, positive pressure ventilation decreases effort of breating by applying a positive counter-pressure and thus decreasing the relative amount of intrathoracic pressure which must be generated by the patient's muscles. This decreases the work of breathing. Additionally, it splints the constricted airways, allowing improved CO2 clearance. IPAP increases the pressure gradient during inspiration, improving the flow of gas agains the resistance of the constricted airways. The tight-fitting mask ensures a consistent delivery of the prescribed FiO2.

d)  BiPAP fails and the patient is successfully intubated. Following intubation, airway pressures rise and the chest becomes more silent. List other interventions may you consider.

  • Airway:
    • Check ETT position (rule out intubation of right main bronchus)
    • Check for ETT kinking or blockage
  • Breathing:
    • Rule out pneumothorax with physical examination, bedside ultrasound or CXR
    • Sedate the patient, and paralyse them with cisatracurium
    • Ventilate with mandatory ventilaton using a low respiratory rate, square pressure waveform and low I:E ratio, 1:4 or similar
    • Consider nebulised adrenaline or small IV adrenaline boluses
    • Consider IV ketamine and IV magnesium infusions
    • Consider volatile anaesthetic agents
    • Consider Heliox
    • Consider ECMO if normoxia cannot be maintained in the face of severe bronchospasm
  • Circulation:
    • correct hypovolemia
    • Watch for dynamic hyperinflation and associated loss of preload;
      • may be necessary to disconnect the patient form the ventilator and manually decompress their chest by external pressure

References

UpToDate: Evaluation of wheezing illness other than asthma in adults

Oddo, Mauro, et al. "Management of mechanical ventilation in acute severe asthma: practical aspects." Intensive care medicine 32.4 (2006): 501-510.

Phipps, P., and C. S. Garrard. "The pulmonary physician in critical care• 12: Acute severe asthma in the intensive care unit." Thorax 58.1 (2003): 81-88.

 

Question 6.1 - 2010, Paper 2

The following data was obtained from a 30 year old spontaneously  breathing tachypnoeic individual. His GCS was15.

Test

Value

Normal Range

pH*

7.47

(7.36 –7.44)

PCO2*

30 mm Hg

(36 –44)

PAO2

60 mm Hg

PaO2

55 mm Hg

Hb

130 G/L

(130 – 150)

a)  What is the likely explanation for the above set of data?

College Answer

a)  What is the likely explanation for the above set of data?

High altitude or breathing a gas mixture containing low FiO2, the combination of a low PAO2 and a normal A-a gradient makes these the likely possibilities.

Discussion

The A-a gradient in this man is very odd. The college gives us the calculated alveolar O2 tension, and it is an oddly low number.

Furthemore, the A-a gradient is only 5, which makes one think that there is no gas exchange deficit.

So, lets leave the patient out of this and turn instead to blame the atmosphere.

Lets consider that this person's alveolar O2 partial pressure should be about 112 at 760mmHg:

PAO2 = 0.21 × (760 - 47) - (PaCO2 × 1.25) = 112.2

Irrespective of the actual alveolar O2 tension, the fraction of O2 should still be 21% if the patient is breathing room air, is not on Mars, and is not somehow actively secreting oxygen.

So, the patient is breathing a gas mixture with a decreased FiO2, for whatever reason.

One can calculate that if 60mmHg is in fact 21% of the total gas mixture, then the atmospheric pressure must be something like 285mmHg, equivalent to the pressure expected at an altitude of about 7.5km above sea level.

References

Peacock, Andrew J. "ABC of oxygen: oxygen at high altitude." BMJ: British Medical Journal 317.7165 (1998): 1063.

Question 6.2 - 2010, Paper 2

The following set of arterial blood gases were obtained from a patient admitted to the ICU after a suicide attempt.

Test

Value

Normal Range

pH*

6.84

(7.36 – 7.44)

PCO2*

94 mm Hg

(36 – 44)

PO2

140 mm Hg

P50

24 mm Hg

Standard base excess*

-16.0 mmol/L

(-2.0 – +2.0)

a)     What  anomaly  do  you  notice  in  the  blood  gas  report?  (Apart  from  the hypercapnia and the acidosis).

b)     List 2 other investigations you would perform to elucidate the cause of the anomaly.

College Answer

a)     What  anomaly  do  you  notice  in  the  blood  gas  report?  (Apart  from  the hypercapnia and the acidosis).

A left shifted curve despite a high PCO2 and a low pH.

b)     List 2 other investigations you would perform to elucidate the cause of the anomaly.

•    CoHb
•    Measure temperature
•    Measure 2,3 DPG

Discussion

This ABG represents a mixed respiratory and metabolic acidosis.

By the standard equation of CO2 to pH relationship (Change in pH = 7.40 - (pCO2 x 0.008)) the pH should be 7.04.

Thus, there is also a metabolic acidosis in play, driving the pH lower.

The anomaly, as pointed out by the college answer, is in the low p50 value.

The p50 is the partial pressure of oxygen which will result in a 50% oxygen saturation of hemoglobin.

Acidosis tends to drive this value higher; this "right shift" of the oxyhemoglobin dissociation curve is known as the Bohr effect.

In essence, the lower the pH, the lower the affinity of hemoglobin for oxygen, and the higher the partial pressure of oxygen required to saturate 50% of the hemoglobin. This facilitates the transport of oxygen out of hemoglobin and into the tissues.

Thus, a low P50 value suggests that the affinity of hemglobin for oxygen is actually quite high (because only a small amount of oxygen is required to saturate it to 50%).

This, in the context of acidosis, is odd.

Thus we come to the real question the college is asking: "What are the causes of a left-shift of the oxygen-hemoglobin dissociation curve?"

The answer is temperature and 2,3-DPG.

Hypothermia and low 2,3-DPG levels can force the curve to the left in spite of acidosis.

Additionally, the p50 can be affected by the presence of any hemoglobin type which has an altered affinity for hemoglobin, whatever the pH. These are the methemoglobins, carboxyhemoglobin, sulfhaemoglobin, foetal hemoglobin, and so on and so forth. If the proportion of such altered haemoglobin is high enough, the total oxyhemoglobin dissociation curve will look weird. The college has only opted to test for one type (COHb) and perhaps for now one should leave it at that.

Other causes of a shifted p50 are listed elsewhere.

References

LIFL have an excellent summary.

Another excellent summary of how this can be easily taught can be found at PubMed:

Julian Gomez-Cambronero "The Oxygen Dissociation Curve of Hemoglobin: Bridging the Gap between Biochemistry and Physiology." Journal of chemical education 78, no. 6 (2001): 757.

 

A specific article related to critical illness is available from CICM itself

Morgan, T. J. "The oxyhaemoglobin dissociation curve in critical illness." Critical Care and Resuscitation 1.1 (1999): 93.

 

The association of oxygen-hemoglobin dissociation and carboxyhemoglobin can be found here:

Rovida, E., et al. "Carboxyhemoglobin and oxygen affinity of human blood."Clinical chemistry 30.7 (1984): 1250-1251.

 

Seminal papers on this subject are still available.

Aberman, A., et al. "An equation for the oxygen hemoglobin dissociation curve."Journal of applied physiology 35.4 (1973): 570-571.

 

Forbes, W. H., and F. J. W. Roughton. "The equilibrium between oxygen and hæmoglobin I. The oxygen dissociation curve of dilute blood solutions." The Journal of physiology 71.3 (1931): 229-260.

Question 6.3 - 2010, Paper 2

A 58 year old woman ventilated in intensive care for a week following a motor vehicle accident was noted to drop her oxygen saturation suddenly, requiring an increase in FiO2 from 0.4 to 0.6.

The nursing staff have performed an arterial blood gas.

Test

Value

Normal Range

FiO2

0.6

pH*

7.48

(7.36 – 7.44)

PCO2

41 mm Hg

(36 – 44)

PO2

86 mm Hg

Ventilator data

Tidal Volume                        700 ml 
Respiratory rate                   14 
Peak pressures                     28 cm H2O
Plateau pressures                 18 cm H2O 
PEEP                                     7.5 cm H2O

SpO2                                        94% 
EtCO2                                      28 mm Hg

a)  What  is  the  most  likely  diagnosis  diagnosis?  List  your  reasons  for  the diagnosis.

College Answer

a)  What  is  the  most  likely  diagnosis  diagnosis?  List  your  reasons  for  the diagnosis.

The most likely diagnosis is a pulmonary embolus. The reasons are as follows:

Sudden onset of hypoxemia raises a number of possibilities – mucus plugging, pneumothorax, LVF, aspiration etc. However, the ventilation data indicate preserved compliance, normal peak pressures (argue against a pneumothorax or plugging or LVF) as well as there is increased dead space, (raised A-et CO2 gradient)

Discussion

This question is identical to Question 13.4 from the first paper of 2014. It relies on the candidate to be able to quickly perform a calculation of the A-a gradient. However, even without maths, one can arrive at the conclusion that the PO2 is way too low for an inspired fraction of 60%.

One could rabbit on about the other causes, but the ventilator data is pristine. The patient has normal peak airway pressures, so nothing is blocked, and normal plateau pressures, demonstrating reasonably normal lung compliance. This is a defect of perfusion, not ventilation.

Lastly, the candidate is presented with an end-tidal CO2 measurement, which is substantially lower than the arterial CO2 measurement, suggesting that there is a large area of lung which is not participating in gas exchange, i.e. it is dead space.

Capnometry and the arterial-expired carbon dioxide gradient is discussed elsewhere.

References

Question 9.1 - 2011, Paper 1

A 52 year old female with systemic lupus erythematosus (SLE) and worsening dyspnoea on exertion presents with the following respiratory function tests:

Test

Actual

Predicted

FEV1

1.96 litres

2.66 litres

FVC

2.52 litres

3.11  litres

FEV1/FVC

78%

85%

PEF

7.50 L/sec

6.47  L/sec

FRC

2.18 litres

2.77  litres

RV

1.08 litres

1.84  litres

TLC

3.64 litres

5.17  litres

DLco

10.4 ml/min/mmHg

24.7  ml/min/mmHg

KCO (DlCO/VA)

2.85 ml/min/mmHg

4.77  1/min/mmHg

Describe and explain the results of the respiratory function tests.
Suggest 1 possible diagnosis.

College Answer

Describe and explain the results of the respiratory function tests.
Suggest 1 possible diagnosis.

•    Moderate restrictive defect
•    High peak expiratory flow; due to fibrotic lung stretching airways open on full inspiration
•    Small  residual  volume;  due  to  cellular  infiltration  /  fibrosis  resulting  in reduced lung compliance

•    Reduced DLco (impaired gas transfer) due to both; A) Reduced lung expansion (restriction) and B) Damage to the lung parenchyma

Diagnosis: Pulmonary fibrosis.

Discussion

This question closely resembles Question 21.2 from the second 2013 paper.

However, this incarnation of the question also includes a nice diagram of the flow/volume curve.

This was abandoned in the 2013 paper probably because it is superfluous.

This question relies on some understanding of formal lung function tests. An excellent overview of this can be found in a 2005 article by Pellegrino et al.

The reduced DLCO and KCO (transfer coefficient for carbon monoxide) strongly suggests that there is a diffusion defect.

This would suggest pulmonary fibrosis.

The college also report that there is a moderate restrictive defect.

According to the 2005 ATS guidelines, a restrictive defect is defined as a TLC below the 5th percentile of the predictive, with a normal FEV1/FVC. This patient has an FEV1/FVC which is still above the 70% cut-off, and is therefore classified as "normal". The TLC percentile bands are not offered by the college, but one can see that it is well below the predicted value ( 3.64 L instead of  5.17 L).

According to the 2010 GOLD guidelines, a restrictive defect is characterised by a normal (or mildly reduced) FEV1, an FVC below 80% of predicted, and a normal (>70%) FEV1/FVC ratio. In the data above, the FVC is 81% of the predicted value, so by this standard the patient is just outside the borders of being classified as restrictive lung disease.

The major diference in this system of classification is the use of a fixed lower limit of normal (LLN), which is easier to remember and more convenient for resource-poor environments (where COPD is prevalent). Unfortunately it seems the use of such fixed cutoffs tends to incorrectly classify up to 20% of patients, particularly at the extremes of age (Miller et al, 2011). The glorious oracle of UpToDate recommends the use of computerised algorithms for predictive values, wherever they are available (i.e. using as the cutoff value the fifth percentile of the predicted FEV1/FVC ratio).

References

Pellegrino, Riccardo, et al. "Interpretative strategies for lung function tests."European Respiratory Journal 26.5 (2005): 948-968.

Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines - 2010

American Thoracic Society (ATS) guidelines for pulmonary function testing

Miller, Martin R., et al. "Interpreting lung function data using 80% predicted and fixed thresholds misclassifies more than 20% of patients." CHEST Journal 139.1 (2011): 52-59.

Question 13 - 2011, Paper 1

An  Anaesthetist   from  a  provincial  hospital  has  a  20  year  old  man  with suspected fat embolism syndrome following an isolated femoral fracture that was repaired  earlier  that day. The patient  has become  increasingly  hypoxic and  difficult  to  ventilate,  but  transfer  to  a  metropolitan  centre  has  been delayed for 12 hours due to bad weather.

His arterial blood gases on SIMV mode of ventilation are as follows: FiO2  1.0, pH 7.21, PaO2  65 mmHg (8.6 kPa), PaCO2  72 mmHg (9.3 kPa), HCO3  28 mmol/L. He has a four quadrant infiltrate on his chest X-Ray.

Outline  the advice  that you would  give to help your colleague  manage  this patient’s ventilation.

College Answer

General
•    Confirm Diagnosis
- ARDS criteria: CXR, PF ratio, Etiology, no overload

•    exclude  other etiologies  - where is the ETT (not RMB), no pneumothorax, aspiration etc.
•    What  ventilator  is  he  using,  are  you  familiar  with  it’s  modes    (such  as pressure control, volume control)
•    Ventilatory strategy –pressure and volume limitation to minimise barotrauma)
•    PEEP increments to effect, ensuring Plateau Pressure < 30 cm H20
•    Heavy  sedation   and  paralysis   to  minimize   O2  consumption   and  CO2 generation to GCS 3 and no spontaneous ventilation
•    Targets for ventilation SpO2 > 90-95 and PO2 > 60
•    permissive hypercapnia as long as pH > 7.1
•    prone position probably not appropriate (if staff not experienced)
•    recruitment manoeuvres

Fluids
-CVP only to ~PEEP+2 as maximum
- consider frusemide if CVP PEEP +5
-use inotrope to maintain MAP > 60 - suggest noradrenaline
-Transfuse only for Hb approaching 7

•    Reassure him and make yourself available for advice 24/7 (Mention of NO, liquid ventilation, surfactant, TGI – no role in this setting)

Discussion

This is a pretty realistic scenario; as if you were on call and managing a patient over the phone, giving advice to your registrar.

The patient is acidotic, hypoxic and hypercapneic.

What do you do?..

Supportive management:

  • Confirm that the ETT is in the right position and is not blocked up with secretions
  • Confirm diagnosis of ARDS by performing a TTE, looking for significant cardiac dysfunction
  • Exclude immediately reversible problems, eg. pneumothorax

Specific ARDS ventilation strategies and supportive non-ventilation strategies:

Initial ventilator strategy:

Additional ventilator manoeuvres to improve oxygenation:

Non-ventilator adjunctive therapies for ARDS:

Ventilator strategies to manage refractory hypoxia

  • Prone ventilation, for at least 16 hours a day (PROSEVA, 2013)
  • High frequency oscillatory ventilation may not improve mortality among all-comers (OSCAR, 2013) or it may actually increase mortality (OSCILLATE, 2013) but some authors feel that there were problems with methodology.

Non-ventilator adjuncts to manage refractory hypoxia

  • Nitric oxide was a cause for some excitement, but is no longer recommended.
  • Prostacyclin is still a cause for excitement, and is still vaguely recommended.
    • Neither agent improves mortality, but prostacyclin can improve oxygenation.
  • ECMO may improve survival (CESAR, 2009) but again there were problems with methodology.
  •  

Note how useless it would have been to digress into specifics of management for fat embolism syndrome.

References

Question 30 - 2011, Paper 1

(A) List 2 causes for this end-tidal CO2 pattern.

(B) List 2 causes for this end-tidal CO2 pattern

(C) Draw and label a pressure-time ventilator waveform showing-

(i) normal followed by
(ii) increased airway resistance.

(D) Draw and label a pressure-volume loop (volume targeted ventilation) showing-

(i) normal lung compliance
(ii) decreased lung compliance
(iii) increased lung compliance.

(E) Draw and label the following for a patient with a large cuff leak-

(i) Flow-time waveform
(ii) Volume-time waveform

College Answer

(A) List 2 causes for this end-tidal CO2 pattern.

♦  Kinked/partially occluded tube
♦  Foreign body in airway
♦  Obstruction of expiratory limb of breathing circuit
♦   Bronchospasm

(B) List 2 causes for this end-tidal CO2 pattern

♦  Decreased respiratory rate
♦  Decreased tidal volume
♦  Increasing metabolic rate (fever, shivering, etc)

(C) Draw and label a pressure-time ventilator waveform showing- (i) normal followed by
(ii) increased airway resistance.

pressure-time waveform from Question 30 - Paper 1 of 2011

(D) Draw and label a pressure-volume loop (volume targeted ventilation) showing-

(i) normal lung compliance
(ii) decreased lung compliance
(iii) increased lung compliance.

pressure-volume loop from Question 30 - Paper 1 of 2011

(E) Draw and label the following for a patient with a large cuff leak-

(i) Flow-time waveform
(ii) Volume-time waveform

flow and volume-time waveform from Question 30 - Paper 1 of 2011

Discussion

Helpfully, the college answer provides us with some model diagrams. Unhelpfully, the college question omits the EtCO2 curves. I have tried to put together some EtCO2 curves to remedy this. So long as everybody is aware that this is not the college image.

Though this is a simple pattern recognition question, some references seem in order. The following local chapters discuss waveform interpretation:

End-tidal CO2 patterns are also discussed on this website by Carefusion.

References

Question 14 - 2011, Paper 2

A 44-year-old man with morbid obesity (BMI 68 kg/m2 ) presents to the Emergency Department with respiratory failure. He is obtunded with an arterial blood gas (ABG) showing

  • pH 7.25,
  • pCO2 75 mmHg (10kPa),
  • PO2 53 mmHg (7 kPa),
  • HCO3 32 mmol/L on FiO2 0.3.

Chext X-Ray reveals cardiomegaly and clear lung fields.
Describe your management of this problem for the first 24 hours.

College Answer

Management includes simultaneous resuscitation and assessment with history and examination,
investigations, (appropriate and interpreted) and ongoing fluid therapy (including triage, monitoring,
pharmacology and non-pharmacological interventions).


ABG information given confirms type 1 and type 2 respiratory failure.


Cardiomegaly may relate to AP portable semi-erect film but cardiomyopathy and ?pericardial effusion
should be considered.


Other causes of decreased conscious state in addition to hypercapnia and hypoxia should be
considered, such as drug toxicity, metabolic / endocrine / electrolyte disturbances.


Resuscitation consists of ensuring adequate airway, ventilatory support as needed, ensuring
adequate circulation and assessment of other, readily reversible causes of decreased conscious state
such as opiates, hypoglycaemia.


Airway support may be by simple measures such as positioning and airway adjuncts as needed and
conscious level permits (nasopharyngeal airway better tolerated than oropharyngeal).


NIV if maintaining airway and protective reflexes present but invasive ventilation if NIV not appropriate
or fails.


Assessment of difficulty of intubation. Invasive ventilation potentially hazardous given morbid obesity.
Appropriate ventilator settings accepting high peak pressures needed to overcome chest wall mass
and intra-abdominal pressure (transpulmonary pressure [Palveolar – Pintrapleural pressure] will be
normal).


History and examination should suggest/exclude any diagnoses including: ischaemic heart disease,
cardiac failure (left and right), COAD, venous thromboembolism, respiratory tract infection, CNS
disorder (Stroke, haemorrhage), diabetic conditions, any other endocrine problems eg
hypothyroidism, and potential for drug related problems.


Simple investigations should be ordered and reviewed to assist above differential diagnosis and assist
treatment (FBC U&E, blood sugar, ECG)


Specific treatment should be directed at clinical suspicions and continued supportive treatment with
ventilatory and haemodynamic support,


General treatment of ICU patient with nutritional support, ulcer prophylaxis, thromboprophylaxis and
sedation/analgesia with modification of doses for morbid obesity.

Additional considerations for management of morbidly obese ICU patient - special beds, hoists,
difficulty with procedures, pressure area care, increased risk of complications.

Discussion

This question does not seem to stem from any specific guidelines.

 Let us deconstruct the gospel answer.

"Management includes simultaneous resuscitation and assessment with history and examination,
investigations, (appropriate and interpreted) and ongoing fluid therapy (including triage, monitoring, pharmacology and non-pharmacological interventions). "

This can be viewed as a "motherhood statement". No examiner would disagree with the fact that management should include triage, history, examination, investigations, and simultaneous management of emergent problems.

The next parts of the answer deal with the ABG result. Yes, its acute on chronic hypercapnic respiratory failure, and the patient is hypoxic; but could there be any other reason for this obtundation?

Drug toxicity, metabolic endocrine and electrolyte disturbances are mentioned.

The answer then moves on to airway support and NIV, mentioning the use of simple airway adjuncts and the airway reflex protection caveat for NIV before discussing the difficulty of intubation.

Thus, one might say:

  1. - Assess airway patency;
  2. - if airway is not protected, introduce simple airway devices and assess their effect on airway patency
  3. - if airway reflexes are intact, commence NIV paying attention to the dangers of the high pressures which will be required in an obese patient
  4. - if airway reflexes are intact, assess for intubation and solicit expert help for intubation.
  5. - assess any rapidly reversible causes of obtundation such as opioid intoxication and hypo/hyperglycaemia
  6. - if no rapidly reversible cause is found, mechanical ventilation must commence while the process of investigation continues
  7. - once airway patency is established and some form of mechanical ventilation is in progress, other causes for the reduced level of consciousness must be pursued and managed, including intracranial causes, thromboembolism, electrolyte abnormalities, cardiac failure, hypothyroidism etc.
  8. - at the same time, management of the possible causes of hypercapneic respiratory failure must commence (therapies specifically directed at COPD and OSA)
  9. - at the same time, standard management protocols for the care of an obese ICU patient must be followed, including thromboprophylaxis, pressure area care, the use of specialised bariatric equipment, and ulcer prophylaxis.

References

One struggles to find references for something like this.

l can only refer to the Oh's Manual chapter 26 (acute respiratory failure in COPD).

 

Question 17 - 2011, Paper 2

You are asked to admit a 48-year-old woman for the management of respiratory failure, who received an allogeneic bone marrow transplant 2 weeks ago for acute myeloid leukaemia. A Chest X-Ray demonstrates a diffuse pulmonary infiltrate.

Initial observations

  • GCS 14
  • Temp 38.4 ºC
  • PR 140 /min, BP 90/40mm Hg
  • RR 35, SaO²
  • 88% on 10 lpm O²

.
The full blood count report from yesterday is at the bedside.

  • Hb 68 g/L
  • WCC 0.2 No differential
  • Plt 39

Comment - Occasional tear drops, Occasional elliptocytes, Occasional lymphocyte and
neutrophil seen.


a) List your differential diagnosis for the respiratory failure

b) List your immediate management priorities (i.e. within the first two hours) of the patient on admission to ICU

College Answer

a) List your differential diagnosis for the respiratory failure

Infective – Severe sepsis in a patient with pancytopenia and agranulocytosis
Nosocomial pneumonia
– Bacterial –Gm negative –e.coli, Pseudomonas, Klebsiella,
– Gm positive –Strep, Staph epi
– Fungal -Aspergillus, Candida, Cryptococcus
– Atypical – Legionella, mycoplasma
– Viral –CMV, HSV, RSV, Influenza, H1N1, VZV
– PCP, toxoplasmosis
– TB (depending on background)
Sepsis due to other site and ARDS

Non- infective
- Idiopathic pneumonia syndrome
- Cardiac failure (cardiotoxicity due to induction chemo)
- Diffuse alveolar haemorrhage
- GVH – too early unless this is second graft
- Non cardiogenic capillary leak syndrome
- Chemo induced ALI / pneumonitis (methotrexate)
- TRALI
- Fluid overload

b) List your immediate management priorities (i.e. within the first two hours) of the patient on admission to ICU

Hypoxic respiratory failure
Non-invasive respiratory support commencing with CPAP progressing to BiPAP / invasive ventilation
as indicated

Circulatory support
Judicious fluid resuscitation +/- inotropes to restore circulation
Central access with platelet cover

Severe sepsis
Early commencement of broad-spectrum antibiotic cover or, if already on antibiotics, review existing
microbiology results, antibiotic duration and broaden or target antibiotic cover and add antifungal
therapy
Review and consider removal of existing indwelling vascular devices

Pancytopenia with agranulocytosis
Reverse barrier nursing in single room
Transfusion of blood products

Investigations
CXR, ABG, Biochemistry, FBC, coagulation profile, blood cultures, sputum, urine MC&S, viral
serology, echo

Discussions re prognosis
Liaison with treating haematologist to ascertain likely outcome from primary disease and BMT and
also discuss with patient and family high risk of deterioration and mortality

Discussion

This question refers to the management of neutropenic sepsis in the ICU. It asks: what organisms are likely to be causing pneumonia or ARDS in a neutropenic patient? And what are you going to do about it?

 This is a pre-engraftment patient with neutropenic sepsis. One can already generate a list of differentials for which pathogens are likely to be active here. Hint: its pretty much all of them. One could not go too wrong simply regurgitating a list of pathogens.

The non-infectious causes of widespread pulmonary infiltrate and shock are also a standard panel.

The management within the first two hours is a reference to the Surviving Sepsis campaign recommendations.

The management of hypoxic respiratory failure here begs a mention of NIV, and its mortality-reducing utility in this setting.

The establishment of central venous access should occur with platelet cover; then, one may pursue goal-directed resuscitation with vasopressors and fluids.

The removal of old lines is a part of source control and should also be mentioned

The commencement of early antibiotics should be mentioned, with the emphasis on "early"; one ought to also mention the collection of multiple blood culture specimens.

A responsible candidate will also rattle off a list of investigations, mention the need for blood products, and comment on the usefulness of a haematologist in the management of a haematology patient.

Ultimately, the prognosis for these people is very poor, and the answer should finish with a call to contact the family and discuss the potential need to set treatment limitation.

References

Here is a list of references from my notes on sepsis in the immunocompromised host, and specifically in the bone marrow transplant recipient:

Leather HL, Wingard JR. Infections following hematopoietic stem cell transplantation. Infect Dis Clin North Am. Jun 2001;15(2):483-520.

Thiéry G, Azoulay E, Darmon M, Ciroldi M, De Miranda S, Lévy V, Fieux F, Moreau D, Le Gall JR, Schlemmer B. Outcome of cancer patients considered for intensive care unit admission: a hospital-wide prospective study. J Clin Oncol. 2005 Jul 1;23(19):4406-13.

Hilbert, Gilles, et al. "Noninvasive ventilation in immunosuppressed patients with pulmonary infiltrates, fever, and acute respiratory failure." New England Journal of Medicine 344.7 (2001): 481-487.

Antonelli M, Conti G, Rocco M, et al. A comparison of noninvasive positive-pressure ventilation and conventional mechanical ventilation in patients with acute respiratory failure. N Engl J Med 1998;339:429-435

Afessa, Bekele, and Elie Azoulay. "Critical care of the hematopoietic stem cell transplant recipient." Critical care clinics 26.1 (2010): 133.

Soubani AO, Kseibi E, Bander JJ, et al. Outcome and prognostic factors of hematopoietic stem cell transplantation recipients admitted to a medical ICU. Chest 2004;126(5):1604–11.

Scales, Damon C., et al. "Intensive care outcomes in bone marrow transplant recipients: a population-based cohort analysis." Crit Care 12.3 (2008): R77.

 

Question 2 - 2012, Paper 1

You are asked to assist and help in the emergency management of a 69-year-old who presented to your emergency department with massive haemoptysis.

a) List six major disease categories that cause massive haemoptysis and give one example of each.

b) Outline the emergency management of massive haemoptysis.

College Answer

a) Major disease categories

  • Infective – lung abscess, TB, Bronchiectasis, Fungal, Necrotising pneumonia
  • Neoplastic - primary or secondaries
  • Cardiac – Mitral Stenosis, Congenital heart Disease, Tricuspid Endocardidis
  • Vascular – Pulmonary embolism, Pulmonary infaction, Pulm Hxt, AVM
  • Systemic Disease – Wegeners, Goodpastures, SLE and other causes of vasculitis
  • Haematological – Any severe coagulopathy including acquired causes – DIC, drugs etc
  • Iatrogenic/Post Surgical – Swann Ganz, Pulmonary procedures
  • Trauma – blunt or penetrating injury, tracheo-innominate artery fistula, ruptured bronchus

b) Emergency management

  • Manage ABC, volume resuscitate
  • Correct coagulopathy if relevant
  • Role of intubation- life- threatening i.e. airway compromise, desaturation or shock. Maybe required if intervention planned
  • How to intubate- large size tube (>7.5) if possible so fibre optic bronchoscopy can be performed if needed, single lumen if life threatening, consider double lumen if controlled circumstances and unilateral pathology
  • Post intubation- can be nursed lateral decubitus with bleeding lung down to prevent soiling of non-bleeding lung
  • Role of bronchoscopy – rigid or flexible – may be needed urgently to place balloon tipped catheter endobronchially to tamponade bleeding
  • Bronchial artery embolization- effective non-surgical management
  • Surgery- lobectomy or pneumonectomy after resuscitation if other measures fail or not available or for etiologies like A- V malformations, trauma, extensive fungal abscess
  • Antimicrobial therapy for underlying infective causes
  • Immunosuppression therapy for underlying vasculitis
 

Discussion

This question interrogates the candidate's ability to form differentials, and then exposes their understanding of pulmonary haemorrhage management.

The list of differentials presented by the college is exhaustive. However, an even more insane list is presented in the article on the role of bronchoscopy in the management of masive haemoptysis. I reproduce this table here:

Causes of Haemoptysis

Infectious

  • Mycobacteria (particularly tuberculosis)
  • Fungal infections (including mycetoma)
  • Necrotizing pneumonia and lung abscess (Klebsiella pneumoniae, Pseudomonas aeruginosa,Staphylococcus aureus, Streptococcus pneumoniae, other Streptococcus spp. and Actinomyces spp.)
  • Bacterial endocarditis with septic emboli
  • Parasitic (paragonimiasis, hydatid cyst)

Neoplastic

  • Bronchogenic carcinoma
  • Endobronchial tumors (carcinoid, adenoid cystic carcinoma)
  • Pulmonary metastases
  • Sarcoma

Pulmonary

  • Bronchiectasis (including cystic fibrosis)
  • Chronic bronchitis
  • Alveolar hemorrhage and underlying causes

Vascular

  • Pulmonary artery aneurysm (Rasmussen aneurysm, mycotic, arteritis)
  • Bronchial artery aneurysm
  • Pulmonary infarct (embolism)
  • Pulmonary hypertension
  • Congenital cardiac or pulmonary vascular malformations
  • Airway-vascular fistula
  • Arteriovenous malformations
  • Mitral stenosis
  • Left-ventricular failure

Vasculitis

  • Wegener's granulomatosis
  • Goodpasture's syndrome
  • Behçet's disease
  • Systemic lupus erythematosus

Trauma

  • Induced by diagnostic bronchoscopy (brushing/biopsy)
  • Related to interventional pulmonology procedures (dilation, metallic stent placement, high-dose brachytherapy)
  • Catheter-induced PA rupture
  • Blunt or penetrating chest injury
  • Transtracheal procedures

Hematological

  • Coagulopathy (congenital, acquired or iatrogenic)
  • Platelet disorders

Drugs and toxins

  • Penicillamine
  • Solvents
  • Crack cocaine
  • Trimellitic anhydride
  • Bevacizumab

Miscellaneous

  • Endometriosis
  • Lymphangioleiomatosis
  • Broncholithiasis
  • Cryptogenic
  • Foreign body aspiration
  • Lung transplantation

As for the management: the college answer is complete but could be arranged in a more eye-pleasing fashion.

1) Control the airway.

  • Intubate the patient with a large-bore tube to permit bronchoscopy
  • If you are skilled and the pathology is unilateral, a dual-lumen tube could be considered

2) Control the breathing.

  • Ventilate the patient with the bad lung dependent, to prevent contralateral lung soiling.
  • Increase the PEEP, to get the benefit of whatever tamponade effect it might provide.

3) Control the circulation.

  • Replace the lost blood and stabilise the hemodynamic variables

4) Control the bleeding

  • Reverse any coagulopathy
  • Perform bronchoscopy
    • Suck out any obvious clots
    • Place a balloon-tipped catheter to put pressure on the bleeder
    • Burn the bleeder with argon plasma (if you have the tools)
  • Perform angio-embolisation if bleeding is not controlled
  • Send the patient to thoracotomy if angio-embolisation is impossible

5) Control the cause

  • Antibiotics for tuberculosis and fungal abscesses
  • Surgery or radiotherapy for cancers
  • Immunosuppression for vasculitis
  • Surgery for AVMs

Angio-embolisation is a pretty cool modality, with a low complication rate.

References

Adlakha, Amit, et al. "LONG-TERM OUTCOME OF BRONCHIAL ARTERY EMBOLISATION (BAE) FOR MASSIVE HAEMOPTYSIS.Thorax (2011).

 

Talwar, D., et al. "Massive hemoptysis in a respiratory ICU: causes, interventions and outcomes-Indian study." Critical Care 16.Suppl 1 (2012): P81.

 

Sakr, L., and H. Dutau. "Massive hemoptysis: an update on the role of bronchoscopy in diagnosis and management." Respiration 80.1 (2010): 38-58.

Question 5.1 - 2012, Paper 1

Figure 1:

flow%20waveform%20with%20bubbling%20secretions.jpg

a) Give a cause for the abnormality seen in the expiratory phase of the waveforms in figure 1.

College Answer

a) Either of the following answers acceptable 
• Water in circuit 
• Secretions in trachea or circuit 

 

Discussion

This is a pattern recognition question which relies on the candidate's familiarity with troubleshooting equipment. Unfortunately, the college has removed the images, so nobody can recognise the patterns, but we've all seen this, surely. 

The expiratory waveform which is described in (a) probably looks like this, and represents the bubbling of fluid in the airway or in the ventilator circuit.

The picture I used to replace Figure 1 is duplicated from an excellent paper by Correger et al, which actually summarises all sorts of useful ventilator waveform patterns. It is an important resource.

References

Correger, E., et al. "Interpretation of ventilator curves in patients with acute respiratory failure." Medicina Intensiva (English Edition) 36.4 (2012): 294-306.

Question 10 - 2012, Paper 1

Outline the potential mechanisms of ventilator associated lung injury in patients with Acute Respiratory Distress Syndrome and the steps that can be taken to minimise them.

College Answer

Injury

Mechanism

Minimisation Strategy

Volutrauma

Non-homogenous lung injury 
Over-distension of normal alveolar units to trans- pulmonary pressures above ~30 cm H2O (that corresponds to approximate total lung volume) 
causes basement membrane stretch and stress on intracellular junctions.

Avoid over-distending the “baby lung” of ARDS:


(a) Maintain Plateau Airway 
pressure under 30 cm H20


(b) Use Tidal volumes 6ml/kg (4- 8ml/kg)


Good evidence to support this 
strategy (ARDSNet)

Barotrauma

Increasing the trans-pulmonary pressures above 
50 cm H2O will cause disruption of the basement 
membranes with classical barotrauma

Biotrauma

Mechanotransduction and tissue disruption leads to upregulation and release of chemokines and 
cytokines with subsequent WBC attraction and activation resulting in pulmonary and systemic inflammatory response and multi-organ dysfunction

Protective lung ventilation 
strategies


?Use of neuromuscular blockers 
may ameliorate

Recruitment / 
Derecruitment Injury

The weight of the oedematous lung in ARDS contributes to collapse of the dependant portions of the lung 
Repetitive opening and closing of these alveoli with tidal ventilation will contribute to lung injury.

Consider recruiting collapsed lung +/- employing an open lung ventilation strategy. 
This may be achieved by: 
(a) Ventilation strategies: Sigh / APRV / “Higher PEEP” 
(b) A recruitment manoeuvres: e.g. CPAP 40/40, or stepwise PCV (c) Prone Positioning (gravitational recruitment manoeuvre) Good theoretical support and case series / few trials inconclusive 
outcomes

Shearing 
injury

 This occurs at junction of the collapsed lung and ventilated lung. The ventilated alveoli move against the relatively fixed collapsed lung with high shearing force and subsequent injury.

Oxygen 
toxicity

Higher than necessary FiO2 overcomes the ability of the cells to deal with free oxygen free radicals and leads to oxygen related free radical related 
lung injury. High FiO2 may contribute to collapse through absorption atelectasis.

Limit FiO2 through the use of 
recruitment, higher PEEP and 
accepting SaO2 / PaO2 that 
correspond the the “shoulder” of the oxyhaemoglobin dissociation curve (SaO2 88-94)

Discussion

This question interrogates one's understanding of ARDS ventilation strategies.

Its difficult to add to the already comprehensive list of answers provided by the college.

Here is a good review article on ventilator-associated lung injury in general.

more recent discussion is also available.

The combination of these two articles was the source of my own summary, which was supposed to trim the theoretical fat away, and leave behind dry factual bones... Pity it never turns out like that. I think the word count of this "summary" far exceeds the combined word count of both the publications.

References

Rocco PR, Dos Santos C, Pelosi P. Pathophysiology of ventilator-associated lung injury. Curr Opin Anaesthesiol. 2012 Apr;25(2):123-30

 

Caironi P et al, Lung opening and closing during ventilation of acute respiratory distress syndrome. Am J Respir Crit Care Med. 2010;181(6):578.

 

The Acute Respiratory Distress Syndrome Network.Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301.

 

Brower RG, Lanken PN, MacIntyre N, et al: Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 351:327–336, 2004.

 

Pinhu, Liao, et al. "Ventilator-associated lung injury." The Lancet 361.9354 (2003): 332-340.

 

Tremblay, Lorraine N., and Arthur S. Slutsky. "Ventilator-induced lung injury: from the bench to the bedside." Applied Physiology in Intensive Care Medicine 1. Springer Berlin Heidelberg, 2012. 343-352.

Question 5 - 2012, Paper 2

Critically evaluate the role of thrombolytic therapy in massive pulmonary embolism.

 

College Answer

1.  Define the rationale for thrombolysis

Standard therapy for pulmonary embolism is anticoagulation, which prevents additional thrombus from forming, but does not directly dissolve the clot that already exists. Thrombolysis theoretically gives primary treatment as it dissolves fibrin

2.  Define massive PE

Massive PE has traditionally been used to describe clot burden on radiology, but this was of little use clinically. Massive PE is more conventionally defined as a cardiogenic shock or SBP <90mmHg due to PE, either confirmed or strongly suspected on clinical grounds.

3.  Discuss the evidence in massive PE

The evidence for thrombolysis to improve mortality in massive PE is not strong, but there is a trend towards improved mortality and resolution of shock with thrombolysis. Most guidelines advocate the use of thrombolysis unless absolutely contraindicated i.e. intracranial haemorrhage

4.  Discuss the other options if thrombolysis can’t be done in massive PE

If thrombolysis is not possible or contraindicated then the other options for massive PE are surgical embolectomy or catheter embolectomy and fragmentation.

5.  Statement of candidate’s approach to thrombolysis in massive PE

Discussion

This is one of those "critically evaluate" questions; a structured approach is favoured:

Introduction

Massive PE is defined as a pulmonary embolism of sufficient size to cause systemic arterial hypotension. A submassive PE, in contrast, is one which only causes right heart dysfunction, without obstructive shock.

Rationale for thrombolysis

  • Thrombolysis may decrease clot burden, in addition to what anticoagulation alone can accomplish.
  • This may lead to the improvement of pulmonary blood flow
  • Systemic haemodynamics may improve
  • A long-term benefor of thrombolysis is the prevention of severe pulmonary hypertension which inevitably develops in the wake of large scale pulmonary emboli.

Evidence for benefits

Evidence for risks

  • In the same meta-analysis, it was found that in comparison to heparin alone thrombolysis doubles the risk of major bleeding from 12% to 22% (which makes some sort of perverse sense, as it tends to halve PE-associated mortality).
  • Real-world registry data suggests that this risk of bleeding is probably underestimated by clinical trial data, given how spotlessly perfect their patient selection is (whereas at the coalface, in the ED and ICU, a fair few patients are retrospectively, posthumously, discovered to have had some contraindication to thrombolysis).
  • In short, the risk of death from bleeding is significant, and should be presented to the patient and family as a real possibility.

Alternative treatments

  • Surgical embolectomy is a possibility, but good outcomes are only seen when a strong and organised purpose-built team is looking after the process, rather than some ad-hoc on-call cardiothoracic surgeon. Furthermore, the patients need to be carefully selected, and the sort of patient most in need of embolectomy are also the patients least likely to be selected for surgery (i.e. they are in florid cardiogenic shock, or worse yet they failed thrombolysis and are now full of alteplase).
  • Clot fragmentation,
  • Catheter embolectomy
  • Catheter-directed thrombolysis

Conclusion

Thrombolysis is an important and potentially lifesaving step in the management of massive PE. If the patient does not meet criteria for thrombolysis, urgent percutaneous or open surgical embolectomy should be considered.

References

Kucher, Nils, et al. "Massive pulmonary embolism." Circulation 113.4 (2006): 577-582.

Jerjes-Sanchez, Carlos, et al. "Streptokinase and heparin versus heparin alone in massive pulmonary embolism: a randomized controlled trial." Journal of thrombosis and thrombolysis 2.3 (1995): 227-229.

Kucher, Nils, and Samuel Z. Goldhaber. "Management of massive pulmonary embolism." Circulation 112.2 (2005): e28-e32.

Wan, Susan, et al. "Thrombolysis compared with heparin for the initial treatment of pulmonary embolism a meta-analysis of the randomized controlled trials." Circulation 110.6 (2004): 744-749.

Kasper, Wolfgang, et al. "Management strategies and determinants of outcome in acute major pulmonary embolism: results of a multicenter registry." Journal of the American College of Cardiology 30.5 (1997): 1165-1171.

Question 15.2 - 2012, Paper 2

The image below is of a 76-year-old lady who presents with dyspnoea

(The college did not include a picture. A suitable replacement image has been found by Google search, and the source file can be viewed here. )

  • List three abnormalities on observation.
  • What are two likely causes of her dyspnoea?

College Answer

a)

Previous Right mastectomy

Marked erythema left breast and anterior chest wall on right

2 Ulcerated lesions on the anterior chest wall near the axilla

Ectatic vessels of chest wall

b)

Radiation induced tissue injury with radiation induced pulmonary fibrosis

Superimposed Infection

Tumour recurrence / lymphangitis carcinomatosis

Discussion

Sorry people; I could find no image with ectatic vessels. It is difficult to add anything more to the college answer. One could also consider direct tumour invasion of the chest wall and pleura, superior vena cava obstruction by metastasis, and pleural effusion (it is surprising that the college did not come up with that one, as it is the most likely cause of dyspnoea in the cancer patient). Pulmonary embolism would also have to be on the list.

References

Question 27 - 2012, Paper 2

A 20-year-old, 80 kg man presents to the ED with acute severe asthma. In ED he has a respiratory arrest and is intubated. He is then transferred to your ICU with the following ventilator settings:

  • Mode                          SIMV 
  • FiO2                           1.0 
  • Vt                                500 ml
  • Respiratory rate        16 breaths/min 
  • Inspiratory flow         20 litres per min 
  • PEEP                         5 cmH2O

He has a tachycardia 130 bpm and a BP of 80/60. Arterial blood gas analysis shows pH 7.1, PCO2 93 mmHg (12.3 kPa), PO2 69 mmHg (9.0 kPa), HCO3 28 mmol/L SaO2 90%.

  • What additional measurements would you take to assist ventilator management?
  • Comment on the ventilator settings, and describe what change (if any) you would make in each case.
  • List the likely causes of this patient’s hypotension

College Answer

a)

Peak pressure, plateau pressure and total PEEP (auto PEEP and intrinsic PEEP acceptable terms)

b) SIMV

Leave unchanged. No benefit for PCV, and risks of hyperinflation with rapid changes in resistance. Will need sedation and probably paralysis to tolerate. (If candidates change to PCV must explain risks)

FiO2 
Obviously, leave.

Vt 
Probably satisfactory; may be able to increase Vt if necessary to help control pCO2

(allowing for adequate expiratory time); “lung protective” strategy not strictly necessary for this situation. High PCO2 most probably relates to gas trapping and is best controlled by changes in flow rate and respiratory rate.

Rate

16 b/min is too high. The hypotension suggests significant dynamic hyperinflation. Rate should be immediately reduced to 10 or fewer. This rate with Inspiratory flow rate of 20 L/min and Vt 500 ml gives I:E of 1:1.5. I:E should be 1:3. Optimal respiratory rate to limit hypercapnia is balance between that which limits gas trapping (lower rate) and that which limits hypoventilation (higher rate)

Inspiratory flow

20 L/min is too low, causing prolonged inspiratory time (1.5 sec for Vt 500 ml). Flow should be adjusted up to minimise inspiratory time. Peak pressure will rise, but this should be tolerated so long as plateau pressure is safe.

PEEP 
Extrinsic PEEP in this situation is controversial.

b)

  • Dynamic hyperinflation
  • Tension pneumothorax
  • Hypovolaemia – unlikely as sole cause but may be a contributing factor
  • Myocardial depression from intubating / sedating drugs
  • R ventricular dysfunction secondary to lung pathology with septal shift compromising L ventricular function
  • Sepsis possible

Discussion

The patient is hypoxic, hypercapneic, and hypotensive.

What additional measurements would you take to assist ventilator management?

  • Expiratory hold manoeuvre to assess autoPEEP
  • Expiratory flow waveform analysis to assess for gas trapping
  • Inspiratory hold manoeuvre to assess the contribution of airway resistance to peak pressure (an indirect way of assessing the resposne to bronchodilators)
  • Plateau pressure to assess actual lung compliance
  • CXR to look for pneumothorax

Comment on the ventilator settings, and describe what change (if any) you would make in each case.

  • Mode                          SIMV
  • Leave this alone; SIMV is appropriate givent that you are about to paralyse the patient
  • FiO2                           1.0
  • Leave this alone; 100% FiO2 is appropriate given the level of hypoxia
  • Vt                                500 ml
  • This may be too low, and may need to be up-titrated depending on the plateau pressure
  • Respiratory rate        16 breaths/min
  • This is probably too fast, and needs to be decreased to allow for CO2 clearance. One may even need to adjust the I:E ratio to allow a longer expiratory phase
  • Inspiratory flow         20 litres per min
  • This is probably too low, and needs to be increased to decrease the inspiratory time (so that more time is allowed for expiration)
  • PEEP                         5 cmH2O
  • The optimal PEEP is difficult to assess - the patient is intubated and so there is no point trying to counteract intrinsic PEEP with extrinsic PEEP, as the respiratory effort now belongs to the ventilator (lets say the patient is paralysed). All one can say is that high PEEP is not indicated, and may be counterproductive in the setting of such hypotension.

List the likely causes of this patient’s hypotension

  • Hypovolemia due to decreased oral intake, associated with worsening asthma symptoms prior to presentation
  • AutoPEEP(dynamic hyperinflation) resulting in decreased venous return to the heart
  • Tension pneumothorax
  • Right heart failure
  • Sepsis
  • PE

References

This reference seems almost tailor-made for this topic:

Oddo, Mauro, et al. "Management of mechanical ventilation in acute severe asthma: practical aspects." Intensive care medicine 32.4 (2006): 501-510.

Question 29 - 2012, Paper 2

You are called to the Emergency Department to assist in the management of a 45-year-old man with respiratory distress. He is a known HIV patient with Pneumocystis jiroveci pneumonia and an allergy to sulphonamides.

On examination: 
Temperature 38.8ºC 
Mucous membranes appear cyanotic

Respiratory rate 35/min 
Heart rate 125/min

Blood pressure 90/50 mmHg 
SpO2 82% on 8L/min oxygen via Hudson mask

Initial arterial blood gas analysis (ABG) is as follows:

Parameter

Result

Normal Range

pH

7.32

7.35 – 7.45

PCO2

27.6 mmHg (3.6 kPa)

35 – 45 (4.6 – 6.0)

PO2

84.6 mmHg (11 kPa)

HCO3

13.9 mmol/L

22 – 27

Standard Base Excess

11.0

-2 – +2

Hb

62 G/L

110 – 165

SpO2

93.4%

FCOHb

0.5%

FHHb

5.4%

FMetHb

18.4%

FO2Hb

75.7%

  • Interpret the ABG report.
  • What is the likely diagnosis?
  • Outline your management of this patient

College Answer

a)

ABG:

Metabolic acidosis 
Respiratory compensation

Anaemia 
Marked MetHb

b) 
What is the likely diagnosis?

Drug related (dapsone as known sensitivity to sulphonamides) methaemoglobinaemia. Haemolytic anaemia likely in this setting

c) 
Outline your management of this patient

ABCs.

Empirical antimicrobial therapy until sepsis is excluded

Cease Dapsone

Use ABG with co-oximetry rather than pulse oximetry in the initial period to monitor response. Oximeter will not be reliable due to MetHb so there will be a reliance on clinical signs and gases.

Optimize tissue oxygen delivery – evidence on ABG that tissue Oxygen delivery is inadequate with lactataemia.

Transfuse - Hb 62 and functionally ~50- transfusion reasonable option

Ensure Hb maximally oxygenated – target high FHbO2 pending resolution of MetHbaemia so pO2 target high (eg >80mmHg)

Methylene Blue infusion 1-2 mg/kg (ideally do a rapid G6PD screen prior)

Exogenous glucose

Exchange transfusion if other measures fail or unavailable

N- acetylcysteine, cimetidine, ketoconazole - experimental

Discussion

ABG analysis:

  • There is acidaemia
  • There is an attempt at respiratory compensation
  • The bicarbonate is low, suggesting that there is a metabolic acidosis.
  • The respiratory compensation for this metabolic acidosis: (1.39 × 1.5) + 8 = 28.8; thus the acidosis is well compensated.

Information for the calculation of anion gap and delta ratio is not supplied, but it is irrelevant. The lactate is probably very high. The massive elephant in the room is the methaemoglobinaemia and anaemia, which are causing a significant tissue hypoxia.

The culprit must be dapsone. The man clearly has some sort of chronic suppression therapy for Pneumocystis, and is allergic to sulfonamides. Apart from classical sulfonamides, dapsone is essentially the only dihydrofolate reductase inhibitor useful for this purpose. It is a sufficiently structurally distinct molecule, and many sulfa-allergic people will not react to it

The commonest side effects of dapsone include methaemoglobinaemia, haemolytic anaemia, and agranulocytosis. Dapsone is converted by the cytochrome P-450 system into a hydroxylamine, which then oxidizes haemoglobin - forming methaemoglobin -and in the process regenerates itself back into dapsone, so that the cycle can repeat.

So, how does one treat methaemoglobinaemia?

  • Use a co-oximeter to measure oxygen saturation - the pulse oximeter will read about 82%.
  • Increase the oxygen carrying capacity of blood by transfusion of PRBCs
  • Aim for a high PaO2
  • Infuse methylene blue to reduce all the Fe3+ back into Fe2+
  • Infuse glucose - it is essential for the hexose monophosphate shunt, which produces the NADPH required for methylene blue to be effective

References

Ward, Kristina E., and Michelle W. McCarthy. "Dapsone-induced methemoglobinemia." Annals of Pharmacotherapy 32.5 (1998): 549-553.

 

Wright, Robert O., William J. Lewander, and Alan D. Woolf. "Methemoglobinemia: etiology, pharmacology, and clinical management."Annals of emergency medicine 34.5 (1999): 646-656.

 

All about dapsone from inchem.org

Question 3.1 - 2012, Paper 2

A 49-year-old female, with a history of pulmonary vasculitis is found collapsed in the ward with shallow breathing and a GCS of 6.

An initial arterial blood gas on room air (FiO2 0.21) reveals:

Parameter

Result

 

Normal Range

Barometric pressure

760 mmHg (100 kPa)

 

pH

7.13*

 

PCO2

80 mmHg (10.5 kPa)*

 

35– 45 (4.6 – 6.0)

PO2

38 mmHg (5.0 kPa)

 

Bicarbonate

26 mmol/L

 

22 – 27

Base Excess

+2 mmol/L

-2 – +2

What is the cause of the hypoxia?

Give the reason for your answer

 

College Answer

Hypoventilation.

No reason to believe there is parenchymal disease / vasculitis as the A-a gradient is 13 mmHg. This fits with the clinical picture of coma, shallow breathing and hypercapnia

Discussion

This question, though it is a blood gas interprestation question, has been placed into the category of respiratory failure SAQs because there is no complex acid-base disorder to diagnose.

However, it relies on the candidate knowing the alveolar gas equation. Here it is:

PAO2 = (0.21 x (760 - 47)) - (PaCO2 x 1.25)

Essentially, at 760mmHg barometric pressure, there should be about 150mmHg occupied by oxygen and carbon dioxide in the alveolus- given that in the alveolus the water vapour pressure is 47mmHg, and FiO2 remains 21%.

Thus, PAO2 can be expressed as 150 - (PaCO2 x 1.25)

Thus, if the PaCO2 is 80, the O2 should be around 50.

Thus, if the PaO2 is 38, one might surmise that the A-a gradient is 12.

With a normal A-a radient, the only possible explanation for the hypoxia is hypoventilation. Identifying such situations is is almost the only effective use of the A-a gradient in critical care. As with other tension-based indices of oxygenation, this value gives little information about the oxygen content of the blood.

References

Here is an intersting digression about the alveolar gas equation:

Cruickshank, Steven, and Nicola Hirschauer. "The alveolar gas equation."Continuing Education in Anaesthesia, Critical Care & Pain 4.1 (2004): 24-27.

Question 4 - 2012, Paper 2

A 65-year-old man had an out of hospital cardiac arrest secondary to a large anterior ST elevation myocardial infarction. His ICU stay has been complicated by aspiration pneumonia. He is now day 14 from admission, with a tracheostomy in situ, and has started weaning from ventilation.
You have been asked to review him as he is communicating that he ‘can’t get enough air’ despite ongoing mechanical ventilatory support.
How would you manage this patient who reports being breathless on a ventilator?

 

College Answer

Urgent attention to A, B, C – Give 100% oxygen and exclude/treat immediate threats to life

Focused history and examination considering differential diagnoses:

Patient factors 
Airway / trache – blocked, displaced or too small diameter

Respiratory eg pneumonia, PE, PTX 
Cardiac – ongoing ischaemia, cardiac failure, fluid overload

Neuromuscular – weakness, fatigue 
Sepsis

Metabolic 
Central – increased respiratory drive, pain, agitation

Ventilator factors 
Unsuitable mode

Triggering threshold too high 
Inadequate flow

Prolonged inspiratory time 
Inappropriate cycling

Inadequate pressure support 
Ventilator malfunction

Treatment:

100% O2, suction trachy, exclude obstruction/malposition, end tidal CO2 etc

Assess ventilation

Mode, respiratory rate and pattern 
Spontaneous and delivered TV / MV / airway pressures

Expiratory flow-time curve, PEEPi (if possible)

Titrated pain relief

May need to carefully sedate to gain control of the situation if he is very distressed and agitated. Rarely need to paralyse after sedation

Investigations

Basic Investigations – eg ABG, ECG, CXR, cultures 
Further investigations as indicated – eg Echo, CTPA, BNP, Troponin etc

Discussion

This question lends itself well to a systematic approach.

  • Immediate management:
    • Increase the FiO2 to 100%
    • consider disconnecting the patient from the ventilator, and manually bag-ventilating them
    • Simultaneously assess and manage threates to life in a systematic manner:
  • Airway
    • machine factors:
      • check for condensation in the ventilator tubing
      • change HME and ventilator filter
    • patient factors:
      • check tracheostomy diameter (too narrow?)
      • check inner cannula (encrusted with inspissated secretions?)
      • check tracheostomy patency (blocked with secretions?)
      • Check tracheostomy position (dislodged during last turn?)
      • suction the patient, loking for fresh blood and clots (unrecognised pulmonary haemorrhage?)
  • Breathing
    • machine factors
      • Check for ventilator malfunction
      • Look for patient-ventilator dyssynchrony and adjust the settings accordingly;
        • is the trigger insufficiently sensitive, or over-sensitive?
        • is the tidal volume and inspiratory flow sufficient to satisfy patient demand?
        • Is the mode inappropriately mandatory?
    • patient factors
      • Assess lung compliance by observing ventilator peak pressures, or qualitatively by manually bag-ventilating the patient
      • Examine the patient and organise an ABG and chest Xray, looking for evidence of...
        • bronchospasm
        • pneumothorax
        • pulmonary oedema
        • impaired gas exchange
          • consider a CTPA if an unexplained A-a gradient has been discovered
        • metabolic acidosis, driving respiratory effort
        • cardiac dysfunction, eg. MI or new arrhythmia
  • Circulation
    • Organise an ECG and bedside TTE, looking for evidence of
      • MI
      • Pulmonary oedema
      • arrhythmia
      • new onset of heart failure
      • evidence of right heart strain
  • Neurology
    • look for muscle weakness or new neurological deficit
    • Look for evidence of poorly controlled pain driving the respiratory effort
    • Assess for delirium and agitation as the primary driver of increased respiratory effort

References

Question 2 - 2013, Paper 1

With regards to the use of high-flow nasal oxygen therapy in adults:

a) Describe the mechanisms by which high flow nasal oxygen therapy is believed to exert its beneficial effects.

b) List two potential adverse effects associated with the use of high-flow nasal oxygen therapy.

c) List two relative contraindications to the use of high-flow nasal oxygen therapy.

College Answer

a)

  • Precise mechanism of benefit is yet to be elucidated.
  • Increased FiO2:
    • Gas inlet flow limits secondary room air entrainment.
    • Provides anatomic oxygen reservoir in nasopharynx and oropharynx.
    • Rinsing of airway deadspace with oxygen.
  • CPAP effect:
    • decreases atelectasis and improves V-Q matching.
    • improves compliance.
    • decreases work of breathing by counteracting intrinsic PEEP.
  • Greater comfort:
    • Warmed and humidified oxygen can be better tolerated, therefore better compliance from patients.

b)

  • Pressure areas in the nose. Epistaxis.
  • Possible gastric distension.

c)

  • Nasal fracture.
  • Upper airway haemorrhage. Base of skull fracture.
  • Recent upper airway or aerodigestive tract surgery.

Discussion

There is a great article available (Ricard et al, 2012) which dissects this oxygen delivery system.

Describe the mechanisms by which high flow nasal oxygen therapy is believed to exert its beneficial effects.

  • PEEP effect
    • Though it seems to only be about 3cm H2O with 60L/min flow, when the mouth is open
    • If it works, then it has all the benefits of PEEP - recruitment of atelectatic lungs, decreased work of breathing, and so forth.
    • On top of that, it is supposed to overcome the "nasopharyngeal resistance" of obese OSA patients
    • In fact the benefits seem to be most pronounced in the obese patients- and the degree of improvement in gas exchange tends to be related to the degree of increase in end-expiratory lung volume, which suggests that there is a real alveolar recruitment effect.
  • Increased FiO2 -
    • The upper airways are "rinsed" with humidified oxygen; this is called the "pharyngeal dead space washout"; each breath drags more of this oxygenated air from this anatomical dead space and into the lungs.
    • The delivery of high flow oxygen at a high concentration cannot be accomplished reliably by oher low-flow means, such as the Venturi mask.
  • Increased comfort -
    • Apparently, its comofortable. The main reason for this is the fact that the mouth is left alsone, unlike most forms of CPAP.
    • Addtionally, the humidification of oxygen tends to decrease the nasty side effects of oxygen therapy, such as raw stripped mucosa

List two potential adverse effects associated with the use of high-flow nasal oxygen therapy.

  • Overdistension of the alveoli, and barotrauma
  • Discomfort associated with the device, its flow or the high temperature/humidity
  • Nasal mucosal damage due to high flow
  • Pressure areas due to the device
  • Failure to achieve the desired effect because of mouth-breathing
  • Overabundance of secretions (Velasco et al, 2014) - though some might view this as a desired effect
  • Epistaxis
  • Time-wasting (delaying the inevitable intubation)
  • Aspiration of food or upper airway secretions
  • Aspiration of circuit condensation water (there's no evidence that this causes pneumonia, but people complained about it in a survey of paediatric ICUs conducted by Manley et al, 2012)

List two relative contraindications to the use of high-flow nasal oxygen therapy.

References

Groves, Nicole, and Antony Tobin. "High flow nasal oxygen generates positive airway pressure in adult volunteers." Australian Critical Care 20.4 (2007): 126-131.

Ricard, J. D. "High flow nasal oxygen in acute respiratory failure." Minerva Anestesiol 78.7 (2012): 836-841.

Locke, Robert G., et al. "Inadvertent administration of positive end-distending pressure during nasal cannula flow." Pediatrics 91.1 (1993): 135-138.

O’Brien, Bj, J. V. Rosenfeld, and J. E. Elder. "Tension pneumo‐orbitus and pneumocephalus induced by a nasal oxygen cannula: Report on two paediatric cases." Journal of paediatrics and child health 36.5 (2000): 511-514.

Baudin, Florent, et al. "Modalities and complications associated with the use of high-flow nasal cannula: experience in a pediatric ICU." Respiratory care 61.10 (2016): 1305-1310.

Question 21.1 - 2013, paper 2

The following image is a snapshot of ventilator graphics for an 80kg patient in the ICU intubated and mechanically ventilated.

ventilator waveform

a) Describe the abnormalities displayed in this image.

b) What changes (if any) would you make to the ventilator settings?

c) Give three possible causes for the appearance of the pattern demonstrated by the pressure time curve.

College Answer

a)

Resistance to inspiratory flow - peak inspiratory pressure approx. 40 cmH2O and plateau pressure less than 20 – high peak to plateau pressure

Prolonged expiration with low peak flow indicative of expiratory resistance

Expiratory flow not returned to baseline at end of expiration indicating auto-PEEP / gas trapping / dynamic hyperinflation

b)

  • Reduce rate
  • Reduce T insp
  • Reduce VT
  • (Check intrinsic PEEP)

c)

  • Kinked tubing / blocked filter
  • Kinked / blocked ETT
  • Asthma

Discussion

a)

The ventilator graphic I have created to replace the one which the college has omitted is designed to yield the answer to somebody who understands ventilator pressure waveforms.

The peak pressure is very high, and during the inspiratory pause one glimpses the plateau pressure, which is comparatively low- this suggests that airway resistance is to blame. The flow waveform confirms this - the flow curve never reaches zero in expiration, suggesting that the passive expiratory gas flow is occurring agaisnt some sort of resistance. This is evidence of autoPEEP. In short, specific features of bronchospasm seen here are:

  • High peak airway pressure, but a normal plateau pressure
  • Slow return of the flow-time curve to baseline
  • The flow-time curve does not reach baseline (indicating that emptying is incomplete)

b)

The college makes sensible suggestions. One would need to decrease the respiratory rate in order for the flow to reach zero, to prevent gas trapping. One may also consider decreasing the tidal volume, while understanding the the combination of these two manoeuvrs may actually create even greater hypercapnea. Reducing the inspiratory time may result in increased peak airway pressure, but will help increase the expiratory time, thereby increasing the total CO2 clearance.

c)

Differentials for this revolve around the airway resistance, and to a lesser extent the compliance of the whole circuit. This could be approached systematically:

  • Machine problems:
    • kinked ventilator tubing
    • "rain-out" in the ventilator tubing
    • old waterlogged HME
    • kinked or obstructed ETT
    • old expiratory filter in the ventilator
  • Patient problems
    • biting and chewing on the tube
    • increased upper airway resistance due to some sort of sputum plug
    • bronchospasm (most likely)
    • increased chest wall rigidity, eg. due to massive fentanyl bolus, or hypothermia.

References

No specific references exist, but there is a good broadoverview article which touches upon the troubleshooting process and has some waveforms :

Santanilla, Jairo I., Brian Daniel, and Mei-Ean Yeow. "Mechanical ventilation."Emergency medicine clinics of North America 26.3 (2008): 849-862.

Question 21.2 - 2013, paper 2

A 54-year-old female with scleroderma and worsening dyspnoea on exertion presents with the following respiratory function tests:

Test

Actual

Predicted

FEV1

1.96 litres

2.66 litres

FVC

2.52 litres

3.11 litres

FEV1/FVC

78%

85%

PEF

7.50 L/sec

6.47 L/sec

FRC

2.18 litres

2.77 litres

RV

1.08 litres

1.84 litres

TLC

3.64 litres

5.17 litres

DLco

10.4 ml/min/mmHg

24.7 ml/min/mmHg

KCO (DlCO/VA)

2.85 ml/min/mmHg

4.77 1/min/mmHg

a) Describe and explain the results of the respiratory function tests.

b) Suggest a possible cause.

College Answer

a)

  • Moderate restrictive defect
  • High peak expiratory flow; due to fibrotic lung stretching airways open on full inspiration
  • Small residual volume; due to cellular infiltration / fibrosis resulting in reduced lung compliance
  • Reduced DLco (impaired gas transfer) due to both:
    • Reduced lung expansion (restriction) and
    • Damage to the lung parenchyma

b)

Pulmonary fibrosis

Discussion

a)

This question relies on some understanding of formal lung function tests. An excellent overview of this can be found in a 2005 article by Pellegrino et al.

The reduced DLCO and KCO (transfer coefficient for carbon monoxide) strongly suggests that there is a diffusion defect.

This would suggest pulmonary fibrosis.

The college also report that there is a moderate restrictive defect.

According to the 2005 ATS guidelines, a restrictive defect is defined as a TLC below the 5th percentile of the predictive, with a normal FEV1/FVC. This patient has an FEV1/FVC which is still above the 70% cut-off, and is therefore classified as "normal". The TLC percentile bands are not offered by the college, but one can see that it is well below the predicted value ( 3.64 L instead of  5.17 L).

According to the 2010 GOLD guidelines, a restrictive defect is characterised by a normal (or mildly reduced) FEV1, an FVC below 80% of predicted, and a normal (>70%) FEV1/FVC ratio. In the data above, the FVC is 81% of the predicted value, so by this standard the patient is just outside the borders of being classified as restrictive lung disease.

The major diference in this system of classification is the use of a fixed lower limit of normal (LLN), which is easier to remember and more convenient for resource-poor environments (where COPD is prevalent). Unfortunately it seems the use of such fixed cutoffs tends to incorrectly classify up to 20% of patients, particularly at the extremes of age (Miller et al, 2011). The glorious oracle of UpToDate recommends the use of computerised algorithms for predictive values, wherever they are available (i.e. using as the cutoff value the fifth percentile of the predicted FEV1/FVC ratio).

 

References

Pellegrino, Riccardo, et al. "Interpretative strategies for lung function tests."European Respiratory Journal 26.5 (2005): 948-968.

Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines - 2010

American Thoracic Society (ATS) guidelines for pulmonary function testing

Miller, Martin R., et al. "Interpreting lung function data using 80% predicted and fixed thresholds misclassifies more than 20% of patients." CHEST Journal 139.1 (2011): 52-59.

Question 2 - 2014, Paper 1

Briefly outline the role of each of the following in the diagnosis of pulmonary embolism in the critically ill:

a) Echocardiography

b) CT pulmonary angiogram (CTPA)

c) Serum troponin

d) D-dimer levels

College Answer

Echo
 Bedside test, rapid.
 Avoids transport, radiation exposure, IV contrast.
 Only 30-40% with PE have suggestive changes. Changes more likely if massive.
 Signs of right heart failure with shock and known PE may be an indication for thrombectomy / thrombolysis.

CTPA
 Spiral CT scan with IV contrast.
 Ability to also detect alternative pulmonary abnormalities.
 Issues of transport, radiation exposure, IV contrast (versus bedside tests (e.g. leg duplex U/S, ECHO) and/or empiric anticoagulation).
 PIOPED II – suggested that CTPA requires concomitanTrt pre-test probability assessment (Wells) to be effective tool in diagnosing or excluding. Positive and negative predictive values differed significantly at different pre-test probabilities.
 Positive predictive value varies with extent of PE and pre-test probability – v good (97%) with main or lobar, falling with smaller; v good with high pre-test probability (96%), falling with lower (NEJM 2006).
 More recent studies with newer generation scanners suggest CTPA better at excluding PE than in PIOPED II - if good quality negative CTPA in an experienced centre, representation with thromboembolism is 1 – 2% at 3 months. In high risk patients, closer to 5TTE%. (J Thromb Haemost 2009).

Troponin
 Not useful for diagnosis of PE.
 Elevated in 30 – 50% with moderate/large PE.
 Presumably from acute RV strain/overload.
 Associated with poorer prognosis.

D-dimer
 Degradation product of cross-linked fibrin.
 Detected in serum (ELISA or agglutination assay).
 Multitude of causes of raised D-dimer other than PE.
 Good sensitivity.
 Good negative predicative value – increased further if use clinical pre-test probability (e.g. Wells).
 Poor specificity and positive predictive value.
 Main role is to exclude PE if low pre-test probability and negative D-dimer.
 No use in the critically ill population as elevated in elderly, post-op, infection, trauma.

Examiners' comments: Candidates did not answer the question as asked.

Discussion

It was not a "compare and contrast" question, but judging by the examiner's comments it was treated as one by many candidates.  However, the college answer to this question still discusses the advantages and disadvantages of these investigations. So, here is a "compare and contrast" sort of table, which incorporates both the model college answer and the 2014 ESC guidelines.

Investigations for Pulmonary Embolism
Test Rationale and advantages Limitations and disadvantages
History and clinical examination
  • Cheap and rapidly available
  • Screening for predisposing factors and associated features is effective in building pre-test probability (Well's rule or the Geneva score)
  • Clinical features of PE (eg. chest pain, dyspnoea, tachycardia) are highly non-specific.
ECG features of RV strain
  • These are
    - inverted T waves in V1-V4
    - S1Q3T3 pattern
    - RBBB
  • Only present in very severe cases
  • Frequently, sinus tachycardia is the only ECG feature
TTE
  • Rapid bedside test
  • No contrast or radiation exposure
  • May reveal RV dysfunction, which would be an indication for thrombolysis
  • Interpreter-dependent accuracy
  • Only 30-40% with PE have suggestive changes; thus a negative result does not exclude PE
CTPA
  • Rapid and easily available
  • May reveal alternative chest pathology
  • New scanners are better at excluding PE
  • The college mentions PIOPED II (2006):
    • sensitivity of 83%
    • specificity of 96%
  • Both contrast and radiation exposure
  • Risk of transport to and from the scanner
  • What if you find a small sub-segmental PE? What clinical significance does this finding have?
Troponin
  • New high-sensitivity tests are good at excluding RV injury
  • Troponin is elevated in 30 – 50% with moderate/large PE.
  • A raised troponin in PE is associated with a poorer prognosis.
  • Poor specificity: will be elevated in a number of situations apart from PE.
D-dimer
  • Good sensitivity: a negative D-dimer excludes PE.
  • Good way of excluding PE in well patientsd with a low pre-test probability
  • Three-month thromboembolic risk was less than 1% in patients left untreated
    on the basis of a negative test result.
  • Poor specificity: will be elevated in a number of situations apart from PE.
  • Critically ill populations invariably have an elevated D-dimer.
  • NNT (number needed to test) is 3 in the ED, but over 10 in other scenarios
Lung scintigraphy (V/Q scan)
  • IV injection of Tc99m-labelled macroaggregated albumin particles are used in the perfusion scan
  • Xe133 gas is then used as a ventilation scan.
  • Total radiation exposure (1.1mSv) is much lower than in a CTPA
  •  it is safe to withhold anticoagulant  therapy in patients with a normal perfusion scan.
  • Not available everywhere
  • Will not detect small PEs
  • Not available for urgent pre-thrombolysis confirmation of PE
     
     

References

Oh's Intensive Care manual: Chapter 34   (pp. 392) Pulmonary  embolism by Andrew  R  Davies  and  David  V  Pilcher

Anderson, Frederick A., and Frederick A. Spencer. "Risk factors for venous thromboembolism." Circulation 107.23 suppl 1 (2003): I-9.

Konstantinides, Stavros V., et al. "2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism." European Heart Journal (2014): ehu283.

Kucher, Nils, et al. "Massive pulmonary embolism." Circulation 113.4 (2006): 577-582.

Jerjes-Sanchez, Carlos, et al. "Streptokinase and heparin versus heparin alone in massive pulmonary embolism: a randomized controlled trial." Journal of thrombosis and thrombolysis 2.3 (1995): 227-229.

Kucher, Nils, and Samuel Z. Goldhaber. "Management of massive pulmonary embolism." Circulation 112.2 (2005): e28-e32.

Wan, Susan, et al. "Thrombolysis compared with heparin for the initial treatment of pulmonary embolism a meta-analysis of the randomized controlled trials." Circulation 110.6 (2004): 744-749.

Kasper, Wolfgang, et al. "Management strategies and determinants of outcome in acute major pulmonary embolism: results of a multicenter registry." Journal of the American College of Cardiology 30.5 (1997): 1165-1171.

Kline, J. A., et al. "Treatment of submassive pulmonary embolism with tenecteplase or placebo: cardiopulmonary outcomes at 3 months: multicenter double‐blind, placebo‐controlled randomized trial." Journal of Thrombosis and Haemostasis 12.4 (2014): 459-468.

Sharifi, Mohsen, et al. "Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT” Trial)." The American journal of cardiology 111.2 (2013): 273-277.

Stein, Paul D., et al. "Multidetector computed tomography for acute pulmonary embolism." New England Journal of Medicine 354.22 (2006): 2317-2327.

Question 4 - 2014, Paper 1

Outline the principles of, and strategies for management of a persisting broncho-pleural fistula (BPF) in a mechanically ventilated patient.

Include in your answer the advantages and disadvantages of each strategy.

College Answer

Principles of Management:
1. Drainage
 Adequate drainage of the fistula with an intercostal catheter of adequate size to manage a large air leak.
 May require multiple catheters, and ability to manage large flow rates.
 Minimise suction.

2. Ventilatory management
 Aim is to reduce mean airway pressure to reduce flow through fistula tract.
 Low tidal volume and PEEP.
 Low mandatory breath rate.
 Permissive hypercapnoea.
 Short inspiratory time.
 Attempt to wean to spontaneous breathing mode from mandatory ventilation as soon as practicable and preferably from ventilatory support altogether.

3. General measures
 Standard ICU supportive management
 Broad spectrum antibiotic cover
 Attention to nutritional requirements – patients usually catabolic.

Strategies for Managing Large Leaks:
1. Independent Lung Ventilation
 Advantages: - May minimise leak in injured lung whilst preserving gas exchange with conventional parameters in normal lung.
 Disadvantages: -requires some form of double lumen tube – difficult to place and secure.
 May not be tolerated in hypoxic patients.
 Requirement for two ventilators –either synchronous or asynchronous – technically demanding and complex.

2. High Frequency Ventilation
 Advantages are that it may reduce peak air pressures and theoretically reduce air leak.
 Disadvantages - not widely available. Recent evidence suggesting an increase in mortality for this ventilatory technique in ARDS patients.

3. Surgery
 Advantages – Definitive management strategy. May be only option to seal leak.
 Disadvantages – Patient may not be fit enough to tolerate.

4. Endobronchial Occlusion
 Advantages – Widely available, can be definitive treatment.
 Disadvantages – may be technically challenging, not feasible with multiple leaks.

5. Application of PEEP to intercostal catheter
 Advantages – may decrease leak volume and maintain intra-thoracic PEEP.
 Disadvantages – compromise drainage, risk of tension, not feasible with multiple tubes.

6. ECMO
 Advantages – may be only option to treat hypoxia.
 Disadvantages – not widely available, complex, little experience.

Examiners' comments: Overall, candidates had poor knowledge of this topic.

Discussion

This answer would benefit from a tabulated format:

Management Strategies for Bronchopleural Fistula
Strategy Advantages Disadvantages
Drainage
- large-bore drain
- or, multiple drains
- minimise suction
  • easy and readily available
  • Usually well tolerated
  • Does not interfere with weaning of ventilation
  • Risk of damaging more lung and creating larger leaks
  • Potentially, perpetuates the fistula by negative pressure suction
  • Invasive
Ventilator strategy:
- low VT
- low PEEP
- low resp rate
- short insp. time
- tolerate high PCO2
- wean rapidly
- extubate early
 
  • easy and readily available
  • Usually well tolerated
  • Early extubation is the ideal step to aim for, as spontaneous negative pressure breathing is better for BPF healing than positive pressure ventilation.
  • The BPF itself may frustrate weaning off ventilation
  • Mandatory mode may prolong ventilation time
  • Permissive hypercapnea may lead to respiratory acidosis, which is not ideal for the patient with traumatic brain injury
Independent lung ventilation
- dual-lumen tube
- or, bronch blocker
 
  • Isolation of one lung permits the selective low-volume low-pressure ventilation of the affected lung, and more rapid higher volume ventilation of the unaffected lung.
  •  PCO2 levels may be easier to control in this manner
  • Technically difficult: DLT insertion is one thing; running two ventilators is another.
  • There may be leak of gas and pressure from one lung to another if the seal is imperfect
  • Sedation requirements will  be higher, to tolerate the larger tube and the very unnatural respiratory pattern
  • Local pressure effects of the DLT are also more problematic
     
Surgical repair
  • The affected lung can be surgically repaired. USually, this means segmental lobectomy (for alveolar leaks) or patching and oversowing of the bronchial leak
  • Apparently, success rates are between 80 and 95%
  • It may be impossible to find the leak intraoperatively
  • It may be unfeasible to remove so much lung
  • It may be impossible if there are multiple leaks
  • The patient must tolerate one-lung ventilation
  • This approach requires thoracotomy
Bronchial stenting
  • The affected bronchus can be stented over bronchoscopically, thereby blocking the leak.
  • This is a minimally invasive alternative to surgical patch repair
  • You need to be sure of where the leak is
  • The leak must be in an accessible bronchus.
  • This may not work if there are multiple leaks
  • The procedure requires technical expertise
  • The patient must be fit to tolerate the bronchoscopy
Bronchial occlusion
  • Similarly to surgery, the affected pronchus is blocked with either a one-way valve or a plug. In fact, the Lois article lists options such as blood clot, cyanoacrylate glue, fibrin, lead shot,  gel foam, calf bone, and various others.
  • You need to be sure of where the leak is
  • The leak must be in an accessible bronchus
  • A major part of the lung may be sacrificed
  • The atelectatic lung may develop infection
Application of PEEP to the ICC
  • The equal intra and extrathoracic PEEP decreases the leak volume
  • Maintained intra-thoracic PEEP permits higher PEEP levels to be used
  • Drainage is compromised
  • There is a major risk of rapid tension pneumothorax
HFOV
  • May reduce peak pressures
  • Certainly reduces tidal volume (to ~50ml)
  • Thus, theoretically reduces flow across the BPD, allowing it to heal
  • This is avery unnatural form of ventilation, and may be poorly tolerated
  • Large amounts of sedation or paralysis will be required
ECMO
  • This may be the only option for severely hypoxic patients
  • With ECMO, one can limit or totally abolish gas flow through the BPF
  • All the risks of ECMO apply, as it is a maximally invasive therapy
  • It is not widely available.
  • There is little experience with this in BPF.

References

Question 13.1 - 2014, Paper 1

a) What does the following pressure-volume loop indicate?

b) What is the likely underlying diagnosis?

College Answer

a) Shift of the pressure volume loop to the left suggestive of increased lung compliance.

b) Emphysema (COPD).

References

Question 13.2 - 2014, Paper 1

The following pressure-volume loop was obtained from a mechanically ventilated patient.

a) What does it indicate?

b) What changes would you make to the ventilator settings to correct the abnormality?

College Answer

a) "Beaking" pattern of lung over-distension, where airway pressure continues to rise without much increase in tidal volume.

b) Reduce the applied tidal volume.

References

Question 13.3 - 2014, Paper 1

Outline four causes for the capnograph trace (shown below) obtained from a critically ill patient.

College Answer

1. Ventilator disconnection
2. Esophageal intubation
3. Cardiac/respiratory arrest
4. Apnoea test in a brain dead patient
5. Capnograph obstruction

Discussion

Reasons for a flat or nearly flat CO2 trace include the following:

  • The patient is dead
  • Cardiac / respiratory arrest
  • Apnoea test in a brain dead patient
  • Oesophageal intubation has occurred
  • Ventilator disconnection
  • Airway obstruction (eg. patient suddenly bit down on the tube)
  • ETT perforation (the end tidal gas is escaping via the hole before it gets to the capnograph)
  • Capnograph disconnection or obstruction
  • Water droplet contamination of capnography module

References

Question 13.4 - 2014, Paper 1

A 58-year-old female ventilated in intensive care for a week following a motor vehicle accident was noted to drop her oxygen saturation suddenly, requiring an increase in FiO2 from 0.4 to 0.6.

The nursing staff has performed an arterial blood gas.

Parameter

Patient Value

Normal Adult Range

FiO2

0.6

pH

7.48*

7.36 – 7.44

PCO2

41 mmHg (5.4 KPa)

35 – 45 (4.6 – 6.0)

PO2

86 mmHg (11.3 kPa)

Ventilator data:

Tidal Volume 700 mL
Respiratory rate 14 breaths/min
Peak pressures 28 cm H2O
Plateau pressures 18 cm H2O
PEEP 7.5 cm H2O
SpO2 94%
EtCO2 28 mmHg

What is the most likely diagnosis? Give the reasons for your diagnosis.

College Answer

The most likely diagnosis is a pulmonary embolus.

The reasons are as follows:
 Sudden onset of hypoxemia raises a number of possibilities – mucus plugging, pneumothorax, LVF, aspiration etc. However, the ventilation data indicate preserved compliance, normal peak pressures (argue against a pneumothorax or plugging or LVF) and there is increased dead space, (raised A-et CO2 gradient)

Discussion

There are numerous possible causes for "sudden onset hypoxemia" in a trauma patient recovering from surgery. The college practically give this one away by offering the candidate an end-tidal CO2 measurement, which is substantially lower than the arterial CO2 measurement, suggesting that there is a large area of lung which is not participating in gas exchange, i.e. it is dead space.  Capnometry and the arterial-expired carbon dioxide gradient is discussed elsewhere.

Of course, one should still go though the motions of calculating the A-a gradient.

PAO2 = 0.6 × (760 - 47) - (PaCO2 × 1.25) = 376.55;

thus, A-a = 290.55

References

Question 16 - 2014, Paper 1

a) Give the differential diagnosis for hypercapnic respiratory failure.
 
b) Outline features from the clinical examination that assists in making a diagnosis/diagnoses.

College Answer

Differential Diagnosis:
1. CNS:
1. Drugs (prescription, illicit, deliberate ingestion/OD)
2. Brain stem lesion
3. Any intra cranial lesion with mass effect (haemorrhagic stroke or traumatic brain injury),
4. Central Sleep Apnoea
2. Spinal Cord:
1. Cervical spinal cord injury/tumour
3. Peripheral Neuro-muscular:
1. Polio, MND, Guillan Barre, Myopathies, Myasthaenia Gravis
4. Chest wall:
1. Kyphoscoliosis, ankylosing spondylitis
2. Obesity-hypoventilation syndrome
5. Respiratory:
1. Asthma/COPD
2. Obstructive sleep apnoea
3. Re-breathing / increased dead space
6. Cardiovascular:
1. Acute severe left heart failure

Clinical examination
1. Neurological:
a. Cranial nerves
b. UMN and LMN signs.
2. Chest wall and rib cage mechanics:
a. Evaluation of thoracic cage component
b. Effect of obesity on ventilation
3. Respiratory:
a. Signs of acute on chronic bronchospasm, chronic lung disease
4. Cardiovascular:
a. Signs of Cor Pulmonale
b. Signs of Left heart failure (dilated cardiomyopathy/valvular heart disease)

Discussion

Causes of Hypercapnia
Decreased minute ventilation

Central nervous system

  • Drugs affecting respiratory drive, eg. opiates
  • Brainstem or cortical lesion affecting consciousness
  • Central sleep apnoea
  • Spinal cord injury

Neuromuscular

  • Neuropathy, eg. Guillain-Barre
  • NMJ disorder, eg. myasthenia gravis
  • Myopathy

Respiratory

  • Decreased lung compliance, eg. pulmonary oedema
  • Decreased chest wall compliance, eg. kyphosis or obesity
  • Increased airway resistance, eg. COPD or asthma

Metabolic, endocrine and environmental

  • Metabolic alkalosis
  • Hypothyroidism
  • Hypothermia
Increased dead space

Increased anatomical dead space

  • Unusually long ventilator circuit (eg. while down in MRI)

Increased alveolar dead space (i.e. ventilated but not perfused)

  • Bullous emphysema, COPD
  • Interstitial pulmonary fibrosis
  • Large pulmonary embolism
Increased CO2 production

Increased metabolic rate

  • Hyperthermia (including malignant hyperthermia)
  • Hyperalimentation
  • Hyperthyroidism
  • Seizures, status epilepticus
   

Features of clinical examination that assist in making a diagnosis:

Observation:

  • Obesity
  • Short fat neck of OSA
  • Cushingoid appearance (OSA, but also suspicious of long term steroids for some sort of autoimmune condition, or COPD)
  • Wasting and cachexia of severe CCF, end-stage COPD or cancer
  • Abnormal breathig pattern (eg. the abdominal breathing of a C-spine quad)

Start with the hands.

  • Clubbing (suggestive of chronicity)
  • Cyanosis
  • Unilateral small muscle wasting (lung mass invading brachial plexus)
  • Pulse (collapsing pulse of AR?)

Axillae and neck

  • Lymph nodes
  • JVP (cardiac causes of ventilation failure)
  • Dissection scars from lymph node clearance; radiotherapy tattoos

Face and cranial nerves

  • Plethoric "mitral facies"
  • Droop, cranial nerve signs of stroke
  • Horner's syndrome (malignancy or stroke)
  • Temporalis wasting (malnutrition)

Chest

  • Abnormal chest wall movement (eg. flail segment or unilateral phrenic nerve paralysis)
  • Subcutaneous emphysema on palpation, suggestive of pneumothorax
  • Percussion findings (eg. dullness of an effusion)
  • Auscultation findings of wheeze or creps (spasm or APO)

Abdomen

  • Recent abdominal wounds (is pain or infection preventing diaphragm excursion?)
  • Distension (Gas? Poop? Ascites?)

Lower limbs

  • Oedema of CCF or prolonged bed stay
  • Muscle wasting of quads (another feature of malnutrition)

References

Question 20 - 2014, Paper 1

A 57-year-old female has required intubation and mechanical ventilation for hypoxaemic respiratory failure with symptoms of cough and dyspnoea that have been gradually progressive over 4 weeks. There is a diffuse bilateral infiltrate on CXR.
She has a history of rheumatoid arthritis and is receiving treatment with methotrexate and prednisolone and has no previous history of respiratory disease.

a) List the likely differential diagnosis.

b) Briefly outline the specific management issues relating to diagnosis and treatment of this patient, excluding acute resuscitation.

College Answer

a) Differential Diagnosis:
1. Bacterial/atypical Pneumonia
2. Opportunistic Infections:
a. Viral: Influenza/CMV/other Herpes Viruses
b. Fungal: Aspergillus/Cryptococcus
c. Other Organisms: PCP/PJP
3. Related to Rheumatoid Arthritis:
a. Methotrexate-induced pneumonitis
b. Rheumatoid Lung Disease

4. Acute cardiac failure e.g. secondary to valvular heart disease, ischaemic cardiomyopathy

b) Management issues:
1. Diagnostic investigations:
a. HRCT/CTPA
b. Bronchoscopy +/- lung biopsy (level of respiratory support may determine whether these investigations are possible)
c. Echo
2. Cease methotrexate
3. Steroids
a. Consider increasing the dose of steroid to cover "stress response"
b. Consider treatment dose associated with PCP/PJP treatment
c. Consider high-dose pulse of steroids
4. Empirical anti-infective treatment (complex decision, treatment may be associated with toxicity)
a. Broad spectrum antibiotic e.g. 3rd generation cephalosporin/aminoglycoside
b. Atypical cover
c. Oseltamivir
d. High dose Co-trimoxazole: monitor for Myelotoxicity
e. Gangcyclovir: monitor for Retinitis, Myelotoxicity
5. Specific treatment for cardiac disease

Discussion

Differential diagnosis for bilateral pulmonary infiltrates should at first glance fall into the "is it infection or is it heart failure" territory. That would be the sensible approach. However, instead here is a long list of differentials.

Differential Diagnosis for Diffuse Bilateral Pulmonary Infiltrates

Vascular:

  • Pulmonary haemorrhage
  • Cardiogenic pulmonary oedema

Infectious

  • Bacterial
  • Viral
  • Fungal
  • PJP

Neoplastic

  • Lymphangitis
  • Infiltrative neoplasm

Idiopathic

  • ARDS

Drug-induced

  • Eosinophilic pneumonitis
  • BOOP
  • Alveolar haemorrhage
  • Methotrexate-induced

Autoimmune

  • Goodpastures (haemorrhagic)
  • Rheumatoid pneumonitis
  • TRALI
  • Graft vs host disease in BMT
  • Engraftment syndrome

Traumatic

  • Bilateral atelectasis
  • Pulmonary contusions

The college then asked for "specific management issues relating to diagnosis and treatment", which according to their model answer called for a salad of recommendations ranging from stopping immunosuppresive therapies ("cease methotrexate") to starting more immunosuppressive therapies ("consider high dose pulse of steroids").  It is of course difficult to assess the situation or determine what specific management or investigations are called for, even with the relatively extensive history given here. Unusually, the examiners have furnished us with some very relevant details:

  • Relatively young patient with no past respiratory problems
  • Severe hypoxia (must be, because she needed to be intubated)
  • Cough and dyspnoea (whereas dyspnoea on its own would lead you down a slightly different path)
  • Sub-acute onset, over 4 weeks
  • History of fairly heavy-handed immunosuppression

The problem of non-specific lung disease appearing randomly and lethally among patients with poor immune systems is sufficiently common in the ICU, to the effect that multiple articles pop up if one searches for "diffuse pulmonary infiltrates in the immunocompromised". 

To exclude non-infectious causes:

  • A transthoracic echo will inevitably be informative, but the finding of a poor systolic function is not going to exclude infectious aetiology (which could easily co-exist with heart failure, as a wet lung is the devil's playground)
  • HRCT is suggested by the college, and this may give some information regarding the pattern of the disease, while not being particularly diagnostic (the CTPA would reveal emboli, but surely a gradual onset over four weeks does not particularly resemble the natural history of a PE)
  • A "vasculitic screen", whatever that might be in the local parlance - mainly to exclude something like Wegener's or Goodpasture's syndromes (though these are made unlikely by the immunosuppression) 

To investigate infectious causes:

  • Perform a bronchoscopy and send lavage specimens for multiple tests:
    • Bacterial cultures and gram stain
    • Acid-fast bacilli
    • Cell count (also looking for weird stuff like eosinophilic pneumonitis)
    • P.carinii PCR
    • Aspergillus PCR
    • Respiratory viral nucleic antigen tests, including CMV, HSV and VZV
    • Cryptococcal antigen
  • Urinary antigens for Streptococcus and Legionella
  • Atypical pneumonia serology, looking for antibodies to mycobacteria, ChlamydiaCoxiella, etc.

Reasonable steps to prevent deterioration:

  • Cease methotrexate. The disease process progressed while the patient (presumably) continued to dutifully take her methotrexate and steroids; ergo it is less likely to be an autoimmune disease driven by B-cells and auto-antibodies.
  • Be moderate with fluid resuscitation, as this has been demonstrated to have a negative impact in ARDS
  • Ventilate the patient with lung-protective low tidal volumes, high PEEP and minimal driving pressures

Some empirical management to cover for the usual suspects:

  • Cover P.carinii with therapeutic dose of sulfamethoxazole/trimethoprim; 
  • Cover gram-positive and gram-negative organisms with something broad, as the stakes are high and there will always be opportunity to narrow the antibiotics once cultures are available. Some combination of meropenem azithromycin and either vancomycin or linezolid are recommended by various guideline-writers (eg. the parts of the 2016 IDSA guidelines which mention "critically ill patients")
  • Antifungal therapy might become relevant if fungi are implicated by culture results
  • Antiviral therapy (oseltamivir) is suggested by the college; the evidence in support of this is very weak, but proponents might argue that those trials don't enrol patients like this, that we have nothing to lose by giving it, and that observational studies (eg. Rodriguez et al, 2011) have suggested that there might be a benefit.

If things are not going as planned (i.e. it's a week down the track and the patient is not getting better), a lung biopsy might be indicated. Apparently, it often identifies steroid-responsive pathology (Gerard et al, 2018), in which case the college's suggestion (massive doses of methylprednisolone) becomes relevant. 

References

Blanco, Silvia, and Antoni Torres. "Differential Diagnosis of Pulmonary Infiltrates in ICU Patients." www.antimicrobe.org

Danés, Cristina, et al. "Pulmonary infiltrates in immunosuppressed patients: analysis of a diagnostic protocol." Journal of clinical microbiology 40.6 (2002): 2134-2140.

Staszewski, Harry. "Diffuse pulmonary infiltrates in immunocompromised patients: Reconciling theory and practice." Postgraduate medicine 94.1 (1993): 69-78.

Fijen, J. W., et al. "Diffuse pulmonary infiltrates in immunocompromised patients." The Netherlands journal of medicine 55.1 (1999): 23-28.

Yousem, Samuel A., Thomas V. Colby, and Charles B. Carrington. "Lung biopsy in rheumatoid arthritis." American Review of Respiratory Disease 131.5 (1985): 770-777.

Gerard, Ludovic, et al. "Open Lung Biopsy in Nonresolving Acute Respiratory Distress Syndrome Commonly Identifies Corticosteroid-Sensitive Pathologies, Associated With Better Outcome." Critical care medicine 46.6 (2018): 907-914.

Mandell L.A, et al; "Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines on the Management of Community-Acquired Pneumonia in Adults"  Clinical Infectious Diseases, Volume 44, Issue Supplement_2, 1 March 2007, Pages S27–S72, https://doi.org/10.1086/511159

Rodríguez, Alejandro, et al. "Impact of early oseltamivir treatment on outcome in critically ill patients with 2009 pandemic influenza A." Journal of antimicrobial chemotherapy66.5 (2011): 1140-1149.

Question 28 - 2014, Paper 1

The following questions relate to the ventilatory management of a critically ill adult 
patient with asthma. 

(Assume the patient has adequate sedation and analgesia, and that optimum 
treatment for bronchospasm has commenced.) 

a) Outline your optimal initial ventilator settings for volume control ventilation. 
Explain your rationale. 

b) Outline the utility of the following three ventilatory measures in monitoring for 
dynamic hyperinflation (DHI). Explain your reasoning. (Assume patient on volume 
controlled mode). 

i. Peak airway Pressure (Ppk) 

ii. Intrinsic or Auto PEEP (PEEPi) 

iii. Plateau Pressure (Ppl) include in your answer how Ppl is measured

College Answer

a) 
Key concept is to avoid dynamic hyperinflation (DHI) - most effectively done by reducing 
minute volume (Ve), <10l/min
 to provide "controlled hypoventilation". Tolerate 
hypercapnia and ensure oxygenation. Settings must be individualised as dictated by 
measures of DHI. 

 Suggested start up settings: Mode; Volume-controlled; High inspiratory flow rate 
60 – 80 L/min (also reduces inspiratory time), long expiratory time ( Exp time 4 – 
5s or I:E > 1:3) achieved by low respiratory rate 8 – 12 breaths/min (may need 
lower), & Small Vt 6 – 8 (10) mL/kg, extrinsic PEEP usually set at 0 (use of PEEP 
controversial however), FIO2 for SpO2 > 90% (oxygenation not usually major 
issue in pure asthma) , set Ppeak limit to 40 – 45 cmH2O, maybe higher. 

b) 
i. Peak Pressure: Not useful for assessing DHI. Ppk represents the sum of pressures 
required to overcome the elastic recoil pressure of the inflated respiratory system and 
to overcome resistance in the airway. Changes in airway resistance and inspiratory 
flow may alter Ppk without affecting DHI. In particular, an increase in flow used to 
shorten inspiratory time in an effort to promote sufficient expiratory time may increase 
Ppk even though DHI decreases. 

ii. PEEPi: May underestimate end expiratory alveolar pressure – marked DHI may 
occur despite low levels of PEEPi, especially at low respiratory rates. This may be 
due to widespread airway closure that prevents accurate assessment of alveolar 
pressure at end expiration. 

iii. Plateau Pressure: The best assessment of DHI. Alveolar pressure will increase as 
lung volume goes up so Pplat reflects gas trapping. Measure at end inspiration with a 
2s pause – pressure falls from peak (static plus resistive) to Pplat (static). Must be no 
leaks in system and patient generally sedated paralysed to get reliable measure. Aim 
< 25 – 30 cmH2O. 

Discussion

a) Initial settings for ventilation of the severe bronchospasm with volume control ventilation
  • Use the largest tube possible.
  • Use lowest FiO2 to achieve SpO2 of 90-92%
  • Use a small tidal volume, 5-7ml/kg
  • Use a slow respiratory rate, 10-12 breaths per minute (or even less!)
  • Use a long expiratory time, with I:E ratio 1:3 or 1:4
  • Increase inspiratory flow rate to maximum. .
  • Reset the pressure limits (i.e. ignore high peak airway pressures).  .
  • Use heavy sedation.
  • Use neuromuscular blockade.
  • Minimise the duration of neuromuscular blockade.
  • Use a volume-control mode of ventilation.
  • Use minimal PEEP.
  • Keep the Pplat below 25cmH2o to prevent dynamic hyperinflation. 
  • Titrate PEEP to work of triggering once the patient is breathing spontaneously.
a) Management strategies for DHI:
  • Reverse reversible patient factors; eg.  bronchospasm can be treated with bronchodilators and steroids
  • correct machine factors, eg. empty the water out of the tubes, cheange the HME, change the ventilator valve
  • Suction ETT, ensure patency
  • Increase expiratory time by decreasing respiratory rate and decreasing I:E ratio
  • Apply PEEP to counteract the increased work of breathing
  • Decrease tidal volume
  • Exotic last-line measures may be deployed:
    • Heliox, to reduce the viscosity of the respiratory gas mixture
    • ECCO2R, to manage the resulting hypercapnea
    • High-frequency oscuillation
b) Outline the utility of Peak airway Pressure (Ppk) in monitoring for DHI
  • Peak airway pressure has not value in monitoring for DHI.
  • It may increase due to numerous factors, of which DHI is only one:
    • Increased inspiratory flow rate
    • Increased airway resistance
    • Decreased lung compliance (for which DHI is one of the causes)
b) Outline the utility of Intrinsic or Auto PEEP (PEEPi) in monitoring for DHI
  • PEEPi is measured using an expiratory hold manoeuvre.
  • An expiratory breath hold stops all flow in the airways; so you can eliminate the expiratory airway resistance (the flow dependent component of intrinsic PEEP).
  • Thus you are able to measure the "static PEEP", the PEEP due to the elastic recoil of the lungs putting pressure on the gas trapped inside them.
  • Ideally, this should be measured in a totally paralysed patient, at zero extrinsic PEEP.
  • Under ideal conditions, the trapped gas will equilibrate in the circuit and one should see the true intrinsic PEEP appear after 1 second of expiratory hold.
  • In reality, at expiration many of the smaller airways end up closed (particularly in bronchospasm) with the result that the expiratory hold manoeuvre may be ineffective. Only the most "open" (least bronchospastic) lung units will reveal their intrinsic PEEP by this method, and the really spastic lung units with the highest intrinsic PEEP will not be observed.
  • Thus, significant DHI may be present, but the PEEPi may not be elevated.
b) Outline the utility of Plateau Pressure (Ppl)) in monitoring for DHI
  • Plateau pressure is measured with the inspiratory hold manoeuvre
  • The high pressure at the plateau ensures all the little airways are splinted open
  • This allows the intrinsic PEEP to equlibrate across the entire respiratory circuit.
  • The college recommend to read the plateau pressure after a 2s pause; the ideal pressure is as usual, under 25-30 cmH2O.
  • Caveats include the need for a paralysed patient, and a circuit without significant leak.

References

Maltais, F., et al. "Comparison of static and dynamic measurements of intrinsic PEEP in mechanically ventilated patients." American journal of respiratory and critical care medicine 150.5 (1994): 1318-1324.

Milic-Emili, J. "Dynamic pulmonary hyperinflation and intrinsic PEEP: consequences and management in patients with chronic obstructive pulmonary disease.Recenti progressi in medicina 81.11 (1990): 733-737.

Brochard, Laurent. "Intrinsic (or auto-) PEEP during controlled mechanical ventilation." Intensive care medicine 28.10 (2002): 1376-1378.

Question 30.3 - 2014, Paper 1

The following set of arterial blood gases were obtained from a patient admitted to the ICU after a suicide attempt.

Parameter

Patient Value

Normal Adult Range

pH

6.84*

7.36 – 7.44

PCO2

94 mmHg* (12.3 kPa)

36 – 44 (4.6 – 5.9)

PO2

140 mm Hg (18.4 kPa)

P50

24 mm Hg

Standard base excess

-16.0 mmol/L*

-2.0 – +2.0

FiO2

0.4

a) In addition to the hypercapnia and the acidosis, what anomaly do you notice in the blood gas report?
b) List two other investigations you would perform to elucidate the cause of the anomaly.

College Answer

a)
A left shifted curve despite a high PCO2 and a low pH.
 
b)
 CoHb
 Measure temperature
 Measure 2,3 DPG

Discussion

This question can be rephrased as "what are the causes of a shifted oxygen-haemoglobin dissociation curve"? The college called attention to the obvious abnormality by putting a p50 value into the question, whereas all the other ABGs in the exam never report this variable.

Anyway: In the adult, the normal p50 should be 24-28mmHg.

  • Causes of a right shift in the oxygen-hemoglobin dissociation curve
  • Causes of a left shift in the oxygen-hemoglobin dissociation curve
    • Alkalosis
    • decreased PaCO2
    • Decreased temperature
    • Decreased 2,3-DPG (eg. in stored blood)
    • Carboxyhaemoglobin
    • Methaemoglobin

References

Question 22 - 2014, Paper 1

A 62-year-old male is admitted to the ICU post-operatively having undergone a transthoracic oesophagectomy for squamous cell carcinoma of the oesophagus. The patient was extubated at the end of the operation but requires re-intubation two days post-surgery due to respiratory failure.

a) List the likely underlying causes of respiratory failure specific to this clinical situation.

b) List the pros and cons of non-invasive ventilation in this clinical situation.

c) Briefly outline the principles of management of an anastomotic leak in this patient.

College Answer

a)
 Pre-existing COAD.
 Diminished airway protection /Altered mental status.
 Chronic aspiration due to impaired preoperative oesophageal function.
 Postoperative aspiration due to recurrent laryngeal nerve compromise and/or inability to swallow.
 Surgical complication including anastomotic breakdown or conduit ischaemia.
 Postoperative pain.
 Pleural effusion.
 Chylothorax.
 Myocardial ischaemia.
 Cardiac failure.
 Weakness due to pre-existing malnutrition.

b)
Pros
 May reduce need for invasive ventilation
 Decreased need for sedation as opposed to invasive ventilation
 Many of the these patient have COAD – reduces work of breathing
 May decrease risk of VAP

Cons
 Oesophageal anastomosis might be compromised and oesophageal leak is a devastating complication
 Many of these patients are at high risk of aspiration

c)
 Assurance of adequate perfusion – maintain good MAP, maintain euvolemia, (avoid vasopressors if possible).
 Adequate source control- all leaks must be adequately drained by re-operation or percutaneous drainage.
 Cessation of contamination – Nil by mouth and well positioned NG tube with free drainage.
 Appropriate nutritional support e.g. enteral feed via jejunostomy
 Endoscopy to assess graft viability if concerned.
 Consider oesophageal stent
 Broad-spectrum antibiotics such as Tazocin and consider anti-fungals – Fluconazole after culture of blood and other secretions.
 In general, cervical leaks can be managed with drainage of neck wound at the bedside, while thoracic leaks are likely to need open re-exploration and drainage

References

Question 24 - 2014, paper 2

The following questions relate to separation from invasive mechanical ventilation:

a) With reference to a spontaneous breathing trial (SBT):
i. What is an SBT?
ii. Over what duration should it occur?
iii. Why would you perform an SBT in a mechanically ventilated patient?
iv. List three methods of performing an SBT.

b) What is the rapid shallow breathing index (RSBI) and how should it ideally be measured?

c) Briefly outline the role of prophylactic (planned) non-invasive ventilation (NIV) immediately following extubation. Explain how this differs from therapeutically applied (rescue) NIV used in the same context.

College Answer

a)
The SBT is the most direct way to assess a patient’s performance or tolerance of unassisted
breathing 
without ventilatory support.
OR
A procedure in which a mechanically ventilated patient is given a trial of spontaneous breathing
without ventilatory support for a limited time without extubation or formal liberation from the ventilator.
Optimal SBT duration has been examined and good evidence supports that 30minutes is
equivalent to 120 minutes with either T piece or PSV.

The SBT can be used to either assess the patient’s suitability for liberation from MV or used
daily as a weaning strategy
. Multiple studies have found that patients tolerant of SBTs were found
to have successful discontinuations at least 77% of the time.
It can be performed using either: Low level Pressure Support (PSV < 7cm H2O), CPAP circuit, or
unassisted via a simple T-piece.

b)
The RSBI is the ratio of frequency of breathing to tidal volume (f/Vt). Rapid shallow breathing as
reflected by f/Vt predicts weaning failure with a threshold of about 105 breaths per minute per litre
(Yang and Tobin). It is less predictive in those ventilated > 8d.It should be measured during the
first minute of a T piece trial using a spirometer to measure Vt. It is of limited value when
measured during trials of pressure support ventilation.
Note: references cited are not expected for marks

c)
Prophylactic NIV: the use immediately after extubation in absence of respiratory failure-High
risk 
patients may benefit (CHF, COPD, high severity scores).
 Ferrer et al , Am J Res and Crit Care Med, 2006 ~ Early NIV avoided respiratory failure and
decreased ICU mortality - in this study NIV appeared useful mainly in a subset of hypercapnic
patients with chronic respiratory disorders.

 However, of no benefit if applied indiscriminately in unselected patients, see Su et al, Resp.
Care. 2012.

Therapeutic NIV: Used post extubation in the presence of established or evolving respiratory
failure- it has no proven benefit in the overall population of patients in this context- it may even
increase mortality by delaying re intubation, see Esteban, NEJM, 2004.

Discussion

a) a Spontaneous Breathing Trial:

  • "Assessment of the patient’s ability to breathe spontaneously" - Boles et al (2007)
  • The simulation of extubated respiratory workload in a still-intubated patient
  • Support during the SBT: Low level Pressure Support (PSV < 7cm H2O), CPAP circuit, or
  • unassisted via a simple T-piece- all of these seem to be equivalent.
  • Duration of the SBT: the college says 30 minutes is equivalent to 120 minutes. This is probably based on a 1999 study by Esteban et al, who compared two 30- and 120-min trial groups (about 250 patients in each) and found no difference between them in terms of outcome or reintubation.
  • SBT failure is identified by the following features:
    • Agitation and anxiety
    • Diaphoresis
    • Cyanosis
    • Evidence of increasing respiratory effort
    • Hypoxia (eg. SpO2 <90%)
    • Hypercapnea (eg. PaCO2 >50mmHg)
    • Unsatisfactory  RSBI: an  fR/VT more than 105 breaths.min-1L-1
    • Resp rate over 35/min, or increased by more than 50%
    • Hypotension, hypertension, or tachycardia
    • Cardiac arrhythmia

b)  rapid shallow breathing index (RSBI):

  • The RSBI is the ratio of frequency of breathing to tidal volume (fR/VT).
  • The seminal Yang and Tobin (1991) paper is mentioned:  they found that RSBI had the best sensitivity and specificity (1.00 and 0.64, respectively) for extubation failure, among all tested  predicitive indices. 

Specific features of the classical  RSBI:

  • You have to be on a T-piece (that's what Yang and Tobin used)
  • You have to measure it during the first minute of the SBT
  • You are supposed to use a spirometer
  • The calculation is: resp rate divided by VT in litres
  • Thus, if you have a resp rate of 30 and your VT is 300ml (0.3L), your RSBI is 100 and you have almost but not quite completely failed your SBT.

You might not need to use a T-piece trial. A recent study by Zhang et al (2014) suggests that you can use pressure support ventilation (with PEEP = 5 and PS = 5-7); the failure threshold is a value of 75 breaths.min-1L-1

c) prophylactic post-extubation NIV:

The examiners quote several studies in their model answer:

  • Ferrer et al (2006):  RCT; 162 patients who tolerated a spontaneous breathing trial (i.e. not in respiratory failure) who had at least one risk factor for post-extubation respiratory failure (eg. age over 65, APACHE-II score over 12 on the day of extubation, or cardiac failure as the cause of intubation). The investigators found reduced rates of respiratory failure in the electively NIVed group, but the 90 day mortality was only improved in the hypercapneic group.
  • Su et al (2012): RCT, 406 patients who tolerated a spontaneous breathing trial randomised to NIV or standard care, looking at their rate of reintubation at 72 hours. There were no differences in extubation failure (13.2% in control and 14.9% in NIV), intensive care unit or hospital mortality. The conclusion reached by these investigators was that routine use of elective NIV will not prevent extubation failure.
  • Esteban et al (2004): RCT, 221 unselected patients being extubated - randomised to NIV or standard therapy. There no difference in reintubation rate. However, recruitment was terminated early when interim analysis discovered an increased mortality rate in the NIV group, and a delay to intubation (i.e. more time was wasted on NIV, from the diagnosis of respiratory failure until the pointlessly delayed reintubation). However, only 10% of the patients in this study had COPD- the outcome would probably have been different if all of them had COPD, as in this highly positie Cochrane review of immediate elective NIV in extubated COPD patients.

In conclusion:

  • Cooperative hypercapneic high-risk patients may benefit from elective NIV immediately following extubation.
  • COPD patients probabyl benefit the most
  • Normocapneic patients may still benefit, but their mortality may not be affected.
  • Patients without risk factors for post-extubation respiratory failure will not benefit.
  • There is no point in doing this routinely, and it may actually be dangerous, as it may delay re-intubation, and promote aspiration.

References

Ferrer, Miquel, et al. "Early noninvasive ventilation averts extubation failure in patients at risk: a randomized trial." American journal of respiratory and critical care medicine 173.2 (2006): 164-170.

Su, Chien-Ling, et al. "Preventive use of noninvasive ventilation after extubation: a prospective, multicenter randomized controlled trial." Respiratory care 57.2 (2012): 204-210.

Esteban, Andrés, et al. "Noninvasive positive-pressure ventilation for respiratory failure after extubation." New England Journal of Medicine 350.24 (2004): 2452-2460.

 
 

Question 4 - 2014, paper 2

With respect to open or video-assisted thorascopic surgical lung biopsy in the management of respiratory failure in the critically ill, discuss the indications, advantages, limitations and complications.

College Answer

Indications
Not common.
Usually performed in setting of progressive and non resolving respiratory failure/ARDS where no
aetiologic diagnosis has been reached by conventional testing such as:
 Radiological techniques
 Microbiological/serological/histological examination of sputum and secretions
o Bronchoscopic samples required
 Radiologically guided (CT or ultrasound) biopsies
 Serological testing

Decision to perform lung biopsy based on:
The need to make a specific diagnosis and thereby direct specific treatment
With-hold potentially harmful or ineffective empiric treatment when other investigations including biopsy obtained by less invasive techniques have been inconclusive
Provide important prognostic information

Diagnostic/therapeutic advantages
May be useful in identifying a range of potentially treatable pathologies

  • Infectious
    • Bacterial
    • Viral
    • Fungal
    • Other e.g. PJP
  • Inflammatory
    • COP (cryptogenic organising pneumonia aka BOOP)
    • Other interstitial pneumonias
    • Connective tissue disease
    • Capillaritis etc.

May diagnose other less treatable pathologies that may alter directions of treatment (limitation of care
or palliation)
 Malignant disease
 Fibrotic disease e.g. IPF
 Other : e.g. veno-occlusive disease

Potentially avoid administration of high dose steroids or other potent immunosuppressants if concern
exists about a possible infectious aetiology.

Also may allow cessation of unnecessary/toxic anti-infective medications.
 However, if all such treatments are initiated empirically then it is often argued that the
procedure is unnecessary (see “limitations” below)
Obtain larger and/or multiple samples
Ability to treat co-existing pathology e.g. perform pleurodesis, drain empyema simultaneously

Limitations
May be difficult to know where best to biopsy (especially if radiology unhelpful) or the most likely
useful area may be inaccessible to the surgeon.
May not give useful diagnostic information especially if not performed early enough,
If all treatment modalities are administered empirically, the value of the test is debatable.

Potential complications

General
Bleeding, infection, poor wound healing etc.

Specific
Increased analgesia requirements post open procedure
Pneumothoraces (persistent/tension etc.)
Persistent air leak (may be prolonged >7 days)(difficult to treat): most common Cx
Haemothorax, massive haemorrhage, pseudotamponade, circulatory collapse
Serous effusions, empyema
Need for single lung ventilation during surgery (VATS)
 Respiratory decompensation intra/post procedure
Death
May not obtain adequate sample

Summary statement (for example)
There is no high-grade evidence for its utility in this context. However, there are multiple case series in the literature that describe high rates of specific diagnostic yield (65-95%), with results leading to treatment alterations in the majority of cases (42 – 89%). All series had a low serious complication rate, and air leaks were the commonest complication.

Additional Examiners’ Comments: Some candidates misread the question as ‘compare and contrast’

Overall well answered.

Discussion

The LITFL lung biopsy page is a definitive resource for the time-poor exam candidate.

In summary:

  • Only do it if the other modalities have failed.
  • If you're going to do it, do it early.
  • It may have no impact on mortality, even if you achieve the correct diagnosis.

Rationale for an open lung biopsy

  • Diagnosis of lung disease cannot be established by less invasive means (eg. BAL, bronchoscopic biopsy, HRCT, serological testing and PCR analysis of secretions)
  • The lung disease is not responding to the current management
  • Management for the differentials is substantially different and a tissue diagnosis will alter the course of management
  • The management suggested has significant side effects, and a biopsy may prevent such management
  • Prognosis will be influenced by tissue diagnosis, and may be grounds for a palliative course of management
  • "While you're there": at the same time as the biopsy, some sort of helpful treatment may be performed in theatre (eg. drainage of an empyema or talc pleurodesis)

Potential findings from a lung biopsy:

  • Pointless and late: a small amount of non-diagnostic necrotic lung was biopsied.
  • Infectious aetiology
    • Bacterial
    • Viral
    • Fungal
    • Other e.g. PJP
  • Inflammatory aetiology
    • COP (cryptogenic organising pneumonia aka BOOP)
    • Other interstitial pneumonias
    • Connective tissue disease
    • Capillaritis etc.
  • Untreatable aetiology (resulting in a change of the goals of care)

Complications of lung biopsy

  • pneumothorax
  • bronchopleural fistula
  • haemothorax
  • major vessel damage
  • failure to establish a diagnosis due to poor sampling
  • Failure of procedure (aborted procedure) due to poor tolerance of single-lung ventilation
  • death
  • The biopsy must be performed in several regions of the lung, and must yield specimens which offer a representative sample, without sampling any areas of irreversible fibrosis or uninformative necrosis.  It cannot be performed in patients who cannot be ventilated on one lung for prolonged periods. Risks and contraindications of of thoracotomy apply.

Evidence in support of lung biopsy

In their answer, the college mention some numbers from "multiple case series in the literature". It would be lovely if they gave a reference.

  • High rates of specific diagnostic yield (65-95%)
  • Results leading to treatment alterations in the majority of cases (42 – 89%).

Even in 1976 (Hill et al) the mortality rate from this procedure was zero, and the morbidity rate was around 4%. In that ancient case series, 33% of the patients enjoyed some sort of positive change in their management because of the biopsy result.

Flabouris and Myburgh (1999) reported something similar. Their complication rate was higher (21%) but these were "proper" mechanically ventilated ICU patients. "Open lung biopsy-guided alteration of therapy directly benefited 39%, and withdrawal was possible in 8.4% of the patients". However, the change to management did not discriminate survivors from non-survivors (i.e. it didn't matter that you changed to an appropriate therapy, the patient died anyway).

A  retrospective series by Lim et al (2007) also reported that a specific diagnosis was achieved in 86% of the biopsied patients, and that in 64% changes to management occurred. Those who were biopsied earlier (within 1 week of intubation) did better in terms of mortality (63% survival vs 11%), which contrasts with the earlier studies.

References

UpToDate has a nice article about lung biopsy.

Bensard, Denis D., et al. "Comparison of video thoracoscopic lung biopsy to open lung biopsy in the diagnosis of interstitial lung disease." CHEST Journal103.3 (1993): 765-770.

Hill, J. D., et al. "Pulmonary pathology in acute respiratory insufficiency: lung biopsy as a diagnostic tool." The Journal of thoracic and cardiovascular surgery 71.1 (1976): 64-71.

Nguyen, W., and K. C. Meyer. "Surgical lung biopsy for the diagnosis of interstitial lung disease: a review of the literature and recommendations for optimizing safety and efficacy." Sarcoidosis vasculitis and diffuse lung disease 30.1 (2013): 3-16.

Flabouris, Arthas, and John Myburgh. "The utility of open lung biopsy in patients requiring mechanical ventilation." CHEST Journal 115.3 (1999): 811-817.

Lim, Seong Y., et al. "Usefulness of open lung biopsy in mechanically ventilated patients with undiagnosed diffuse pulmonary infiltrates: influence of comorbidities and organ dysfunction." Critical care 11.4 (2007): R93.

Question 20 - 2014, paper 2

A 51-year-old male has just been transferred to ICU from the surgical ward with worsening shortness of breath five days post-oesophagectomy, and a presumed anastomotic leak.

On arrival in ICU he is tachypnoeic and extremely agitated.

Arterial blood gas analysis on FiO2 0.6-0.8 via reservoir (non-rebreathing) mask shows:

Parameter Patient Value Normal Adult Range
pH 7.12* 7.35 – 7.45
PaO2 50 mmHg (6.6 kPa)  
PaCO2 50 mmHg (6.6 kPa)* 35 – 45 (4.6 – 6.0)
HCO3 16 mmol/L* 22 – 28

Chest X-ray shows bilateral pulmonary infiltrates.

a) List the possible causes for his respiratory failure.

The patient is intubated and mechanical ventilatory support is initiated.

b) Describe the ventilator settings you will prescribe, giving the rationale for your decision.

Following intubation, there is no immediate improvement in the patient’s oxygenation

c) List the initial strategies that may be used to improve oxygenation.

College Answer

a) List the possible causes for his respiratory failure.

Differential diagnosis should include:
 ARDS secondary to sepsis from any source or other inflammatory insult including the following
 Pneumonia (hospital-acquired)
 Aspiration
 Atelectasis/pleural effusions/empyema
 Fluid overload secondary to resuscitation, renal failure
 Exacerbation of pre-existing condition e.g. heart failure, valvular heart disease, post-op
ischaemia/MI, arrhythmia
 Lung diseases e.g. lymphangitis carcinomatosis

The patient is intubated and mechanical ventilatory support is initiated.

b) Describe the ventilator settings you will prescribe, giving the rationale for your decision.

 Use a mode with which one is familiar and aim to limit ventilator-associated lung injury, i.e
oxygen toxicity, barotrauma, volutrauma, shear stress and biotrauma
 Choice of mode (any appropriate answer acceptable e.g. APRV for recruitment benefit, or
volume assist control as staff familiarity and no one mode shown to have benefit over another)
 Avoid over-distention of alveoli by keeping tidal volumes at 6-8 ml/kg (predicted body weight
which in the ARDSnet studies was ~20% below actual body weight and calculated by a formula
linking height and sex)
 Use PEEP to minimise alveolar collapse and derecruitment.
 Titrate PEEP to achieve a PaO2 of 60 mmHg with lowest FiO2 that is needed using decremental
PEEP trial post recruitment manoeuvre.
 I:E ratio of  1:1
 Permissive hypercapnea to avoid large minute volumes and alveolar injury through collapse and expansion of lung units

Following intubation, there is no immediate improvement in the patient’s oxygenation

c) List the initial strategies that may be used to improve oxygenation.

 High FiO2 (titrated to lowest possible level to limit toxicity)
 Confirm ETT position and patency
 Exclude readily reversible cause of hypoxia e.g. PTX, mucus plug, large effusion
 Increased inspiratory time
 Increased PEEP
 Recruitment manoeuvre with decremental PEEP trial
 Prone positioning for at least 16/24 hours per day
 Ensure adequate cardiac output

Discussion

a) List the possible causes for his respiratory failure.

In the chapter on the definition, causes and differential diagnosis of ARDS there is this table:

Differential Diagnosis for Diffuse Bilateral Pulmonary Infiltrates

Vascular:

  • Pulmonary haemorrhage
  • Cardiogenic pulonary oedema

Infectious

  • Bacterial
  • Viral
  • Fungal
  • PJP

Neoplastic

  • Lymphangitis
  • Infiltrative neoplasm

Idiopathic

  • ARDS

Drug-induced

  • Eosinophilic pneumonitis
  • BOOP
  • Alveolar haemorrhage
  • Methotrexate-induced

Autoimmune

  • Goodpastures (haemorrhagic)
  • Rheumatoid pneumonitis

Traumatic

  • Bilateral atelectasis
  • Pulmonary contusions

The next question asks the candidate to describe the ventilator settings you will prescribe, giving the rationale for your decision.  After those settings fail to work, the college asks for strategies that may be used to improve oxygenation. Overall this question is asking about  Ventilation strategies for ARDS. These are discussed in greater detail elsewhere. A brief summary may be offered:

Initial ventilator strategy:

Additional ventilator manoeuvres to improve oxygenation:

Non-ventilator adjunctive therapies for ARDS:

Ventilator strategies to manage refractory hypoxia

  • Prone ventilation, for at least 16 hours a day (PROSEVA, 2013)
  • High frequency oscillatory ventilation may not improve mortality among all-comers (OSCAR, 2013) or it may actually increase mortality (OSCILLATE, 2013) but some authors feel that there were problems with methodology.

Non-ventilator adjuncts to manage refractory hypoxia

  • Nitric oxide was a cause for some excitement, but is no longer recommended.
  • Prostacyclin is still a cause for excitement, and is still vaguely recommended.
    • Neither agent improves mortality, but prostacyclin can improve oxygenation.
  • ECMO may improve survival (CESAR, 2009) but again there were problems with methodology.

References

Blanco, Silvia, and Antoni Torres. "Differential Diagnosis of Pulmonary Infiltrates in ICU Patients." www.antimicrobe.org

ARDS Definition Task Force. "Acute Respiratory Distress Syndrome." Jama307.23 (2012): 2526-2533.

Question 1 - 2015, Paper 1

You are called to review a 29-year-old male with confirmed asthma in the Emergency Department. He has been unwell for 2 days with increasing cough, wheeze and shortness of breath. He has just been intubated.

a) Describe what ventilator settings you will initially set and give the reasons for your answer. (40% marks)

Two hours later he has become increasing difficult to ventilate. You quickly assess and exclude all other causes except severe bronchospasm.

b) Briefly outline your management of this situation. (60% marks)

College Answer

a)

Ventilator settings Rationale
FiO2 = 1.0

Correct/prevent hypoxia. Adjust as indicated from SpO2

PEEP = 0 or <3 cmH2O

Gas trapping obviates need for PEEP in patients with no spontaneous respiratory effort. A school of thought that PEEP splints airways open and reduces airflow obstruction

Low Respiratory rate

Allow enough time for expiration and prevent gas trapping with adequate minute ventilation, accepting permissive hypercapnia

Tidal volume = 6-8 ml/kg IBW

Adequate Vt for minute ventilation but at ‘safe’ volumes to reduce risk of VALI

I:E = 1:4

Allow enough time for expiration and prevent gas trapping. Accept permissive hypercapnia

High inspiratory flow rate

Allow delivery of target Vt in relatively short inspiratory time. Accept high peak pressures

Reset airway pressure alarm limits

Peak pressures reflect airway resistance and high values are not a concern. Lung compliance in asthma is normal and so elevated plateau pressures represent gas trapping

Ensure adequate sedation:

  • Ketamine +/- propofol +/- analgesia
  • Preferentially use non histamine releasing analgesia – fentanyl

Muscle relaxation:

  • Non steroid/non histamine releasing agents – ideally cisatracurium

Bronchodilator therapy

  • Regular inhaled salbutamol – MDI, nebuliser
  • IV infusion salbutamol
  • IV adrenaline infusion
  • Anticholinergic therapy – Ipratropium bromide inhaled regularly
  • Magnesium infusion – aiming for Mg 1.5-2.5 mmol/L
  • Methylxanthine therapy – Aminophylline infusion

Steroid therapy

  • 100 mg 6 hrly hydrocortisone (or any reasonable steroid / dose)

Ventilation

  • Confirm ventilator settings
  • Tidal volume 6-8 mL/kg
  • Check plateau (rather than peak) inspiratory pressure with inspiratory pause in volume control mode and paralysed patient
  • Reduce respiratory rate if possible
  • Minimise PEEP
  • Check for evidence of dynamic hyperinflation with expiratory hold in paralysed patient
  • Permissive hypercapnia

Other strategies

  • Inhaled volatile anaesthetic agents
  • Heliox if available
  • Consider ECCO2 removal / ECMO

Additional comments:
Common scenario and should be basic knowledge. Some candidates gave a poor explanation
for  their choice  of  ventilator  settings  in  part  a).  Candidates  who  failed  the  question  had
knowledge gaps and inadequate detail in their answer.

Discussion

In the revision section chapter on ventilation strategies for status asthmaticus, a detailed discussion of these strategies is available, with references. Below is a summary cut and pasted from the front of this chapter.

a)

Ventilation strategy

  • Use the largest tube possible.
  • Use lowest FiO2 to achieve SpO2 of 90-92%
  • Use a small tidal volume, 5-7ml/kg
  • Use a slow respiratory rate, 10-12 breaths per minute (or even less!)
  • Use a long expiratory time, with I:E ratio 1:3 or 1:4
  • Increase inspiratory flow rate to maximum. .
  • Reset the pressure limits (i.e. ignore high peak airway pressures).  .
  • Use heavy sedation.
  • Use neuromuscular blockade.
  • Minimise the duration of neuromuscular blockade.
  • Use a volume-control mode of ventilation.
  • Use minimal PEEP.
  • Keep the Pplat below 25cmH2o to prevent dynamic hyperinflation. 
  • Titrate PEEP to work of triggering once the patient is breathing spontaneously.

b) Some of the other, non-ventilator strategies for the management of status asthmaticus:

First-tier therapies with strong supporting evidence

  • Humidified oxygen titrated to SpO2 90-92%
  • Nebulised beta-agonist bronchodilators
  • Nebulised anticholinergic drugs
  • Steroids: IV hydrocortisone or oral prednisone

Second-tier therapies with weak supporting evidence

  • Intravenous beta-agonist bronchodilators for refractory bronchospasm
  • Methylxanthines
  • Nebulised adrenaline
  • Magnesium sulfate
  • Helium-oxygen mixture

Third-tier therapies without any supporting evidence

  • Ketamine
  • Volatile anaesthetics
  • ECMO in asthma

References

Oh's Intensive Care manual: Chapter 35   (pp. 401) Acute  severe  asthma by David  V  Tuxen  and  Matthew  T  Naughton.

Stow, Peter J., et al. "Improved outcomes from acute severe asthma in Australian intensive care units (1996–2003)." Thorax 62.10 (2007): 842-847.

Sekiya, Kiyoshi, et al. "Clinical evaluation of severe asthma attacks requiring tracheal intubation and mechanical ventilation." Allergology International 58 (2009): 289-294.

Sandford, Andrew J., et al. "Polymorphisms in the IL4, IL4RA, and FCERIB genes and asthma severity." Journal of Allergy and Clinical Immunology 106.1 (2000): 135-140.

McFadden Jr, E. R. "Acute severe asthma." American journal of respiratory and critical care medicine 168.7 (2003): 740-759.

Bousquet, Jean, et al. "Uniform definition of asthma severity, control, and exacerbations: document presented for the World Health Organization Consultation on Severe Asthma." Journal of Allergy and Clinical Immunology126.5 (2010): 926-938.

Perrin, Kyle, et al. "Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma." Thorax 66.11 (2011): 937-941.

Rodrigo, Gustavo J., et al. "Effects of Short-term 28% and 100% Oxygen on Paco2 and Peak Expiratory Flow Rate in Acute AsthmaA Randomized Trial."CHEST Journal 124.4 (2003): 1312-1317.

Sellers, W. F. S. "Inhaled and intravenous treatment in acute severe and life-threatening asthma." British journal of anaesthesia 110.2 (2013): 183-190.

Cates, C. J., E. J. Welsh, and B. H. Rowe. "Holding chambers (spacers) versus nebulisers for delivery of beta-agonist relievers in the treatment of an asthma attack." (2013).

Teoh, Laurel, et al. "Anticholinergic therapy for acute asthma in children."Cochrane Database Syst Rev 4 (2012).

Coupe, M. O., et al. "Nebulised adrenaline in acute severe asthma: comparison with salbutamol.European journal of respiratory diseases 71.4 (1987): 227-232.

Albertson, T. E., et al. "Pharmacotherapy of critical asthma syndrome: current and emerging therapies." Clinical reviews in allergy & immunology (2014): 1-24.

Powell, Colin, et al. "Magnesium sulphate in acute severe asthma in children (MAGNETIC): a randomised, placebo-controlled trial." The Lancet Respiratory Medicine 1.4 (2013): 301-308.

Shan, Zhilei, et al. "Intravenous and nebulized magnesium sulfate for treating acute asthma in adults and children: a systematic review and meta-analysis."Respiratory medicine 107.3 (2013): 321-330.

Wigmore, T., and E. Stachowski. "A review of the use of heliox in the critically ill." Critical Care and Resuscitation 8.1 (2006): 64.

Rodrigo, G., et al. "Heliox for nonintubated acute asthma patients." Cochrane Database Syst Rev 4 (2006).

Jat, Kana R., and Deepak Chawla. "Ketamine for management of acute exacerbations of asthma in children." Cochrane Database of Systematic Reviews 11 (2012).

Howton, Joseph C., et al. "Randomized, double-blind, placebo-controlled trial of intravenous ketamine in acute asthma." Annals of emergency medicine 27.2 (1996): 170-175.

Vaschetto, R., et al. "Inhalational anesthetics in acute severe asthma." Current drug targets 10.9 (2009): 826-832.

Lobaz, S., and M. Carey. "Rescue of acute refractory hypercapnia and acidosis secondary to life-threatening asthma with extracorporeal carbon dioxide removal (ECCO2R)." JICS 12.2 (2011): 140-142.

Leiba, Adi, et al. "Early administration of extracorporeal life support for near fatal asthma." IMAJ-RAMAT GAN- 5.8 (2003): 600-602.

Samaria, J. K. "Role Of Niv In Acute Respiratory Failure Due To Asthma: Effectiveness And Predictors Of Failure." Am J Respir Crit Care Med 183 (2011): A1365.

Op't Holt, Timothy B. "Additional Evidence to Support the Use of Noninvasive Ventilation in Asthma Exacerbation." Respiratory care 58.2 (2013): 380-382.

Lim, Wei Jie, et al. "Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma." The Cochrane Library Published Online: 12 DEC 2012

Gupta, Dheeraj, et al. "A prospective randomized controlled trial on the efficacy of noninvasive ventilation in severe acute asthma." Respiratory care 55.5 (2010): 536-543.

Williams, Trevor J., et al. "Risk factors for morbidity in mechanically ventilated patients with acute severe asthma." The American review of respiratory disease146.3 (1992): 607-615.

Lacomis, David, Thomas W. Smith, and David A. Chad. "Acute myopathy and neuropathy in status asthmaticus: case report and literature review." Muscle & nerve 16.1 (1993): 84-90.

Hermans, Greet, et al. "Clinical review: critical illness polyneuropathy and myopathy." Crit Care 12.6 (2008): 238.

Question 12 - 2015, Paper 1

You are called to urgently review a 73-year-old female who is ventilated following admission with severe community-acquired pneumonia. She had a tracheostomy five days ago. She has now acutely desaturated and developed high airway pressures.

Outline your management of this problem.

College Answer

This is an emergency situation with the risks of hypoxia, hypoventilation and/or barotrauma.

Management consists of concurrent resuscitation and focussed assessment to identify the underlying cause with definitive management as indicated.

The differential diagnosis includes:

  • Ventilator malfunction
  • Obstruction/kinking of circuit including filter
  • Displacement/blockage trache tube
  • Increased airway resistance e.g. bronchospasm
  • Decreased lung or chest wall compliance e.g. pneumothorax, lung collapse, intra-abdominal hypertension

Stepwise response (does not have to be in this order)

  • Increase FiO2 to 1.0
  • Assess patient for severity of insult – is there haemodynamic instability? Is the patient peri-arrest?
  • Call for help and crash trolley / difficult airway trolley if indicated
  • Disconnect patient from the ventilator and manually ventilate with FiO2 1.0 and assess resistance/compliance
  • If resistance/compliance seems normal with reduction in airway pressures and improvement in saturations 
then cause is due to ventilator malfunction or inappropriate settings. Replace ventilator and/or review settings
  • If resistance/compliance seems abnormal then systematic approach to look for cause
  • Check circuit and filter for kinking/blockage and unkink/replace as indicated
  • Assess trache for position and patency – remove inner cannula and pass suction catheter. If not patent and 
not cleared by suction or if displaced (may be evidence of subcutaneous emphysema) remove trache tube, occlude stoma and ventilate initially with bag-valve-mask and subsequently re-intubate with oral endotracheal tube
  • If trache tube patent and correctly placed assess chest expansion and air entry to confirm/exclude bronchospasm, pneumothorax, lobar collapse, pleural effusion etc.
  • Treat as appropriate – bronchodilators, thoracocentesis, physio, bronchoscopy, pleural drainage
  • If decreased chest wall compliance consider sedation
  • If increased intra-abdominal pressure, treat appropriately e.g. gastric decompression
  • Re-assess patient after definitive management with investigations as indicated e.g. ABG and CXR.
  • Review 
ventilator settings
  • Be aware there may be more than one cause.
 If there is an obvious precipitating cause e.g. pneumothorax complicating difficult CVC insertion, tracheostomy displacement then treat this directly but then re-assess patient for resolution of hypoxia and high airway pressures

Additional comments:
Candidates were expected to describe a systematic approach and consider the possibility of multiple causes

Discussion

Contrary to the above comment, some of these steps do have to be in order. A good algorithm is suggested in Chapter 3 of  Emergency Department Resuscitation of the Critically Ill,  "The Crashing Ventilated Patient" by Jairo Santanilla.

The following approach has been adopted from the above.

Immediate management:

  • Increase the FiO2 to 100%
  • Disconnect from the ventilator, and manually bag-ventilate them.
  • Simultaneously assess and manage threats to life in a systematic manner.
  • If the lung compliance is good, the patient's ventilator or its tubing is the problem, and you can keep bagging the patient until the ventilator is changed.
  • if the bag ventilation is difficult, one must conclude that the patient or the tube are the problem.

If the bag ventilation is easy and the patient improves with it:

  • Machine factors are to blame.
  • Check the circuit:
    • Check for condensation in the ventilator tubing
    • Change HME 
    • Change the expiratory filter
    • If there is nothing obviously wrong with the tubing, the ventilator may be malfunctioning. Change the ventilator while manually bagging the patient.

If the bag ventilation is difficult and the patient is still unwell:

  • Patient factors are to blame.
  • Either the airway or the rest of the respiratory system is somehow compromised.
  • Address the airway first:
    • In the intubated patient:
      • Is the ETT blocked?
      • Pass a suction catheter down and suction the patient
      • Ensure the patient is not biting the tube.
      • Has the ETT migrated? Is there a cuff  herneation?
      • Auscultate both lungs; ensure equal air entry
      • Listen for cuff leak
      • Ensure satisfactory cuff pressure
    • In the tracheostomy patient:
      • check tracheostomy diameter (too narrow?)
      • check inner cannula (encrusted with inspissated secretions?)
      • check tracheostomy patency (blocked with secretions?)
      • Check tracheostomy position (dislodged during last turn?)
      • Check for subcutaneous emphysema
      • Suction the patient, loking for fresh blood and clots (unrecognised pulmonary haemorrhage?)
  • Let's say the airway is fine. The rest of the respiratory system must be somehow compromised.  The possibilities include:
    • Bronchial occlusion, eg. by sputum plug or clot
    • Bronchospasm
    • Pulmonary embolism
    • Pulmonary oedema
    • Pleural pathology, eg. pneumothorax, haemothorax or pleural effusion
    • Abdominal pathology, eg. massive distension
  • These possibilities need to be investigated systematically:
    • Auscultation of the chest will immediately identify lateralising pathology, and may reveal pulmonary oedema
    • A bedside chest ultrasound will immediately confirm or exclude pneumothorax, haemothorax or large pleural effusion.
    • A bedside TTE should immediately exclude severe LV failure and massive PE.
    • ECG will exclude MI
    • ABG will identify metabolic acidosis
    • CXR to confirm/exclude large bronchus obstruction
    • Bronchoscopy to relieve this mechanical obstruction
  • If there is no problem with the respiratory system, but the patient is still "impossible to ventilate", consider the following extrapulmonary possibilities:
    • Patient-ventilator dyssynchrony
    • Pain of respiration (eg. in context of rib fractures or thoracotomy)
    • Increased ventilatory demand:
      • Severe agitation
      • Seizures
      • Fever and rigors
      • Metabolic acidosis

References

Jairo I. Santanilla "The Crashing Ventilated Patient"; Chapter 3 in Emergency Department Resuscitation of the Critically Ill, American College of Emergency Physicians, 2011.

Question 16 - 2015, Paper 1

Critically evaluate the role of thrombolysis in pulmonary embolism.

College Answer

Theory:

  • Thrombolytic agents activate plasminogen to plasmin and can be used to accelerate clot lysis in pulmonary embolus.
  • Can be given systemically or catheter directed via a pulmonary artery catheter.
  • By reducing clot burden, aim is to decrease pulmonary hypertension, decrease right ventricular dysfunction and improve mortality
  • Side effects of thrombolysis therapy can be devastating and include intracranial haemorrhage and massive GI or other bleeding.
  • Potential benefits of thrombolysis weighed up against risks of haemorrhage.
  • Usual contraindications to thrombolysis: recent intracranial haemorrhage, recent major surgery, active bleeding etc

Evidence:

Systemic Thrombolysis

  • Large randomized controlled trials supporting the use of systemic thrombolytics in pulmonary embolus are lacking
  • Meta-analysis of thrombolysis revealed that in subgroup of haemodynamically unstable patients (n = 154) thrombolysis decreased the composite end point of death or recurrent pulmonary embolus.
  • A commonly accepted indication is persistent hypotension (Massive PE) in a number of guidelines (Level of evidence not great – 2C)
  • More controversial is the role of thrombolysis in haemodynamically stable patients.
  • Recent meta-analysis: no difference in recurrent PE or mortality but increased major bleeding

In the following groups:

  • Submassive PE:
    • Definition: pulmonary embolus with SBP >90 mmHg andmyocardial necrosis or right ventricular dysfunction  on echocardiography – worse prognosis than without pulmonary hypertension/EV dysfunction.
  • Evidence of mortality benefit is lacking.
  • Recent NEJM article showed thrombolysis prevented deterioration in RV dysfunction with no mortality benefit. Increased haemorrhage and stroke rate vs heparin anticoagulation.
  • Cardiopulmonary resuscitation
  • Evidence of benefit is lacking from clinical trials – based on case reports and series
  • Large clot burden
  • Lower dose (“safe dose”) thrombolysis has been investigated in this group and found improvement in pulmonary hypertension (persisted until 28months) but no improvement in mortality and no increased risk of bleeding

Catheter directed thrombolysis:

  •  Can be directed via PAC.
  • Can be used in patients where systemic thrombolytics have failed or risk of systemic thrombolysis considered too great.
  • Evidence of mortality benefit is lacking but may be improved RV dysfunction
  • Small studies

In practice:

  • Usually thrombolysis for patients with massive PE (i.e. Persistent hypotension)
  • Consider on a case by case basis patients with submassive PE (right ventricular dysfunction on echocardiography)
  • Consider safe dose thrombolysis for patients with large clot burden.
  • Consider thrombolysis in CPR
  • Role of catheter directed thrombolysis uncertain.

Additional comments:

This is an area of enormous practical significance AND a common problem. Candidates were not expected to know the details of individual studies, but to be able to show a reasonable understanding of the state of play of the evidence.

A satisfactory answer was expected to include the following:

  • Rationale for using thrombolysis with risks and benefits
  • Indications
  • Discussion of use in sub-massive PE and cardiac arrest
  • Reference to evidence

In general, candidates who failed gave either clearly inaccurate statements or superficial answers.

Discussion

The following topic headings were structured according to the examiner's impression of what a "satisfactory answer" might contain.

Rationale:

  • Plasminogen activators can produce clot lysis
  • Clot bulk is the major pathophysiological contributor to the mortality and morbidity from PE
  • Other thrombotic diseases (eg. AMI and stroke) seem to benefit from thrombolytic therapy
  • Ergo, thrombolysis should reduce mortality and morbidity from PE.

Benefits:

  • Decrease clot burden
  • Improve systemic haemodynamics by improving LV filling
  • Prevent further RV injury
  • Prevent progression to pulmonary hypertension
  • Relieve mechanical obstruction in obstructive cardiac arrest due to PE

Risks:

Indications:

Practical application

  • The dose of alteplase is 0.9mg/kg:
    • 10% of the dose over 1 minute;
    • 90% of the dose over the subsequent hour
    • Maximum dose is 90mg.
  • For cardiac arrest, as little as 10mg (bolus) is required to overcome the mechanical obstruction (Gabrilovich, 2013) - then,  CPR should continue for 30 minutes.

Evidence in support of thrombolysis for massive PE:

  • 2004 meta-analysis (Wan et al);  small sub-group (n = 154) of haemodynamically unstable PE patients.
  • Within this small subgroup thrombolytic therapy reduced the risk of their composite endpoint of death and recurrent PE (from 19% to 9%).
  • On the basis of this, all current guidelines seem to recommend thrombolysis for haemodynamically unstable massive PE.

Evidence for and against thrombolysis in sub-massive PE:

  • PEITHO trial (2014) - referred to it as "a recent NEJM article" in the model answer. Improved haemodynamics but unchanged 7-day mortality and a greatly increased risk of  major haemorrhage and haemorrhagic stroke.
  • TOPCOAT trial (2014) - with thrombolysis, fewer adverse outcomes, better functional capacity, and greater quality of life at 3 months.
  • MOPETT trial (2013) - referred to in the model answer ("lower dose (“safe dose”) thrombolysis has been investigated"). Much less pulmonary hypertension was observed at 28 months, but there was no effect on mortality.
  • Risk is greater than benefit, as mentioned in the model answer: "recent meta-analysis" looking at the use of thrombolysis in haemodynamically stable patients (they probably meant this 2014 paper by Riera-Mestre et al) found that NNT to avoid one death was 125 patients., but NNH for a major bleed were 27, and for ICH were 91.

References

Oh's Intensive Care manual: Chapter 34   (pp. 392) Pulmonary  embolism by Andrew  R  Davies  and  David  V  Pilcher

Anderson, Frederick A., and Frederick A. Spencer. "Risk factors for venous thromboembolism." Circulation 107.23 suppl 1 (2003): I-9.

Konstantinides, Stavros V., et al. "2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism." European Heart Journal (2014): ehu283.

Kearon, Clive, et al. "Antithrombotic therapy for VTE disease: antithrombotic therapy and prevention of thrombosis: American College of Chest Physicians evidence-based clinical practice guidelines." CHEST Journal 141.2_suppl (2012): e419S-e494S.

Kucher, Nils, et al. "Massive pulmonary embolism." Circulation 113.4 (2006): 577-582.

Jerjes-Sanchez, Carlos, et al. "Streptokinase and heparin versus heparin alone in massive pulmonary embolism: a randomized controlled trial." Journal of thrombosis and thrombolysis 2.3 (1995): 227-229.

Kucher, Nils, and Samuel Z. Goldhaber. "Management of massive pulmonary embolism." Circulation 112.2 (2005): e28-e32.

Wan, Susan, et al. "Thrombolysis compared with heparin for the initial treatment of pulmonary embolism a meta-analysis of the randomized controlled trials." Circulation 110.6 (2004): 744-749.

Kasper, Wolfgang, et al. "Management strategies and determinants of outcome in acute major pulmonary embolism: results of a multicenter registry." Journal of the American College of Cardiology 30.5 (1997): 1165-1171.

Kline, J. A., et al. "Treatment of submassive pulmonary embolism with tenecteplase or placebo: cardiopulmonary outcomes at 3 months: multicenter double‐blind, placebo‐controlled randomized trial." Journal of Thrombosis and Haemostasis 12.4 (2014): 459-468.

Sharifi, Mohsen, et al. "Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT” Trial)." The American journal of cardiology 111.2 (2013): 273-277.

Stein, Paul D., et al. "Multidetector computed tomography for acute pulmonary embolism." New England Journal of Medicine 354.22 (2006): 2317-2327.

Meneveau, Nicolas. "Therapy for acute high-risk pulmonary embolism: thrombolytic therapy and embolectomy." Current opinion in cardiology 25.6 (2010): 560-567.

Riera-Mestre, Antoni, et al. "Thrombolysis in hemodynamically stable patients with acute pulmonary embolism: A meta-analysis." Thrombosis research 134.6 (2014): 1265-1271.

Meyer, Guy, et al. "Fibrinolysis for patients with intermediate-risk pulmonary embolism." New England Journal of Medicine 370.15 (2014): 1402-1411.

Gabrilovich, Michael, Susan McMillen, and Marcus Romanello. "1319: Use of thrombolytics for pulmonary embolism in refractory cardiac arrest." Critical Care Medicine 41.12 (2013): A340.

Logan, Jill K., et al. "Evidence-based diagnosis and thrombolytic treatment of cardiac arrest or periarrest due to suspected pulmonary embolism." The American journal of emergency medicine 32.7 (2014): 789-796.

Lavonas, Eric J., et al. "Part 10: Special Circumstances of Resuscitation 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care." Circulation 132.18 suppl 2 (2015): S501-S518.

Question 4 - 2015, Paper 2

A 42-year-old male is admitted to your intensive care day 4 post induction chemotherapy for acute promyelocytic leukemia (AML-M3). The patient was initially treated with idarubicin and all-trans retinoic acid (ATRA). He has progressively become more dyspnoeic in the ward. A chest X-Ray demonstrates a bilateral, diffuse pulmonary infiltrate.

Initial examination reveals:

  • RR 40 breaths/min, SpO2 88% on 10 L/min O2 by face mask
  • Glasgow Coma Scale 14 (E4 M6 V4)
  • Temperature 38.9 ºC
  • Heart rate 144 beats/min
  • Blood pressure 95/50 mmHg

Full blood count is as follows on admission:

Parameter

Patient value

Normal Adult Range

Haemoglobin

88 g/L*

135 – 180

White Cell Count

26 x 109/L* ( no differential)

4.0 – 11.0

Platelets

22 x 109/L*

150 – 400

Comment: Blasts visible

International normalised ratio (INR)

3.2

a)   Give your differential diagnosis for his respiratory failure.        (40% marks)
b)   What are the major issues in this patient and how would you manage them?    (60% marks)

College Answer

a)

Sepsis in a patient with immune compromise secondary to leukaemia. Nosocomial pneumonia

–   Bacterial –Gm negative –E.coli, Pseudomonas, Klebsiella
–   Gm positive: Strep, Staph epi
–   Fungal:  Aspergillus, Candida, Cryptococcus
–   Atypical:  Legionella, mycoplasma
–   Viral:  CMV, HSV, RSV, Influenza, H1N1, VZV
–   PCP:  Toxoplasmosis
–   TB (depending on background)

Non- infective
-    Idiopathic pneumonia syndrome
-    Cardiac failure (cardiotoxicity due to induction chemo)
-    Diffuse alveolar haemorrhage
-    Non cardiogenic capillary leak syndrome

-    Chemo induced ALI / pneumonitis
-    Retinoic Acid Syndrome

b)
Major issues are:

1.    Hypoxic respiratory failure

Probable nosocomial pneumonia now requiring respiratory support and is likely to be progressive

Problem with invasive respiratory support carrying very high mortality and complications including barotrauma, further nosocomial infections

Management - Non-invasive respiratory support commencing with CPAP progressing to BiPAP using the lowest FiO2 to maintain PaO2 above 60 mmHg. Attempt to avoid invasive respiratory support if possible.

2.    Possible Sepsis

May rapidly progress to septic shock in this patient Possible unusual infective agent

Early commencement of Broad cover (Cefepime / Ceftazadime / Tazocin and Vancomycin + Voriconazole / caspofungin / liposomal amphotericin + acyclovir + Bactrim.) Discussion with ID and haematology specialists for prior antimicrobial therapy, CMV status, previous aspergillus infection etc

Removal of indwelling intravenous catheters that are in anyway suspicious for infection

Central access (with platelet cover), consideration of inotropes after transfusion of blood products and IV fluids preferentially using Albumin containing solutions.

Steroids.

3.    Prognosis from acute promyelocytic leukemia (AML-M3).

Management is to liaise early with treating haematologist to ascertain likely outcome from primary disease and also discuss with family and patient the significant risk of deterioration and mortality.

4.    Other

Treatment of coagulopathy- Vit K, Platelets, FFP
Difficulties in making definitive diagnosis

Possible atypical infection with low yield probable from cultures Significant other non-infective differential diagnosis.

Management includes having a high degree of suspicion for resistant or unusual organism and managing with broad cover.

Additional Examiners’ Comments:

Candidates were expected to give some indication of treatment strategies e.g. antibiotics, reversal of coagulopathy rather than just writing D/W ID, haematology etc.

Discussion

a)
A long list of differenials  for a diffuse pulmoanry infiltrate is given in the chapter on the causes of ARDS. After this question came out, the list was amended to include ATRA syndrome, which is a freakishly rare thng and unlikely to ever be seen by anyobne outside of a major bone marrow transplant centre. The list mainly comes from an excellent article from Silvia Blanco and Antoni Torres (antimicrobe.org).

Differential Diagnosis for Diffuse Bilateral Pulmonary Infiltrates

Vascular:

  • Pulmonary haemorrhage
  • Cardiogenic pulonary oedema

Infectious

  • Bacterial
  • Viral
  • Fungal
  • PJP

Neoplastic

  • Lymphangitis
  • Infiltrative neoplasm

Idiopathic

  • ARDS
  • Idiopathic pneumonia syndrome

Drug-induced

  • Eosinophilic pneumonitis
  • BOOP
  • Alveolar haemorrhage
  • Methotrexate-induced

Autoimmune

  • Goodpastures (haemorrhagic)
  • Rheumatoid pneumonitis
  • TRALI
  • Graft vs host disease in BMT
  • Engraftment syndrome
  • ATRA syndrome

Traumatic

  • Bilateral atelectasis
  • Pulmonary contusions
  • Chemical pneumonitis

ATRA syndrome (or "retinoic acid syndrome", or "differentiation syndrome") listed in the differentials above is a complication of therapy with all-trans-retinoic acid. A good references for those interested is a 2008 paper by Patatanian and Thompson. The authors describe this complication of ATRA therapy as "unpredictable but frequent" and offer little in the way of aetiological information.

Idiopathic pneumonia syndrome (also mentioned in the college list of differentials) is a (probably autoimmune) complication of bone marrow transplant, which is well covered in this 2011 article by Panoskaltsis et al. Characteristic features consist of pneumonia-like infiltrates and a demonstrated absence of respiratory tract infection.

b)

"What are the major issues in this patient and how would you manage them?" This part of the question requires a structured answer. There are many ways to structure an answer like this. The suggested answer below is organised by important systems.

Issues:

  • Airway: The need to avoid intubation
  • Respiratory: Hypoxic respiratory failure
  • Circulatory: Haemodynamic instability: likely, septic shock (HR 144, BP 95/50)
  • Neuro: A decreased level of consciousness (GCS 14)
  • Haematological: anaemia, thrombocytopenia, likely neutropenia, and coagulopathy.
  • Infectious: High fever (38.9°C) and raised WCC (26)
  • Definitive diagnosis:  cause of respiratory failure is uncertain
  • Social: prognosis and family understanding of the situation, medical consensus

Plans:

  • Airway plan:
    • Avoid intubation- unless it is clear that the patient is failing. See the non-invasive ventilation chapter for the rationale behind this. In short, recommendations to avoid intubation in immunosuppressed patients are based on early trials (eg. Scales et al, 2008) which do not reflect the recent improvements in critical care for such patients. The college answer to Question 11 from the second paper of 2018 reflects this fact; they actually say "Invasive ventilation is not routinely avoided given overall good prognosis". This is very interesting, as in this 2015 version of the question, the college model answer recommended to avoid intubation. To digress briefly on this important topic, in a more recent review Lueck et al (2018) found markedly improved outcomes (eg. 1-year survival up from 14% to 32%) in BMT patients admitted to ICU. 
    • Keep patient fasted (nil by mouth) in the event intubation is required
  • Respiratory support plan:
    • Commence CPAP NIV
    • Aim for SpO2 >90%, PaO2 > 60mmHg
    • Breaks every 2 hours for chest physiotherapy (on high flow nasal prongs)
    • Ensure humidified circuit
    • Ensure frequent cough; encourage expectoration of sputum
  • Circulatory support plan:
    • Assess for fluid responsiveness using dynamic parameters
    • If fluid responsive, resuscitate with 20% albumin
    • If fluid resuscitation is ineffective, maintain MAP >65 with noradrenaline
    • Consider stress dose steroids (unless steroids are already being given)
  • Neurological plan:
    • Avoid sedating analgesics
    • Change NIV mode to BiPAP if hypercapnea develops
  • Haematological:
    • Transfuse to Hb >70 (TRISS)
    • Correct platelets for CVC insertion
    • Administer Vitamin K and FFP for correction of the INR
    • Seek clarification re. WCC differential (All neutrophils? All blasts?)
  • Infectious:
    • Fungal cover with voriconazole or caspofungin
    • PJP cover with Bactrim
    • Viral cover with aciclovir
    • Atypical cover with azithromycin
    • Gram negative and anaerobe cover with meropenem
    • Gram-positive cover with vancomycin
  • Definitive diagnosis:
    • Blood and sputum cultures
    • Atypical pneumonia serology
    • Urinary legionella and pneumococcal antigens
    • Sputum culture
    • TTE to exclude the contribution of cardiac failure to shock and hypoxia
    • Discussion with haematology team regarding the use of high dose steroids for ATRA syndrome (10mg bd of dexamethasone for 3 days, or addition of cytarabine to the chemotherapy cocktail to suppress the bone marrow).
  • Social:
    • Schedule family discussion
    • Confer with haematology regarding prognosis

 

References

Panoskaltsis-Mortari, Angela, et al. "An official American Thoracic Society research statement: noninfectious lung injury after hematopoietic stem cell transplantation: idiopathic pneumonia syndrome." American journal of respiratory and critical care medicine 183.9 (2011): 1262-1279.

Patatanian, E., and D. F. Thompson. "Retinoic acid syndrome: a review." Journal of clinical pharmacy and therapeutics 33.4 (2008): 331-338.

Lee, Hwa Young, Chin Kook Rhee, and Jong Wook Lee. "Feasibility of high-flow nasal cannula oxygen therapy for acute respiratory failure in patients with hematologic malignancies: A retrospective single-center study." Journal of critical care 30.4 (2015): 773-777.

Scales, Damon C., et al. "Intensive care outcomes in bone marrow transplant recipients: a population-based cohort analysis." Critical Care 12.3 (2008): R77.

Lueck, Catherina, et al. "Improved short-and long-term outcome of allogeneic stem cell recipients admitted to the intensive care unit: a retrospective longitudinal analysis of 942 patients." Intensive care medicine 44.9 (2018): 1483-1492.

Question 18 - 2015, Paper 2

a)    List and briefly describe the different mechanisms by which an ICU ventilator may detect (and thus is triggered by) a spontaneous inspiratory effort.

Include in your answer the utility and potential disadvantages of each mechanism.    (60% marks)

b)    Outline the mechanisms by which an ICU ventilator may cycle from inspiration to expiration. (40% marks)

College Answer

a)

Pressure triggering: the ventilator triggers in response to a fall in pressure by a user defined value below set PEEP or CPAP.

Requires a respiratory muscle contraction against a static load (closed inspiratory limb) to generate a negative pressure below the threshold set value before fresh gas flow can occur. The imposed work of triggering is high, and may exceed the patient’s reserve, resulting in missed triggers. Working against a static load may cause patient distress. There is significant delay between the initiation of respiratory effort and the onset of any fresh gas flow.

Flow triggering: the ventilator triggers in response to a user defined change in flow during the expiratory phase. The exact mechanism is ventilator specific and differs between ventilator types. Obviates some of the disadvantages of pressure triggering. A constant fresh gas flow is available for any inspiratory effort, eliminating patient effort against a static load. However there still remains a delay between inspiratory effort and the onset of support. Auto triggering and cardiac triggering can occur if the flow is too sensitive.

Neural Assistance, (NAVA): specific to Maquet Servo ventilators, diaphragmatic EMG is detected by a specific nasogastric tube with an array of bipolar electrodes positioned across the oesophago-gastric junction when the tube is placed correctly.

NAVA improves patient-ventilator synchrony when compared with commonly used PSV.

Patients ventilated with NAVA do not experience the increased tidal volumes and reduced ventilatory frequency seen at higher levels of PSV.

NAVA prevents dynamic hyperinflation which has been implicated as the major factory in asynchrony.

NAVA eliminates ‘wasted efforts’ where a patient makes inspiratory effort but fails to trigger the ventilator.

Requires specific nasogastric tube

b)

Time cycled.

Once the time programmed for inspiration (inspiratory flow time plus inspiratory pause time) is completed, the ventilator automatically cycles to expiration. This occurs independent of any patient effort or other variables.

Flow cycled.

Once flow has decreased to a pre-determined minimum value, (eg 25% maximum flow rate), the ventilator cycles to expiration. In lungs with poor compliance, the cycling threshold will be reached more quickly, resulting in a shorter time for inspiration and a smaller tidal volume. Used more in spontaneous modes

Pressure cycled.

Once a set pressure is reached, the ventilator will cycle to expiration. Non-compliant lungs will have smaller tidal volumes than compliant lungs. The most common application for this mode is as an alarm setting as a safety feature to prevent sustained or excessive high pressures.

Volume cycled

Once a set volume is reached, the ventilator will cycle to expiration (or inspiratory pause).

Additional Examiners’ Comments:

Overall there was a lack of knowledge on the core topic of ventilator triggering and cycling and inadequate explanation of basic concepts. Some candidates confused pressure with volume and/or flow. Most answers were incomplete and few candidates scored well

Discussion

Methods of triggering, their advantages and disadvantages:

Triggering method Mechanism Advantages Disadvantages
Pressure triggered by a patient-generated drop in pressure, from  PEEP.
  • Prevents cardiac auto-triggering
  • By gradually increasing respiratory workload, one may theoretically  "train" the respiratory muscles to perform more work
  • May be useful as a part of extubation assessment (a high pressure trigger is lke a quasi-MIP measurement)
  • Requires the patient to inhale against a closed inspiratory valve. This increases the work of breathing.
  • The patient may not be able to generate such pressure, and may be unable to trigger
  • Between the initiation of effort and the actual delivery opf gas, there is a delay (however long it takes for the patient to generate that sort of pressure)
Flow Triggered by a patient-generated change in fresh gas flow though a circuit
  • Little effort is required: the patient's respiratory workload is decreased
  • Rapid triggering: little delay between initiated effort and the triggered breath
  • May have auto-triggering by cardiac oscillations
  • Still no rapid enough (some delay exists between initiated effort and the delivered breath)
NAVA Triggered by a change in diaphragmatic EMG, detected by a properly positioned electrode array on a special NGT
  • Least amount of patient effort is wasted
  • Patient-ventilator synchrony is improved compared to PSV
  • Dynamic hyperinflation is prevented
  • A special NG tube is required
  • It must be positioned correctly; if it is slightly dislodged the system does not work.

References

BANNER, MICHAEL J., PAUL B. BLANCH, and ROBERT R. KIRBY. "Imposed work of breathing and methods of triggering a demand-flow, continuous positive airway pressure system." Critical care medicine 21.2 (1993): 183-190.

Sassoon, Catherine SH. "Triggering of the ventilator in patient-ventilator interactions." Respiratory Care 56.1 (2011): 39-51.

Question 1 - 2015, Paper 2

Critically evaluate the role of non-invasive ventilation (NIV) in critically ill patients.

College Answer

Rationale

NIV provides ventilatory support for patients with respiratory failure via a sealed face-mask, nasal mask, mouthpiece, full face visor or helmet without the need for intubation. Ventilatory support may be with CPAP or bi-level modes and delivered by a range of ventilators from specifically designed devices to full-service ICU ventilators.

NIV decreases resource utilisation compared with invasive ventilation and avoids the associated complications.

Patient selection and a well-designed clinical protocol are important to avoid delaying intubation in patients who are not suitable for and/or failing NIV.

Indications

  • APO – alveolar recruitment, decreased afterload, decreased work of breathing
  • COPD – decrease work of breathing and unload respiratory muscles
  • Immunosuppressed
  • Planned strategy post extubation in selected patients
  • OSA / Obesity hypoventilation syndrome
  • Asthma
  • Patients with not for intubation/ treatment limitation orders who may qualify for HDU admission or admission to respiratory care units
  • Post-operative patients – in selected patients
  • Rib fractures
  • Cystic fibrosis as bridge to transplantation

Evidence for its use:

  • APO – studies show decreased intubation rate and faster time to resolution of respiratory failure and reduction in mortality and hospital length of stay
  • COPD – RCTs and Cochrane review (14 RCTs) showed significant improvement in intubation rates, complications, length of hospital stay and mortality rates for NIV compared with invasive ventilation
  • Immunocompromised - – 2 studies, one looking at solid organ transplant recipients and one looking at patients with haematological malignancy showed benefit with NIV, i.e. fewer intubations, complications and reduced ICU and hospital mortality
  • Asthma – probably beneficial but limited evidence
  • Rib fractures – fewer episodes of pneumonia but no mortality benefit and limited evidence

Evidence against its use:

  • Use as rescue strategy for failed extubation – delays time to re-intubation. May be of benefit as part of weaning strategy and planned intervention post extubation especially in COPD patients
  • ARDS – not recommended as first line therapy

Predictors of success

  • Younger age
  • Unimpaired conscious state
  • Moderate rather than severe hypercarbia
  • Rapid improvement in physiological parameters

Contra-indications

  • Coma
  • Cardiac / respiratory arrest
  • Cardiac instability – shock, ventricular dysrhythmias, severe acute myocardial ischaemia GI bleeding
  • Intractable vomiting
  • Inability to protect airway – poor cough, excessive secretions, decreased conscious state Upper airway obstruction
  • Following upper GI surgery (some debate about this)

Complications

  • Facial and nasal trauma and pressure sores
  • Gastric distension
  • Dry mucous membranes
  • Aspiration of gastric contents

Alternatives

  • Invasive ventilation
  • HFNP – may provide CPAP 5mm Hg

Summary statement / My Practice

Such as:

  • Role of NIV in critically ill includes APO and respiratory failure in COPD and immunosuppressed patients. In my practice I use NIV as a planned strategy post-extubation in selected patients and as ventilatory support for patients with respiratory failure and treatment directives limiting care. I do allow its use to delay or withhold intubation in those who need this.

Additional Examiners’ Comments:

NIV is a fundamental part of intensive care practice and the overall level of understanding was poor. Few candidates were able to demonstrate detailed knowledge of this core therapy.

Candidates were not expected to include as much detail to score good marks. Essential points included indications, some mention of evidence for and against, contra-indications and complications. Candidates were given credit if they included valid points not in the answer template.

Discussion

There is no way anybody could write all that in ten minutes unless they had a prefabricated answer all loaded and ready to go in their head.  

Rationale for NIV

  • Positive pressure ventilation in general has benefits which are common to both NIV and IPPV.
  • NIV has advantages when compared to IPPV:
    • Decreased cost
    • Better tolerated (no need for sedation)
    • More convenient
    • Better availability outside of the ICU setting (eg. domiciliary)
    • Ability to interrupt therapy for breaks allows easier weaning from mechanical support

Strong indications for NIV

  • Cardiogenic pulmonary oedema: improves survival, decreases rate of intubation (Cochrane review)
  • COPD: halves mortality when compared to invasive ventilation (Cochrane review)
  • Obesity hypoventilation sydrome: mainstay of chronic maintenance and rescue for acute respiratory failure (Carrillo et al, 2012)
  • Rib fractures and chest trauma: reduced mortality, intubation rate and infections (Chiumillo et al, 2013)

Weak indications for NIV

  • Asthma:  no mortality benefit, but prevents intubation, decreases ICU stay and imrpoves delivery of nebulised drugs (Lim et al, 2012)
  • Weaning COPD patients from invasive ventilation: improves mortality, reduces VAP risk (Cochrane review)
  • Elective extubation of patients without respiratory failure: Cooperative hypercapneic high-risk patients may benefit (Ferrer et al, 2006) but not all-comers (Su et al, 2012) and it may actually be dangerous in unselected patients (Esteban et al, 2004) as waiting for NIV to work in a patient who clearly requires re-intubation is a pointless time-wasting exercise with an associated increase in mortality.
  • Ventilation for cystic fibrosis patients awaiting lung transplant: based on small-scale observational studies (Bright-Thomas et al, 2013)
  • Community-acquired pneumonia: useful in patients with pre-existing cardiac or respiratory disease (Carrillo et al, 2012)
  • Post-operative respiratory failure- "prophylactic NIV" - little data in support of this (Jaber et al, 2012)
  • Lung infection in the neutropenic patient: improves survival when compared to intubation (one small trial
  • Limitations of therapy: if the patient requires intubation but is "not for " intubation; NIV provides comfort (Azoulay et al, 2010)

Disadvantages when compared to invasive ventilation

  • More difficult to manage with an uncooperative patient
  • Cannot be used in physically restrained patients (what if they vomit? They cannot remove the mask)
  • Prevents the effective clearance of secretions and impairs physiotherapy access for suctioning
  • Cannot be performed on patients with a decreased level of consciousnes
  • Mask-face interface is difficult to manage: "one size fits all" masks do not in fact fit all; patients with unusual anatomy or little facial soft tissue (eg. in cachexia) will have more difficulty
  • Mask leak is uncomfortable and decreaseas the effectiveness of the therapy
  • Work of breathing may be increased

Contraindications for NIV

  • Decreased level of consciousness
  • Respiratory arrest
  • Vomiting
  • Hemodynamic instability
  • Poor clearance of secretions, eg. absent cough and gag
  • large sputum load and/or pneumonia
  • surgical or traumatic damage to the airways or oesophagus

Complications of NIV

  • Mask intolerance, agitation and claustrophobia
  • Increased need for sedation
  • Delay of intubation
  • Aspiration
  • Poor clearance of secretions
  • Hypotension of hypovolemic patients
  • Facial pressure areas
  • Raised intracranial pressure
  • Aerophagy
  • Damage to facial, nasal and oesophageal surgical sites or traumatic injuries, leading to surgical emphysema, pneumothorax and pneumomediastinum

References

Gay, Peter C. "Complications of noninvasive ventilation in acute care."Respiratory care 54.2 (2009): 246-258.

Hore, Craig T. "Non‐invasive positive pressure ventilation in patients with acute respiratory failure." Emergency Medicine 14.3 (2002): 281-295.

Lightowler, Josephine V., et al. "Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis." BMJ: British Medical Journal 326.7382 (2003): 185.

Ram, F. S., et al. "Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease." Cochrane Database Syst Rev 3.3 (2004).

Gay, Peter C. "Complications of noninvasive ventilation in acute care."Respiratory care 54.2 (2009): 246-258.

Carrillo, Andres, et al. "Noninvasive ventilation in acute hypercapnic respiratory failure caused by obesity hypoventilation syndrome and chronic obstructive pulmonary disease." American journal of respiratory and critical care medicine 186.12 (2012): 1279-1285.

Chiumello, D., et al. "Noninvasive ventilation in chest trauma: systematic review and meta-analysis." Intensive care medicine 39.7 (2013): 1171-1180.

Lim, Wei Jie, et al. "Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma." The Cochrane Library Published Online: 12 DEC 2012

Alonso, Ana Souto, Pedro Jorge Marcos Rodriguez, and Carlos J. Egea Santaolalla. "Long-Term Noninvasive Ventilation Among Chronic Respiratory Failure Diseases (Cystic Fibrosis and Other Diseases) Awaiting Lung Transplantation: Key Determinants and Practical Implications." Noninvasive Mechanical Ventilation. Springer International Publishing, 2016. 771-779.

Gupta, Dheeraj, et al. "A prospective randomized controlled trial on the efficacy of noninvasive ventilation in severe acute asthma." Respiratory care 55.5 (2010): 536-543.

Williams, Trevor J., et al. "Risk factors for morbidity in mechanically ventilated patients with acute severe asthma." The American review of respiratory disease146.3 (1992): 607-615.

Carrillo, Andres, et al. "Non-invasive ventilation in community-acquired pneumonia and severe acute respiratory failure." Intensive care medicine 38.3 (2012): 458-466.

Jaber, Samir, Gerald Chanques, and Boris Jung. "Postoperative non-invasive Ventilation." Intensive Care Medicine. Springer New York, 2008. 310-319.

Azoulay, Élie, et al. "Palliative noninvasive ventilation in patients with acute respiratory failure." Intensive care medicine 37.8 (2011): 1250-1257.

Azoulay, Élie, et al. "Noninvasive mechanical ventilation in patients having declined tracheal intubation." Intensive care medicine 39.2 (2013): 292-301.

Ferrer, Miquel, et al. "Early noninvasive ventilation averts extubation failure in patients at risk: a randomized trial." American journal of respiratory and critical care medicine 173.2 (2006): 164-170.

Su, Chien-Ling, et al. "Preventive use of noninvasive ventilation after extubation: a prospective, multicenter randomized controlled trial." Respiratory care 57.2 (2012): 204-210.

Esteban, Andrés, et al. "Noninvasive positive-pressure ventilation for respiratory failure after extubation." New England Journal of Medicine 350.24 (2004): 2452-2460.

Bright-Thomas, Rowland J., and Susan C. Johnson. "What is the role of noninvasive ventilation in cystic fibrosis?." Current opinion in pulmonary medicine 20.6 (2014): 618-622.

 
 

Question 21 - 2016, Paper 1

Critically evaluate the use of neuromuscular blocking agents in severe respiratory failure due to acute respiratory distress syndrome (ARDS).

College Answer

Rationale & Theoretical Benefits

  • In general will reduce O2 consumption & CO2 production
  • Avoids patient ventilator dys-synchrony
  • Allows evaluation of respiratory mechanics
  • Generally required to perform a recruitment manoeuvre
  • In patients with pronounced spontaneous respiratory effort:
    • They may draw large spontaneous tidal volumes well in excess of appropriate ARDSnet values (pulmonary stress)
    • They may generate large spontaneous negative trans-pulmonary pressures during controlled breaths (pulmonary strain)
    • Spontaneous respiratory activity is difficult to otherwise supress (with sedation only), particularly in the setting of permissive hypercapnia
  • Observationally improves oxygenation in the short term
  • May reduce cytokine release and biotrauma
  • Facilitates prone positioning

Theoretical Problems

  • Contradicts strategies of maintaining spontaneous efforts and respiratory muscle strength.
  • May unmask poor compliance in patients who were generating very negative inspiratory pressures while breathing spontaneously, with consequent difficulties maintaining adequate tidal volume.
  • Potential for awareness during paralysis
  • Risks of ‘Critical Illness Weakness’ associated with use of NMBA. 
  • Risks of accumulation of NMBA drug in critical illness. 
  • Increased risk of positive fluid balance and thromboembolic risks.

Practical Issues

  • Timing / duration of paralysis not known – Papazian used 48 hr
  • Which NMB – non-steroid based may be better for reducing risk of weakness (Papazian used cisatracurium)
  • Train of four monitoring needed

Best Evidence                                                                                                         

  • Single French RCT (Papazian, NEnglJM Sept 2010) 
  • Severe ARDS, P/F < 150
  • Showed mortality improvement at 90 days with paralysis for 48 hrs in early severe ARDS hours (hazard ratio for death 0.68).  No increase in weakness.
  • Evidence for improved oxygenation beyond period of paralysis. 
  • Criticisms:
    • 25% of eligible patients enrolled, limits external validity
    • study used low levels of PEEP (lower than the control of several high vs. low PEEP
    • trials)

Practice statement

Anything reasonable – for example:

I do not use NMBs routinely in severe ARDS but in selected patients e.g. those difficult to ventilate / oxygenate I use cistracurium infusion with train of four monitoring

Discussion

Rationale for the use of neuromuscular blockade in ARDS

  • Improve chest wall compliance: The lung compliance is already poor enough; removing chest wall compliance from the equation helps to prevent absurdly high peak pressures
  • Improved patient-ventilator synchrony: Many of these patients end up ventilated with such perverse pressure/volume combinations that without paralysis there would be a constant and counterproductive battle of patient versus ventilator. True, this is something one could achieve with haemodynamically disastrous doses of sedation, but ... why would you?
  • Recruitment manoeuvres  generally require paralysis for the abovementioned reasons; if the patient tries to exhale or cough during one of these manoeuvres, a pneumothorax may occur.
  • Prone ventilation usually requires paralysis
  • Decrease skeletal muscle metabolism: this is a hidden benefit, which is frequently overlooked. Neuromuscular blockade prevents the skeletal muscle from performing anything but the very barest baseline of metabolic work; the ATP production in the muscle fibres drops to whatever is required to maintain ionic concentration gradients. This decreases the oxygen extraction ratio for a large percentage of your patients tissues. Oxygenated blood, formerly directed into muscles, is redistributed into splanchnic vascular beds. Indeed, in a study performed on ICU patients with respiratory failure, the oxygen extraction ratio was found to by decrease 5% (from 36% to 31%).
  • Improved assessment of respiratory mechanics: without the interference of respiratory muscles, the lung compliance can be assessed more correctly, and the pressure-volume loops are more meaningful

Disadvantages of sustained neuromuscular blockade

  • This strategy is contrary to the normal strategy of ventilating patients with the most spontaneous mode possible, to preserve their muscle strength and to increase their comfort.
  • Longer duration of ventilation and longer ICU stay (Arroliga et al, 2005)
  • Increased risk of critical illness polyneuromyopathy
  • Increased risk of pressure areas
  • Increased risk of DVTs
  • Accumulation of paralytic agents (unless you use something like cisatracurium)
  • Risk of paralysed awareness
  • Increased nursing care

Evidence for the efficacy of neuromuscular blockade in ARDS

  • Papazian et al, 2010 -  a 48 hour course of cisatracurium early in the progress of severe ARDS. The authors found a 10% absolute risk reduction of 90-day mortality (31.6% vs 40.7%) associated with the use of neuromuscular blockade, without any increase in the risk of ICU-acquired weakness. , This places cisatracurium in the rare category of things which have been supported by positive trials.  Alongside low tidal volume ventilation and low delta-P, this is one of the strategies which can be strongly recommended. Unfortunately, as the college mention, the study has several weak points:
    • Papazian et al only enrolled 25% of the eligible patients. 10% of patients excluded due to 'other reason', whatever that means.
    • 21% of the patients had PA catheters, which is totally contrary to modern Australian practice
    • 30% of the patients received nitric oxide, which has been thoroughly discredited in the literature and has fallen into disuse in Australia
    • Papazian et al used a surprisingly low PEEP, around 9 cmH2O on average.
    • The groups differed in their use of steroids (39% in treatment arm, 45% in placebo)
    • The mortality from ARDS was much lower than predicted, which underpowered the study.
  • Blanch et al, 2015 - a prospective study which observed that ventilator asynchrony is associated with a higher in-hospital mortality.

References

Papazian, Laurent, et al. "Neuromuscular blockers in early acute respiratory distress syndrome." N Engl J Med 363.12 (2010): 1107-1116.

Neto, Ary Serpa, et al. "Neuromuscular blocking agents in patients with acute respiratory distress syndrome: a summary of the current evidence from three randomized controlled trials." Annals of intensive care 2.1 (2012): 1-8.

Question 23 - 2016, Paper 1

Outline the strategies for management of a persisting broncho-pleural fistula (BPF) in a mechanically ventilated patient. Include in your answer, where relevant, the advantages and disadvantages of the strategies listed.

College Answer

Principles of Management:

1. Drainage                                                                                                                                                 

  • Adequate drainage of the fistula with an intercostal catheter of adequate size to manage a large air leak.
  • May require multiple catheters, and ability to manage large flow rates.
  • Minimise suction.                                                                                                                                                                 

2.Ventilatory management                                                                                                    

  • Aim is to reduce mean airway pressure to reduce flow through fistula tract.
  • Low tidal volume and PEEP.
  • Low mandatory breath rate.
  • Permissive hypercapnoea.
  • Short inspiratory time.
  • Attempt to wean to spontaneous breathing mode from mandatory ventilation as soon as practicable and preferably from ventilatory support altogether.

3. Independent Lung Ventilation                                                                                           

  • Advantages: - May minimise leak in injured lung whilst preserving gas exchange with conventional parameters in normal lung.
  • Disadvantages: -requires some form of double lumen tube – difficult to place and secure.
  • May not be tolerated in hypoxic patients.
  • Requirement for two ventilators –either synchronous or asynchronous – technically demanding and complex.                                                            

4.High Frequency Ventilation                                                                                                                

  • Advantages are that it may reduce peak air pressures and theoretically reduce air leak.
  • Disadvantages - not widely available. Recent evidence suggesting an increase in mortality for this ventilatory technique in ARDS patients.      

5.Surgery                                                                                                                                  

  • Advantages – Definitive management strategy. May be only option to seal leak.  Disadvantages – Patient may not be fit enough to tolerate.                             

6. Endobronchial Occlusion                                                                                                                    

  • Advantages – Widely available, can be definitive treatment.
  • Disadvantages – may be technically challenging, not feasible with multiple leaks.

7. Application of PEEP to intercostal catheter                                                   

  • Advantages – may decrease leak volume and maintain intra-thoracic PEEP.
  • Disadvantages – compromise drainage, risk of tension, not feasible with multiple tubes.

8. ECMO                                                                                                                                                      

  • Advantages – may be only option to treat hypoxia.
  • Disadvantages – not widely available, complex, little experience.

Discussion

Management Strategies for Bronchopleural Fistula
Strategy Advantages Disadvantages
Drainage
- large-bore drain
- or, multiple drains
- minimise suction
  • easy and readily available
  • Usually well tolerated
  • Does not interfere with weaning of ventilation
  • Risk of damaging more lung and creating larger leaks
  • Potentially, perpetuates the fistula by negative pressure suction
  • Invasive
Ventilator strategy:
- low VT
- low PEEP
- low resp rate
- short insp. time
- tolerate high PCO2
- wean rapidly
- extubate early
 
  • easy and readily available
  • Usually well tolerated
  • Early extubation is the ideal step to aim for, as spontaneous negative pressure breathing is better for BPF healing than positive pressure ventilation.
  • The BPF itself may frustrate weaning off ventilation
  • Mandatory mode may prolong ventilation time
  • Permissive hypercapnea may lead to respiratory acidosis, which is not ideal for the patient with traumatic brain injury
Independent lung ventilation
- dual-lumen tube
- or, bronch blocker
 
  • Isolation of one lung permits the selective low-volume low-pressure ventilation of the affected lung, and more rapid higher volume ventilation of the unaffected lung.
  •  PCO2 levels may be easier to control in this manner
  • Technically difficult: DLT insertion is one thing; running two ventilators is another.
  • There may be leak of gas and pressure from one lung to another if the seal is imperfect
  • Sedation requirements will  be higher, to tolerate the larger tube and the very unnatural respiratory pattern
  • Local pressure effects of the DLT are also more problematic
     
Surgical repair
  • The affected lung can be surgically repaired. USually, this means segmental lobectomy (for alveolar leaks) or patching and oversowing of the bronchial leak
  • Apparently, success rates are between 80 and 95%
  • It may be impossible to find the leak intraoperatively
  • It may be unfeasible to remove so much lung
  • It may be impossible if there are multiple leaks
  • The patient must tolerate one-lung ventilation
  • This approach requires thoracotomy
Bronchial stenting
  • The affected bronchus can be stented over bronchoscopically, thereby blocking the leak.
  • This is a minimally invasive alternative to surgical patch repair
  • You need to be sure of where the leak is
  • The leak must be in an accessible bronchus.
  • This may not work if there are multiple leaks
  • The procedure requires technical expertise
  • The patient must be fit to tolerate the bronchoscopy
Bronchial occlusion
  • Similarly to surgery, the affected pronchus is blocked with either a one-way valve or a plug. In fact, the Lois article lists options such as blood clot, cyanoacrylate glue, fibrin, lead shot,  gel foam, calf bone, and various others.
  • You need to be sure of where the leak is
  • The leak must be in an accessible bronchus
  • A major part of the lung may be sacrificed
  • The atelectatic lung may develop infection
Application of PEEP to the ICC
  • The equal intra and extrathoracic PEEP decreases the leak volume
  • Maintained intra-thoracic PEEP permits higher PEEP levels to be used
  • Drainage is compromised
  • There is a major risk of rapid tension pneumothorax
HFOV
  • May reduce peak pressures
  • Certainly reduces tidal volume (to ~50ml)
  • Thus, theoretically reduces flow across the BPD, allowing it to heal
  • This is avery unnatural form of ventilation, and may be poorly tolerated
  • Large amounts of sedation or paralysis will be required
ECMO
  • This may be the only option for severely hypoxic patients
  • With ECMO, one can limit or totally abolish gas flow through the BPF
  • All the risks of ECMO apply, as it is a maximally invasive therapy
  • It is not widely available.
  • There is little experience with this in BPF.

References

Lois, Manuel, and Marc Noppen. "Bronchopleural fistulas: an overview of the problem with special focus on endoscopic management." CHEST Journal 128.6 (2005): 3955-3965.

Baumann, Michael H., and Steven A. Sahn. "Medical management and therapy of bronchopleural fistulas in the mechanically ventilated patient." CHEST Journal 97.3 (1990): 721-728.

Pierson, David J., et al. "Management of bronchopleural fistula in patients on mechanical ventilation." (2012) - from UpToDate.

Question 23 - 2016, Paper 2

A 65-year-old male is in ICU following an out of hospital cardiac arrest secondary to a large anterior ST elevation myocardial infarction. His ICU stay has been complicated by aspiration pneumonia. He is now day 14 from admission, with a tracheostomy in situ, and has started weaning from the ventilator.

You have been asked to review him as he is communicating that he 'can't get enough air' despite on-going mechanical ventilatory support.

Outline your approach to this problem.

College answer

Urgent attention to A, B, C – Give 100% oxygen and exclude/treat immediate threats to life. 
 
Focused history and examination considering differential diagnoses: 
  
Patient factors 
Airway / trache – blocked, displaced or too small diameter 
Respiratory e.g. pneumonia, PE, PTX 
Cardiac – ongoing ischaemia, cardiac failure, fluid overload 
Neuromuscular – weakness, fatigue 
Sepsis 
Metabolic 
Central – increased respiratory drive, pain, agitation 
 
Ventilator factors 
Unsuitable mode 
Triggering threshold too high 
Inspiratory flow rate too low 
Prolonged inspiratory time 
Inappropriate cycling 
Inadequate pressure support 
Inadequately set tidal volume 
Ventilator malfunction 
 
Treatment: 
100% O2, suction trache, exclude obstruction/malposition, end tidal CO2 etc. 
 
Assess ventilation 
Mode, respiratory rate and pattern 
Spontaneous and delivered TV / MV / airway pressures 
Expiratory flow-time curve, PEEPi (if possible) 
 
Titrated pain relief  
May need to carefully sedate to gain control of the situation if he is very distressed and agitated. Rarely need to paralyse after sedation 
 
Investigations 
Basic Investigations – e.g. ABG, ECG, CXR, cultures 
Further investigations as indicated – e.g. Echo, CTPA, BNP, Troponin etc.  
 
Management of underlying cause: 
Change trache if indicated 
Consider change ventilator settings or mode  
Increase pressure support etc 
ACV Vs SIMV Vs BiLevel 
 
An acceptable answer included the following elements: 
Resuscitation 
Address causes of dyssynchrony 
     Patient factors 
     Ventilator factors 
Approach to management 

 
Additional Examiners‟ Comments: 
Most candidates put together a reasonable answer. Some treated it only as a blocked airway question. Many were not well organised for such a common and important clinical question that has been asked previously. Few candidates thought broadly. 

 

Discussion

Apart from slightly different wording, this question closely resembles Question 4 from the second paper of 2012. The discussion section from that question is therefore reporduced below, with minimal modification.

This question lends itself well to a systematic approach.

  • Immediate management:
    • Increase the FiO2 to 100%
    • consider disconnecting the patient from the ventilator, and manually bag-ventilating them
    • Simultaneously assess and manage threates to life in a systematic manner:
  • Airway
    • machine factors:
      • check for condensation in the ventilator tubing
      • change HME and ventilator filter
    • patient factors:
      • check tracheostomy diameter (too narrow?)
      • check inner cannula (encrusted with inspissated secretions?)
      • check tracheostomy patency (blocked with secretions?)
      • Check tracheostomy position (dislodged during last turn?)
      • suction the patient, loking for fresh blood and clots (unrecognised pulmonary haemorrhage?)
  • Breathing
    • machine factors
      • Check for ventilator malfunction
      • Look for patient-ventilator dyssynchrony and adjust the settings accordingly;
        • is the trigger insufficiently sensitive, or over-sensitive?
        • is the tidal volume and inspiratory flow sufficient to satisfy patient demand?
        • Is the mode inappropriately mandatory?
    • patient factors
      • Assess lung compliance by observing ventilator peak pressures, or qualitatively by manually bag-ventilating the patient
      • Examine the patient and organise an ABG and chest Xray, looking for evidence of...
        • bronchospasm
        • pneumothorax
        • pulmonary oedema
        • impaired gas exchange
          • consider a CTPA if an unexplained A-a gradient has been discovered
        • metabolic acidosis, driving respiratory effort
        • cardiac dysfunction, eg. MI or new arrhythmia
  • Circulation
    • Organise an ECG and bedside TTE, looking for evidence of
      • MI
      • Pulmonary oedema
      • arrhythmia
      • new onset of heart failure
      • evidence of right heart strain
  • Neurology
    • look for muscle weakness or new neurological deficit
    • Look for evidence of poorly controlled pain driving the respiratory effort
    • Assess for delirium and agitation as the primary driver of increased respiratory effort

References

Jairo I. Santanilla "The Crashing Ventilated Patient"; Chapter 3 in Emergency Department Resuscitation of the Critically Ill, American College of Emergency Physicians, 2011.

Question 29 - 2016, Paper 2

With respect to positive end-expiratory pressure (PEEP) in a ventilated patient with acute respiratory distress syndrome (ARDS):

a) Describe the possible approaches to setting PEEP. (80% marks)

b) List the disadvantages of excessive PEEP in this situation. (20% marks)

College answer

a) 
•    PEEP setting adjusted to FiO2, increasing with increasing FiO2 according to the ARDSNet studies (low Vt study NEJM 2000, PEEP 5 – 20+ with FiO2 0.3 – 1.0 and ALVEOLI high PEEP study NEJM 2004 PEEP 5 – 24 with FiO2 0.3 – 1.0) or clinical assessment 
•    Use of lung mechanics to set PEEP – requires the static measurement of P-V curve e.g. using super-syringe. Patient sedated and paralysed and ventilated at FiO2 1.0 and zero PEEP with lung inflation in 50-100ml increments from FRC using a super-syringe followed by deflation in similar steps. Pressure and volume are recorded simultaneously and the P-V curve is constructed from the data. 
Typically requires identification of lower infection point on P-V curve (on VC mode) and setting of PEEP 2 cm H2O above the LIP. 
•    PEEP adjusted to maximise static compliance  
(C = Vt / (Pplateau – PEEP) 
•    Optimal (or best) PEEP – a level of PEEP that optimizes PaO2 and compliance without interfering with tissue oxygen delivery – ideally achieved during or immediately after recruitment manoeuvre, e.g. in Staircase Recruitment Manouevre best PEEP is 2.5 cmH2O above derecruitment point 
•    Transpulmonary pressures (TPP) to guide setting of PEEP – this requires real time measurement of oesophageal pressures (by placement of an oesophageal balloon) to keep the TPP (Paw-Pes) < 25 cm H2O at end inspiration and between 0 – 10 cm H2O at end expiration, while applying the low tidal volume ARDSNet ventilation strategy.  
 
b)      Disadvantages of excessive PEEP in patients with ARDS 
•    Overdistention of non-diseased alveoli resulting in further injury (VILI) 
•    Increased risk of barotrauma 
•    Increased dead space effect due to over-distension and also due to reduction in blood flow to alveoli • CO2 retention 
•    Reduced venous return to the heart, decreased cardiac output and a fall in blood pressure, vital organ perfusion. 
•    May decrease venous return from the abdomen, increasing renal/portal vein pressure and decreasing perfusion of kidneys/gut and increasing IAP 
•    Increased ICP 
•    May increase right to left shunt (increased pulmonary vascular resistance) 
 
Additional Examiners' Comments: 
Overall there was poor understanding of this topic and some candidates were unable to provide basic details. In the responses to part (a) there was generally good breadth in regard to the options of setting best PEEP, however there was often little depth in the options given. In part (b) most answers focused on the cardiorespiratory complications. There were very few candidates who mentioned increased intra-abdominal and intra-cranial pressures as potential complications. 

 

Discussion

a)

These issues undergo a thorough exploration in the chapter on how to determine the optimal PEEP for open lung ventilation in ARDS.

In brief:

  • Use an arbitrarily high PEEP: set to 15-20cmH2O.
    • Meta-analysis of LOVS, ALVEOLI and PROGRESS has suggested that severe ARDS patients (P/F ratio under 200) benefit from higher PEEP settings.
    • CT data suggests that in most ARDS patients the optimal PEEP is around 16cm H2O
  • Use the ARDSNet PEEP/FiO2 escalation tables (setting the PEEP according to the severity of the oxygenation failure)
    • The tables were used in the ARMA and LOVS trials, and are therefore associated with improved survival in ARDS
    • However, the main hypothesis of those trials was related more to tidal volumes and not to PEEP selection.
    • Recently, there has been a move away from oxygenation-based PEEP selection, and towards an "open lung" approach with PEEP being selected on the basis of ideal end-expiratory lung unit recruitment
  • Titrate PEEP according to maximum compliance, i.e. set the PEEP which achieves the highest static compliance
    • This has the advantage of being tailored to each specific patient
    • The physiological basis is sound (maximum compliance should occur when maximum recruitment but minimal overdistension has occurred).
    • No strong literature evidence exists
  • Set the PEEP using the lower inflection point of the pressure volume curve
    • On the pressure volume curve, the lower inflection point indicates the pressure at which alveolar recruitment is maximal (i.e. fewest alveoli are collapsed).
    • It is unclear where this point is on any given real-life curve
    • It is unclear whether we should use the lower (inspiratory) inflection point or the upper (expiratory) inflection point, and there are good theoretical arguments for each.
    • The measurement requires paralysis and - ideally - serial static measurements
  • Use a staircase recruitment (or derecruitment) manoeuvre to find the lowest PEEP at which the maximal oxygenation is maintained.
    • This has the advantage of having a very pragmatic endpoint, SpO2.
    • One recruits the lung, and then decreases PEEP incrementally until SpO2 begins to drop
    • The minimum PEEP which maintains the highest SpO2 is then selected as the "ideal" PEEP
    • The problem is, this PEEP may still expose some of the lung regions to cyclic atelectasis, and will not prevent biotrauma. As long as oxygenation is preserved, those lung regions will be ignored by this technique.
  • Using a PA catheter, titrate PEEP to achieve the smallest intrapulmonary shunt
    • Shunt will increase with atelectasis or derecruitment
    • Shunt will also increase with overdistension
    • Monitoring the intrapulmonary shunt is possible only by using a PA catheter
    • These days this technique is at least as unpopular as the PA catheter
  • Titrate PEEP according to the transpulmonary pressure
    • Oesophageal pressure (Pes) derived from an oesophageal balloon manometer is a satisfactory surrogate for pleural pressure.
    • Transpulmonary pressure = (Pplat - Pes)
    • This variable ca be used to titrate PEEP as well as tidal volume, as it relates to derecruitment and overdistension.
    • The ideal TPP is 0-10 in end-expiration and no more than 25 in inspiration
  • Using electrical impedance tomography, titrate PEEP to achieve the highest electrical impedance in the thorax (i.e. the greatest amount of aerated lung)
    • This is promising bu still largely experimental
    • No hard outcomes adata is available, only animal and "feasibility" studies.
  • Sequential CT scans to visually determine a PEEP at which the greatest volume of lung is recruited during end-expiration
    • CT volumetric measurements are the gold standard of recruitment research
    • The disadvantages are related to safety and logistics, i.e. transport to and from the CT scanner as well as radiation exposure.

b)

Disadvantages of excessive PEEP are discussed in the chapter on ventilator-associated lung injury, as excessive pressure at end-expiration is pathologically indistinguishable from excessive pressure at inspiration, except in terms of magnitude. The short statement about each issue borows heavily from the college answer to  Question 10 from the first paper of 2012 . In summary, the problems are:

  • Volutrauma
    • Over-distension of normal alveolar units to trans pulmonary pressures above ~30 cm H2O
      causes basement membrane stretch and stress on intracellular junctions.
  • Barotrauma
    • Increasing the trans-pulmonary pressures above 50 cm H2O will cause disruption of the basement membranes
  • Biotrauma
    • Mechanotransduction and tissue disruption leads to upregulation and release of chemokines and  cytokines with subsequent WBC attraction and activation resulting in pulmonary and systemic inflammatory response and multi-organ dysfunction.
  • Cardiovascular effects
    • Excessive PEEP results in increased pulmonary pressure, increased right ventricular afterload and decreased cardiac preload.
    • Right heart failure may lead to haemodynamic instability.
  • Extrathoracic effects
    • Excessive PEEP decreases cardiac output by decreasing preload, and increases central venous pressure
    • The net result is decreased organ perfusion pressure, and therefore poorer organ function (including renal hepatic and splanchnic)

References

Cisneros, J. M., et al. "Pneumonia after heart transplantation: a multiinstitutional study." Clinical infectious diseases 27.2 (1998): 324-331.

Reichenspurner, Hermann, et al. "Stanford experience with obliterative bronchiolitis after lung and heart-lung transplantation." The Annals of thoracic surgery 62.5 (1996): 1467-1473.

Gao, Shao-Zhou, et al. "Accelerated coronary vascular disease in the heart transplant patient: coronary arteriographic findings." Journal of the American College of Cardiology 12.2 (1988): 334-340.

Yusuf, S. A. L. I. M., et al. "Increased sensitivity of the denervated transplanted human heart to isoprenaline both before and after beta-adrenergic blockade."Circulation 75.4 (1987): 696-704

Question 3 - 2017, Paper 1

Critically evaluate the use of High Flow Nasal Prongs (HFNP) in adult ICUs.

College answer

Definition & Equipment:
Variable FiO2 high flow (20L/min or more), humidified and heated to 37oC applied by specific nasal 
cannulae. The cannulae are soft, and have a wide aperture; such that the gas velocity is less for a 
given flow than conventional cannulae; this aids in patient tolerance.

Use:
• Varied and has become common and widespread
• Hypoxaemic respiratory failure of any cause
• Post extubation
• Maintenance of oxygenation during procedures (intubation, bronchoscopy, 
TOE, GI endoscopy)
• Paediatrics
• May be used in hypercapnic respiratory failure as reduces dead space; less 
evidence in this group
• Oxygen therapy in treatment limitation / palliation / not for intubation settings

Rationale & Physiologic Advantages:
• High flow “washes” dead space
• Mechanical splinting of nasopharynx prevents supraglottic collapse
• Small amount of CPAP with effects on work of breathing
• Well tolerated generally, and therefore
• Consistent oxygenation
• Known and titratable FiO2; potentially reduces periods of hypoxia and hyperoxia
• Humidification may be of benefit in reducing epithelial injury in patients with hyperpnoea

Disadvantages:
• PEEP is variable and difficult to measure
• PEEP drops to ~2 cmH2O when mouth open
• More costly and more complex to set up than standard nasal cannulae

Adverse effects:
• Local trauma, discomfort and pressure areas 
• Epistaxis
• Gastric distension
• Secretions block cannulae
• May delay intubation and lead to worse outcomes 
• Excessive PEEP may cause PTX in neonates

Evidence:
• NEJM Study; Frat et al (France) 2015 (DOI: 10.1056/NEJMoa1503326)
o Multicenter
o NIV vs FMO2 vs HFNP
o No change in intubation rates
o Mortality advantage over NIV and face mask O2
o Favourable editorial at the time

• Other studies:
o Some have shown decreased re-intubation rates
o THRIVE as pre-oxygenation may be better than RSI
o Delays intubation (Kang, 2015)
o o THRIVE (Anaesthesia, Pateal, 2015) Mean apnoea time in difficult intubations 14min, 
but PREOXYFLOW (Vour’ch, 2015) lowest SpO2 no better than high flow face mask
o Post extubation HFNP x24h equivalent to NIV (Hernandez, JAMA 2016)

Summary statement and personal practice opinion.

Additional Examiners Comments: 
Many candidates failed to list the indications for this therapy and the knowledge of the evidence and patient groups studied was poor.

Discussion

Question 2 from the first  paper of 2013 asked for indications, contraindications and complications of high flow nasal prong therapy. To cover all bases, the High Flow Nasal Prongs revision chapter was written to answer Question 2 as if it were a "critically evaluate" style SAQ. Then, in this paper, that effort was justified by an actual "critically evaluate" SAQ.

Thus:

Rationale for the use of high flow nasal prongs (HFNP)

  • Pharyngeal dead space washout
  • Improved oxygenation by PEEP effect (minor though it may be)
  • Improved oxygenation by oxygen dilution reduction (at high resp rates)
  • Benefits of humidification
  • Increased comfort
  • HFNP may be appropriate in circumstances where NIV is not (eg. oesophageal surgery)
  • HFNP may be used for apnoeic oxygenation as an alternative to the standard mask (eg. PREOXYFLOW and THRIVE trials )

Clinical applications

  • As a stand-alone therapy for hypoxic respiratory failure, in which case it could be used in any sort of respiratory failure
  • Instead of NIV:
    • When positive pressure is contraindicated, eg. oesophagectomy
    • When the patient is intolerant of NIV (eg. delirium)
    • When clearance of secretions must be maintained, but the patient is too hypoxic for conventional oxygen delivery devices (eg. in pneumonia)
  • Instead of intubation:
    • In patients whom it is inappropriate to intubate (i.e. as a palliative measure)
    • In patients for whom intubation is associated with a worse outcome, eg. febrile neutropenic patients and those recovering from bone marrow transplant.
  • Prior to intubation, as preoxygenation
    • May significantly improve preoxygenation and reduce episodes of hypoxia (Miguel-Montanes et al, 2015)- but not all trials have been able to confirm this.

Limitations of HFNP and contraindications to their use

  • The patient must be able to protect their airway
  • The nose must be intact (i.e. its not obstructed, fractured, or
  • The base of skull should be intact (in base of skull fracture you might induce a pneumocephalus and god knows what else)
  • There should be no epistaxis (or the blood will end up being aspirated)
  • If there has been recent nasal surgery, HFNP may do damage the operative site
  • If there has been recent oesophageal surgery, use of HFNP must be weighed against the risk of anastomotic breakdown (though it could still be used, and is safer than NIV)
  • There is some PEEP, but it is not measured, and is completely unpredictable
  • If the patient requires intubation and intubation is delayed because of people wasting time experimenting with HFNP, the outcome may be worse.

Potential adverse events associated with HFNP

  • Overdistension of the alveoli, and barotrauma
    • In fact, in neonates this may lead to pneumothorax - and it is slightly thrilling that the college mention this (it was a part of the old Deranged Physiology HFNP article; did an examiner read it, or did we all arrive at the same answers simultaneously? Either way, it leads to mildly raised neck-hairs).
  • Nasal mucosal damage due to high flow
  • Pressure areas due to the device
  • Aspiration of food
  • Patient discomfort, including irritation by the annoying hissing sound

Evidence in the literature:

Parke et al (2011) one of the first studies comparing HFNP and standard high-flow face mask

  • 60 patients randomised to either normal mask or HFNP
  • Main outcome measure was having to resort to NIV
  • HFNP group did much better (10% rate of NIV vs. 30% for the standard mask)

FLORALI trial (2015): multicenter open-label trial, 310 patients

  • Only hypoxic patients were selected (P/F ratio <300) - hypercapnea was excluded
  • Primary outcome was intubation rate, secondary outcome was mortality
  • HNFP was compared to standard oxygen and NIV
  • There was no difference in intubation rate, but somehow there was a improvement in 90 day mortality associated with the use of high-flow oxygen.
  • The NIV group had 9ml/kg tidal volumes, which may have influenced their mortality by exacerbating their lung injury
  • Of the intubated and NIV patients, more died of shock rather than respiratory failure.

PREOXYFLOW (2015): multicenter open-label trial,124 patients

  • Randomised to either high flow oxygen mask (removed at the end of intubation) or high flow nasal prongs (kept on during the whole process).
  • The main point was to see whether an apnoeic patient would benefit from high flow oxygen blowing into their airway; theoretically they should desaturate more slowly during the intubation attempt because pure oxygen from the HFNP-irrigated upper airways will be entrained into the lung by mass transfer.
  • No such effect was seen (a statistically insignificant difference of 1% SpO2 was found).

THRIVE (2014): observational case series of 25 patients with difficult airways

  • HFNP was commenced prior to the induction of anaesthesia
  • While maintaining jaw thrust, HFNP delivered oxygen to the apnoeic patient (apnoea time was counted from the administration of muscle relaxant)
  • Median apnoea time was 14 minutes (ranging from 9 to 19 minutes) and the patients did not desaturate beyond 90%.
  • Given that half of these patients were obese and a third had stridor, this is an outstanding result. Amazed authors concluded that this technique "has the potential to transform the practice of anaesthesia".

S68 Hi-Flo study (2014): Randomised controlled trial of 72 babies under 18 months of age

  • Bronchiolitis was the specific pathology under investigation
  • Comparison of 2L vs 8L O2
  • There was a minor improvement of clinical parameters (a modified Tal score), but no real difference otherwise

BiPOP (2015)Multicenter, randomized trial in 830 post-op cardiothoracic patients

  • Inclusion criteria were respiratory failure after surgery, or those who were "deemed at risk" of this following extubation
  • The patients were then randomised to either HFNP or NIV
  • HFNP was non-inferior: the rate of reintubation was the same in both groups
  • There was also no difference in ICU mortality.
  • NIV produced more skin pressure areas, but was otherwise equivalent.

References

Groves, Nicole, and Antony Tobin. "High flow nasal oxygen generates positive airway pressure in adult volunteers." Australian Critical Care 20.4 (2007): 126-131.

Ricard, J. D. "High flow nasal oxygen in acute respiratory failure." Minerva Anestesiol 78.7 (2012): 836-841.

Locke, Robert G., et al. "Inadvertent administration of positive end-distending pressure during nasal cannula flow." Pediatrics 91.1 (1993): 135-138.

O’Brien, Bj, J. V. Rosenfeld, and J. E. Elder. "Tension pneumo‐orbitus and pneumocephalus induced by a nasal oxygen cannula: Report on two paediatric cases." Journal of paediatrics and child health 36.5 (2000): 511-514.

Corley, Amanda, et al. "Oxygen delivery through high-flow nasal cannulae increase end-expiratory lung volume and reduce respiratory rate in post-cardiac surgical patients." British journal of anaesthesia (2011): aer265.

Boyer, Alexandre, et al. "Prognostic impact of high-flow nasal cannula oxygen supply in an ICU patient with pulmonary fibrosis complicated by acute respiratory failure." Intensive care medicine 37.3 (2011): 558-559.

Stéphan, François, et al. "High-flow nasal oxygen vs noninvasive positive airway pressure in hypoxemic patients after cardiothoracic surgery: a randomized clinical trial." JAMA (2015).

Miguel-Montanes, Romain, et al. "Use of high-flow nasal cannula oxygen therapy to prevent desaturation during tracheal intubation of intensive care patients with mild-to-moderate hypoxemia*." Critical care medicine 43.3 (2015): 574-583.

Kang, Byung Ju, et al. "Failure of high-flow nasal cannula therapy may delay intubation and increase mortality." Intensive care medicine 41.4 (2015): 623-632.

Frat, Jean-Pierre, et al. "High-Flow Oxygen through Nasal Cannula in Acute Hypoxemic Respiratory Failure." New England Journal of Medicine (2015).

Vourc’h, Mickaël, et al. "High-flow nasal cannula oxygen during endotracheal intubation in hypoxemic patients: a randomized controlled clinical trial." Intensive care medicine (2015): 1-11.

Patel, A., and S. A. R. Nouraei. "Transnasal Humidified Rapid‐Insufflation Ventilatory Exchange (THRIVE): a physiological method of increasing apnoea time in patients with difficult airways." Anaesthesia 70.3 (2015): 323-329.

Hathorn, C., et al. "S68 The Hi-flo Study: A Prospective Open Randomised Controlled Trial Of High Flow Nasal Cannula Oxygen Therapy Against Standard Care In Bronchiolitis." Thorax 69.Suppl 2 (2014): A38-A38.

Parke, Rachael L., Shay P. McGuinness, and Michelle L. Eccleston. "A preliminary randomized controlled trial to assess effectiveness of nasal high-flow oxygen in intensive care patients." Respiratory Care 56.3 (2011): 265-270.

Vourc’h, Mickaël, et al. "High-flow nasal cannula oxygen during endotracheal intubation in hypoxemic patients: a randomized controlled clinical trial." Intensive care medicine 41.9 (2015): 1538-1548.

 
 

Question 7 - 2017, Paper 1

You are asked to urgently review a 48-year-old male who has been in ICU for three weeks tollowing an episode of severe community-acquired pneumonia. He had a percutaneous tracheostomy sited one week ago and has now developed sudden bleeding out of his airway.

List the possible causes for the bleeding.       (30% marks)

Outline your assessment and management of the situation.            (70% marks)

College answer

a) Possible causes

Medical

  • Coagulopathy
    • Coagulation factor deficiency
      • (related to vitamin k def from antibiotics)
    • Excess anticoagulation medication
    • Thrombocytopaenia
    • DIC from sepsis
    • Antiplatelet medications
  • Complication of pneumonia
    • Abscess
    • Neoplasm causing pneumonia now bleeding
  • Less likely
    • Non-airway – blood from mouth, nose (post NGT) or GI tract tracking past trache tube cuff
    • Cardiac – mitral stenosis, tricuspid endocarditis
    • Vascular – PE, pulmonary infarction, AVM
    • Systemic disease – Wegeners, Goodpastures, SLE

Surgical

  • Tracheostomy site
    • Granulation tissue in track
    • Innominate artery fistula (not common but very bad)
    • Thyroid artery
    • Anterior jugular vein
  • Trachea
    • Suction trauma

b) This is an emergency situation with risks of hypoxia, aspiration and hypovolaemia

Assessment and management

  • Resuscitation
  • History and examination to determine cause/contributing factors
  • Supportive therapy
  • Specific therapy

Initial management will depend on the volume and extent of bleeding. Even small amounts of bleeding from a tracheostomy are potentially life threatening as may clot and occlude airway.

Resuscitation

  • 100% FiO2
  • Ensure airway clear
    • Pass suction catheter, suction blood only if necessary, repeated suctioning may exacerbate problem, may need to change inner cannula
    • If ventilation not possible via trache, may need to reintubate orally (pass ETT distal to stoma) to allow ventilation and protect distal airway from soiling
  • Ventilate with safe volume and pressure limits as able
  • Nurse in lateral decubitus position with bleeding lung (if known) down
  • Ensure adequate venous access, fluid resuscitation as needed, check coagulation status and platelet count, organise factor replacement as required.
  • In the case of exsanguination/brisk bleeding will need to enlist assistance of ENT +/- cardiothoracic surgery +/- interventional radiology

History and examination

Once initial situation settled, obtain history and perform examination of tracheostomy site to determine likely contributing factors from the above list of potential causes e.g. difficulty performing tracheostomy, progress of pneumonia, medications, recent blood results, comorbidities, suction technique.

Investigations 

  • Fibre-optic bronchoscopy to identify bleeding site
  • Coagulation profile and ROTEM/TEG
  • CXR
  • CT/CTPA if adequately stable

Specific treatment

Will depend on the cause identified:

  • Granulation tissue – as per surgical site bleeding with lower threshold for surgical exploration 
  • Tracheo-inominate artery fistula (TIF) – bronchoscopy and angiography may fail to identify the source. TIF should be suspected in any patient suffering major haemoptysis post tracheostomy insertion. Management consists of over inflation of the tracheostomy cuff. If this fails to control bleeding then distal orotracheal intubation (tip at or beyond carina) followed by digital insertion through the pretracheal space and compression of innominate artery against the manubrium. This should be followed by urgent surgical exploration.
  • Use of bronchial blocker / double lumen tube
  • Bronchial artery embolization
  • Surgical lobectomy or pneumonectomy if embolization fails
  • Correction of coagulopathy – consider TXA
  • Antimicrobial agents for infection
  • Immunosuppression for underlying vasculitis
  • Treatment of less likely causes as indicated

Additional Examiners’ Comments:

Candidates were not expected to provide the level of detail in the answer template. The management component required resuscitation and specific management for pulmonary haemorrhage and tracheostomy related haemorrhage including innominate-tracheal fistula. Several candidates failed to mention this pathology or its management.

Discussion

A more generic discussion of massive haemoptysis is carried out in the linked chapter. The etymology nerd would point out that can't call this airway bleeding "haemoptysis" because strictly speaking the Greek word "ptusis" means "to spit", and the trache patient's bloody cough is bypassing the mouth and lips. 

The list of differentials could be broad, but for a 30% answer one would not go about reproducing the massive table of differentials such as the one offered by Sakr et al in their 2010 article. A short list would suffice. How about this:

Causes related to the tracheostomy:

  • Erosion into tracheal wall
  • Tracheo-innominate fistula
  • Tracheo-oesophageal fistula (i.e. this could be haemtemesis)

Causes related to the pneumonia

  • Lung abscess
  • Mycotic aneurysm of a pulmonary artery

Causes unrelated to either

  • Bronchial AVM
  • Pulmonary embolism
  • Lung tumour
  • Platelet disorder or coagulopathy
  • Coagulopathy

Management is generic, and is cut-and-pasted here from Question 2 from the first paper of 2012.

1) Control the airway.

  • Assess patency of the tracheostomy
    • Replace inner cannula
    • Assess the possibility of bronchoscopy via the tracheostomy
    • If impossible, intubate the patient with a large-bore tube to permit bronchoscopy (i.e. remove the tracheostomy.
    • If you are skilled and the pathology is unilateral, a dual-lumen tube could be considered
  • Position the patient in a Trendelenberg position, or with the bleeding lung dependent.

2) Control the breathing.

  • Ventilate the patient with the bad lung dependent, to prevent contralateral lung soiling
  • Increase the PEEP, to get the benefit of whatever tamponade effect it might provide.

3) Control the circulation.

  • Replace the lost blood and stabilise the hemodynamic variables

4) Control the bleeding

  • Reverse any coagulopathy
  • Perform bronchoscopy
    • Suck out any obvious clots
    • Place a balloon-tipped catheter to put pressure on the bleeder
    • Burn the bleeder with argon plasma (if you have the tools)
  • Perform angio-embolisation if bleeding is not controlled. Angio-embolisation is a pretty cool modality, with a low complication rate.
  • Send the patient to thoracotomy if angio-embolisation is impossible

5) Control the cause

  • Antibiotics for tuberculosis and fungal abscesses
  • Surgery or radiotherapy for cancers
  • Immunosuppression for vasculitis
  • Surgery for AVMs

References

Adlakha, Amit, et al. "LONG-TERM OUTCOME OF BRONCHIAL ARTERY EMBOLISATION (BAE) FOR MASSIVE HAEMOPTYSIS.Thorax (2011).

Talwar, D., et al. "Massive hemoptysis in a respiratory ICU: causes, interventions and outcomes-Indian study." Critical Care 16.Suppl 1 (2012): P81.

Sakr, L., and H. Dutau. "Massive hemoptysis: an update on the role of bronchoscopy in diagnosis and management." Respiration 80.1 (2010): 38-58.

Ibrahim, W. H. "Massive haemoptysis: the definition should be revised." European Respiratory Journal 32.4 (2008): 1131-1132.

Corey, Ralph, and Khin Mae Hla. "Major and massive hemoptysis: reassessment of conservative management." The American journal of the medical sciences 294.5 (1987): 301-309.

Amirana, M., et al. "An Aggressive Surgical Approach to Significant Hemoptysis in Patients with Pulmonary Tuberculosis 1, 2, 3." American Review of Respiratory Disease 97.2 (1968): 187-192.

Question 13 - 2017, Paper 1

A 56-year-old female with idiopathic pulmonary fibrosis (IPF) is transferred to your ICU from a regional hospital having presented with an acute exacerbation and hypoxic respiratory failure. She has been intubated and ventilated, with SP02 88% on a Fi02 1.0.

Outline how you would optimise lung function in this patient.         (50% marks)

Outline the barriers to weaning from mechanical ventilation in this patient.          (50% marks)

College answer

a) Optimise lung function

  • Look for and treat reversible features e.g. fluid overload, infection, bronchospasm, heart failure
    • Diuretics / fluid limitation
    • Appropriate antimicrobial treatment
    • Bronchodilators
  • Disease modifiers – steroids, immunosuppressants, novel agents e.g. tyrosine kinase inhibitors
  • Pulmonary vasodilators
  • Lung protective strategies and be cautious about high PEEP as the more compliant part of the lungs may be over inflated
  • Involvement of respiratory physicians
    • They may know the patient
    • Advice regarding prognostication
  • V-V ECMO as bridge to transplantation, now being pursued in some centres

b) Outline the barriers to weaning in this patient with IPF?

  • Oxygenation can be significantly impaired – set realistic goals of PaO2 / SpO2
  • Compliance can be severely impaired affecting ventilator synchrony – leading to difficulties in sedation
  • Spontaneous respiratory rate can be high, leading to staff wanting to increase analgesia / sedation
  • Muscle strength can be poor
    • Progressive disease
    • Chronic malnutrition
    • Weakness exacerbated by steroids
    • CIPM
  • Immunosuppression can lead to recurrent infections
  • Pulmonary hypertension can lead to significant CVS dysfunction
  • Patient cognition and emotional status
  • Negative attitudes to a bad prognostic disease

Discussion

As far as "optimise lung function" goes, there are three main domains: try to control the disease process, get some gas exchange happening and control the pulmonary hypertension.

Specific management of the disease process

  • High dose corticosteroids
  • Nintendanib, a a receptor blocker for multiple tyrosine kinases
  • Pirfenidone, a collagen synthesis inhibitor

Manipulation of gas exchange

  • Inhaled pulmonary vasodilators may improve shunt (eg. inhaled prostacycline, inhaled nitric oxide)
  • Mechanical ventilation strategies are largely extrapolated from ARDS management protocols, with some notable differences.
    • Use smaller tidal volumes (like ARDS), 6ml/kg
    • Minimise PEEP (unlike ARDS management): Fernandez et al (2008) found that high PEEP settings failed to improve oxygenation and were associated with worse outcome.
    • Avoid recruitment manoeuvres. IPF patients have minimal recruitable lung, and are vulnerable to overdistension injury.
    • Tolerate hypercapnia; use high respiratory rate
    • Use heavy sedation and neuromuscular junction blockers to improve tolerance of this sort of ventilation strategy
    • There is no evidence to promote the use of prone ventilation
    • Unless the patient is being prepared for a lung transplant, VV ECMO would be a bridge to nowhere and therefore should not be offered. 

Management aimed to control pulmonary hypertension

  • There is a concern that any systemically administered pulmonary vasodilators may worsen shunt. 
  • Sildenafil may improve pulmonary haemodynamics, and does not seem to worsen the shunt (Ghofrani et al, 2002)
  • Endothilin receptor antagonists, eg. bosantan (which might also have some sort of antifibrotic properties) have some role to play in long term management (Minai et al, 2008)

Supportive management

  • Anti-acid therapy for chronic microaspiration
    • The microaspiration of gastric content is viewed as one of the potential triggers of these acute exacerbations. Thus, PPI is indicated.
  • Antimicrobial therapy for any pulmonary infective complications (i.e. there may be a treatable component in all this)

Barriers to weaning:

Due to the disease process

  • Impaired lung mechanics due to restrictive lung disease
  • Increased work of breathing due to hypoxia and respiratory acidosis
  • Concomitant right heart failure due to severe pulonary hypertension

Due to side effects of therapy

  • Corticosteroid-induced myopathy
  • Weakness due to prolonged use of neuromuscular junction blockers

Sequelae of prolonged ICU stay

  • ICU-acquired weakness
  • Malnutrition
  • Residual effect of high-dose sedative medication 

Hilariously, the college has included "negative attitudes to a bad prognostic disease" as one of the barriers to weaning, implying that an intensivists' natural apathetic nihilism will sabotage the process of respiratory recovery. Presumably, a vigorous and positive attitude towards IPF influences survival by virtue of generating fewer palliative care referrals.

References

Saydain, Ghulam, et al. "Outcome of patients with idiopathic pulmonary fibrosis admitted to the intensive care unit." American journal of respiratory and critical care medicine 166.6 (2002): 839-842.

Collard, Harold R., et al. "Acute exacerbations of idiopathic pulmonary fibrosis." American journal of respiratory and critical care medicine 176.7 (2007): 636-643.

Liang, Zhan, et al. "Referral to Palliative Care Infrequent in Patients with Idiopathic Pulmonary Fibrosis Admitted to an Intensive Care Unit.Journal of palliative medicine 20.2 (2017): 134-140.

Moran, J. L., and P. Rangappa. "Outcomes of patients admitted to the intensive care unit with idiopathic pulmonary fibrosis." Critical Care and Resuscitation 11.2 (2009): 102.

Raghu, Ganesh, et al. "An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management." American journal of respiratory and critical care medicine 183.6 (2011): 788-824.

Ghofrani, Hossein Ardeschir, et al. "Sildenafil for treatment of lung fibrosis and pulmonary hypertension: a randomised controlled trial." The Lancet 360.9337 (2002): 895-900.

Minai, Omar A., et al. "Vaso-active therapy can improve 6-min walk distance in patients with pulmonary hypertension and fibrotic interstitial lung disease." Respiratory medicine 102.7 (2008): 1015-1020.

Fernández-Pérez, Evans R., et al. "Ventilator settings and outcome of respiratory failure in chronic interstitial lung disease." CHEST Journal 133.5 (2008): 1113-1119.

Juarez, Maya M., et al. "Acute exacerbation of idiopathic pulmonary fibrosis—a review of current and novel pharmacotherapies.Journal of thoracic disease 7.3 (2015): 499-519.

Question 22.1 - 2017, Paper 1

The following ventilator waveforms shown below (Figure 1) are from a female patient, ventilated with a volume preset assist control mode for severe respiratory failure. Her predicted body weight is 55 kg and   her arterial oxygen saturation is 97%.

asthma ventilator screen

Give the likely lung disease for which the patientis being ventilated. (10% marks)

Give three features from this scenario that supports your diagnosis. (30% marks)

 

College answer

a) Asthma • COPD (Although pressures of 68 cmH2O unusual in COPD) 
 
b)  High peak airway pressure • High peak-plateau pressure difference • Continuing expiratory flow at the end of expiratory time (alternatively, 5 l/min flow at endexpiration) • Oxygen requirements (FiO2 0.4) not very high for a patient who requires mechanical ventilation  • PEEP zero 

Discussion

That image is not the official CICM image, as they do not publish those. It was from my own collection. A ghostly reflection of the author with his smartphone can be seen in the background of the photograph. The original college image is very similar, but of a better quality (they also took the photo on a Siemens Servo-I). The settings and parameters in the original image were:

  • Ppeak = 68 cmH2O
  • pPlat = 16 cmH2O
  • Pmean = 14 cmH2O
  • PEEP = 0 cmH2O
  • RR = 16
  • FiO= 40%
  • VT = 360 ml 

Overall, the image as shown here illustrates severe obstructive airways disease. One can ascertain this from the very high peak inspiratory pressure and the relatively low plateau pressure. Other features which suggest that the ventilated patient has severe bronchospasm include a zero PEEP setting (which is what you'd do for severe bronchospasm with gas trapping) and a very unusual I:E ratio, with an intenstionally prolonged expiratory phase designed to promote CO2 clearance.

References

Question 22.2 - 2017, Paper 1

The following ventilator waveforms shown below (Figure 2) are from a patient who is sedated, paralysed and ventilated in a pressure regulated volume control mode (pressure control mode with a target tidal volume). The patient has a history of bronchiectasis.

PRVC - bronchiectasis with secretions

Give the most likely cause for the abnormal oscillations in the waveforms .           (10% marks)

College answer

Secretions in ETT or fluid in circuit.

Discussion

The college image was somewhat unlike the one I have presented here; their oscillations were much more impressive. Some of the settings on the ventilator were also different, and flow/pressure/volume loops were available (showing the exact same oscillations)  However, none of that really does much to change the interpretation of this SAQ. Like a very similar SAQ from long ago (Question 5.1 from the first paper of 2012) this one tends to have only two main interpretations: either it is pus bubbling in the patient's lungs, or this is water "rain-out" collecting in the circuit.

References

Correger, E., et al. "Interpretation of ventilator curves in patients with acute respiratory failure." Medicina Intensiva (English Edition) 36.4 (2012): 294-306.

Question 22.3 - 2017, Paper 1

The following ventilator waveform shown below (Figure 3) is from a patient who is sedated and ventilated    in the pressure regulated volume control mode (a pressure control mode with a target tidal volume). The patient has an arterial oxygen saturation of 94%.

That's obviously not the original college image.
The ventilator settings from the college image were as follows:

  • PRVC mode
  • 30% FiO2
  • 7 PEEP
  • 24 resp rate (actual patient rate was 25, but there were no spontaneous breaths)
  • VT 450ml
  • MVe is 10.7 L/min
  • I:E ratio of 1:2
  • Ppeak of 24
  • Pmean of 7

Give the likely lung pathology.   (10% marks)

Give two features shown in the flow waveform that support your answer. (20% marks)

College answer

a) Less than 24 cm H2O

Flow has not reached zero by the end of inspiration indicating there is still a pressure gradient between the ventilator and the alveoli. As result the alveolar pressure must be less than the inspiratory pressure delivered by the ventilator.  [Note: 24 was not an acceptable answer]         

 b) Obstructive airways disease

High inspiratory flow at the end of inspiration despite adequate inspiratory time
Failure of expiratory flow to return to zero by the end of expiration

Discussion

The examiners had chosen to answer the question "what is the likely lung pathology" with the cryptic phrase "less than 24 cm H2O". To analyse this, one needs to take into context the fact that the college then went on to remark that to merely write "24" would be somehow unacceptable. This leads one to believe that this whole answer is not the product of chance keystrokes accidentally self-assembling into a nonsequitur. We must somehow work "less than 24 cm H2O" into a valid answer to this SAQ. If the author were not well supplied with contraband exam papers, trying to reverse-engineer this and find an appropriate ventilator waveform would have been a painful and ridiculous exercise.

Fortunately, they let you keep your paper at the end. The Siemens Maquet Servo-I model ventilator screen used for this SAQ did in fact have the number "24" on it. That number represented the peak inspiratory pressure, usually seen in the status screen at the top right hand corner of the monitor. The monitor was also alarming "Paw High", and it had been silenced. The SAQ text also gives us the patient's oxygen saturation, a neither-here-nor-there 94%. From these data, we must somehow generate a lung pathology. Not only that, but it must be a pathology which might somehow give rise to "24" as a plausible description.

"Obstructive airways disease" would not be that answer. Nothing about the way this patient is being ventilated fits with that description, and the waveforms did not agree (the expiratory waveform returned to zero, contrary to the examiner's comment). The high inspiratory flow rate at the end of inspiration is correctly identified; in the college image the ventilator cycled to expire at a flow rate which would be about 50% of peak. However, "high inspiratory flow at the end of inspiration despite adequate inspiratory time" is difficult to interpret as a sign of obstructive airways disease, as such disease typically results in low flow rates through the obstructed airways.  

 "Flow has not reached zero by the end of inspiration" is a valid thing to say. However, it is not essential for it to reach zero.  When the mandatory volume is achieved by the decelerating flow ramp and the ramp ends up at zero at the end of inspiration, that probably just means that the lung compliance is poor. 

"As result the alveolar pressure must be less than the inspiratory pressure delivered by the ventilator". This is correct. In fact this statement cannot be challeged because underpins the entire practice of ventilation, as in order for any inspiratory flow to occur there needs to be a pressure gradient where the alveolar pressure is lower than the pressure in the ventilator tubing.  

The ventilator settings are in fact quite bizarre, as they call for a mandatory minute volume of over 10L. The peak pressure is a bit high, and the lung compliance is a bit reduced (~ 26 ml/cmH2O), but the patient is being ventilated with a level of PEEP which does not make sense for an ARDS patient, for example. 

Thus far, Dr Hyde has offered the most reasonable explanation for the bizarre college answer. In his opinion, the answer "less than 24" is the vestigial remnant of an deleted first question to this SAQ,  which has become trapped in the official paper through poor proofreading. 

"I wonder if they initially had a 3rd question in there that got vetted out just before the paper was published. I can imagine there being 3x 10% questions there, and question a) being along the lines of "what's the alveolar pressure?" - which would then make sense of their answer of <24 as we know that at a Pplat of 24 there is still ongoing flow before the breath cycles."

I am grateful for this explanation, as is the only one which makes sense. 

References

Question 22.4 - 2017, Paper 1

The following ventiator waveform shown below (Figure 4) is from a patient who is sedated and ventilated in the pressure regulated volume control mode (a pressure control mode with a target tidal volume).The patient has an arterial oxygen saturation of 94%.

Give the likely underlying lung pathology. (10% marks)

Give one feature shown in the flow waveform that supports your answer. (10% marks)

College answer

a) Any lung pathology associated with poor compliance such as severe restrictive pathologies 
 
b) Inspiratory flow drops sharply very early in inspiration 

Discussion

The original college image also had 100% FiO2, but the other settings were:

  • PRVC mode (not SIMV PRVC)
  • PEEP 6
  • RR 30
  • VT 260
  • Mve 7.6
  • Ppeak 33
  • Pmean 19

In every other respect, "any lung pathology associated with poor compliance" applies equally well to both images. 

References

Question 25 - 2017, Paper 1

With respect to trans-pulmonary pressure (TPP):

Explain what is meant by the phrase "trans-pulmonary pressure (TPP)".                (10% marks)

Describe the technique of measurement, including any limitations.          (30% marks)

Discuss the rationale for its clinical use.  (40% marks)

Briefly outline the evidence for its role in the management of patients with acute respiratory distress syndrome (ARDS). (20% marks)

College answer

TPP
TPP is the difference between the alveolar pressure (Palv) and pleural pressure (Ppl).
TPP is the net distending pressure applied to the lung.

Rationale for TPP measurements
By measuring TPP the effects of chest wall compliance are negated and a true measure of lung
distension is obtained. This may allow the safe tolerance of higher plateau pressures; with the
assumption that it is lung distension that is important in generating lung injury
Current therapies target Paw (<30 cmH2O) to minimise volutrauma or barotrauma. More accurate prevention of ventilator associated lung injury may be obtained by using TPP, e.g.:

  • Limit recruitment maneuvers to TPP 25 cmH2O
  • Setting PEEP to TPP 0-10 cmH2O
  • Limiting volutrauma by setting VT to a TPP 25 cmH2O
  • Determination of respiratory muscle work in spontaneous ventilation
  • Assessment of ventilator dys-synchrony
  • Estimation of auto-PEEP in spontaneously breathing patients

Measurement
In ventilated patients Ppl is estimated from oesphageal pressure (Pes.) with a thin wall latex
oesophageal ballon inserted via the NG or OG route. Its measurement is prone to error.

  • Malposition – gastric (one of third balloon placements in study below challenging)
  • Positioning: supine vs erect (addition of mediastinal weight)
  • Assumption that pleural pressures even through the chest
  • Extrinsic factors – obesity, rising intra-abdominal pressure

Measurement is automated on some ventilators.
Palv difficult to measure instantaneously during flow, but equalises to airway pressure at states of zero flow with airway occluded. Classically measured as inspiratory pause pressure after complete tidal volume.

Evidence, Talmor, NEJM 2008
61 patients ARDS / ALI – ARDSNet vs TPP targeted ventilation

  • TPP group had higher PEEP, better oxygenation, higher Pplat
  • Trends to better compliance, better mortality

No established role in general management.
May have a role in obesity, raised intra-abdominal pressure and air trapping.
Other techniques can compensate for inability to measure TPP e.g. best PEEP may be estimated by measuring respiratory compliance or oxygenation during a recruitment manoeuvre.

Amato’s re-analysis of the ARDS net data showed convincingly that total respiratory driving pressure (Pplat-PEEP) correlated most strongly with mortality. Total respiratory driving pressure may correlate with TPP.


Additional Examiners’ Comments:
Many candidates had little/no concept of either the utility or rationale for measuring transpulmonary  pressure. Candidates confused terminology when discussing pleural pressure and alveolar pressure  and could not give precise definitions

Discussion

a) Explain what is meant by the phrase "trans-pulmonary pressure (TPP)"

The college defined TPP as "the difference between the alveolar pressure (Palv) and pleural pressure (Ppl)", or as "the net distending pressure applied to the lung". In fact this may be a sub-optimal definition according to Loring et al (2016), who would call the (Palv-Ppl) difference "elastic recoil pressure of the lung". However, in the ICU the TPP is usually measured in the absence of flow (i.e. in an inspiratory hold and at end-expiration). This means the pressure drop across the airway can be neglected (it is zero), and one does not need to consider it. 

b) Describe the technique of measurement, including any limitations. 

Technique:

  • Insert the oesophageal manometer into the patient up to around 60cm 
  • Inflate the balloon with ~ 0.5ml of air
  • Transduce the pressure
  • Ballot the stomach: a properly positioned transduced catheter will "feel" your abdominal poking
  • Withdraw the catheter into the oesophagus (to a depth of around 40cm)
  • Confirm placement with "cardiac oscillations" on the monitor

c) Discuss the rationale for its clinical use.  (40% marks)

In general:

  • Airway pressure alone may be misleading
  • TPP offers a more accurate asssement of stress upon the lung parenchyma
  • TPP has the advantage of separating chest wall compliance from lung compliance.
  • Customisation of PEEP and VT settings is possible, particularly for the morbidly obese and patients with high abdominal compartment pressure. 
  • The measurement of TPP by oesophageal manometry is fairly non-invasive

In management of ventilation:

  • Perform smarter recruitment manoevres, eg. using TPP of 25
  • Set the PEEP in ARDS to prevent atelectasis (TPP 0-10)
  • Set  the VT in ARDS to prevent volutrauma (TPP <25)
  • Set the ventilator in morbidly obese patients, those with abdominal compartment syndrome or with some sort of rapidly changing abdominal pressure (pregnant, undergoing laparsocopy, etc).
  • Detect "respiratory entrainment" or reverse triggering, a form of patient-ventilator dyssynchrony where the mandatory inspiration causes the patient's respiratory muscles to contract, as if in protest. 
  • Detect ineffective respiratory efforts
  • Improve the synchrony of SIMV with weak patient efforts
  • Improve the cohesion between ventilator inspiratory time and the patients respiratory time
  • Auto-PEEP can be measured using this method 
  • It may provide a simple measure of patient effort in weaning from mechanical ventilation

d) Briefly outline the evidence for its role in the management of patients with acute respiratory distress syndrome (ARDS).

The college have quoted Talmor et al (2008): "Mechanical ventilation guided by esophageal pressure in acute lung injury." This was a randomised controlled study of 61 ARDS patients, of whom the TPP-guided group has better survival. The primary endpoint was oxygenation, and this too was better when PEEP was guided by TPP. Unfortunately the study sample was too small for the results to reach statistical significance. Apart from this study, the EpVent Trial (Fish et al, 2014) is under way and plans to enrol 200 patients. There seems to be little else.

References

Sarge, T., and D. Talmor. "Targeting transpulmonary pressure to prevent ventilator induced lung injury." Minerva Anestesiol 75.5 (2009): 293-299.

Sahetya, Sarina K., and Roy G. Brower. "The promises and problems of transpulmonary pressure measurements in acute respiratory distress syndrome." Current opinion in critical care 22.1 (2016): 7-13.

Loring, Stephen H., George P. Topulos, and Rolf D. Hubmayr. "Transpulmonary pressure: the importance of precise definitions and limiting assumptions." American journal of respiratory and critical care medicine194.12 (2016): 1452-1457.

Grasso, Salvatore, et al. "ECMO criteria for influenza A (H1N1)-associated ARDS: role of transpulmonary pressure." Intensive care medicine 38.3 (2012): 395-403.

Lee, Hans J., et al. "Comparison of pleural pressure measuring instruments."Chest 146.4 (2014): 1007-1012.

Chiumello, Davide, et al. "The assessment of transpulmonary pressure in mechanically ventilated ARDS patients.Intensive care medicine 40.11 (2014): 1670-1678.

Talmor, Daniel, et al. "Esophageal and transpulmonary pressures in acute respiratory failure." Critical care medicine 34.5 (2006): 1389.

Talmor, Daniel S., and Henry E. Fessler. "Are esophageal pressure measurements important in clinical decision-making in mechanically ventilated patients?.Respiratory Care 55.2 (2010): 162-174.

Talmor, Daniel, et al. "Mechanical ventilation guided by esophageal pressure in acute lung injury." New England Journal of Medicine 359.20 (2008): 2095.

Ferris, Benjamin G., Jere Mead, and N. Robert Frank. "Effect of body position on esophageal pressure and measurement of pulmonary compliance."Journal of Applied Physiology 14.4 (1959): 521-524.

Mauri, Tommaso, et al. "Esophageal and transpulmonary pressure in the clinical setting: meaning, usefulness and perspectives.Intensive care medicine 42.9 (2016): 1360-1373.

Eichler, Lars, et al. "Intraoperative Ventilation of Morbidly Obese Patients Guided by Transpulmonary Pressure.Obesity Surgery (2017): 1-8.

Fish, Emily, et al. "The Esophageal Pressure-Guided Ventilation 2 (EPVent2) trial protocol: a multicentre, randomised clinical trial of mechanical ventilation guided by transpulmonary pressure." BMJ open 4.10 (2014): e006356.

Rodriguez, Pablo O., et al. "Transpulmonary pressure and gas exchange during decremental PEEP titration in pulmonary ARDS patients." Respiratory Care 58.5 (2013): 754-763.

Terragni, Pier Paolo, et al. "Accuracy of plateau pressure and stress index to identify injurious ventilation in patients with acute respiratory distress syndrome.The Journal of the American Society of Anesthesiologists 119.4 (2013): 880-889.

Akoumianaki, Evangelia, et al. "The application of esophageal pressure measurement in patients with respiratory failure." American journal of respiratory and critical care medicine 189.5 (2014): 520-531.

Akoumianaki, Evangelia, et al. "Mechanical ventilation-induced reverse-triggered breaths: a frequently unrecognized form of neuromechanical coupling." Chest 143.4 (2013): 927-938.

Question 11.2 - 2017, Paper 2

List four potential causes for auto-triggering during pressure support ventilation. (40% marks)

College answer

•    Trigger set too low (too sensitive) 
•    Cardiac impulse 
•    ETT leak/circuit leak 
•    Chest drain 
•    Condensation in circuit 

Discussion

Auto-triggering can be broadly defined as "unintended initiation of breath delivery by the ventilator". The breadth of the term unintended may give rise to a large possible list of reasons, which includes:

  • Myoclonoc jerks
  • Cardiac oscillations
  • Leak from the circuit
  • Leak from the chest drain (eg. a bronchopleural fistula)
  • Inappropriate sensitivity settings
  • Water condensation sloshing and bubbling in the circuit
  • Large volume of respiratory secretions, eg. bronchiectasis
  • Swallowing or vomiting
  • Peristalsis in a massive hiatus hernia or intrathoracic bowel loops
  • Muscle contractions due to external pacing (or misplaced leads in transvenous pacing)
  • Transmitted movement from patient transport or repositioning
  • IABP

In truth, this list answers the question "what are the causes of auto-triggering in a patient who is on a flow-triggered mode" as it is harder to come up with a list of non-diaphragmatic causes for pressure-based auto-triggering, apart from severe myoclonus and hiccups. 

References

Arnaud W. Thille, MD, and Laurent Brochard, MD. Promoting Patient-Ventilator Synchrony (Clin Pulm Med 2007;14: 350 –359)

Petrof BJ, Legare M, Goldberg P et al. Continuous positive airway pressure reduces work of breathing and dyspnea during weaning form mechanical ventilation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis 1990; 141: 281–9.

Arbour, Richard. "170: Ventilator Autotriggering Consequent To Intra-aortic Balloon Pump Counterpulsation.Critical Care Medicine 46.1 (2018): 68.

Question 11.3 - 2017, Paper 2

The waveform below (Figure 1) is from a ventilator with the following settings:

Volume control SIMV, PS 10, PEEP 5. 

The bedside nurse informs you that the patient appears to be "struggling against the ventilator".

a) Given the appearance of the waveform, what is the likeliest cause of the patient's distress?

(10% marks) 

The following waveform (Figure 2) is from a ventilator with the following settings:

Volume control SIMV, PS 10, PEEP 5. 

The bedside nurse informs you that the airway pressures have increased.


b) Given the appearance of the waveform, what is the likeliest cause of the increased airway
pressure and how would you treat it? 

The waveform below (Figure 3) is from a ventilator with the following settings:

Volume control SIMV, PS 10, PEEP 5.

The patient has ARDS and the bedside nurse informs you that the patient appears to be "working hard on the ventilator".


c) Given the appearance of the waveform, what is the likely cause of the increased work of
breathing? 

College answer

(i)    Patients effort to initiate a breath is not recognised by the ventilator           
 
(ii)    Double triggering- Two breaths occur in less than half mean inspiratory time. Occurs when patient demand outlasts set inspiratory time. 
Treat by increasing tidal volume, increasing inspiratory time, increasing sedation or paralysis 
                                                             
(iii)    Flow starvation. Patients inspiratory demand is greater than that delivered by ventilator resulting in scooped out appearance of pressure waveform.      
 

Discussion

Though the college have removed the images from their official paper, some effort was made by the author to reproduce them faithfully enough to 

a) is a form of dyssynchrony best described as "wasted effort"; the patient is clearly making efforts to breathe but the ventilator is not triggering. This is because the trigger is insufficiently sensitive (or, the patient is significantly weakened).

b) is a case "breath stacking" and gas trapping. There is air hunger: the patient wants a deeper and longer breath, and when the ventilator cycles to expiration the patient takes another breath immediately. The college recommend changing some of the control variables or increasing sedation; however an alternative solution may also be to give the patient more control over their ventilation by changing them to a patient-triggered flow-cycled mode like PSV on the Servo-I.

c) is a case of flow being insufficient to meet demand,; the patient's inspiratory effort as trying to add to the tidal volume, which creates negative pressure - this gives the pressure waveform its "scalloped" appearance.

References

Arnaud W. Thille, MD, and Laurent Brochard, MD. Promoting Patient-Ventilator Synchrony (Clin Pulm Med 2007;14: 350 –359)

Petrof BJ, Legare M, Goldberg P et al. Continuous positive airway pressure reduces work of breathing and dyspnea during weaning form mechanical ventilation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis 1990; 141: 281–9.

Question 23 - 2017, Paper 2

A 42-year-old miner has been transferred to the unit after an industrial accident in a remote location. He was entrapped in a fire underground.

He arrives 30 hours after injury, weighs  70 kg  and is 1.75m tall.
He is intubated and ventilated. His admission chest x-ray shows widespread bilateral pulmonary infiltrates.

His initial arterial blood gas shows the following:

Fi02 1.0  
pH 6.93* 7.35 - 7.45
p02 55 mmHg (7.3 kPa)  
pC02 78.0 mmHg (10.4 kPa)* 35.0 - 45.0 (4.6 - 6.0)
Sp02 87%  
Bicarbonate _ 16.0 mmol/L* 22.0 - 26.0
Base Excess -14.0 mmol/L* -2.0 - +2.0

His current ventilator settings are as follows:

Fi02 
Respiratory rate 
Tidal volume
Peak lnspiratory Pressure
PEEP
1.0
12 breaths/min
650 ml
38 cmH20
5 cmH20


a) List six possible causes for his hypoxaemia. (20% marks)

b) Outline your management strategies for the treatment of his hypoxaemia. (80% marks)

College answer

a)                                                         
•    Aspiration pneumonitis 
•    Blast Injury 
•    Smoke inhalation 
•    Misplaced ETT 
•    Fluid overload 
•    Pulmonary oedema 
•    Restrictive defect from circumferential burn 
 
b) General ventilator strategies based on ARDS net criteria 
•    Check adequate placement of ETT (no R endobronchial intubation) 
•    ARDS net ventilation Vt 6mls/kg = 420mls best PEEP.  
Use of recruitment maneuvers with derecruitment to assess best PEEP 
CPAP 40/40 or step wise recruitment maneuvers 
Use of flow loops 
Aim Plateau <30cm H2O avoid baro trauma 
Increase I:E ratio towards 1:1 and increase rate if tolerated 
Check for autoPEEP and use of broncho dilators  
Treat reversible causes like PTX 
C- rule out cardiomyopathy and improve V:Q match as cardiac function can be depressed in the severe inflammatory state. 
 
General adjunctive measures 
•    Physio. Suctioning. Consider bronchoscopy  
•    Sedation, heavy sedation will be required. In advanced Hypoxia may require paralysis. 
•    Treat factors increasing metabolic demand (removal of eschar, treatment of sepsis, high risk of pneumonia) 
•    Optimize Hb and oxygen carrying capacity. 
•    If patient has been over resuscitated may require diuresis 
 
General Rescue therapies 
•    Prone positioning- may not be practical in a burns patient 
•    Alternative ventilation strategies - prolonged  
•    ECMO in severe cases 
•    Nitric oxide or inhaled prostacyclin 
 
Burns specific measures 
Bronchodilators 
      B2 agonists such as Adrenaline or Salbutamol 
      Adrenaline reduces blood flow to injured/obstructed airways improving V:Q mismatch 
 
Muscarinic receptor antagonists – reduction of cytokines, reduction of mucus secretions 
NAC 
Inhaled fibrinolytics for reduction of fibrin casts in volume and plugging. 
 
Bronchial Toileting. 
•    bronchoscopy for cast removal and prevention and treatment of mechanical obstruction and plugging 
***rule out toxidromes, cyanide, CO, may need or antidote.**** 
•    Ensure chest expansion not impeded by eschar 
•    May require escharotomies for free chest movement
 

Discussion

This is hypoxia in a miner pulled from an underground fire. His ABG result demonstrates a severe metabolic and respiratory acidosis. Specific elements which arouse concern in that setting are:

  • He's a miner, and therefore possibly exposed to exotic substances. Who knows what he was mining in there?
  • He was underground, which as an enclosed space has two major consequences:
    • It amplifies blast waves
    • It concentrates heat
    • It limits the oxygen supply

The differentials therefore are:

  • Inhalational burns injury
  • Corrosive agent inhalation
  • Asphyxiant agent exposure (eg. carbon monoxide or cyanide)
  • "Blast lung" due to primary blast injury.
  • Aspiration due to a decreased level of consciousness
  • Pulmonary oedema due to primary myocardial damage
  • Barotrauma due to profoundly stupid ventilator settings.

The ventilator settings are mildly inappropriate This guy is being ventilated like a elective theatre case. The college clearly wanted the candidates to discuss the standard approach to ARDS ventilation

In brief:

Initial ventilator strategy:

Additional ventilator manoeuvres to improve oxygenation:

Non-ventilator adjunctive therapies for ARDS:

Ventilator strategies to manage refractory hypoxia

  • Prone ventilation, for at least 16 hours a day (PROSEVA, 2013)
  • High frequency oscillatory ventilation may not improve mortality among all-comers (OSCAR,2013) or it may actually increase mortality (OSCILLATE, 2013) but some authors feel that there were problems with methodology.

Non-ventilator adjuncts to manage refractory hypoxia

  • Nitric oxide was a cause for some excitement, but is no longer recommended.
  • Prostacyclin is still a cause for excitement, and is still vaguely recommended.
    • Neither agent improves mortality, but prostacyclin can improve oxygenation.
  • ECMO may improve survival (CESAR, 2009) but again there were problems with methodology.

References

Tredget, EDWARD E., et al. "The role of inhalation injury in burn trauma. A Canadian experience." Annals of surgery 212.6 (1990): 720.

Kimmel, Edgar C., and Kenneth R. Still. "Acute lung injury, acute respiratory distress syndrome and inhalation injury: an overview." Drug and chemical toxicology 22.1 (1999): 91-128.

Gorguner, Metin, and Metin Akgun. "Acute inhalation injury." The Eurasian journal of medicine 42.1 (2010): 28.

Question 3 - 2017, Paper 2

A 76-year-old male returns to the ICU following a right sided thoracotomy and right upper lobectomy. He is extubated but has a large air leak from the intercostal catheter.

a) Describe your assessment and specific management of the air leak. (50% marks)

b) The patient desaturates and requires re-intubation. Describe your management of his ventilation (50% marks)

College answer

  1. Describe your assessment and specific management of the air-leak.                          
    • History: discuss with the surgeon and anaesthetist the intraoperative course and any airleak at the end of the operation
    • Assess his respiratory state-respiratory rate and pattern, saturations and oxygen. Support this as indicated but with awareness that re-intubation and PPV will likely worsen the airleak
    • Examine the patient-are the drains connected correctly, are they on suction, what is the suction set at, is the suction entraining air through the chest wall?

Investigations: ABG and urgent CXR

Management:

    • Assess the degree of right lung expansion on the postoperative CXR 
    • Consider removing or reducing the suction on the drain if lung expanded
    • If lung not expanded check icc patency and insert another icc if needed
    • Discuss with the surgeon any operative interventions         
  1. The patient desaturates and requires re-intubation. Describe your ventilatory management.
    • High ventilation pressures will worsen any air leak so low to no PEEP, low peak airway pressures and toleration of hypercarbia
    • Spontaneous patient triggered ventilator modes with pressure support may reduce the airleak compared with mandatory modes
    • Consider: 
      •  Potential need for lung isolation/bronchial blocker 
      • Oscillation
      • ECMO

Examiners comments:  

Many candidates answered part A as if the patient was already intubated, having not read the stem carefully. Very few referred to suction on the drain, or principles in managing broncho pleural fistula. There was little emphasis on additional drains and importance of try to reinflate lung.

Discussion

Assessment and specific management of this air leak would have to involve some answer to the question,  "does this patient need to go back to the operating theatre?". 

Possible causes of air leak: there are only two. 

  • It's coming from the patient's lung
  • It's coming from the extrathoracic air

First, assess the patient to ensure they are safe:

  • Ensure that they are not in respiratory distress (examine them and assess respiratory rate, pulse oximetery, subcutaneous emphysema, tracheal deviation, etc) - look for immediately lifethreatening issues first.
  • Ensure normoxia and normal metabolic parameters (perform ABG )
  • Assess for haemoptysis (an early feature of operative site breakdown)

Second: equipment issues can be easily excluded: the first step will be to examine the chest drain and ensure that all of the side holes are inside the chest.

Third: If the chest drain is mechanically intact (i.e not tracked) truly well inside the chest,  it is bubbling significantly because there is really an air leak from some respiratory structure into the pleural cavity. This could be because of:

  • The operative site leaking (i.e. the bronchus of the right upper lobe)
  • A new pneumothorax from the remaining lung
  • Air gaining entry through the thoracotomy wound

Further assessment would then consist of:

  • Quantification of the leak:
    • Ask the patient to cough
    • Ask the patient to speak
    • Observe the quantity of bubbles.
    • If bubbling is constantly happening while the patient is speaking, the leak is significant.
    • If the bubbling is only present with cough and diminishes with ssutained coughing, the leak is probably small. 
  • CXR to confirm drain position and assess the size of the pneumothorax; and if this is equivocal or uninformative, a chest CT to clearly define the structures and help surgical planning

Management options would consist of:

  • Do nothing. Keep the drain on suction and wait for it to settle down. Most do within 3 days of the surgery. Generally, about 50% of post-lobectomy patients will have some sort of air leak postoperatively, but this tends to settle down by day 3 or so. 
  • Decrease the level of suction. Cerfolio et al (1998) dropped the suction down from the usual 20cm H2O down to 10cm H2O if there was airt leak on Day 2.
  • Provocative chest drain clamping: the air leak may settle down more easily if the pressure in the pleural space is less negative.
  • Permissive chest tube removal: essentially an irreversible alternative to clamping the chest drain; the advantage is that by doing this one eliminates another hole in the chest cavity which might be bringing in extrathoracic air. 
  • Outpatient management with a chest tube and a Heimlich valve is a legitimate option for patients unsuitable for further surgery.
  • Talc pleurodesis  (60ml of a water/talc slurry is injected via the chest drain) Alternative agents mentioned in the literature included tetracycline and silver nitrate.
  • Blood patch is an alternative to talk, but is not as sclerosant. 
  • Pneumoperitoneum  is an option (actually a preventative measure which is most effective when performed intraoperatively) immediately following lobectomy. 
  • Intrabronchial valve which is placed bronchoscopically. It is invasive, has the potential to dislodge, and can act as a nidus for infection. Moreover, you'd need to remove it a few weeks later.
  • Surgical revision is the ultimate solution for a leak which is not resolving with conservative measures in a patient suitable for surgery. The most aggressive solution (hopefully avoidable) would be a pneumonectomy. 

Ventilatory management of a patient with bronchopleural fistula follows a standard set of principles:

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References

Lois, Manuel, and Marc Noppen. "Bronchopleural fistulas: an overview of the problem with special focus on endoscopic management." CHEST Journal 128.6 (2005): 3955-3965.

Baumann, Michael H., and Steven A. Sahn. "Medical management and therapy of bronchopleural fistulas in the mechanically ventilated patient." CHEST Journal 97.3 (1990): 721-728.

Pierson, David J., et al. "Management of bronchopleural fistula in patients on mechanical ventilation." (2012) - from UpToDate.

Mueller, Michael Rolf, and Beatrice A. Marzluf. "The anticipation and management of air leaks and residual spaces post lung resection." Journal of thoracic disease 6.3 (2014): 271.

Cerfolio, Robert J., et al. "A prospective algorithm for the management of air leaks after pulmonary resection." The Annals of thoracic surgery 66.5 (1998): 1726-1730.

Question 11.1 - 2017, Paper 2

In relation to describing the mode of mechanical ventilation, define the following terms:

a) Flow triggered.

b) Pressure limited.

c) Time cycled

(30% marks)

College answer

a)    Flow Triggered:                                          
•    The signal to start inspiration is a change in flow, i.e. a change in flow results in opening of the inspiratory valve 
 
b)    Pressure Limited: 
•    Pressure is factor that limits the way gas flows into the lung during inspiration. The pressure within the lung cannot exceed the set limit.  
 
c)    Time Cycled: 
•    Time is the signal that stops inspiration i.e. the inspiratory valve closes and the expiratory valve opens OR Inspiration switches to expiration once the set inspiratory time elapses. 
 

Discussion

Triggering, limits and cycling are what is called "phase variables" of mechanical ventilation. "Egan's Fundamentals of Respiratory Care" is what I used for these definitions, it being the bible for respiratory therapists in America. Locally we have no such bible, but Oh's Manual contains within it the definitive "Mechanical Ventilation" chapter by Andrew Bersten which does not define these variables.

Anyway: Egan's defines these variables quite well around pages 1012-1014 of the 11th edition.  The definitions offered there are similar to, and possibly non-inferior to, the canonic college definitions.

In short:

Flow triggering is where the difference in flow between the expiratory and inspiratory limb of the ventilator is used as the trigger variable to initiate a mechanical breath

Pressure limit is the pressure at which the ventilator opens the expiratory valve regardless of which phase of ventilation is occuring at the time. Pressure limited ventilation 

Time cycling means the expiratory flow valve is opened after a preset time interval has elapsed, and the inspiratory valve is closed.

References

Travers, Colm P., et al. "Classification of Mechanical Ventilation Devices." Manual of Neonatal Respiratory Care. Springer International Publishing, 2017. 95-101.

Heuer, Albert J., James K. Stoller, and Robert M. Kacmarek. "Egan's Fundamentals of Respiratory Care." (2016).

Question 8 - 2018, Paper 1

Critically evaluate the role of ventilatory recruitment manoeuvres in the critically ill.

College answer

Introductory statement

  • Recruitment maneuvers are ventilator manipulations to improve oxygenation in moderate to severe ARDS. Often used as part of an open lung strategy.

 Rationale

  • In ARDS, collapsed/consolidated alveoli are unable to take part in gas exchange. In addition, the recurrent opening and closing of units can contribute to atelectrauma.
  • Recruitment maneuver is a temporary increase in pulmonary pressures to open collapsed alveoli. Subsequent PEEP titration aims to prevent cyclical opening/closing of these units. 

 Advantages

  • May lead to improved oxygenation, compliance and markers of inflammation (decreased). Cheap, Simple, quick c.f. ECMO, iNO

 Disadvantages

  • Need for sedation/paralysis
  • Transient oxygenation response
  • Risk barotrauma
  • VILI
  • Worsening of shunt
  • Cardiovascular instability
  • No consensus on how they should be performed.

 Evidence

  • Studies in mod – severe ARDS, including a Meta-analysis have failed to demonstrate patient-centred outcome benefit. Trials generally of poor quality, high risk of bias.
  • Latest trial ART: showed increased 6/12 mortality, barotrauma and length of mechanical ventilation in group undergoing RMs cf no RMs (and there were 3 cardiac arrests during RMs). Considered a large well designed trial, potential weaknesses include inability to blind and the use of stepwise PEEP recruitment.
  • PHARLAP – another large trial examining this issue has now ceased recruitment in the light of the ART results.

Own practice

Anything reasonable here including “I do not perform recruitment maneuvers”

If a candidate was unaware of the ART trial and described a routine use of Recruitment Maneuvers they were should be marked down at the examiners discretion.

 Examiners Comments:

 This question was overall answered well by many candidates. A logical explanation of the rationale for recruitment and its benefits as well as possible harm along with a mention of recent literature was required to score marks. Good candidates understood that although oxygenation may improve with recruitment maneuvers mortality benefit was not demonstrated in any trials. The risk of possible harm from the ART study as well PHARLAP ceasing recruitment due to this was noted by some candidates.

Discussion

Introduction/definition

  • A recruitment manoeuvre is any technique that transiently increases alveolar pressure above normal tidal ventilation, and sustains that pressure beyond the normal inspiratory time (Hodgson et al, 2016)

Rationale for the use of recruitment manoeuvres

  • ARDS is characterised by heterogeneity of lung disease (Gattinoni & Pesenti, 2006)
  • Some areas of lungs may be collapsed/atelectatic and not be participating in gas exchange
  • These regions may be reinflated by the application of enough positive transpulmonary pressure
  • If these regions can subsequently be kept inflated by an open-lung (high PEEP) strategy, an improvement in gas exchange should result
  • An improvement in gas exchange should decrease hypoxia, produce a decrease in the required FiO2, and therefore decrease oxygen toxicity and organ dysfunction due to hypoxia and hypercapnea.  

Advantages of recruitment manoeuvres

  • They are easy to perform (all you need is a ventilator)
  • Compared to other techniques of improving oxygenation, this is the cheapest (followed by prone position). Other techniques either require expensive consumables (inhaled nitric oxide, prostacycline) or equipment (high frequency oscillation, ECMO).
  • There is a range of different manoeuvres in the literature, which means one is not restricted to one technique. It is possible to tailor the therapy to the patient and vary the technique depending on the degree of atelectasis, haemodynamic performance and expected friability of the lungs.
  • Oxygenation may improve. This is the one thing which is consistently demonstrated by all the studies, including those which did not find any beneficial effect on mortality.
  • The patient with ARDS will usually already be paralysed and sedated, i.e. it is not inconvenient to sedate and paralyse them just for this procedure
  • In the prone position, recruitment manoeuvres are more effective.

Disadvantages of recruitment manoeuvres

  • Nobody can agree on how much pressure to use, or for how long (i.e. the fact that there is a range of techniques is a mixed blessing)
  • They may not be appropriate in all conditions, eg. the classically fragile lung in PJP pneumonia
  • If the patient has already had a pneumothorax, obviously it will get worse 

Possible complications

  • Barotrauma and ventilator-induced lung injury
    • Pneumothorax
    • Subcutaneous emphysema
    • Pneumomediastinum
    • ​​​​​​Cyclic atelectasis (i.e. with repeated recruitment manoeuvres, after each the reinflated lung may just collapse again)
    • The pressure will first be selectively distributed to well-aerated lung, potentially damaging those alveoli which were previously performing well as gas exchange units. After such an assault, these lung units may have impaired gas exchange. 
  • Poor or unexpectedly opposite effect on oxygenation:
    • The recruitment manoeuvre may be ineffective because the pressure used may be insufficient, and a sufficient pressure may be comically excessive. 
    • The effect on oxygenation is only transient: 
    • The effect of increasing pressure may produce worsening shunt (i.e. instead of recruiting the collapsed lung regions, you push more blood flow into them, increasing the shunt fraction and therefore degrading oxygenation).
  • Haemodynamic effects
    • Because of increased intrathoracic pressure, RV afterload increases and RV preload decreases. The consequence of this is a decrease in cardiac output. In the critically ill patient, this will manifest as a marked fall in blood pressure
    • A cytokine/endotoxin shower may be produced by the shunt. The blood shunted through diseased lung will incrrease the systemic delivery of bacterial toxin and cytokines, contributing to haemodynamic instability which may be sustained even after the manoeuvre is completed.

Evidence for and against recruitment manoeuvres

  • Experimental animal models have demonstrated improved lung mechanics and gas exchange (summarised by Moran et al, 2003), which encouraged human studies
  • Small-scale trials have demonstrated benefits in specific patient categories and scenarios, but this evidence has been inconsistent and patchy. For example, post-suctioning recruitment manoeuvres work really well in pigs (Kasim et al, 2009) but not in human children (Morrow et al, 2007)
  • The 2016 Cochrane review by Hodgson et al found that only low-quality evidence supported the use of recruitment manoeuvres, in terms of improved ICU mortality (but not hospital mortality). In total, data from 1658 trial participants were compiled.
  • The ART trial (Cavalcanti et al, 2017) enrolled 1010 patients and found an increased 28-day all-cause mortality associated with recruitment manoeuvres to 50-60 cmH2O. ​​​​​​​
  • The PHARLAP trial (Hodson et al, 2019) was stopped early because the steering committee lost equipoise following the publication of ART. What data they managed to collect did not suggest any improvement in patient-centred outcomes.

References

Cavalcanti, Alexandre Biasi, et al. "Effect of Lung Recruitment and Titrated Positive End-Expiratory Pressure (PEEP) vs Low PEEP on Mortality in Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial." Jama 318.14 (2017): 1335-1345.

Hodgson, Carol L., et al. "A randomised controlled trial of an open lung strategy with staircase recruitment, titrated PEEP and targeted low airway pressures in patients with acute respiratory distress syndrome." Critical care 15.3 (2011): R133.

Hodgson, Carol, et al. "Recruitment manoeuvres for adults with acute respiratory distress syndrome receiving mechanical ventilation." The Cochrane Library (2016).

Villar, Jesús, Fernando Suárez-Sipmann, and Robert M. Kacmarek. "Should the ART trial change our practice?." Journal of thoracic disease 9.12 (2017): 4871.

Cavalcanti, Alexandre Biasi, Marcelo Britto Passos Amato, and Carlos Roberto Ribeiro de Carvalho. "Should the ART trial change our practice?." Journal of thoracic disease 10.3 (2018): E224.

Moran, I., et al. "Recruitment manoeuvres in acute lung injury/acute respiratory distress syndrome." European Respiratory Journal 22.42 suppl (2003): 37s-42s.

Gattinoni, Luciano, and Antonio Pesenti. "The concept of “baby lung”." Applied Physiology in Intensive Care Medicine. Springer, Berlin, Heidelberg, 2006. 303-311.

Rocco, Patricia RM, Paolo Pelosi, and Marcelo Gama De Abreu. "Pros and cons of recruitment maneuvers in acute lung injury and acute respiratory distress syndrome." Expert review of respiratory medicine 4.4 (2010): 479-489.

Kasim, Ihsan, et al. "A recruitment breath manoeuvre directly after endotracheal suction improves lung function: An experimental study in pigs.Upsala journal of medical sciences 114.3 (2009): 129-135.

Morrow, Brenda, Merle Futter, and Andrew Argent. "A recruitment manoeuvre performed after endotracheal suction does not increase dynamic compliance in ventilated paediatric patients: a randomised controlled trial." Australian Journal of Physiotherapy 53.3 (2007): 163-169.

Hodgson, Carol L., et al. "Maximal recruitment open lung ventilation in acute respiratory distress syndrome (PHARLAP). A phase II, multicenter randomized controlled clinical trial." American journal of respiratory and critical care medicine 200.11 (2019): 1363-1372.

Question 1 - 2018, Paper 1

During the transport of an intubated, ventilated patient, the end—tidal carbon dioxide (ETCO2) trace on the transport monitor indicates that CO2 is no longer detectable. List the possible causes and outline your response.

College answer

  • Patient related possibilities 
    • Airway issue – blockage or dislodgement of ETT o Patient disconnected from ventilator/ventilator tubing 
    • Patient not ventilating – for example pneumothorax or high peak pressures resulting in transport ventilator ‘cutting out’ flow
    • CO2 not being produced by the patient – cardiac arrest, massive pulmonary embolism
  • Equipment related possibilities 
    • Capnography calibrating
    • Disconnection of ventilator/ventilator tubing (no mark if already mentioned above) o Transport monitor/cable failure
    • Capnography related problem – for example disconnection of ETCO2 tubing or H2O within the tubing/capnography
  • Response 
    • Immediate patient assessment – check pulse, check ventilating
    • May need to modify transport to enable thorough assessment and treatment if needed – for example to gain access to the patient.
    • If patient issue:
      • CPR if arrest, or resuscitation as indicated 
      • Change to bag mask ventilation
      • Check ETT position/blockage – reintubation if necessary
      • Treat if intrinsic lung pathology – thoracostomy for pneumothorax.
    • If confident patient is stable check equipment for disconnection or leak

Decision on continuation of transport to be made if equipment faulty; whether to continue or abort transfer will depend on factors including patient stability, reason for and urgency of transfer and estimated time remaining.

Examiners Comments:

 Overall done reasonably well. Few candidates considered transport related issues or gave a good systematic approach.

Discussion

So, the capnography trace; it is no longer detectable. If one iholds onto the belief that college questions undergo careful review and are very precisely worded, then this specific choice of phrase gains a particular significance. The trace did not peter out and go flat, it disappeared entirely. The possible causes and response to this therefore fall into "blame the patient" and "blame the equipment" categories. The college classification is sufficiently brief and comprehensive, so that minimal mprovement on the college answer can be offered. One is merely able to rearrange the wording somewhat, to make it easier for the time-poor candidate to score more points.

In short:

  • Patient causes:
    • Airway
      • Upper obstruction (eg. patient suddenly bit down on the tube)
      • Lower obstruction (eg. anaphylaxis, bronchospasm)
    • Breathing
      • No expired gas
        • Apnoea; you forgot to switch the patient to a mandatory mode
        • No ventilation; no flow is being delivered because of some sort of catastrophic respiratory problem, eg. pneumothorax or severe bronchospasm
      • No CO2 in the expired gas (oesophageal intubation, though the scenario we are given makes this unlikely)
    • Circulation
      • No CObeing circulated to the alveolus (massive PE)
      • No CObeing produced (cardiac arrest)
  • Equipment causes:
    • Ventilator
      • Powered down (battery loss)
      • Empty (gas supply failure)
    • Circuit
      • Disconnected
      • Kinked
    • Endotracheal tube
      • Perforation (the end tidal gas is escaping via the hole before it gets to the capnograph)
      • Cuff leak 
    • EtCO2 monitor
      • Disconnected infra-red monitoring module
      • Disconnected or waterlogged entrainment port of an inline monitor
    • Monitoring display
      • The plug has fallen out
      • Miscalibrated monitor (waveform exists but is out of the display scalar range)

A possible systematic response to this might consist of:

  • Check the patient:
    • Other monitoring on the screen: does it support the diagnosis of cardiac arrest or massive PE?
    • Airway: is the ETT obstructed or leaking?
    • Breathing:
      • is there evidence of pneumothorax or bronchospasm?
      • is there air entry, or is the patient not ventilating for some reason?
    • Circulation: is there still pulsatile blood flow?
  • Check the equipment
    • Pass a suction catheter down the ETT to make sure it is not blocked
    • Check the tubing to make sure the capnometry module is intact and atached
    • Check the monitor atachments to make sure all the plugs are in place
    • Check the monitor to make sure it is properly scaled
    • Recalibrate the monitor
  • Check your transport progress
    • Is this transport so vital that it can't wait for equipment that works?

In terms of published evidence, there is little literature out there to guide one's written response to this question, except for papers which support the intra-transport CO2 monitoring. For example, Silvestri et al (2005) determined that it is helpful on the basis of the fact that among the patients who were monitored in this way, none ended up having undetected oesophageal intubation. However, unlike other such situations (eg. the tracheostomy patient who just won't ventilate) this scenario has not yeat attracted the attention of anybody who might create a flowchart management algorithm.

References

Question 25 - 2018, Paper 1

A 51 -year-old male has just been transferred to the ICU from the surgical ward with worsening shortness of breath five days post-oesophagectomy, and a presumed anastomotic leak.

On arrival in ICU, he is tachypnoeic and extremely agitated.

Arterial blood gas analysis on FiO2 0.6 — 0.8 via reservoir (non-rebreathing) mask shows the following:

Parameter

Patient Value

Adult Normal Range

7.12*

7.35 - 7.45

PaO2

50 mmH 6.6 kPa

PaCO2

50 mmH 6.6 kPa *

35-45 4.6 -6.0

HCO3

16 mmol/L*

22 - 28

Chest X-ray shows bilateral pulmonary infiltrates.

  1. List the possible causes for his respiratory failure.    (20% marks)

The patient is intubated and mechanical ventilatory support is initiated.

  1. Describe the ventilator settings you will prescribe, giving the rationale for your decision.

(60% marks)

Following intubation, there is no immediate improvement in the patient's oxygenation.

  1. List the initial strategies that may be used to improve oxygenation. (20% marks)

College answer

a)  

Differential diagnosis should include:

  • ARDS secondary to sepsis from any source or other inflammatory insult including the following
  • Pneumonia (hospital-acquired)
  • Aspiration
  • Atelectasis/pleural effusions/empyema 
  • Fluid overload secondary to resuscitation, renal failure
  • Exacerbation of pre-existing condition e.g. heart failure, valvular heart disease, post-op ischaemia/MI, arrhythmia
  • Lung diseases e.g. lymphangitis carcinomatosis

b)  

  • Use a mode with which one is familiar and aim to limit ventilator-associated lung injury, i.e. oxygen toxicity, barotrauma, volutrauma, shear stress and biotrauma
  • Choice of mode (any appropriate answer acceptable e.g. APRV for recruitment benefit, or volume assist control as staff familiarity and no one mode shown to have benefit over another)
  • Avoid over-distention of alveoli by keeping tidal volumes at 6-8 ml/kg (predicted body weight which in the ARDSnet studies was ~20% below actual body weight and calculated by a formula linking height and sex)
  • Use PEEP to minimise alveolar collapse and derecruitment. 
  • Titrate PEEP to achieve a PaO2 of 60 mmHg with lowest FiO2 that is needed 
  • Permissive hypercapnea to avoid large minute volumes and alveolar injury through collapse and expansion of lung units

c)

  • High FiO2 (titrated to lowest possible level to limit toxicity)
  • Confirm ETT pos

     

    ition and patency
  • Exclude readily reversible cause of hypoxia e.g. PTX, mucus plug, large effusion
  • Increased inspiratory time
  • Increased PEEP
  • Prone positioning for at least 16/24 hours per day
  • Ensure adequate cardiac output

 

Examiners Comments:

Answered well overall. Lack of detail and structure in some answers.

Discussion

a) List the possible causes for his respiratory failure.    

Tandon et al (2001) mention that this happened to over 14% of their oesophagectomy patients, with a 50% mortality. Why is this post-oesophagectomy patient so hypoxic, and what are those infiltrates? One might classify this into two broad categories:

  • Related to the oesophagectomy
    • ARDS due to sepsis
    • Aspiration, eg. even some sort of tracheo-oesophageal fistula
    • Atelectasis/pleural effusions/empyema 
    • Massive blood transfusion
  • Unrelated to the surgery
    • Pulmonary haemorrhage
    • Hospital-acquired pneumonia
    • Lymphangitis carcinomatosis
    • Drug-related (eg. eosinophilic) pneumonitis
    • Autoimmune pulmonary vasculitis
    • Pulmonary oedema due to MI, valve disease or fluid overload
    • Pancreatitis

b) Describe the ventilator settings you will prescribe, giving the rationale for your decision.

c) List the initial strategies that may be used to improve oxygenation. 

Let's assume you've excluded sophomoric errors like right bronchial intubation and sputum plugging. Other strategies may include:

Additional ventilator manoeuvres to improve oxygenation:

Ventilator strategies to manage refractory hypoxia

  • Prone ventilation, for at least 16 hours a day (PROSEVA, 2013)
  • High frequency oscillatory ventilation may not improve mortality among all-comers (OSCAR, 2013) or it may actually increase mortality (OSCILLATE, 2013) but some authors feel that there were problems with methodology.
  • ECMO may improve survival (CESAR, 2009) but again there were problems with methodology, and in any case the upper GI surgeon may have a big problem with heparinising the circuit.

References

Tandon, S., et al. "Peri‐operative risk factors for acute lung injury after elective oesophagectomy." British journal of anaesthesia 86.5 (2001): 633-638.

ARDS Definition Task Force. "Acute Respiratory Distress Syndrome." Jama307.23 (2012): 2526-2533.

Marini, John J. "Point: is pressure assist-control preferred over volume assist-control mode for lung protective ventilation in patients with ARDS? Yes." CHEST Journal 140.2 (2011): 286-290.

Esteban, Andrés, et al. "Prospective randomized trial comparing pressure-controlled ventilation and volume-controlled ventilation in ARDS." CHEST Journal 117.6 (2000): 1690-1696.
 
Gainnier, Marc, et al. "Effect of neuromuscular blocking agents on gas exchange in patients presenting with acute respiratory distress syndrome*."Critical care medicine 32.1 (2004): 113-119.

Watling, Sharon M., and Joseph F. Dasta. "Prolonged paralysis in intensive care unit patients after the use of neuromuscular blocking agents: a review of the literature." Critical care medicine 22.5 (1994): 884-893.

Armstrong Jr, Bruce W., and Neil R. MacIntyre. "Pressure-controlled, inverse ratio ventilation that avoids air trapping in the adult respiratory distress syndrome." Critical care medicine 23.2 (1995): 279-285.

Hodgson, Carol, et al. "Recruitment manoeuvres for adults with acute lung injury receiving mechanical ventilation." Cochrane Database Syst Rev 2.2 (2009).

Zavala, Elizabeth et al.Effect of Inverse I: E Ratio Ventilation on Pulmonary Gas Exchange in Acute Respiratory Distress Syndrome Anesthesiology: January 1998 - Volume 88 - Issue 1 - p 35–42

Brower RG, Lanken PN, MacIntyre N, et al; National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Higher versus lower positive endexpiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351(4):327-336.

Meade MO, Cook DJ, Guyatt GH, et al; Lung Open Ventilation Study Investigators. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):637-645.

Mercat A, Richard JC, Vielle B, et al; Expiratory Pressure (Express) Study Group. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646- 655.

Briel, Matthias, et al. "Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome." JAMA: the journal of the American Medical Association 303.9 (2010): 865-873.

De Campos, T. "Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network." N Engl J Med342.18 (2000): 1302-130g.

Putensen, Christian, et al. "Meta-analysis: ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury." Annals of internal medicine 151.8 (2009): 566-576.

de Durante, Gabriella, et al. "ARDSNet lower tidal volume ventilatory strategy may generate intrinsic positive end-expiratory pressure in patients with acute respiratory distress syndrome." American journal of respiratory and critical care medicine 165.9 (2002): 1271-1274.

Kahn, Jeremy M., et al. "Low tidal volume ventilation does not increase sedation use in patients with acute lung injury*." Critical care medicine 33.4 (2005): 766-771.

Hodgson, Carol L., et al. "A randomised controlled trial of an open lung strategy with staircase recruitment, titrated PEEP and targeted low airway pressures in patients with acute respiratory distress syndrome." Crit Care 15.3 (2011): R133.

MANCINI, MARCO, et al. "Mechanisms of pulmonary gas exchange improvement during a protective ventilatory strategy in acute respiratory distress syndrome." American journal of respiratory and critical care medicine 164.8 (2012).

Amato, Marcelo Britto Passos, et al. "Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome." New England Journal of Medicine 338.6 (1998): 347-354.

Chu, Eric K., Tom Whitehead, and Arthur S. Slutsky. "Effects of cyclic opening and closing at low-and high-volume ventilation on bronchoalveolar lavage cytokines*." Critical care medicine 32.1 (2004): 168-174.

Amato, Marcelo BP, et al. "Driving pressure and survival in the acute respiratory distress syndrome." New England Journal of Medicine 372.8 (2015): 747-755.

Guérin, Claude, et al. "Prone positioning in severe acute respiratory distress syndrome." New England Journal of Medicine 368.23 (2013): 2159-2168.

Young D, et al. " High-frequency oscillation for ARDS". N Engl J Med 2013, 368:806-813

Ferguson, Niall D., et al. "High-frequency oscillation in early acute respiratory distress syndrome." New England Journal of Medicine 368.9 (2013): 795-805.

Pathmanathan, N., et al. "Five-year single-centre review of ARDS patients receiving high-frequency oscillatory ventilation." Critical Care 18.Suppl 1 (2014): P338.

Long, Yun, et al. "Positive end-expiratory pressure titration after alveolar recruitment directed by electrical impedance tomography." Chinese medical journal 128.11 (2015): 1421.

Question 11 - 2018, Paper 2

A 42-year-old male is admitted to your ICU day 4 post-induction chemotherapy for acute promyelocytic leukemia (AML-M3). The patient was initially treated with idarubicin and all-trans retinoic acid (ATRA). He has progressively become more dyspnoeic in the ward. A chest X-ray demonstrates a bilateral, diffuse pulmonary infiltrate. 

Initial examination reveals:

Respiratory Rate      

40 breaths/min, SpO2 88% on 10 L/min O2 by face mask

Glasgow Coma Scale 

14 (E4 M6 V4)

Temperature            

38.9ºC 

Heart rate                

144 beats/min 

Blood pressure         

95/50 mmHg 

Full blood count is as follows on admission:

Parameter

Patient Value

Adult Normal Range

Haemoglobin

88 g/L*

135 – 180 

White Cell Count

26.0 x 109/L* ( no differential)

4.0 – 11.0

Platelets

22 x 109/L*

150 – 400 

Comment: Blasts visible

International normalised ratio (INR)

3.2

  1. Give your differential diagnosis for his respiratory failure.   
    (40% marks) 
  1. What are the major issues in this patient and how would you manage them?
    (60% marks)

College answer

Differential for respiratory failure

          Infection

                    *common CAP/HAP bacteria

                    *resistant organisms/less virulent bacteria (given immunosuppression,                                        hospitalisation)

              *PJP/toxoplasmosis (although probably not yet immunosuppressed for long 

                              enough)

                    *fungal

                    *viral

          Non-infective

                    *Differentiation syndrome (previously called ATRA syndrome)

                    *Pulmonary haemorrhage

                    *Drug induced pneumonitis

                    Aspiration

                    TRALI

                    Cardiogenic pulmonary oedema

                    Non-cardiogenic capillary leak syndrome

Major issues and management

During early phase there is usually DIC and high risk of haemorrhage (especially pulmonary heamorrhage and ICH). After ATRA or ATO there is risk of differentiation syndrome. Despite this the overall prognosis is better than all other types of AML with cure rates ~90%. Hence, it would generally be appropriate to offer routine ICU supportive care (including invasive ventilation).

Specific issues and management:

  1. Infection: seek and treat infection (usually a broad septum anti-pseudomonal B-lactam and vancomycin would be appropriate empiric antimicrobials). It is probably too early for fungal infection but there would usually be fungal prophylaxis (e.g. voriconazole or fluconazole) prescribed and viral prophylaxis prescribed (e.g. aciclovir). CMV status relevant. Septrin if PJP. Advice from haematology and ID should be sought. Cultures should be sent.
  2. Differentiation syndrome: Steroids (e.g. dexamethasone 10 mg bd) for differentiation syndrome 3. Coagulopathy: Factor replacement is more aggressive given risk of bleeding from DIC (aim fib >1.5, pats >30-50).
  1. Management of respiratory failure: Optimise oxygenation/ventilation (Invasive ventilation is not routinely avoided given overall good prognosis).
  2. Routine supportive care. Seek and treat shock (most likely septic, other types possible (haemorrhagic, hypovolaemic, cardiogenic, obstructive). Stress ulcer prophylaxis given high dose steroids and coagulopathy. Nutritional support – enteral feeding (oral if possible). No thrombophophylaxis required. Consultation with haematologist and ID specialist.
  3. Haematologic management: Routine cytotoxic precautions for staff if cytotoxic (e.g. idarubicin given). WCC maybe mainly blasts and patient maybe neutropenic. Should have routine neutropaemic precautions. Role of G-CSF controversial given potential to stimulate malignant clone. Usually continue ATRA but discontinue chemotherapy.

Examiner’s Comments:

Many candidates listed coagulopathy and differentiation syndrome in their differential, but few discussed the management of these problems.

Discussion

This question is identical to Question 4 from the second paper of 2015, including not only the history but also the wording of the questions. However, weirdly, the college model answer is different. Even more weirdly, it is a different answer which is not obviously better than the previous one. Confidently, the author presents the same identical discussion section for both of these SAQs, as it is unclear as to why they might need to be different. 

Issues:

  • Airway: The need to avoid intubation
  • Respiratory: Hypoxic respiratory failure
  • Circulatory: Haemodynamic instability: likely, septic shock (HR 144, BP 95/50)
  • Neuro: A decreased level of consciousness (GCS 14)
  • Haematological: anaemia, thrombocytopenia, likely neutropenia, and coagulopathy.
  • Infectious: High fever (38.9°C) and raised WCC (26)
  • Definitive diagnosis:  cause of respiratory failure is uncertain
  • Social: prognosis and family understanding of the situation, medical consensus

Plans:

  • Airway plan:
    • Avoid intubation- unless it is clear that the patient is failing. See the non-invasive ventilation chapter for the rationale behind this. In short, recommendations to avoid intubation in immunosuppressed patients are based on early studies (eg. Scales et al, 2008) which do not reflect the recent improvements in critical care for such patients. The college answer reflects this fact. This is very interesting, as in the 2015 version of the question the college model answer recommended to "attempt to avoid invasive respiratory support if possible". Generally, mortality rates for BMT patients in the ICU are improving (from 14% survival at 1 year to 32%, according to ), but mechanical ventilation is still one of the most important negative prognostic indicators (in the series by Al-Zubaidi from 2018, it was associated with a 90% mortality at 1 year, not much different to 92% in Scales et al ten years ago).
    • Thus: keep patient fasted (nil by mouth) in the event intubation is required.
  • Respiratory support plan:
    • Commence CPAP NIV
    • Aim for SpO2 >90%, PaO2 > 60mmHg
    • Breaks every 2 hours for chest physiotherapy (on high flow nasal prongs)
    • Ensure humidified circuit
    • Ensure frequent cough; encourage expectoration of sputum
  • Circulatory support plan:
    • Assess for fluid responsiveness using dynamic parameters
    • If fluid responsive, resuscitate with 20% albumin
    • If fluid resuscitation is ineffective, maintain MAP >65 with noradrenaline
    • Consider stress dose steroids (unless steroids are already being given)
  • Neurological plan:
    • Avoid sedating analgesics
    • Change NIV mode to BiPAP if hypercapnea develops
  • Haematological:
    • Transfuse to Hb >70 (TRISS)
    • Correct platelets for CVC insertion
    • Administer Vitamin K and FFP for correction of the INR
    • Seek clarification re. WCC differential (All neutrophils? All blasts?)
  • Infectious:
    • Fungal cover with voriconazole or caspofungin
    • PJP cover with Bactrim
    • Viral cover with aciclovir
    • Atypical cover with azithromycin
    • Gram negative and anaerobe cover with meropenem
    • Gram-positive cover with vancomycin
  • Definitive diagnosis:
    • Blood and sputum cultures
    • Atypical pneumonia serology
    • Urinary legionella and pneumococcal antigens
    • Sputum culture
    • TTE to exclude the contribution of cardiac failure to shock and hypoxia
    • Discussion with haematology team regarding the use of high dose steroids for ATRA syndrome (10mg bd of dexamethasone for 3 days, or addition of cytarabine to the chemotherapy cocktail to suppress the bone marrow).
  • Social:
    • Schedule family discussion
    • Confer with haematology regarding prognosis

References

Panoskaltsis-Mortari, Angela, et al. "An official American Thoracic Society research statement: noninfectious lung injury after hematopoietic stem cell transplantation: idiopathic pneumonia syndrome." American journal of respiratory and critical care medicine 183.9 (2011): 1262-1279.

Patatanian, E., and D. F. Thompson. "Retinoic acid syndrome: a review." Journal of clinical pharmacy and therapeutics 33.4 (2008): 331-338.

Lee, Hwa Young, Chin Kook Rhee, and Jong Wook Lee. "Feasibility of high-flow nasal cannula oxygen therapy for acute respiratory failure in patients with hematologic malignancies: A retrospective single-center study." Journal of critical care 30.4 (2015): 773-777.

Scales, Damon C., et al. "Intensive care outcomes in bone marrow transplant recipients: a population-based cohort analysis." Critical Care 12.3 (2008): R77.

Lueck, Catherina, et al. "Improved short-and long-term outcome of allogeneic stem cell recipients admitted to the intensive care unit: a retrospective longitudinal analysis of 942 patients." Intensive care medicine 44.9 (2018): 1483-1492.

Al-Zubaidi, Nassar, et al. "Predictors of outcome in patients with hematologic malignancies admitted to the intensive care unit." Hematology/oncology and stem cell therapy (2018).

Question 26.1 - 2018, Paper 2

The following question is based on the shown pulmonary function tests (PFTs). Assume in each case that the test result is adequate and reproducible.

Key:

FVC

L

Forced Vital Capacity

FEV1

L

Forced Expiratory volume in 1 second

FEV1/FVC

%

Ratio of the above

RV

L

Residual volume at end expiration

TLC

L

Total Lung Capacity

DLCO corr

ml/min/mmHg

Diffusing capacity for carbon monoxide, corrected for Hb

You are asked to evaluate a previously well, 36-year-old male who has presented to Emergency Department (ED) with shortness of breath and increased work of breathing. This has been progressive over the past week. He has had PFTs performed recently as an outpatient: 

Predicted

Actual

% Predicted

Post Bronchodilator

% Change

FVC (L)

4.20

3.15

75

3.62

+15

FEV1 (L)

3.40

2.14

63

2.56

+20

FEV1/FVC (%)

80

68

71

+4

RV (L)

2.31

3.03

131

TLC (L)

6.41

6.53

102

  1. What pattern of abnormality is shown?
  1. Should it become necessary, what implications will this have for your ventilation strategy?  (30% marks)

College answer

Obstructive, reversible, evidence of gas trapping but not hyperinflation (1 mark)   
At risk of dynamic hyperinflation, may need high inspiratory pressures, low PEEP, long expiratory time (3 Marks) 

Discussion

Formal pulmonary function tests have also been asked about in Question 21.2 from the first  paper of 2014  and the identical Question 9.1 from the first  paper of 2011. 

To approach this systematically:

  • FVC is the forced vital capacity, and here it is decreased, which ordinarily simply means that the spirometry effort was poor, but the college assure us that each test was "adequate and reproduceable" so the patient must truly have reduced FVC.
  • FEV1 is the forced expired volume over 1 second, and is a measure of maximal air flow. A decreased FEV1 which improves with bronchodilators demonstrates a reversible obstructive pattern.
  • FEV1/FVC ratio is a measure of airway resistance which incorporates both the abovementioned metrics.
  • RV is the residual volume. A high RV suggests end-expiratory gas trapping or bullous dead space. This patient's RV is clearly increased; on the basis of this the college say there is "evidence of gas trapping" .
  • TLC is the total lung capacity. In this case, the TLC is near normal. On the basis of this, the college say that there is no hyperinflation.

The ventilation strategy for somebody with such an obstructive pattern of respiratory function and such propensity to hyperinflation resembles that which might be used for status asthmaticus, and would consist of the following strategies:

  • Use the largest tube possible.
  • Use lowest FiO2 to achieve SpO2 of 90-92%
  • Use a small tidal volume, 5-7ml/kg
  • Use a slow respiratory rate, 10-12 breaths per minute (or even less!)
  • Use a long expiratory time, with I:E ratio 1:3 or 1:4
  • Increase inspiratory flow rate to maximum. .
  • Reset the pressure limits (i.e. ignore high peak airway pressures).  .
  • Use a volume-control mode of ventilation.
  • Use minimal PEEP.
  • Keep the Pplat below 25cmH2o to prevent dynamic hyperinflation. 
  • Titrate PEEP to work of triggering once the patient is breathing spontaneously.

References

Pellegrino, Riccardo, et al. "Interpretative strategies for lung function tests."European Respiratory Journal 26.5 (2005): 948-968.

The American Thoracic Society has a page which features an excellent bibliography of the articles which support their interpretation standards.

Question 26.2 - 2018, Paper 2

The following question is based on the shown pulmonary function tests (PFTs). Assume in each case that the test result is adequate and reproducible.

Key:

FVC

L

Forced Vital Capacity

FEV1

L

Forced Expiratory volume in 1 second

FEV1/FVC

%

Ratio of the above

RV

L

Residual volume at end expiration

TLC

L

Total Lung Capacity

DLCO corr

ml/min/mmHg

Diffusing capacity for carbon monoxide, corrected for Hb

A 39-year-old female has presented in ED with severe, acute on chronic shortness of breath, now affecting her at rest. She has a 15-pack year history of smoking. She has had PFTs performed recently as an outpatient. Her chest X-ray shows marked bi-basal hyper-lucency.

Predicted

Actual

% Predicted

Post Bronchodilator

% Change

FVC (L)

3.15

1.50

48

0.83

-10

FEV1 (L)

2.65

0.52

20

0.53

+2

FEV1/FVC (%)

83

54

14

RV (L)

1.49

3.13

210

TLC (L)

4.44

4.74

107

DLCO corr

(ml/min/mmHg)

24.85

6.70

27

  1. What pattern of abnormality is shown?
  1. Suggest two likely diagnoses.                                                                   (20% marks)

College answer

Severe, non-reversible obstructive lung disease     
Smoking related lung disease  
Alpha 1 antitrypsin deficiency                          (2 marks) 

Discussion

Formal pulmonary function tests have also been asked about in Question 21.2 from the first paper of 2014  and the identical Question 9.1 from the first paper of 2011. 

To approach this systematically:

  • FVC is the forced vital capacity, and here it is significantly decreased, which ordinarily simply means that the spirometry effort was poor, but the college assure us that each test was "adequate and reproduceable" so the patient must truly have reduced FVC.
  • FEV1 is the forced expired volume over 1 second, and is a measure of maximal air flow. A decreased FEV1 which fails to improve with bronchodilators demonstrates a irreversible obstructive pattern.
  • FEV1/FVC ratio is a measure of airway resistance which incorporates both the abovementioned metrics.
  • RV is the residual volume. A high RV suggests end-expiratory gas trapping or bullous dead space. This patient's RV is significantly increased, but the college do not make any specific comment on this.
  • TLC is the total lung capacity. In this case, the TLC is 107% of normal. On the basis of this, one might say that there is hyperinflation of the lungs. The college do not mention this.
  • DLCO is the diffusing capacity for carbon monoxide, a measure of the efficiency of the lung as a gas exchange surface. In this case, the DLCO is 27% of predicted, demonstrating a significant diffusion defect (which is probably not a measurement error, given the normal TLC). The "corr" in the SAQ refers to the correction of the DLCO for the patient's haemoglobin value, which we are not supplied with.

In summary, this patient has hyperinflated lungs with a severe irreversible obstructive pattern. The history we are given (smoker, but too young to have such severe bibasal bullous emphysema) suggests something might be congenitally broken in her lungs. As such, the college offer α-1 antitrypsin deficiency as one of the differentials. A list of (vaguely) plausible differentials might include:

References

Pellegrino, Riccardo, et al. "Interpretative strategies for lung function tests."European Respiratory Journal 26.5 (2005): 948-968.

The American Thoracic Society has a page which features an excellent bibliography of the articles which support their interpretation standards.

Question 26.3 - 2018, Paper 2

The following question is based on the shown pulmonary function tests (PFTs). Assume in each case that the test result is adequate and reproducible.

Key:

FVC

L

Forced Vital Capacity

FEV1

L

Forced Expiratory volume in 1 second

FEV1/FVC

%

Ratio of the above

RV

L

Residual volume at end expiration

TLC

L

Total Lung Capacity

DLCO corr

ml/min/mmHg

Diffusing capacity for carbon monoxide, corrected for Hb

A 46-year-old female has presented with several months of progressive shortness of breath and lethargy compromising her previously active lifestyle. She is markedly hypoxic, with a resting SpO2 of 88% in air. She has had PFTs performed recently as an outpatient

Predicted

Actual

% Predicted

Post Bronchodilator

% Change

FVC (L)

3.56

3.35

94

2.77

-6

FEV1 (L)

2.88

2.70

93

2.31

-4

FEV1/FVC (%)

81

82

83

RV (L)

1.90

2.03

107

TLC (L)

5.22

5.11

98

DLCO corr

(ml/min/mmHg)

23.25

7.96

34

  1. What pattern of abnormality is shown?
  1. List two differential diagnoses.                                                                  (20% marks)

College answer

Normal lung function, markedly impaired diffusion of gases  
Problem is not in the lungs but with the blood flow i.e. pulmonary vascular disease/pulmonary hypertension

Any 2 of: 
idiopathic or familial PAH    
cardiac disease - L sided 
connective tissue disease /SLE 
drug induced 
chronic thromboembolic disease                    (2 marks) 
 

Discussion

Formal pulmonary function tests have also been asked about in Question 21.2 from the first paper of 2014  and the identical Question 9.1 from the first paper of 2011. 

To approach this systematically:

  • FVC is the forced vital capacity, and here it is normal.
  • FEV1 is the forced expired volume over 1 second, and is a measure of maximal air flow. Here, it is normal.
  • FEV1/FVC ratio is a measure of airway resistance which incorporates both the abovementioned metrics.
  • RV is the residual volume. A high RV suggests end-expiratory gas trapping or bullous dead space. This patient's RV is normal.
  • TLC is the total lung capacity. In this case, the TLC is essentially normal.
  • DLCO is the diffusing capacity for carbon monoxide, a measure of the efficiency of the lung as a gas exchange surface. In this case, the DLCO is 34% of predicted, demonstrating a significant diffusion defect (which is probably not a measurement error, given the normal TLC). The "corr" in the SAQ refers to the correction of the DLCO for the patient's haemoglobin value, which we are not supplied with. Normal  spirometry and lung volumes associated with a decreased haemoglobin-corrected DLCO suggest that something is wrong with the pulmonary vasculature and blood flow.

An isolated defect in the diffusing capacity for carbon monoxide could be anaemia, but the "corr" in the SAQ refers to the correction of the DLCO for the patient's haemoglobin value, which excludes this as a differential. Other possible causes (according to UpToDate) include:

  • Pulmonary hypertension:
    • Chronic thromboembolic
    • Primary
    • Secondary to left-sided cardiac disease (eg.. MR)
    • Secondary to vasculitis, pulmonary fibrosis, etc
  • Hepatopulmonary syndrome
  • High carboxyhaemoglobin level
  • Early interstitial lung disease (i.e. fiborisis is already occurring, but the the TLC and FVC have not had time to change)

References

Pellegrino, Riccardo, et al. "Interpretative strategies for lung function tests."European Respiratory Journal 26.5 (2005): 948-968.

The American Thoracic Society has a page which features an excellent bibliography of the articles which support their interpretation standards.

Question 26.4 - 2018, Paper 2

26.4 – due to a transcription error this section did not include enough information in the stem to provide an adequate answer. As a result, only answers to sections 26.1-26.3 contributed to marks for this question. 

College answer
 

Discussion

With any luck, this "transcription error" did not waste the time of any marginal candidate, causing them to lose the one mark they needed to pass.

References

Question 8 - 2018, Paper 2

A 67-year-old male is admitted to ICU with a 5-day history of increasing shortness of breath, nonproductive cough and acute respiratory failure. He has a background of COPD with a long history of smoking. He is not on home oxygen therapy. Recent pulmonary function tests have demonstrated a severe non-reversible obstructive pattern of impairment.

He has been on non-invasive ventilation (NIV) for 2 hours.

Discuss in detail how you would make a decision about whether to offer invasive mechanical ventilation to this patient, should he fail the trial of NIV. 

College answer

Broad overview
The decision to ventilate severe COPD requires careful consideration, especially in patients who may
be near-end-stage lung disease. Quality of life in such patients may not justify aggressive treatment.
This decision hinges on a firm understanding of the outcome of ARF in COPD.
Factors to be considered
Severity of COPDbased on Spirometry, lifestyle score, dyspnea score
Patient/surrogate wishes/ advance directives
Presence of severe comorbidities
especially cardiovascular and malignancy
Cause of the exacerbatione.g. PE, presence of overlap syndrome (COPD + OSA)
Previous respiratory specialist opinione.g. severe disease, or transplant candidate

Description of above factors

Conclusion
Difficult decision
IMV if unsure and change to terminal care
Global score 

Sample Answer
The decision to ventilate severe COPD requires careful consideration, especially in patients who may
be near-end-stage lung disease. Quality of life in such patients may not justify aggressive treatment.
This decision hinges on understanding of the outcome of ARF in COPD. Patients with COPD requiring
IMV have a hospital mortality of up to 25%, rising to 33% in those needing IMV after failing NIV
(Chandra et al AJRCCM 2012, Roberts et al, Thorax 2010).

a) Severity of COPD, based on spirometry, life style score and dyspnoea scores

The global initiative for Obstructive lung disease (GOLD) criteria for severity of COPD based on
spirometry results help with decision making and prognosis. This criterion takes into account
FEV1/FVC % (all less than 70%) and % of predicted FEV1 (>80, 80-50, 50-30, <30%) to classify
COPD severity into four groups. This man would classify as GOLD 4 (very severe) and have a high
long-term mortality.

BODE index - based on body mass index (<21/>21), MRC dyspnea score (1 to 4, where 4 is
extreme dyspnea on getting dressed, housebound), six-minute walk distance (score 0 to 3, where
3 is <150 m) and FEV1 % predicted (>65 to <35, score 0-3). 4-year survival for those scoring 7-10
in total is only 20% and likely to have even poorer survival if offered IMV.

A life style score of 3 (housebound) or 4 (bedbound/chair bound) had a very poor prognosis
(Menzies et al Chest 1989) and would be difficult to justify IMV in this group.

b) cause of ARF: bronchitis causing an exacerbation has a better prognosis than that due to LV
failure, PE or pneumonia and this will be taken into account in the decision process.

c) severe cardiovascular comorbidities such as unstable angina, severe IHD refractory to
medical therapies, NYHA class 3-4 heart failure would have a high mortality despite aggressive
therapy, as would occult or overt malignancy.

d) existing advance directives and the ability to have a frank discussion with patient surrogates
would impact on the decision to proceed to IMV

e) pre-existing assessment and ongoing follow-up by respiratory physicians will inform the
decision to offer IMV. Existing opinions formed during a stable state precluding IMV is helpful.
Similarly, ongoing smoking and non-engagement with rehabilitation services would make a
decision to offer IMV tenuous. The opposite scenario and future possibility of transplant surgery
may sway the decision to IMV. A documented trajectory of multiple frequent admissions for acute
exacerbations with deteriorating function would affect the decision.
In summary, this is often a difficult decision. A decision to offer IMV would be carefully considered,
collaborative and based on a through collateral history, examination and perusal of existing
referrals and specialist documents. In the event of having to make a precipitous decision, I would
err on the side of offering IMV to buy time for a more considered decision and planned cessation
of IMV (terminal or otherwise).
 

Descriptions of scoring systems and level of detail in template were not expected. Important points
from 
template are bolded.

Discussion

It is unclear how many markes were awarded to the candidates who acknowledged that this is "often a difficult decision", or whether the failure to actually write those words had suggested to the examiners that the candidate felt it was an easy straightforward call. That notwithstanding, there should surely be some structured and systematic way of answering this question, which asks "describe how you would make a decision", not "rant interminably about scoring systems". That's  claearly possible, given that 65.7% of the candidates managed to pass.

Thus:

Establish that intubation is permitted by the circumstances

  • Presence of reversible physiological factors which intubation might address, such as:
    • Respiratory acidosis
    • Decreased level of consciousness
    • Fatigue due to high respiratory workload
  • Absence of existing treatment limitation orders
  • Absence of features which might suggest futility, i.e. where chances of success are impossibly small (eg. multiorgan system failure, severe shock, extreme frailty, etc)
    Insufficient information to guide robust end-of-life decisionmaking (Wildman et al, 2007; prognostic pessimism may deny intubation to potentially salvageable patients)

Consider the possible outcome of intubation: weight factors for and against invasive ventilation

  • Factors which favour a beneficial effect from invasive ventilation:
    • Acute exacerbation of COPD as the cause of respiratory failure -Nevins et al (2001) found that the in-hospital mortality was only 12% for these people, as compared to 28% for the rest of the cohort
    • Higher premorbid FEV1 (over 1.2) - this is the GOLD score (Mannino et al, 2006); GOLD stage 3 or 4 (FEV1/FVC<0.70 and FEV1<50% predicted) is associated with a mortality of around 35% at ten years.
    • Good baseline function  -low BODE index (Celli et al, 2004)
  • Factors which predict a poor outcome from intubation:
    • Failure of NIV, particularly if the patient is elderly - Chandra et al (2012) found that the in-hospital mortality for these people was 33%; non-survivors were largely elderly (over 55% of them were aged 75 or older)
    • Poor baseline function indices - BODE index 7-10 (Low BMI, breathless at rest and unable to walk more than 150m over six minutes, with an FEV1 below 35% of the predicted value) =  20% chance of surviving the next 48 months.
    • Poor global assessment of function -  Menzies et al (1989) found that if the patient is unable to leave their house because of their symptoms, their ICU mortality was with intubation 71%, going up to 75% if they were chronically bedbound or chairbound.
    • Dependence on home oxygen: according to Hajizadeh et al (2015) there is 23% in-hospital mortality, 45% 1-year mortality and  26.8% were discharged to a nursing home within 30 days.
    • Comorbidities (Menzies et al, 1989):
      • Malignancy
      • Cor pulmonale
      • Chronic hypercapnia
      • Left ventricular failure

Discuss with the patient and family, considering that:

  • The patient's autonomy needs to be respected (they may have strong views on the matter)
  • It is important to remain objective - physicians can influence patient opinion significantly depending on how they "spin" their explanation of intubation and mechanical ventilation ( Sullivan et al, 1996)
  • For some scenarios, invasive ventilation has a good chance of success (ICU mortality for the "pure" COPD cohort from Nevins et al (2001) was actually lower than for other acute respiratory pathologies - 9% ICU mortality and 17% hospital mortality).
  • Survivors of short ICU stay with invasive ventilation rate their post-discharge health as same or better, and 96% responded that they would be willing to undergo similar treatment again (Wildman et al, 2009). These patients stayed in ICU for 6-9 days on average.

If deciding to go ahead with a trial of invasive ventilation, discuss the duration of the "trial", considering that:

  • Successful ventilation episodes are short:
    • For survivors of acute exacerbations of COPD, median duration of ventilation is 3 days (Gadre et al, 2018)
    • Prolonged ventilation has a higher mortality: for Nevins et al (2001), the patients who were still invasively ventilated after 72 hours had an in-hospital mortality of 37%, vs. 16% for the rest.
    • With the development of VAP, the mortality increases to 57% (Rinaudo et al, 2018)
  • Survivors of prolonged ICU stay (according to Huttmann et al, 2018) have a significantly poorer level of independence, report depression, and 32% reported that they would have elected to die in hindsight rather than receive invasive ventilation for a prolonged period.

Discuss "Plan B" 

  • If opting out of invasive ventilation for reasons of patient preference or for reasons of medical apprpriateness, or when discontinuing ventilation because of failure to improve, discuss the palliative scenario.
  • Reinforce the offer for ongoing discussions with the patient and family
  • Explain the symptoms at the end of life and the measures taken to control these

References

Chandra, Divay, et al. "Outcomes of noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease in the United States, 1998–2008." American journal of respiratory and critical care medicine 185.2 (2012): 152-159.

Simonds, A. K. "Ethics and decision making in end stage lung disease.Thorax 58.3 (2003): 272-277.

Gadre, Shruti K., et al. "Acute respiratory failure requiring mechanical ventilation in severe chronic obstructive pulmonary disease (COPD)." Medicine 97.17 (2018).

Lindenauer, Peter K., et al. "Outcomes associated with invasive and noninvasive ventilation among patients hospitalized with exacerbations of chronic obstructive pulmonary disease." JAMA internal medicine 174.12 (2014): 1982-1993.

Nevins, Michael L., and Scott K. Epstein. "Predictors of outcome for patients with COPD requiring invasive mechanical ventilation." Chest 119.6 (2001): 1840-1849.

Stefan, Mihaela S., et al. "Comparative effectiveness of noninvasive and invasive ventilation in critically ill patients with acute exacerbation of COPD." Critical care medicine 43.7 (2015): 1386.

Rinaudo, Mariano, et al. "Impact of COPD in the outcome of ICU-acquired pneumonia with and without previous intubation." Chest 147.6 (2015): 1530-1538.

Sullivan, Karen E., et al. "What do physicians tell patients with end-stage COPD about intubation and mechanical ventilation?." Chest 109.1 (1996): 258-264.

Wildman, Martin J., et al. "Implications of prognostic pessimism in patients with chronic obstructive pulmonary disease (COPD) or asthma admitted to intensive care in the UK within the COPD and asthma outcome study (CAOS): multicentre observational cohort study." Bmj 335.7630 (2007): 1132.

Jerpseth, Heidi, et al. "Considerations and values in decision making regarding mechanical ventilation for older patients with severe to very severe COPD." Clinical Ethics 11.4 (2016): 140-148.

Mannino, David M., Dennis E. Doherty, and A. Sonia Buist. "Global Initiative on Obstructive Lung Disease (GOLD) classification of lung disease and mortality: findings from the Atherosclerosis Risk in Communities (ARIC) study." Respiratory medicine 100.1 (2006): 115-122.

Celli, Bartolome R., et al. "The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease." New England Journal of Medicine 350.10 (2004): 1005-1012.

Menzies, Richard, William Gibbons, and Peter Goldberg. "Determinants of weaning and survival among patients with COPD who require mechanical ventilation for acute respiratory failure." Chest 95.2 (1989): 398-405.

Wildman, Martin James, et al. "Survival and quality of life for patients with COPD or asthma admitted to intensive care in a UK multicentre cohort: the COPD and Asthma Outcome Study (CAOS)." Thorax 64.2 (2009): 128-132.

Wakatsuki, Mai, and Paul Sadler. "Invasive Mechanical Ventilation in Acute Exacerbation of COPD: Prognostic Indicators to Support Clinical Decision Making.Journal of the Intensive Care Society 13.3 (2012): 238-243.

National Institute for Health and Clinical Excellence. Chronic obstructive pulmonary disease: management of chronic obstructive pulmonary disease in adults in primary and secondary care (partial update) London: National Clinical Guideline Centre; 2018

Quinnell, Timothy G., et al. "Prolonged invasive ventilation following acute ventilatory failure in COPD: weaning results, survival, and the role of noninvasive ventilation." Chest 129.1 (2

Question 23 - 2019, Paper 1

Outline the principles of, and strategies for management of a persisting broncho-pleural fistula (BPF) in a mechanically ventilated patient.

Include in your answer the advantages and disadvantages of each strategy.
 

College answer

Principles of Management:

  1. Drainage
    • Adequate drainage of the fistula with an intercostal catheter of adequate size to manage a large air leak.
    • May require multiple catheters, and ability to manage large flow rates.
    • Minimise suction.
  2. Ventilatory management
    • Aim is to reduce mean airway pressure to reduce flow through fistula tract.
    • Low tidal volume and PEEP.
    • Low mandatory breath rate.
    • Permissive hypercapnoea.
    • Short inspiratory time.
    • Attempt to wean to spontaneous breathing mode from mandatory ventilation as soon as practicable and preferably from ventilatory support altogether.
  3. General measures
    • Standard ICU supportive management
    • Broad spectrum antibiotic cover
    • Attention to nutritional requirements – patients usually catabolic.
 

Strategies for Managing Large Leaks:

  1. Independent Lung Ventilation
    • Advantages: - May minimise leak in injured lung whilst preserving gas exchange with conventional parameters in normal lung.
    • Disadvantages: -requires some form of double lumen tube – difficult to place and secure.
    • May not be tolerated in hypoxic patients.
    • Requirement for two ventilators –either synchronous or asynchronous – technically demanding and complex.
  2. High Frequency Ventilation
    • Advantages are that it may reduce peak air pressures and theoretically reduce air leak.
    • Disadvantages - not widely available. Recent evidence suggesting an increase in mortality for this ventilatory technique in ARDS patients.
  3. Surgery
    • Advantages – Definitive management strategy. May be only option to seal leak.
    • Disadvantages – Patient may not be fit enough to tolerate.
  4. Endobronchial Occlusion
    • Advantages – Widely available, can be definitive treatment.
    • Disadvantages – may be technically challenging, not feasible with multiple leaks.
  5. Application of PEEP to intercostal catheter
    • Advantages – may decrease leak volume and maintain intra-thoracic PEEP.
    • Disadvantages – compromise drainage, risk of tension, not feasible with multiple tubes.
  6. ECMO
    • Advantages – may be only option to treat hypoxia.
    • Disadvantages – not widely available, complex, little experience

Examiners Comments:

Answered well. Most candidates could have scored more if they had given greater breath to the strategies used, or greater depth to the strategies they discussed.


 

Discussion

This question is identical to Question 23 from the first paper of 2016 and Question 4 from the first  paper of 2014, which were done extremely poorly. The fact that in 2019 trainees have almost uniformly passed this question suggests that either some sort of fistula epidemic has made it a topical matter on everybody's mind, or that writing practice answers to previous exam questions is a valid exam preparation strategy.

In brief:

Management Strategies for Bronchopleural Fistula
Strategy Advantages Disadvantages
Drainage
- large-bore drain
- or, multiple drains
- minimise suction
  • easy and readily available
  • Usually well tolerated
  • Does not interfere with weaning of ventilation
  • Risk of damaging more lung and creating larger leaks
  • Potentially, perpetuates the fistula by negative pressure suction
  • Invasive
Ventilator strategy:
- low VT
- low PEEP
- low resp rate
- short insp. time
- tolerate high PCO2
- wean rapidly
- extubate early
 
  • easy and readily available
  • Usually well tolerated
  • Early extubation is the ideal step to aim for, as spontaneous negative pressure breathing is better for BPF healing than positive pressure ventilation.
  • The BPF itself may frustrate weaning off ventilation
  • Mandatory mode may prolong ventilation time
  • Permissive hypercapnea may lead to respiratory acidosis, which is not ideal for the patient with traumatic brain injury
Independent lung ventilation
- dual-lumen tube
- or, bronch blocker
 
  • Isolation of one lung permits the selective low-volume low-pressure ventilation of the affected lung, and more rapid higher volume ventilation of the unaffected lung.
  •  PCO2 levels may be easier to control in this manner
  • Technically difficult: DLT insertion is one thing; running two ventilators is another.
  • There may be leak of gas and pressure from one lung to another if the seal is imperfect
  • Sedation requirements will  be higher, to tolerate the larger tube and the very unnatural respiratory pattern
  • Local pressure effects of the DLT are also more problematic
     
Surgical repair
  • The affected lung can be surgically repaired. USually, this means segmental lobectomy (for alveolar leaks) or patching and oversowing of the bronchial leak
  • Apparently, success rates are between 80 and 95%
  • It may be impossible to find the leak intraoperatively
  • It may be unfeasible to remove so much lung
  • It may be impossible if there are multiple leaks
  • The patient must tolerate one-lung ventilation
  • This approach requires thoracotomy
Bronchial stenting
  • The affected bronchus can be stented over bronchoscopically, thereby blocking the leak.
  • This is a minimally invasive alternative to surgical patch repair
  • You need to be sure of where the leak is
  • The leak must be in an accessible bronchus.
  • This may not work if there are multiple leaks
  • The procedure requires technical expertise
  • The patient must be fit to tolerate the bronchoscopy
Bronchial occlusion
  • Similarly to surgery, the affected pronchus is blocked with either a one-way valve or a plug. In fact, the Lois article lists options such as blood clot, cyanoacrylate glue, fibrin, lead shot,  gel foam, calf bone, and various others.
  • You need to be sure of where the leak is
  • The leak must be in an accessible bronchus
  • A major part of the lung may be sacrificed
  • The atelectatic lung may develop infection
Application of PEEP to the ICC
  • The equal intra and extrathoracic PEEP decreases the leak volume
  • Maintained intra-thoracic PEEP permits higher PEEP levels to be used
  • Drainage is compromised
  • There is a major risk of rapid tension pneumothorax
HFOV
  • May reduce peak pressures
  • Certainly reduces tidal volume (to ~50ml)
  • Thus, theoretically reduces flow across the BPD, allowing it to heal
  • This is avery unnatural form of ventilation, and may be poorly tolerated
  • Large amounts of sedation or paralysis will be required
ECMO
  • This may be the only option for severely hypoxic patients
  • With ECMO, one can limit or totally abolish gas flow through the BPF
  • All the risks of ECMO apply, as it is a maximally invasive therapy
  • It is not widely available.
  • There is little experience with this in BPF.

References

Lois, Manuel, and Marc Noppen. "Bronchopleural fistulas: an overview of the problem with special focus on endoscopic management." CHEST Journal 128.6 (2005): 3955-3965.

Baumann, Michael H., and Steven A. Sahn. "Medical management and therapy of bronchopleural fistulas in the mechanically ventilated patient." CHEST Journal 97.3 (1990): 721-728.

Pierson, David J., et al. "Management of bronchopleural fistula in patients on mechanical ventilation." (2012) - from UpToDate.

Mueller, Michael Rolf, and Beatrice A. Marzluf. "The anticipation and management of air leaks and residual spaces post lung resection." Journal of thoracic disease 6.3 (2014): 271.

Cerfolio, Robert J., et al. "A prospective algorithm for the management of air leaks after pulmonary resection." The Annals of thoracic surgery 66.5 (1998): 1726-1730.

Question 2 - 2019, Paper 2

A 49-year-old female is intubated and ventilated in your ICU following a motor vehicle accident. You are called to the bedside when the ventilator low pressure alarm is triggered. List the potential causes and outline your approach to this problem.

College answer

Potential causes:

Most likely air leak:

ETT cuff rupture or incompetent pilot balloon valve, ETT dislodgement,

Disconnection/ defect in ventilator circuit,

Leak into chest drain,

Bronchopleural fistula

Pressure alarm or Tidal Volume set too low

Ventilator failure                                                                                                               (3 marks)

Approach

  1. Examine the patient. – will indicate urgency of problem: e.g.:
    1. SpO2
    2. ET CO2
    3. Chest movement
    4. Breath sounds
    5. Bubbling in chest drains if present
  2. Carefully check ETT
    1. Insertion depth? any change from previous to indicate dislodgement
    2. Air pressure in cuff- re-inflate if low
    3. Audible air leak
    4. If suspect dislodgement have direct look with laryngoscope and reintubate if necessary

(2 marks)

  1. Check ventilator settings and alarms? any inadvertent change to these (1 mark)
  2. Check total length of ventilator circuit, specially connections and any access ports

(1 mark)

Depending on status of patient may have to take off ventilator and hand-bag patient, +/- exchange ETT if thought to be culprit. (1 mark)

Exchange circuit if necessary. Internal ventilator problem unlikely but may need to change out ventilator.   (1 mark)

Examiners Comments:

Those candidates who clearly identified that a low-pressure alarm is usually associated with an air leak (anywhere in the system/patient) and had a logical approach to managing the problem were able to score good marks. Those who gave a random selection of 'any problem that a patient may develop and may trigger any alarm' did not score so well.

Discussion

Low pressure alarm, eh? Why is this happening?

  • The low pressure alarm on most ventilators is sounded when the circuit pressure drops below a certain pressure value 
  • The alarm is usually set (manually) to about 2cm H2O below the PEEP value.
  • The sensor for this is usually in the afferent (pre-patient) limb of the circuit, and it is involved in a feedback loop with the solenoid flow-limitng valve which contols flow into the circuit
  • The ventilator is usually able to compensate for a depressurised circuit by increasing the flow rate.

So, the low pressure alarm has sounded. This can mean several things:

  • There is no problem:
    • The pressure sensor is malfunctioning
    • The pressure sensor is working fine, but somebody has either set the alarm threshold too high, or has decreased the PEEP without also adjusting the alarm.
  • There is a real probem:
    • The problem is with the circuit
    • The problem is with the patient
    • The ventilator has failed in some fundamental way and is not producing flow (eg. in a turbine-driven ventilator, the turbine has failed)
    • The flow is being "stolen" by the suction set

It's impossible to determine which one it is without doing a bit of troubleshooting. If there is a real problem, it could be:

  • Patient problem:
    • Leak could be around the ETT
      • The tube has migrated out past the cords, and now and there is a massive leak
      • The cuff has deflated, and now there is a cuff leak
      • The ETT itself is damaged, and now there is a leak out of the defect (this is rare, as it takes quite a lot of effort to damage those things).
    • Leak could be via the patient:
      • Large volume air leak via the ICC
  • Circuit problem:
    • Disconnection of the circuit from the ventilator
    • Disconnection of the patient from the circuit
  • Failure of the ventilator

So, the best way to approach this:

1) Ensure the patient is safe:

  • Disconnect the patient from the ventilator and the inline suction set, and bag them manually, noting the pressure generated thereby
  • Note whether there is an audible leak; if yes, then the endotracheal tube is to blame
  • Assure that the patient's oxygenation is adequate
  • Assure that the end-tidal COis still generating a waveform (i.e. the tube is not displaced into the oesophagus)

3) Systematically troubleshoot the circuit

  • Start with the patient
    • Listen to the chest: is there air entry?
    • ETT:
      • Make sure it is at the same depth as was previously documented
      • Check the cuff pressure with the manometer
      • Check for cuff leak
      • Perform laryngoscopy if there is any doubt
    • Check the chest drain: is there now a vigorous air leak?
      May need a chest Xray
    • Check the ventilator: while bagging the patient manually, see if the problem is reproduced with the same circuit and a "test lung".
    • Check the closed suction set: did the trigger valve become disabled by some accident (i.e. is the suction constantly "stealing" airway pressure?)

References

Jairo I. Santanilla "The Crashing Ventilated Patient"; Chapter 3 in Emergency Department Resuscitation of the Critically Ill, American College of Emergency Physicians, 2011.

Raphael, David T. "The Low-Pressure Alarm Condition: Safety Considerations and the Anesthesiologist’s Response." Anesthesia Patient Safety Foundation Newsletter 13.4 (1999).

Question 4 - 2019, Paper 2

Critically evaluate the use of inhaled nitric oxide in the ICU.

College answer

Indications:
Nitric oxide is used as a rescue therapy for ARDS with refractory hypoxemia and right ventricular dysfunction in ICU. Evidence for its use in ICU is limited. However, because of the immediate physiological benefits, it continues to be one of the agents used in ICU in these scenarios.

Mechanism of Action of iNO
o    Causes selective pulmonary arteriolar vasodilatation
o    This leads to a reduction in pulmonary artery pressure and pulmonary vascular resistance.
o    Reduction in PVR leading to reduced afterload on RV→ improvement in right ventricular cardiac output and organ perfusion.
o    Dilates pulmonary vessels in better ventilated areas of the lung which in turn reduces V/Q mismatch and improves oxygenation.

Advantages:
o    Quick onset of effect
o    Minimal systemic hypotension

Disadvantages:
o    Can cause methaemoglobinemia in patients with methaemoglobin reductase deficiency
o    Very expensive
o    Needs specialized/complex equipment to deliver
o    Needs to be weaned slowly as can cause rebound pulmonary hypertension
o    Air filtration rates of 10-12 air exchanges per hour are necessary to prevent accumulation of NO/ NO2 in the ambient air in ICU
o    Decrease platelet aggregation.
 

Evidence
For hypoxemia in ARDS:

Despite obvious physiological benefits iNO has not been shown to change ICU outcomes of mortality, ventilator-free days in large randomised control trials in adult and paediatric patient groups. In a Cochrane Review published in 2016, there were no statistically significant effects of iNO on longest follow-up mortality, 28-day mortality in both adults and children- moderate quality of evidence. There was a statistically significant improvement in P/F ratio and oxygenation index at 24 hours- moderate quality of evidence. There was a statistically significant increase in renal failure in iNO groups- high quality evidence.

For right ventricular dysfunction:
Only small randomised control trials and case series are available. Most of them have been conducted in post-cardiac surgery patients with right heart dysfunction, patients on LVAD, heart transplantation with primary graft dysfunction and patients with pulmonary arterial hypertension. Again all the studies demonstrate a physiological reduction in pulmonary artery pressure and ?increase cardiac output. No randomised trials have demonstrated mortality benefit with iNO.

Other studies on LVAD and heart transplantation are case series only, and there are no randomised clinical trials. Theoretical benefit for ischaemia-reperfusion injury post- lung transplant (decreased leucocyte and platelet aggregation) but no difference in clinical outcomes.

Summary statement
Inhaled nitric oxide in ICU provides short-term physiological benefits to the patients in ICU with refractory hypoxemia and right heart dysfunction. However, none of the studies has shown any mortality benefit. When used for refractory hypoxemia in ARDS, there is strong evidence that it is associated with renal failure. Also, it is an expensive therapy. Candidates might state that they use alternative selective pulmonary vasodilators like inhaled epoprostenol instead of iNO. This is also acceptable.

Examiners Comments:

Some insightful, thoughtful and well-balanced answers. However, there are quite a few candidates who have minimal knowledge of a mainstream agent used in intensive care practice. A structured approach to this type of question i.e. " Critically evaluate " was quite variable; some have practiced this template well whilst others have not thought about this prior to the exam.

Discussion

Somebody at CICM must have a subscription to the British Journal of Pharmacology. After ignoring nitric oxide for over a decade (the last SAQ was Question 14 from the first paper of 2006), the college had decided to spring this topic on its final exam candidates in 2019. Totally coincidentally, the BJP published a special themed issue celebrating the 20th anniversary of  Furchgott Ignarro and Murads' Nobel Prize for the discovery of nitric oxide's role in cell signalling. In this issue, the excellent article by Yu et al (2019) has served as the main source of information for this answer.

Rationale for the use of inhaled nitric oxide:

  • To decrease pulmonary vascular resistance:
    • This decreases right ventricular afterload and may improve the performance of a failing right ventricle
  • To improve V/Q matching (for severe ARDS):
    • Only ventilated regions of lung receive the inhaled agent
    • Therefore pulmonary vessels will only be dilated in the well-ventilated regions of the lung
    • Therefore blood flow will be preferentially directed to those regions
    • In heterogeneous lung disease (eg. ARDS) this may improve shunt

Administration

  • via a uniquely designed gas mixer
  • from its own tank
  • start at 5-10 ppm, go up to 160ppm as needed

Monitoring

  • Monitor PA pressures with PAC and serial TTE
  • monitor response with arterial oxygenation
  • regular CXR, watch for pulmonary haemorrhage
  • Monitor for toxicity, particularly methaemoglobin levels and NO2
  • Observe strict handling safeguards, including gas scavenging and ventilation precautions

Mechanism of action:

  • Nitric oxide is a potent vasodilator; it inhibits vasoconstriction by increasing the amount of cyclic GMP (cGMP) in the cytosol, thus decreasing the amount of cytosolic calcium ions available to sustain smooth muscle contraction.

Advantages

  • Relatively non-toxic
  • Does not require scavenging technology (though if it were used in higher concentration, it would require scavenging)
  • Short-acting (thus, no systemic vasodilation - only pulmonary)
  • Small molecule:
    • diffuses easily to the site of action
    • penetrates well into the alveoli (where aerosols do not)

Disadvantages

  • Expensive
  • Can actually decrease the oxygen-carrying capacity of the blood
  • Though scavenging is not required, a high air flow rate in the room is called for.

Complications

  • Methemoglobinaemia
  • Hypotension
  • Rebound hypoxia after abrupt withdrawal
  • Thrombocytopenia (in as many as 10% of patients)
  • Increased susceptibility to pulmonary infections probably due to NO2 formation
  • Renal failure

Contraindications

  • Left ventricular failure
  • Left to right intracardiac shunt
  • Uncontrolled haemorrhage 
  • Existing methaemoglobinaemia

Evidence

In short, there is little high-quality evidence. What we do know is that there is no benefit in mortality. However:

  • It is an effective pulmonary vasodilator (Sim et al, 2010)
  • It improves oxygenation in ARDS (Albert et al, 2017) 
  • There does not appear to be a surival benefit. One of the papers quoted by the CICM examiners was the 2016 Cochrane review by Gebistorf et al, which looked at ARDS and concluded that the evidence was "insufficient to support INO in any category of critically ill patients". The same study found that nitric oxide caused an apparent increase in the risk of renal failure (RR was ~ 1.59). However, many of the older trials on this application of nitric oxide were performed in the bad old days, before the advent of lung-protective ventilation. 

Other applications:

  • Haemolysis:  Lei et al (2018) were able to demonstrate a marked improvement in the rates of renal failure (from 63% to 50%) among post-cardiac surgical patients receiving inhaled nitric oxide.
  • Post-cardiac surgery pulmonary hypertension: iNO is at least as effective as inhaled prostacycline (McGinn et al, 2015).
  • Sickle cell disease: a single trial did not demonstrate much improvement in symptoms (Gladwin et al, 2011)
  • Cerebral malaria: iNO does not seem to have much of an effect on the outcomes in this disease (Hawkes et al, 2015)

References

Ikaria, the only company which produces this stuff in Australia, has an excellent product information pamphlet.

Barker, Steven J., and John J. Badal. "The measurement of dyshemoglobins and total hemoglobin by pulse oximetry." Current Opinion in Anesthesiology21.6 (2008): 805-810.

Afshari, Arash, et al. "Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) and acute lung injury in children and adults." Cochrane Database Syst Rev 7 (2010).

Gebistorf, Fabienne, et al. "Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) in children and adults." Cochrane database of systematic reviews 6 (2016).

Yu, Binglan, et al. "Inhaled nitric oxide." British journal of pharmacology 176.2 (2019): 246-255.

Sim, Ji-Yeon. "Nitric oxide and pulmonary hypertension." Korean journal of anesthesiology 58.1 (2010): 4.

Albert, Martin, et al. "Comparison of inhaled milrinone, nitric oxide and prostacyclin in acute respiratory distress syndrome." World journal of critical care medicine 6.1 (2017): 74.

Question 22 - 2020, Paper 1

A 48-year-old patient with Guillain Barre Syndrome who has been hospitalised for 30 days was recently re-admitted to your ICU with septic shock. He required mechanical ventilation via his tracheostomy, vasopressor treatment, and is now recovering.

a)    What factors in this patient contribute to an increased risk for nosocomial infections?
(30% marks)

b)    How would you reduce the risk of him acquiring another nosocomial infection while in the ICU?
(70% marks)
 

College answer

This question had several aspects to it that required structure to cover those elements. Candidates were expected to cover elements related to the specific patient care of the individual patient but also to cover general ICU aspects in regard to infection prevention management. Detailed descriptions were not required, as long as the general elements were covered with some relevant examples. Especially important points are underlined.

A)

Recognition that long stay patient in hospital who has a tracheostomy is a high risk patient for exposure to and/or colonisation with potential resistant flora and is therefore at risk for development of nosocomial infections (3 marks)

        1. Increased risk if higher severity of illness, significant comorbidities ,diabetes, malnutrition or immunosuppressed (all critically unwell patients at risk)
        2. Previous or ongoing antibiotic treatment, specifically when complex regimens and/or prolonged duration
        3. Open wounds, pressure sores
        4. Invasive devices – consider timely removal if not required or change when concern of colonisation

B)

  1. Prevention of specific infections in the intensive care unit (3 marks)
    1. Ventilator association pneumonia care bundle
 
      1. Prevention colonisation oral cavity (oral hygiene,
      2. Prevention aspiration (Nursing 30-45 degrees, subglottic aspiration, cuff pressure maintenance)
      3. Minimize duration of ventilation (minimise sedation, early mobilisation)
      4. Endotracheal and circuit care (HME, avoid routine ventilator circuit change, suction when required for secretions).
    1. CLABSI (central line associated blood stream infection) prevention bundle
      1. Insertion: Equipment (including PPE and catheter selection, dressing), preparation (including site selection) and sterile technique;
      2. Care: daily check insertion sites for signs of inflammation, daily review need (and remove when not required), check for lumen patency, hand hygiene and swab hub when handling. Consider timely removal if not required or change when concern of colonisation/infection/inflammation
      3. Documentation
      4. Education (staff experience)
    2. Infective diarrhea
      1. Vigilance/high index of suspicion for symptoms consistent with infective diarrhea, specifically for Clostridioides difficile
      2. Contact precautions/isolation (including hand washing) when C difficile suspected/confirmed
    3. Urinary tract infection
      1. consider timely removal of catheter if not required or change when concern of colonisation

NG tube/sinusitis- consider PEG.

  1. Environmental and personal aspects (2 marks)
    1. Hand hygiene
    2. Aseptic or sterile technique for procedures
    3. Personal protective equipment as per unit/hospital protocol, specifically in case of multi resistant organisms (ESBL, VRE, MRSA)
    4. Environmental hygiene (bench top cleaning, disposable versus non disposable curtains)
    5. Visitor education in regard to hand hygiene
  1. Antimicrobial stewardship – (some mention of appropriate antibiotic choice and de- escalation) multidisciplinary approach to provide correct treatment to patients with infections, improve outcome and to reduce risk of resistance development (2 marks)
    1. Regular screening for colonisation with
      1. Surveillance cultures (tracheal aspirate, urine if catheterised)
      2. Nasal/rectal swabs if concern for multi resistant organisms (VRE, MRSA)
    2. Knowledge of local microbiological data and resistance patterns
    3. Therapeutic guidelines on empiric antibiotic treatment
    4. De-escalation, change from parenteral to enteral antibiotics, avoid long duration when possible

Discussion

Increased risk in GBS patients is hard to discuss, not because the topic is entirely unfamiliar to senior ICU trainees, but rather because the answer requires a structured approach, and with so much to discuss, it is difficult to know how best to structure such a vast amount of information. A certain discipline is also going to be required. A well-informed exam candidate will squander many minutes writing everything they know about this.

Let us consider this in terms of predisposing factors and the possible infection they cause. One way is to organise the factors is according to the infections they promote, and the process which  has caused them. The ideas used to populate this table came from this article by Henderson et al (2003).  

Factors which Contribute to the Increased Risk of Nosocomial Infection among Patients with Guillain-Barre Syndrome
Infectious consequences Contributing factors
VAP
  • Prolonged intubation
  • Gram-negative colonisation of the lower airway
  • Poor oral hygiene (with intubation)
  • Weak cough
Sinusitis
  • Prolonged NGT dwell-time
Hospital-acquired pneumonia
  • Weak cough
  • Impaired airway defence reflexes
  • Prostration and basal atelectasis
Pressure area infections
  • Prolonged immobility
Line-related sepsis
  • Prolonged need for parenteral medications
Urinary tract infection
  • Long term IDC
Increased predisposition to infection
  • Immunosuppressant therapies
  • Malnutrition
Resistant organisms
  • Multiple courses of antibiotics
  • Prolonged hospital stay, and therefore increased risk of cross-contamination

With this exercise behind us, we can easily recombine the contributing factors into a structured list of interventions designed to address them:

Strategies fpr the Prevention of Nosocomial Infection in Patients with Guillain-Barre
Factor Intervention
Prolonged intubation
  • If expecting prolonged ventilation, think about an early tracheostomy
Gram-negative colonisation of the lower airway
  • Consider SDD
  • Upright (30 degrees head up) position
  • Discontinue PPI to maintain lower GI tract acidity
  • Promote gastro-oesophageal sphincter competence by removing NGT when able
Poor oral hygiene
  • Extubate early to give the nurses access
  • Educate nursing staff re. importance of oral hygiene, and promote internal audits of compliance
Weak cough
  • Chest physiotherapy to assist cough
  • Postural drainage
  • Longer suction catheters
Prolonged NGT dwell-time
  • If prolonged swallowing dysfunction is anticipated, a PEG may be a better option
Impaired airway defence reflexes
  • Prevent aspiration by the methods recommended in the VAP prevention section above (eg. head up position, etc)
  • If feeding orally, ensure the fluids are thickened and the diet is puree.
Prostration and basal atelectasis
  • Ensure daily physiotherapy engagement and encourage early passive mobilisation (eg. placing the patient into a chair-like position i bed)
Prolonged immobility
  • Realistically, this is GBS and you can't do much about this. Anecdotally, it appears that larger and earlier doses of IVIG tend to produce a more rapid improvement, but this is really not the topic of discussion here.
Prolonged need for parenteral medications
  • Rationalise IV medications (eg. can't that paracetamol be oral?)
  • Rationalise IV antibiotics
  • Rationalise central access (if it has to be parenteral, can it be peripherally parentral?)
  • If central access is imperative, transition to PICCs
Long term IDC
  • Unless the patient has specific urinary retention problems, the IDC may be superfluous in the later stages of disease
Immunosuppressant therapies
  • Corticosteroids have no role to play and so you shouldn't be using them anyway
Malnutrition
  • Optimal nutrition (including protein intake) may require specialist dietitian consultation and a means of delivering the nutrients safely (eg. PEG)
Resistant organisms
  • Antibiotic stewardship should be practiced
Cross-contamination with MROs
  • Single room with handwashing basin and alcohol handrub for staff
  • Standard contact precautions for all visitors

References

Henderson, R. D., et al. "The morbidity of Guillain-Barré syndrome admitted to the intensive care unit." Neurology 60.1 (2003): 17-21.

Question 28 - 2020, Paper 1

a)    What is meant by the term intermediate risk pulmonary embolism (PE) (submassive PE)?
(30% marks)

b)    Discuss the role of thrombolysis in patients presenting with intermediate risk PE. (70% marks)
 

College answer

Latest definition according to European Society of Cardiology guideline [European Heart Journal (2020) 41, 543_603]

Intermediate Risk Pulmonary embolism can be either:

:PE without haemodynamic instability in a patient with evidence of RV dysfunction (dilatation on ECHO/CT, ECG changes, BNP) and myocardial necrosis (troponin)

or:

PE without haemodynamic instability in a patient who has one or more of the following features- age>80, cancer, Chronic heart failure, PR>110, SBP<100, SaO2< 90%. In addition, they may have either RV dysfunction or elevated cardiac troponin or none of these.

Intermediate Risk Pulmonary embolism is when PE presents without haemodynamic instability (SBP<90mmHg) but with evidence of RV dysfunction (dilatation on ECHO/CT, ECG changes, BNP) or myocardial necrosis (troponin).

 

Rationale for using thrombolysis (reperfusion treatment) is that it leads to faster improvement in pulmonary obstruction. However, the treatment decision needs to be balanced with the risk of life- threatening bleeding.

  1. In High –Risk PE (Cardiac arrest/ Obstructive shock/persistent hypotension), thrombolysis is recommended as it reduces mortality.
  2. Benefits less clear in Intermediate risk PE and thus a difficult clinical decision to make. Low mortality rate for Intermediate risk PE makes it difficult to justify the use of thrombolytic therapy in view of the risk of life-threatening bleed.
  3. In Intermediate risk PE thrombolysis is hypothesised to improve functional outcomes (mainly dyspnoea) and new onset pulmonary hypertension, but there is lack of good quality evidence.
  1. In Intermediate risk PE rescue thrombolysis is recommended only for patients who show signs of haemodynamic deterioration on anticoagulation therapy. All patients with intermediate risk PE should be observed in a monitored area for signs of deterioration.
  1. Establishing multidisciplinary Pulmonary embolism management team may help in the decision-making process ( low level evidence).

Discussion

The first part of this question is easy. The terms are actually interchangeable (Rali & Criner, 2018);  "submassive" appears to be an AHA classification, whereas "intermediate risk" is from the ACCP, but basically both involve the same features:

  • Confirmed PE
  • No shock
  • The presence of either RV dysfunction or elevated biomarkers

The ESC also split the category into "intermediate to low risk" for those who only have one of RV dysfunction and biomarkers, whereas the "intermediate to high risk" group has both.  The college mention the 2019 ESC guidelines, in case anybody needs that reference as a link.

Now, the role of thrombolysis is a more delicate question.

First of all, from an initial reading of the question text did the college mean "systemic" or "catheter directed", or both? One would have to assume both. 

Rationale for thrombolysis in this group: 

  • Prevention of long-term morbidity (eg. VTE-associated pulmonary hypertension).
  • Decrease clot burden
  • Improve systemic haemodynamics by improving LV filling
  • Prevent further RV injury

Full dose systemic thrombolysis for submassive PE:

  • PEITHO trial (2014) - multi-centre RCT, 1005 patients; no mortality benefit, higher risk of bleeding but better haemodynamics. 
  • TOPCOAT trial (2014) - multi-centre RCT, 83 patients randomised: fewer adverse outcomes, better functional capacity, and greater quality of life at 3 months
  • Overall, meta-analysis by Riera-Mestre et al (2014)  found that there was a very slight improvement in mortality; NNT to avoid one death was 125 patients.
  • In contrast, the numbers needed to harm (NNH) for a major bleed were 27, and for an intracranial haemorrhage were 91.
  • Overall, full dose systemic thrombolysis is associated with significant risk in this group.

Low dose systemic thrombolysis for submassive PE

  • MOPETT trial (2013) - single-centre RCT, 121 patients randomised; much less pulmonary hypertension was observed at 28 months (16% vs 57%).
  • Wang et al (2010) found neither any difference in bleeding complications nor in efficacy between the full dose and low dose groups
  • The role for this strategy is unclear; it may have merit in patients who are unable to access catheter-directed thrombolysis

Catheter-directed thrombolysis for submassive PE

  • EXPRESS (D'Auria et al, 2019) 339 patients, low mortality overall but a clear improvement with catheter-directed thrombolysis (3% vs 10%)
  • Pei et al (2019) scraped together 28 studies (total n=2135) into a meta-analysis, the results of which were highly positive:
    • Cardiac index improved by 0.68 L/m2
    • PA pressure reduced by a mean difference of almost 17 mm Hg
    • Very low mortality overall, 2.9% in hospital 
  • Overall, this appears to be the safest and most effective technique of delivering thrombolysis

References

Konstantinides, Stavros V., et al. "2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS) The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC)." European Heart Journal 41.4 (2020): 543-603.

Krishnan, Abhinav C., et al. "Effectiveness of Catheter Directed Thrombolysis for Massive and Submassive Pulmonary Embolism Compared to Systemic Thrombolysis or No Thrombolysis." Circulation 140.Suppl_1 (2019): A17230-A17230.

Bhamani, Amyn, Joanna Pepke-Zaba, and Karen Sheares. "Lifting the fog in intermediate-risk (submassive) PE: full dose, low dose, or no thrombolysis?." F1000Research 8 (2019).

Levis, Joel T. "ECG diagnosis: Pulmonary embolism." The Permanente Journal 15.4 (2011): 75.

Rali, Parth M., and Gerard J. Criner. "Submassive pulmonary embolism." American Journal of Respiratory and Critical Care Medicine 198.5 (2018): 588-598.

Wang, Chen, et al. "Efficacy and safety of low dose recombinant tissue-type plasminogen activator for the treatment of acute pulmonary thromboembolism: a randomized, multicenter, controlled trial." Chest 137.2 (2010): 254-262.

D'Auria, Stephen, et al. "EXPRESS: Outcomes of Catheter-Directed Thrombolysis versus Standard Medical Therapy in a Retrospective Propensity Matched Cohort of Patients with Acute Submassive Pulmonary Embolism." Pulmonary Circulation (2019): 2045894019898368.

Pei, Dorothy T., et al. "Meta-analysis of Catheter Directed Ultrasound Assisted Thrombolysis in Pulmonary Embolism." The American journal of cardiology (2019).

Question 2 - 2020, Paper 1

a) Describe your initial ventilator settings for a patient just intubated for acute severe asthma. Explain the rationale for each of your choices. (50% marks)

b) Hypotension commonly occurs after intubation in an asthmatic. What are the potential aetiologies and what steps would you take to prevent and/or treat them? (50% marks)

College answer

Either volume controlled or pressure controlled modes are acceptable.

Generally spontaneous modes are avoided early and when unstable, needs deep sedation +/- paralysis to facilitate non injurious mode of ventilation

FiO2 1.0 – newly intubated – titrate down asap as risk of O2 toxicity and Aa gradient not usually a

problem

PEEP: – controversial – Conventional teaching advocates a PEEP 0 to minimise high Paw, but there will already be some dynamic hyperinflation with intrinsic PEEP – set PEEP in or around this. Acceptable to mention PEEP titration to pressure/volume curves, but not required.(a discussion around what PEEP would be set with a reasonable justification was required for marks)

VT 4-6ml per kg – limited by plateau pressure < 30 – note PIPs will be high and need to be tolerated,

e.g. up to 50 cmH2O), ventilator alarms will need to be adjusted

RR / T insp. to be minimised to avoid dynamic hyper-inflation (or prolong exp. time) Generally aim Pplat <30cm/H20 and PEEPi <10

Dehydration – unwell by days, inadequate PO intake and then positive intrathoracic pressure – decreasing preload further, minimised by IV fluids loading prior to intubation, and volume loading afterwards to treat.

Afterload reduction/obliteration of sympathetic stimulation – drugs (sedatives and bronchodilators), use vasoconstrictors (titrated metaraminol or noradrenaline), may alter induction drugs or doses used

Dynamic hyperinflation exacerbating the preload reduction. Prevention is with settings targeting lower RR, and shorter insp time, Pplat <30 cmH2O and PEEPi<10. Treat by disconnection of patient from the ventilator and transiently ceasing ventilation. Occasionally manual compression of chest required to aid expiration.

Tension pneumothorax. Prevention is by avoiding high tidal volumes/ mean airway pressures, and accepting high pCO2 if necessary. Paralysis to prevent coughing. Tension pneumothorax is treated with immediate decompression (e.g. with 14 G needle, then early intercostal chest drain).

*If dynamic hyperinflation as a cause of hypotension was not mentioned, a candidate could only score a maximum of 4/10)

Examiners Comments:

Generally, well answered other than the justification for PEEP use.

Discussion

a) 

  • FiO2: lowest possible to achieve SpO2 of 90-92% (this improves V/Q matching)
  • Tidal volume: small, 5-7ml/kg (as there is no reason to use larger volumes; moreover larger volumes may give rise to dynamic hyperinflation)
  • Respiratory rate: slow, 10-12 breaths per minute (or even less - depending on the degree of dynamic hyperinflation; the extra expiratory time should promote lung emptying and CO2 clearance)
  • Long expiratory time, with I:E ratio 1:3 or 1:4 (for the same reason as the decreased resp rate)
  • Use a volume-controlled mode, or any other mode with a square flow waveform (i.e. constant flow) - this decreases the peak airway pressure
  • Reset the pressure limits (i.e. ignore high peak airway pressures) as the peak airway pressure during inspiration is almost completely the product of the increased airway resistance
  • Use minimal PEEP (some PEEP may be beneficial, but a high PEEP will be harmful)
  • Keep the Pplat below 25cmH2o to prevent dynamic hyperinflation. 
  • Titrate PEEP to work of triggering once the patient is breathing spontaneously.

b)

The asthmatic patient, upon intubation, has the tendency to arrest. There are several possible reasons for this. They are presented here in the format of [problem]:[solution], though in all honesty a table would probably work better. 

Preload problems

  • Obstructive shock could result from:
    • Dynamic hyperinflation
    • Tension pneumothorax
  • These are exacerbated by hypovolaemia.
  • The solution would be:
    • Avoid excessive bag-mask ventilation, and use a slow manual respiratory rate
    • Look actively for pneumothorax
    • Volume-load the patient prior to intubation, i.e. give a fluid bolus

Contractility problems

  • Cardiotoxic drugs given during intubation can give rise to haemodynamic instability, as you take away the patient's sympathetic drive by anaesthetising them. 
  • The solution would be to use agents such as ketamine, which are more "cardiostable" in sane induction doses.

Rate and rhythm problems

  • The patient, approaching intubation, will have been recently filled with proarrhythmic medications such as salbutamol, adrenaline or aminophylline
  • The same drugs lower the threshold for arrhythmia by decreasing serum potassium and by promoting metabolic (lactic) acidosis.
  • The additional proarrhythmic effect of post-intubation hypotension could push the patient over into fatal arrhythmias (eg. VF) or merely haemodynamically unproductive ones (SVT).
  • One possible protective strategy would be to ensure the biochemistry and electrolytes are well-corrected, and have sticky defib pads on the patient's chest before the intubation takes place.

Afterload problems

  • Though completely unrelated to asthma, one needs to consider the possibility that the patient is haemodynamically unstable after intubation because they are having an anaphylactic reaction to the induction agents. 

References

Busse, W. W., et al. "Expert panel report 3: Guidelines for the diagnosis and management of asthma." Washington, DC: US Department of Health and Human Services, National Heart Lung and Blood Institute (2007): 1-417.

Stather, David R., and Thomas E. Stewart. "Clinical review: mechanical ventilation in severe asthma." Critical Care 9.6 (2005): 581.

Leatherman, James. "Mechanical ventilation for severe asthma." Chest 147.6 (2015): 1671-1680.https://www.atsjournals.org/doi/abs/10.1164/ajrccm/136.4.872

Laher, Abdullah E., and Sean K. Buchanan. "Mechanically ventilating the severe asthmatic." Journal of intensive care medicine 33.9 (2018): 491-501.

Tuxen, David V., and Susan Lane. "The effects of ventilatory pattern on hyperinflation, airway pressures, and circulation in mechanical ventilation of patients with severe air-flow obstruction." American Review of Respiratory Disease 136.4 (1987): 872-879.

Tuxen, David V. "Detrimental effects of positive end-expiratory pressure during controlled mechanical ventilation of patients with severe airflow obstruction." Am Rev Respir Dis 140.1 (1989): 5-9.

Sarnaik, Ashok P., et al. "Pressure-controlled ventilation in children with severe status asthmaticus." Pediatric Critical Care Medicine 5.2 (2004): 133-138.

Oddo, Mauro, et al. "Management of mechanical ventilation in acute severe asthma: practical aspects." Intensive care medicine 32.4 (2006): 501-510.

Question 13 - 2020, Paper 1

A 45-year-old male with a history of a renal transplant 3 years ago, currently on tacrolimus, mycophenolate and prednisolone is admitted to your ICU with pulmonary infiltrates, hypoxia and worsening renal function.

a)    What are the potential infectious causes of the respiratory failure? Justify what empirical antimicrobial treatment you would commence.    (50% marks)

b)    Describe how you would manage his immunosuppressive therapy.    (50% marks)
 

College answer

  1. Infectious causes: Most likely to be bacterial (e.g. Strep pneumo); however as is immunosuppressed patient consider and cover possible additional causative agents:
    • Bacteria most likely cause
      • Risk of bronchiectasis from mycophenolate → if this may be colonised with Pseudomonas aeruginosa needing cover
      • Early commencement of broad spectrum antibiotics with Pseudomonas coverage as per local sensitivity patterns (e.g. pip-taz, meropenem)
    • Viral pneumonia
      • Esp. influenza/RSV/adenovirus → oseltamivir
      • CMV pneumonia/pneumonitis – less common now with prophylaxis and at 3 years post-transplant; would not routinely investigate for unless other clinical suspicion or high risk (i.e. no prophylaxis immediately after transplant, prophylaxis recently stopped, donor +ve/recipient -ve). Treat with gancyclovir
    • Fungal – Pneumocystis jirovecii (PJP) very common if not on prophylaxis (trimethoprim- sulfamethozazole) –if clinical suspicion treats with Bactrim; otherwise ensure continue prophylaxis even if other cause identified
  1. Management of anti-rejection drugs & immunosuppression
    • Tacrolimus – needs levels monitored; many interactions with other agents including anti- microbials →; if tacrolimus continued dose will likely need to be reduced in renal failure
    • Consider ceasing all anti-rejection drugs and managing with steroids alone during septic period
    • May require stress-dose steroids if septic irrespective of other anti-rejection drug management (i.e. risk of adrenal insufficiency on prednisone)
    • Risk of neutropaenia with mycophenolate + tacrolimus – if present may need to be reduced or ceased during acute infection + G-CSF

Examiners Comments:

Some candidates answered only part of the question. The relevance of the immunosuppression was not appreciated in some answers and a generic list of infectious causes was given.

Discussion

The most likely infectious causes are:

Typical bacteria:

  • Classical community-acquired organisms eg. S.pneumoniae and Haemophilus
  • Gram-negatives, eg. Pseudomonas and Klebsiella

Atypical bacteria:

  • Mycoplasma species, including tuberculosis
  • All the usual community-acquired atypicals (eg. M.pneumoniae, the Chlamydias, Legionella, etc)

Viral

  • Influenza
  • "Common cold" viruses, eg. RSV, parainfluenza, etc
  • CMV

Fungal

  • Pneumocystis jirovecii
  • Aspergillus sp.

Is there any data regarding infectious causes of pulmonary infiltrates in the renal transplant recipient? Sure. Kalra et al (2005) lists multiple organisms, and in fact in most patients several species were simultaneously involved. Tuberculosis, PJP, Candida albicans and swarms of Enterobacteriacea were mentioned. However, these were patients from New Delhi, and so their microbial enemies may differ from those of the Norwegian transplant patients.

Justify your antibiotic choice? Well. 

  • Piperacillin/tazobactam would cover most Gram-positive and Gram-negative nasties
  • Azithromycin would take out any atypicals, apart from TB
  • Bactrim (trimethoprim/sulfamethoxazole) at a "treatment dose", as the risk of PJP is very high
  • The patient is on enough T-cell toxins to have a reasonable risk of viral pneumonitis, and if the suspicion was high enough, ganciclovir could be commenced to cover CMV. Oseltamivir probably has all the therapeutic benefits of coconut water, but the college wanted us to mention it as well. 

Now, how to manage the immunosuppressants. Three major issues are present:

  1. The patient is septic; and
  2. Renal function is impaired, but
  3. The graft is precious and must survive

The KDIGO Clinical practice guideline for the care of kidney transplant recipients and the Australian adaptation thereof are actually somewhat useless for this purpose. Fortunately, there are some good free articles out there (eg. Bafi et al, 2017), as well as paywalled ones (Kalil et al, 2007). In short:

  • Reduction in the immunosuppression is desirable. However:
    • Graft rejection can occur, particularly in renal transplant recipients (hearts and livers seem to be ok with a period of reduced dose immunosuppression)
    • An immune reconstitution syndrome may develop
    • Abrupt cessation of the steroids is obviously undesirable
  • Thus:
    • Continue the steroids, and consider increasing the dose, particularly if the patient is haemodynamically unstable
    • Cease the mycophenolate temporarily 
    • Omit the tacrolimus until the next serum tacrolimus level is available
    • Test levels regularly, as renal function influences clearance.

References

Kalra, Vikram, et al. "Spectrum of pulmonary infections in renal transplant recipients in the tropics: a single center study." International urology and nephrology 37.3 (2005): 551-559.

Bafi, Antônio Tonete, Daniere Yurie Vieira Tomotani, and Flávio Geraldo Rezende de Freitas. "Sepsis in solid-organ transplant patients." Shock 47.1S (2017): 12-16.

Kalil, Andre C., H. Dakroub, and Alison Gail Freifeld. "Sepsis and solid organ transplantation.Current drug targets 8.4 (2007): 533-541.

Question 16 - 2020, Paper 1

A 65-year-old female, with a known medical history of rheumatoid arthritis, and a left mastectomy for breast cancer treated with radiotherapy 7 years ago, presents with respiratory failure requiring intubation and mechanical ventilation. Chest X-ray reveals a large left-sided pleural effusion, into which  an intercostal catheter is placed.

With regard to this patient, discuss how examination of the pleural fluid may assist in identifying the cause of this effusion.
 


 


 

College answer

Appearance                                                                                                              (1.5 marks)

Clear, straw-coloured – more likely transudate (although still may be exudate) Blood-stained – malignancy, pulmonary infarction

Yellow/green – rheumatoid Pus – empyema

Turbid – inflammatory exudate

Transudate vs exudate                                                                                           (3 marks)

Clearly some overlap, but in general terms Transudate – cardiac failure,

Exudate – malignancy, empyema, parapneumonic, , connective tissue disease (e.g. rheumatoid), pulmonary infarction, TB

Based on biochemical analysis

Different diagnostic criteria for distinguishing e.g. Light’s Criteria Rule

Light’s Criteria

Exudate if at least one of the following; Pleural fluid protein / serum protein ratio > 0.5

Pleural fluid LDH / serum protein LDH ratio > 0.6

Pleural fluid LDH > 2/3 of the upper limit of the lab’s normal serum LDH

Pleural fluid pH < 7.30 - exudate, with following differentials more likely; Malignant effusion

Complicated parapneumonic effusion or empyema Rheumatoid pleural disease

(SLE, TB)

pH < 7.2 is predictive of empyema, and is the best marker of a complicated parapneumonic effusion

(1.5 marks)

Glucose – low concentration (< 3.3 mmol/L) or pleural fluid / serum glucose ratio < 0.5 not only supports exudate, but makes following differentials more likely;

 

Malignant effusion

Complicated parapneumonic effusion or empyema

Rheumatoid pleural disease (glucose can be particularly low)                        (1.5 marks)

Microscopy                                                                                                                (1.5 marks)

Nucleated cell counts rarely diagnostic but may be supportive (e.g. >50,000/ml usually only complicated parapneumonic effusion/empyema)

Lymphocytosis – very high lymphocyte ratio (85-95% of total nucleated cells) suggests rheumatoid, TB,

Cytology                                                                                                                     (0.5 marks)

Malignant cells – overall sensitivity of only 60% in malignant effusions. Varies with type of malignancy.

Culture/Sensitivity                                                                                                    (0.5 marks)

Empyema

To achieve high marks candidates needed to demonstrate an understanding of how individual results point to specific diagnoses, rather than simply listing test options.

Examiners Comments:

This question was not answered well. Those who provided a good diagnostic approach to the evaluation of pleural effusion in the clinical context scored higher compared to those who provided only a list of differential diagnoses. Many candidates did not know Light's criteria differentiating exudate from transudate.

Discussion

Biochemistry and cytology are the main things one can order. 

Biochemistry:

  • Pleural fluid protein and LDH;  Serum protein and LDH. Light's own 1972 paper about his criteria is available online. Of course at that stage he never actually called them "Light's criteria". However, 30 years later in his article on pleural effusions for NEJM Richard W Light does refer to his own criteria as "Light's criteria".
    • In short, your effusion is exudative if:
      • The fluid to serum protein ratio is greater than 0.5
      • The fluid LDH is over 200 IU/L
      • the fluid LDH to serum LDH ratio os greater than 0.6
  • Glucose:  an extremely low pleural fluid glucose suggests that something is consuming it. Low pleural fluid glucose suggests TB, pneumonia or malignancy.
  • pH: this is a weird one. Everybody orders pleural fluid pH, and few understand what significance it has. According to the 2000 guidelines from CHEST, pH can determine the need for therapeutic drainage. Anormal pleural pH is about 7.60; a pH of <7.20 is equivalent to a positive gram stain in terms of identifying an effusion which requires drainage. Oesophageal rupture can also cause a low pleural pH.
  • Amylase:  this is elevated in pancreatitis-related effusion and in oesophageal rupture
  • Cholesterol: this reveals the effusion as a chylothorax

Cytology from the cell count:

  • Lymphocytosis = malignancy or tuberculosis. This cell count clue comes from another paper by Light. In his case series, of 31 exudative effusions with a lymphocytic predominance, 30 were due either to tuberculosis or neoplasm.
  • Neutrophilia = parapneumonic effusion or PE.
  • Eosinophilia (more than 10% eosinophils)  usually means there has recently been blood or air in the pleural space; however weird causes include drugs  and environmental toxins (dantrolene, bromocriptine, nitrofurantoin, exposure to asbestos) or autoimmune causes eg.  Churg–Strauss syndrome.
  • Malignant cells, obviously.

 Other tests:

  • Culture. The presence of bugs will identify the effusion as an empyema
  •  Direct visual inspection: although it appears to be highly unreliable (Villena et al, 2004), and one really cannot list it among diagnostic tests (i.e. it may do nothing to "assist in identifying the cause of this effusion").

References

Light, Richard W., et al. "Pleural effusions: the diagnostic separation of transudates and exudates." Annals of Internal Medicine 77.4 (1972): 507-513.

Light, Richard W. "Pleural effusion." New England Journal of Medicine 346.25 (2002): 1971-1977.

Shinto, Richard A., and Richard W. Light. "Effects of diuresis on the characteristics of pleural fluid in patients with congestive heart failure." The American journal of medicine 88.3 (1990): 230-234.

Light, Richard W., Yener S. Erozan, and Wilmot C. Ball. "Cells in pleural fluid: their value in differential diagnosis." Archives of Internal Medicine 132.6 (1973): 854-860.

Colice, Gene L., et al. "Medical and surgical treatment of parapneumonic effusions: an evidence-based guideline." CHEST Journal 118.4 (2000): 1158-1171.

Villena, Victoria, et al. "Clinical implications of appearance of pleural fluid at thoracentesis." Chest 125.1 (2004): 156-159.

Question 5 - 2020, Paper 2

a)    Define massive pulmonary embolism.    (10% marks)

b)    Discuss the advantages and disadvantages of thrombolysis, catheter directed clot removal and surgical embolectomy, in the treatment of massive pulmonary embolism.    (90% marks)


 

College answer

Not available.

Discussion

a) Massive  (or "high risk") PE is defined by the AHA guidelines (2011) as:

  • SBP <90 mmHg for at least 15 minutes;
  • OR requiring inotropic support,
  • AND not due to a cause other than PE, pulselessness, or persistent profound bradycardia.

b)

  Advantages Disadvantages
Thrombolysis
  • Widely available
  • Use is supported by major society guidelines (AHA 2011, ESC 2019)
  • Reduces the risk of death by as much as 55%
  • Minimally invasive (requires a PIVC)
  • Does not require sedation or anaesthesia
  • Substantial risk of lifethreatening bleeding, including ICH
  • Risk of bleeding is probably underestimated by clinical trial data
  • May not work in patients who present following a substantial delay (as the clot has started to organise)

Catheter-directed clot removal

  • Excellent published success rate (~87%), i.e. achieved improvement of hypoxia, haemodynamic stability, and survival
  • Lower risk as compared to systemic thrombolysis
  • May be performed in patients in whom thrombolysis was not completely effective or is contraindicated
  • Can be offered concurrently with antigoagulation
  • Minimally invasive, as compared to surgical embolectomy
  • Can be repeated several times, or thrombolysis can be administered continuously for a sustained period
  • Data regarding efficacy is mainly derived from registries and pooled results from case series
  • Concern re. publication bias and industry sponsorship
  • Requires interventional radiology, which may not be widely available
  • Invasive
  • Substantial radiation and IV contrast exposure
  • May require sedation or an anaesthetic, which could be dangerous in the haemodynamically unstable patient
  • Still may not work in patients who present following a substantial delay (as the clot has started to organise, and would be less friable)
Surgical embolectomy
  • Highly effective even for clots which have become organised
  • Can be offered concurrently with antigoagulation
  • May be an option for patients in whom thrombolysis is contraindicated
  • Outcomes are at least as good as thrombolysis, and rates of rethrombosis or intervention are reduced (mortality rate only 12%) 
  • Cannot be offered to patients who have recently received thrombolysis
  • Maximally invasive and requires anaesthetic plus cardiopulmonary bypass
  • Recovery is prolonged in comparison to other methods
  • Rarely performed, which means staff may be deskilled
  • Only available at centres where cardiothoracic surgery is routinely performed

References

Question 6 - 2020, Paper 2

With regard to mechanical ventilation, describe the mechanism of action of flow and pressure triggering and list the advantages and disadvantages of both.

College answer

Not available.

Discussion

Triggering method Mechanism Advantages Disadvantages
Pressure triggered by a patient-generated drop in pressure, from  PEEP.
  • Prevents cardiac auto-triggering
  • By gradually increasing respiratory workload, one may theoretically  "train" the respiratory muscles to perform more work
  • May be useful as a part of extubation assessment (a high pressure trigger is lke a quasi-MIP measurement)
  • Requires the patient to inhale against a closed inspiratory valve. This increases the work of breathing. Tracheal triggering is apparently better than conventional, but
  • The patient may not be able to generate such pressure, and may be unable to trigger
  • Between the initiation of effort and the actual delivery opf gas, there is a delay (however long it takes for the patient to generate that sort of pressure)
Flow Triggered by a patient-generated change in fresh gas flow though a circuit
  • May have auto-triggering by cardiac oscillations
  • Still no rapid enough (some delay exists between initiated effort and the delivered breath)

References

BANNER, MICHAEL J., PAUL B. BLANCH, and ROBERT R. KIRBY. "Imposed work of breathing and methods of triggering a demand-flow, continuous positive airway pressure system." Critical care medicine 21.2 (1993): 183-190.

Sassoon, Catherine SH. "Triggering of the ventilator in patient-ventilator interactions." Respiratory Care 56.1 (2011): 39-51.

Question 11 - 2020, Paper 2

You are asked to review a 74-year-old female in the Emergency Department who has presented with an infective exacerbation of her Chronic Obstructive Pulmonary Disease (COPD).

On examination she is conscious, but unable to speak in sentences. She has a respiratory rate of 36 breaths/min and oxygen saturations of 88% on high flow nasal prongs (HFNP) with FiO2 = 0.4, and 50 L/min of flow. Heart rate is 108 beats/min and blood pressure 156/84 mmHg.

Her blood gas shows:

pH                 7.34

PaO2              58 mmHg (7.73 kPa)

CO2               52 mmHg (6.93 kPa)

Lactate           3.2 mmol/L

What factors would influence your decision to choose non-invasive ventilation or invasive ventilation in this patient?

College answer

Not available.

Discussion

Suitability for intubation:

  • Presence of reversible physiological factors which intubation might address, such as:
    • Respiratory acidosis
    • Decreased level of consciousness
    • Fatigue due to high respiratory workload
  • Absence of existing treatment limitation orders
  • Absence of features which might suggest futility, i.e. where chances of success are impossibly small (eg. multiorgan system failure, severe shock, extreme frailty, etc)
    Insufficient information to guide robust end-of-life decisionmaking (Wildman et al, 2007; prognostic pessimism may deny intubation to potentially salvageable patients)

Factors which favour a beneficial effect from invasive ventilation:

  • Acute exacerbation of COPD as the cause of respiratory failure -Nevins et al (2001) found that the in-hospital mortality was only 12% for these people, as compared to 28% for the rest of the cohort
  • Higher premorbid FEV(over 1.2) - this is the GOLD score (Mannino et al, 2006); GOLD stage 3 or 4 (FEV1/FVC<0.70 and FEV1<50% predicted) is associated with a mortality of around 35% at ten years.
  • Good baseline function  -low BODE index (Celli et al, 2004)
  • Pneumonia as the cause of this exacerbation would favour HFNP or invasive ventilation instead of NIV, as NIV may even be counterproductive (by impairing the clearance of secretions, for example)

Factors which predict a poor outcome from intubation:

  • Failure of NIV, particularly if the patient is elderly - Chandra et al (2012) found that the in-hospital mortality for these people was 33%; non-survivors were largely elderly (over 55% of them were aged 75 or older)
  • Poor baseline function indices - BODE index 7-10 (Low BMI, breathless at rest and unable to walk more than 150m over six minutes, with an FEV1 below 35% of the predicted value) =  20% chance of surviving the next 48 months.
  • Poor global assessment of function -  Menzies et al (1989) found that if the patient is unable to leave their house because of their symptoms, their ICU mortality was with intubation 71%, going up to 75% if they were chronically bedbound or chairbound.
  • Dependence on home oxygen: according to Hajizadeh et al (2015) there is 23% in-hospital mortality, 45% 1-year mortality and  26.8% were discharged to a nursing home within 30 days.
  • Comorbidities (Menzies et al, 1989):
    • Malignancy
    • Cor pulmonale
    • Chronic hypercapnia
    • Left ventricular failure

Patient and family preferences

  • The patient's autonomy needs to be respected (they may have strong views on the matter)
  • It is important to remain objective - physicians can influence patient opinion significantly depending on how they "spin" their explanation of intubation and mechanical ventilation ( Sullivan et al, 1996)
  • For some scenarios, invasive ventilation has a good chance of success (ICU mortality for the "pure" COPD cohort from Nevins et al (2001) was actually lower than for other acute respiratory pathologies - 9% ICU mortality and 17% hospital mortality).
  • Survivors of short ICU stay with invasive ventilation rate their post-discharge health as same or better, and 96% responded that they would be willing to undergo similar treatment again (Wildman et al, 2009). These patients stayed in ICU for 6-9 days on average.

References

Chandra, Divay, et al. "Outcomes of noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease in the United States, 1998–2008." American journal of respiratory and critical care medicine 185.2 (2012): 152-159.

Simonds, A. K. "Ethics and decision making in end stage lung disease.Thorax 58.3 (2003): 272-277.

Gadre, Shruti K., et al. "Acute respiratory failure requiring mechanical ventilation in severe chronic obstructive pulmonary disease (COPD)." Medicine 97.17 (2018).

Lindenauer, Peter K., et al. "Outcomes associated with invasive and noninvasive ventilation among patients hospitalized with exacerbations of chronic obstructive pulmonary disease." JAMA internal medicine 174.12 (2014): 1982-1993.

Nevins, Michael L., and Scott K. Epstein. "Predictors of outcome for patients with COPD requiring invasive mechanical ventilation." Chest 119.6 (2001): 1840-1849.

Stefan, Mihaela S., et al. "Comparative effectiveness of noninvasive and invasive ventilation in critically ill patients with acute exacerbation of COPD." Critical care medicine 43.7 (2015): 1386.

Rinaudo, Mariano, et al. "Impact of COPD in the outcome of ICU-acquired pneumonia with and without previous intubation." Chest 147.6 (2015): 1530-1538.

Sullivan, Karen E., et al. "What do physicians tell patients with end-stage COPD about intubation and mechanical ventilation?." Chest 109.1 (1996): 258-264.

Wildman, Martin J., et al. "Implications of prognostic pessimism in patients with chronic obstructive pulmonary disease (COPD) or asthma admitted to intensive care in the UK within the COPD and asthma outcome study (CAOS): multicentre observational cohort study." Bmj 335.7630 (2007): 1132.

Jerpseth, Heidi, et al. "Considerations and values in decision making regarding mechanical ventilation for older patients with severe to very severe COPD." Clinical Ethics 11.4 (2016): 140-148.

Mannino, David M., Dennis E. Doherty, and A. Sonia Buist. "Global Initiative on Obstructive Lung Disease (GOLD) classification of lung disease and mortality: findings from the Atherosclerosis Risk in Communities (ARIC) study." Respiratory medicine 100.1 (2006): 115-122.

Celli, Bartolome R., et al. "The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease." New England Journal of Medicine 350.10 (2004): 1005-1012.

Menzies, Richard, William Gibbons, and Peter Goldberg. "Determinants of weaning and survival among patients with COPD who require mechanical ventilation for acute respiratory failure." Chest 95.2 (1989): 398-405.

Wildman, Martin James, et al. "Survival and quality of life for patients with COPD or asthma admitted to intensive care in a UK multicentre cohort: the COPD and Asthma Outcome Study (CAOS)." Thorax 64.2 (2009): 128-132.

Wakatsuki, Mai, and Paul Sadler. "Invasive Mechanical Ventilation in Acute Exacerbation of COPD: Prognostic Indicators to Support Clinical Decision Making.Journal of the Intensive Care Society 13.3 (2012): 238-243.

National Institute for Health and Clinical Excellence. Chronic obstructive pulmonary disease: management of chronic obstructive pulmonary disease in adults in primary and secondary care (partial update) London: National Clinical Guideline Centre; 2018

Quinnell, Timothy G., et al. "Prolonged invasive ventilation following acute ventilatory failure in COPD: weaning results, survival, and the role of noninvasive ventilation." Chest 129.1 (2

Question 7 - 2021, Paper 1

You are called to urgently review a 70-year-old patient who is being ventilated following admission with severe community-acquired pneumonia. She had a tracheostomy five days ago. She has now acutely desaturated with a saturation of 85% and developed high airway pressures but is haemodynamically stable.

Outline your differential diagnosis and initial management of this problem.
 

College answer

Not available.

Discussion

This question is essentially the same as Question 12 from the first paper of 2015, except the patient has aged three years over t, and is now 73. Bewildered, the author could only guess at the significance of this minor change. 

A good algorithm for assessing a patient suddenly impossible to ventilate is suggested in Chapter 3 of  Emergency Department Resuscitation of the Critically Ill,  "The Crashing Ventilated Patient" by Jairo Santanilla.

The following approach has been adopted from the above.

Immediate management:

  • Increase the FiO2 to 100%
  • Disconnect from the ventilator, and manually bag-ventilate them.
  • Simultaneously assess and manage threats to life in a systematic manner.
  • If the lung compliance is good, the patient's ventilator or its tubing is the problem, and you can keep bagging the patient until the ventilator is changed.
  • if the bag ventilation is difficult, one must conclude that the patient or the tube are the problem.

If the bag ventilation is easy and the patient improves with it:

  • Machine factors are to blame.
  • Check the circuit:
    • Check for condensation in the ventilator tubing
    • Change HME 
    • Change the expiratory filter
    • If there is nothing obviously wrong with the tubing, the ventilator may be malfunctioning. Change the ventilator while manually bagging the patient.

If the bag ventilation is difficult and the patient is still unwell:

  • Patient factors are to blame.
  • Either the airway or the rest of the respiratory system is somehow compromised.
  • Address the airway first:
    • In the intubated patient:
      • Is the ETT blocked?
      • Pass a suction catheter down and suction the patient
      • Ensure the patient is not biting the tube.
      • Has the ETT migrated? Is there a cuff  herneation?
      • Auscultate both lungs; ensure equal air entry
      • Listen for cuff leak
      • Ensure satisfactory cuff pressure
    • In the tracheostomy patient:
      • check tracheostomy diameter (too narrow?)
      • check inner cannula (encrusted with inspissated secretions?)
      • check tracheostomy patency (blocked with secretions?)
      • Check tracheostomy position (dislodged during last turn?)
      • Check for subcutaneous emphysema
      • Suction the patient, loking for fresh blood and clots (unrecognised pulmonary haemorrhage?)
  • Let's say the airway is fine. The rest of the respiratory system must be somehow compromised.  The possibilities include:
    • Bronchial occlusion, eg. by sputum plug or clot
    • Bronchospasm
    • Pulmonary embolism
    • Pulmonary oedema
    • Pleural pathology, eg. pneumothorax, haemothorax or pleural effusion
    • Abdominal pathology, eg. massive distension
  • These possibilities need to be investigated systematically:
    • Auscultation of the chest will immediately identify lateralising pathology, and may reveal pulmonary oedema
    • A bedside chest ultrasound will immediately confirm or exclude pneumothorax, haemothorax or large pleural effusion.
    • A bedside TTE should immediately exclude severe LV failure and massive PE.
    • ECG will exclude MI
    • ABG will identify metabolic acidosis
    • CXR to confirm/exclude large bronchus obstruction
    • Bronchoscopy to relieve this mechanical obstruction
  • If there is no problem with the respiratory system, but the patient is still "impossible to ventilate", consider the following extrapulmonary possibilities:
    • Patient-ventilator dyssynchrony
    • Pain of respiration (eg. in context of rib fractures or thoracotomy)
    • Increased ventilatory demand:
      • Severe agitation
      • Seizures
      • Fever and rigors
      • Metabolic acidosis

References

Jairo I. Santanilla "The Crashing Ventilated Patient"; Chapter 3 in Emergency Department Resuscitation of the Critically Ill, American College of Emergency Physicians, 2011.

Question 14 - 2021, Paper 1

A 57-year-old female has required intubation and mechanical ventilation for hypoxaemic respiratory failure with symptoms of cough and dyspnoea that have been gradually progressive over 4 weeks. There is a diffuse bilateral infiltrate on her chest X-ray. She has a history of rheumatoid arthritis and is receiving treatment with methotrexate and prednisolone and has no previous history of respiratory disease.

a)    List the likely differential diagnosis.    (20% marks)

b)    Briefly outline the specific management issues relating to diagnosis and treatment of this patient, excluding acute resuscitation.    (80% marks)
 

College answer

Not available.

Discussion

This question is identical to Question 20 from the first paper of 2014.

List the likely differential diagnosis  here is only worth only 20% which means that a table of this size would be completely unreasonable.

Differential Diagnosis for Diffuse Bilateral Pulmonary Infiltrates

Vascular:

  • Pulmonary haemorrhage
  • Cardiogenic pulmonary oedema

Infectious

  • Bacterial
  • Viral
  • Fungal
  • PJP

Neoplastic

  • Lymphangitis
  • Infiltrative neoplasm

Idiopathic

  • ARDS

Drug-induced

  • Eosinophilic pneumonitis
  • Organising pneumonia
  • Alveolar haemorrhage
  • Methotrexate-induced

Autoimmune

  • Goodpastures (haemorrhagic)
  • Rheumatoid pneumonitis
  • TRALI
  • Graft vs host disease in BMT
  • Engraftment syndrome

Traumatic

  • Bilateral atelectasis
  • Pulmonary contusions

Specific management issues relating to diagnosis and treatment: 

To exclude non-infectious causes:

  • A transthoracic echo will inevitably be informative, but the finding of a poor systolic function is not going to exclude infectious aetiology (which could easily co-exist with heart failure, as a wet lung is the devil's playground)
  • HRCT is suggested by the college, and this may give some information regarding the pattern of the disease, while not being particularly diagnostic (the CTPA would reveal emboli, but surely a gradual onset over four weeks does not particularly resemble the natural history of a PE)
  • A "vasculitic screen", whatever that might be in the local parlance - mainly to exclude something like Wegener's or Goodpasture's syndromes (though these are made unlikely by the immunosuppression) 

To investigate infectious causes:

  • Perform a bronchoscopy and send lavage specimens for multiple tests:
    • Bacterial cultures and gram stain
    • Acid-fast bacilli
    • Cell count (also looking for weird stuff like eosinophilic pneumonitis)
    • P.carinii PCR
    • Aspergillus PCR
    • Respiratory viral nucleic antigen tests, including CMV, HSV and VZV
    • Cryptococcal antigen
    • COVID19 rapid antigen test
  • Urinary antigens for Streptococcus and Legionella
  • Atypical pneumonia serology, looking for antibodies to mycobacteria, ChlamydiaCoxiella, etc.

Reasonable steps to prevent deterioration:

  • Cease methotrexate. The disease process progressed while the patient (presumably) continued to dutifully take her methotrexate and steroids; ergo it is less likely to be an autoimmune disease driven by B-cells and auto-antibodies.
  • Be moderate with fluid resuscitation, as this has been demonstrated to have a negative impact in ARDS
  • Ventilate the patient with lung-protective low tidal volumes, high PEEP and minimal driving pressures

Some empirical management to cover for the usual suspects:

  • Cover P.jirovecii with therapeutic dose of sulfamethoxazole/trimethoprim; 
  • Cover gram-positive and gram-negative organisms with something broad, as the stakes are high and there will always be opportunity to narrow the antibiotics once cultures are available. Some combination of meropenem azithromycin and either vancomycin or linezolid are recommended by various guideline-writers (eg. the parts of the 2016 IDSA guidelines which mention "critically ill patients")
  • Antifungal therapy might become relevant if fungi are implicated by culture results
  • Antiviral therapy (oseltamivir) is suggested by the college in their answer to Question 20 from the first paper of 2014, in the ake of the H1N1 pandemic. In this day and age, one would probably score marks by mentioning remdesivir and baricitinib.

If things are not going as planned (i.e. it's a week down the track and the patient is not getting better), a lung biopsy might be indicated. Apparently, it often identifies steroid-responsive pathology (Gerard et al, 2018), in which case the college's suggestion (massive doses of methylprednisolone) becomes relevant. 

References

Blanco, Silvia, and Antoni Torres. "Differential Diagnosis of Pulmonary Infiltrates in ICU Patients." www.antimicrobe.org

ARDS Definition Task Force. "Acute Respiratory Distress Syndrome." Jama307.23 (2012): 2526-2533.

Esteban, Andrés, et al. "Prospective randomized trial comparing pressure-controlled ventilation and volume-controlled ventilation in ARDS." CHEST Journal 117.6 (2000): 1690-1696.
 
Gainnier, Marc, et al. "Effect of neuromuscular blocking agents on gas exchange in patients presenting with acute respiratory distress syndrome*."Critical care medicine 32.1 (2004): 113-119.

Watling, Sharon M., and Joseph F. Dasta. "Prolonged paralysis in intensive care unit patients after the use of neuromuscular blocking agents: a review of the literature." Critical care medicine 22.5 (1994): 884-893.

Armstrong Jr, Bruce W., and Neil R. MacIntyre. "Pressure-controlled, inverse ratio ventilation that avoids air trapping in the adult respiratory distress syndrome." Critical care medicine 23.2 (1995): 279-285.

Hodgson, Carol, et al. "Recruitment manoeuvres for adults with acute lung injury receiving mechanical ventilation." Cochrane Database Syst Rev 2.2 (2009).

Zavala, Elizabeth et al.Effect of Inverse I: E Ratio Ventilation on Pulmonary Gas Exchange in Acute Respiratory Distress Syndrome Anesthesiology: January 1998 - Volume 88 - Issue 1 - p 35–42

Brower RG, Lanken PN, MacIntyre N, et al; National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Higher versus lower positive endexpiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351(4):327-336.

Meade MO, Cook DJ, Guyatt GH, et al; Lung Open Ventilation Study Investigators. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):637-645.

Mercat A, Richard JC, Vielle B, et al; Expiratory Pressure (Express) Study Group. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646- 655.

Briel, Matthias, et al. "Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome." JAMA: the journal of the American Medical Association 303.9 (2010): 865-873.

De Campos, T. "Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network." N Engl J Med342.18 (2000): 1302-130g.

Putensen, Christian, et al. "Meta-analysis: ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury." Annals of internal medicine 151.8 (2009): 566-576.

de Durante, Gabriella, et al. "ARDSNet lower tidal volume ventilatory strategy may generate intrinsic positive end-expiratory pressure in patients with acute respiratory distress syndrome." American journal of respiratory and critical care medicine 165.9 (2002): 1271-1274.

Kahn, Jeremy M., et al. "Low tidal volume ventilation does not increase sedation use in patients with acute lung injury*." Critical care medicine 33.4 (2005): 766-771.

Hodgson, Carol L., et al. "A randomised controlled trial of an open lung strategy with staircase recruitment, titrated PEEP and targeted low airway pressures in patients with acute respiratory distress syndrome." Crit Care 15.3 (2011): R133.

MANCINI, MARCO, et al. "Mechanisms of pulmonary gas exchange improvement during a protective ventilatory strategy in acute respiratory distress syndrome." American journal of respiratory and critical care medicine 164.8 (2012).

Amato, Marcelo Britto Passos, et al. "Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome." New England Journal of Medicine 338.6 (1998): 347-354.

Chu, Eric K., Tom Whitehead, and Arthur S. Slutsky. "Effects of cyclic opening and closing at low-and high-volume ventilation on bronchoalveolar lavage cytokines*." Critical care medicine 32.1 (2004): 168-174.

Question 17 - 2021, Paper 1

a)    List the indications, contraindications, uses and adverse effects of high-flow nasal cannulae (HFNC).    (40% marks)

b)    Critically evaluate the use of HFNC use in adult ICU patients.    (60% marks)
 

College answer

Not available.

Discussion

The wording of this SAQ might have confused some people, as some trainees would have found it difficult to find the subtle difference between the indications for high flow nasal oxygen and the uses of high flow nasal oxygen. 

Fortunately, this question is a mutant hybrid offspring of Question 2 from the first  paper of 2013  and Question 3 from the first paper of 2017, which means the candidates should have been well prepared for it. Thus:

Indications

  • For hypoxic respiratory failure, especially due to pneumonia
  • For hypercapnic respiratory failure (though the evidence is weaker)
  • Where NIV is poorly tolerated or inappropriate (eg. oesophageal surgery)
  • Where intubation is not appropriate
  • Apnoeic oxygenation pre-intubation

Contraindications:

Complications

  • Overdistension of the alveoli, and barotrauma
  • Discomfort associated with the device, its flow or the high temperature/humidity
  • Nasal mucosal damage due to high flow
  • Pressure areas due to the device
  • Failure to achieve the desired effect because of mouth-breathing
  • Overabundance of secretions (Velasco et al, 2014) - though some might view this as a desired effect
  • Epistaxis
  • Time-wasting (delaying the inevitable intubation)
  • Aspiration of food or upper airway secretions
  • Aspiration of circuit condensation water (there's no evidence that this causes pneumonia, but people complained about it in a survey of paediatric ICUs conducted by Manley et al, 2012)

"Critically evaluate" in 6 minutes or less, omitting elements already covered in the preceding question and stripping a more comprehensive answer down to some kind of bare metal:

  • Rationale:
    • ​​​​​Pharyngeal dead space washout
    • Improved oxygenation by PEEP effect (minor though it may be)
    • Improved oxygenation by oxygen dilution reduction (at high resp rates)
    • Benefits of humidification
    • Increased comfort
  • Advantages:
    • ​​​​​​​Appropriate where NIV and intubation are not
    • Allows high FiO2 otherwise impossible to safely achieve
    • Allows high flow rates of gas, beneficial in patients with increased respiratory effort
  • Limitations:
    • ​​​​​​​​​​​​​​The patient must be able to protect their airway
    • The nose and base of skull must be intact and uninjured
    • Avoided in upper GI surgery (risk to anastomosis)
    • PEEP is not measured, and is completely unpredictable
    • Intubation may be delayed; the outcome may be worse.
  • Evidence:

References

Groves, Nicole, and Antony Tobin. "High flow nasal oxygen generates positive airway pressure in adult volunteers." Australian Critical Care 20.4 (2007): 126-131.

Ricard, J. D. "High flow nasal oxygen in acute respiratory failure." Minerva Anestesiol 78.7 (2012): 836-841.

Locke, Robert G., et al. "Inadvertent administration of positive end-distending pressure during nasal cannula flow." Pediatrics 91.1 (1993): 135-138.

O’Brien, Bj, J. V. Rosenfeld, and J. E. Elder. "Tension pneumo‐orbitus and pneumocephalus induced by a nasal oxygen cannula: Report on two paediatric cases." Journal of paediatrics and child health 36.5 (2000): 511-514.

Corley, Amanda, et al. "Oxygen delivery through high-flow nasal cannulae increase end-expiratory lung volume and reduce respiratory rate in post-cardiac surgical patients." British journal of anaesthesia (2011): aer265.

Boyer, Alexandre, et al. "Prognostic impact of high-flow nasal cannula oxygen supply in an ICU patient with pulmonary fibrosis complicated by acute respiratory failure.Intensive care medicine 37.3 (2011): 558-559.

Stéphan, François, et al. "High-flow nasal oxygen vs noninvasive positive airway pressure in hypoxemic patients after cardiothoracic surgery: a randomized clinical trial.JAMA (2015).

Miguel-Montanes, Romain, et al. "Use of high-flow nasal cannula oxygen therapy to prevent desaturation during tracheal intubation of intensive care patients with mild-to-moderate hypoxemia*." Critical care medicine 43.3 (2015): 574-583.

Kang, Byung Ju, et al. "Failure of high-flow nasal cannula therapy may delay intubation and increase mortality." Intensive care medicine 41.4 (2015): 623-632.

Frat, Jean-Pierre, et al. "High-Flow Oxygen through Nasal Cannula in Acute Hypoxemic Respiratory Failure." New England Journal of Medicine (2015).

Vourc’h, Mickaël, et al. "High-flow nasal cannula oxygen during endotracheal intubation in hypoxemic patients: a randomized controlled clinical trial.Intensive care medicine (2015): 1-11.

Patel, A., and S. A. R. Nouraei. "Transnasal Humidified Rapid‐Insufflation Ventilatory Exchange (THRIVE): a physiological method of increasing apnoea time in patients with difficult airways." Anaesthesia 70.3 (2015): 323-329.

Hathorn, C., et al. "S68 The Hi-flo Study: A Prospective Open Randomised Controlled Trial Of High Flow Nasal Cannula Oxygen Therapy Against Standard Care In Bronchiolitis." Thorax 69.Suppl 2 (2014): A38-A38.

Parke, Rachael L., Shay P. McGuinness, and Michelle L. Eccleston. "A preliminary randomized controlled trial to assess effectiveness of nasal high-flow oxygen in intensive care patients." Respiratory Care 56.3 (2011): 265-270.

Vourc’h, Mickaël, et al. "High-flow nasal cannula oxygen during endotracheal intubation in hypoxemic patients: a randomized controlled clinical trial." Intensive care medicine 41.9 (2015): 1538-1548.

Question 23.1 - 2021, Paper 1

a)    What does the following pressure-volume loop (Figure 23.1) indicate?

b)    What is the likely underlying diagnosis?
(20% marks)

College answer

Not available.

Discussion

Because "(Image removed from exam report.)", and because this abomination of a paper was published without official answers, we have no idea which exact ventilator loop the college chose for this. However, it is possible to guess, on the basis of the fact that the wording of this question is identical to the wording of Question 13.1 from the first paper of 2014. The college answers to that question were:

"a) Shift of the pressure volume loop to the left suggestive of increased lung compliance."

"b) Emphysema (COPD)."

References

Question 23.2 - 2021, Paper 1

The following pressure-volume loop (Figure 23.2) was obtained from a mechanically ventilated patient.

a)    What does it indicate?

b)    What changes would you make to the ventilator settings to correct the abnormality?
(20% marks)

College answer

Not available.

Discussion

Because "(Image removed from exam report.)", and because this abomination of a paper was published without official answers, we have no idea which exact ventilator loop the college chose for this. However, it is possible to guess, on the basis of the fact that the wording of this question is identical to the wording of Question 13.2 from the first paper of 2014.

The college answers to that question were:

a) "Beaking" pattern of lung over-distension, where airway pressure continues to rise without much increase in tidal volume.

b) Reduce the applied tidal volume.

References

Question 23.2 - 2021, Paper 1

Causes of a flat capnograph trace

Outline four causes for the below capnograph trace (Figure 23.3) obtained from a critically ill patient.
(20% marks)
 

College answer

Not available.

Discussion

Because "(Image removed from exam report.)", and because this abomination of a paper was published without official answers, we have no idea which exact ventilator loop the college chose for this. However, it is possible to guess, on the basis of the fact that the wording of this question is identical to the wording of Question 13.2 from the first paper of 2014.

Reasons for a flat or nearly flat CO2 trace include the following:

  • The patient is dead
  • Cardiac / respiratory arrest
  • Apnoea test in a brain dead patient
  • Oesophageal intubation has occurred
  • Ventilator disconnection
  • Airway obstruction (eg. patient suddenly bit down on the tube)
  • ETT perforation (the end tidal gas is escaping via the hole before it gets to the capnograph)
  • Capnograph disconnection or obstruction
  • Water droplet contamination of capnography module

References

Question 23.4 - 2021, Paper 1

A 58-year-old female ventilated in intensive care for a week following a motor vehicle accident was noted to drop her oxygen saturation suddenly, requiring an increase in FiO2 from 0.4 to 0.6. The nurse has performed an arterial blood gas analysis.

Parameter      

Patient Value

Adult Normal Range

FiO2

0.6

pH

7.48*

7.36 – 7.44

PCO2

41 mmHg (5.4 kPa)

35 – 45 (4.6 – 6.0)

PO2

86 mmHg (11.3 kPa)      

Ventilator data:

Tidal Volume            700 mL

Respiratory rate       14 breaths/min

Peak pressure           28 cmH2O

Plateau pressure       18 cmH2O

PEEP                         7.5 cmH2O

SpO2                         94%

EtCO2                       28 mmHg

What is the most likely diagnosis? Give the reasons for your diagnosis.                                                                                                                                (40% marks)

College answer

Not available.

Discussion

This question is identical to Question 13.4 from the first paper of 2014. 

There are numerous possible causes for "sudden onset hypoxemia" in a trauma patient recovering from surgery. The college practically give this one away by offering the candidate an end-tidal CO2 measurement, which is substantially lower than the arterial CO2 measurement, suggesting that there is a large area of lung which is not participating in gas exchange, i.e. it is dead space.  Capnometry and the arterial-expired carbon dioxide gradient is discussed elsewhere.

Of course, one should still go though the motions of calculating the A-a gradient.

PAO2 = 0.6 × (760 - 47) - (PaCO2 × 1.25) = 376.55;

thus, A-a = 290.55

References

Question 5 - 2021, Paper 2

A 75-year-old female has been admitted to the ICU from the rehabilitation ward with respiratory failure due to community acquired pneumonia. She has a background history of chronic obstructive pulmonary disease (COPD) and congestive cardiac failiure (CCF). The resident tells you the patient is now receiving non-invasive ventilation (NIV) on the ward.

a)    Explain how NIV can improve the underlying pathophysiology in this patient.    (50% marks)

b)    Explain how you would assess efficacy of NIV in this patient.    (50% marks)


 

College answer

Not available.

Discussion

This question resembles questions that ask the candidates to critically evaluate NIV, insofar as the answer to both types of question are very similar. However, in an a glorious outburst of good SAQ design, the examiners have wrapped the discussion around a clinical case scenario, and reframed the otherwise very nebulous "critically evaluate" stem into a laudably discrete series of practical questions. This sort of assessment has face validity: you can look at it, and confidently say to yourself that a person who can readily answer this question is probably a good intensivist.

So: this patient has COPD and CCF, which tend to respond well to NIV, and community-acquired pneumonia, which does not tend to respond very well.

How can NIV can improve the underlying pathophysiology in this patient?

  • For respiratory failure in general:
    • Positive pressure ventilation in general has benefits which are common to both NIV and IPPV.
    • Increased inspiratory positive pressure decreases work of breathing by improving lung compliance by recruiting collapsed alveoli
    • Increased FRC due to increased closing capacity improves oxygenation
    • Tight-fitting mask ensures accurate delivery of prescribed FiO2
  • CCF:
    • Increased alveolar pressure decreases the effects of pulmonary oedema on gas exchange
    • Increased intrathoracic pressure improves LV performance:
      • Decreased LV transmural pressure = decreased afterload
      • Decreased venous return = decreased preload
    • Improvement in pulmonary oedema and respiratory distress also indirectly decrease myocardial oxygen demand by moderating the sympathetic response and decreasing the effort of breathing
  • COPD:
    • Increased end-expiratory positive pressure decreases work of breathing vs. intrinsic PEEP
    • Increased expiratory air flow can improve CO2 clearance
    • Increased minute volume can better compensate for the increased dead space of emphysema
    • Splinting open of smaller airways allows better bronchodilator delivery
  • Community-acquired pneumonia:
    • NIV does not tend to benefit this group of patients, because:
      • It can impair secretion clearance
      • It can increase shunt
    • However, the delivery of humidified oxygen by mask can improve secretion clearance
    • In patients with CCF or COPD and pneumonia, NIV can improve mortality ( Carrillo et al, 2012) 

How you could assess efficacy of NIV in this patient:

  • NIV should be viewed as effective if it achieves the desired clinical endpoints over a specified timeframe, and if the patient does not manifest any features suggestive of impending NIV failure during the trial. 
  • To assess the efficacy of NIV, one should:
    • Establish endpoints for this therapy
    • Establish a timeframe for the trial of NIV
    • Monitor for features suggestive of NIV failure throughout this trial
  • Endpoints:
    • Clinical endpoints:
      • Achievement of the SpO2 goal of 88-92%
      • The FiO2 should decrease with NIV (compared to what it was pre-NIV), i.e. the PaO2/FiO2 ratio should improve
      • Improved tachycardia
      • Improvement in the respiratory rate (if the patient was tachypnoeic)
      • Subjective improvement in patient respiratory distress and reported comfort
      • Satisfactory mask tolerance, without the requirement for sedation
      • Improved level of consciousness
    • Gas exchange and pulmonary function:
      • PaCO2 decrease (if the patient was hypercapneic)
      • pH increase (if the patient was acidaemic due to hypercapnia)
      • Improvement of CXR appearance, specifically looking for radiological features of pulmonary oedema
  • Timeframe:
    • Within 1 hour,
      • Resp rate should improve
      • PaO2/FiO2 ratio should improve
      • Heart rate should improve
      • PaCO2 and pH should demonstrate an encouraging trend
        (Nicolini et al, 2014)
    • Within 4 hours,
      • Level of consciousness should improve
    • Within 24 hours,
  • Features suggestive of NIV "failure":
    • Persistent metabolic acidosis
    • Haemodynamic instability
    • Persistently decreased level of consciousness
    • Poor mask tolerance and ventilator dyssynchrony

References

Gay, Peter C. "Complications of noninvasive ventilation in acute care."Respiratory care 54.2 (2009): 246-258.

Hore, Craig T. "Non‐invasive positive pressure ventilation in patients with acute respiratory failure." Emergency Medicine 14.3 (2002): 281-295.

Lightowler, Josephine V., et al. "Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis." BMJ: British Medical Journal 326.7382 (2003): 185.

Ram, F. S., et al. "Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease." Cochrane Database Syst Rev 3.3 (2004).

Gay, Peter C. "Complications of noninvasive ventilation in acute care."Respiratory care 54.2 (2009): 246-258.

Carrillo, Andres, et al. "Noninvasive ventilation in acute hypercapnic respiratory failure caused by obesity hypoventilation syndrome and chronic obstructive pulmonary disease." American journal of respiratory and critical care medicine 186.12 (2012): 1279-1285.

Chiumello, D., et al. "Noninvasive ventilation in chest trauma: systematic review and meta-analysis." Intensive care medicine 39.7 (2013): 1171-1180.

Lim, Wei Jie, et al. "Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma." The Cochrane Library Published Online: 12 DEC 2012

Alonso, Ana Souto, Pedro Jorge Marcos Rodriguez, and Carlos J. Egea Santaolalla. "Long-Term Noninvasive Ventilation Among Chronic Respiratory Failure Diseases (Cystic Fibrosis and Other Diseases) Awaiting Lung Transplantation: Key Determinants and Practical Implications." Noninvasive Mechanical Ventilation. Springer International Publishing, 2016. 771-779.

Gupta, Dheeraj, et al. "A prospective randomized controlled trial on the efficacy of noninvasive ventilation in severe acute asthma." Respiratory care 55.5 (2010): 536-543.

Williams, Trevor J., et al. "Risk factors for morbidity in mechanically ventilated patients with acute severe asthma." The American review of respiratory disease146.3 (1992): 607-615.

Carrillo, Andres, et al. "Non-invasive ventilation in community-acquired pneumonia and severe acute respiratory failure." Intensive care medicine 38.3 (2012): 458-466.

Jaber, Samir, Gerald Chanques, and Boris Jung. "Postoperative non-invasive Ventilation." Intensive Care Medicine. Springer New York, 2008. 310-319.

Azoulay, Élie, et al. "Palliative noninvasive ventilation in patients with acute respiratory failure." Intensive care medicine 37.8 (2011): 1250-1257.

Azoulay, Élie, et al. "Noninvasive mechanical ventilation in patients having declined tracheal intubation." Intensive care medicine 39.2 (2013): 292-301.

Ferrer, Miquel, et al. "Early noninvasive ventilation averts extubation failure in patients at risk: a randomized trial." American journal of respiratory and critical care medicine 173.2 (2006): 164-170.

Su, Chien-Ling, et al. "Preventive use of noninvasive ventilation after extubation: a prospective, multicenter randomized controlled trial." Respiratory care 57.2 (2012): 204-210.

Esteban, Andrés, et al. "Noninvasive positive-pressure ventilation for respiratory failure after extubation." New England Journal of Medicine 350.24 (2004): 2452-2460.

Bright-Thomas, Rowland J., and Susan C. Johnson. "What is the role of noninvasive ventilation in cystic fibrosis?." Current opinion in pulmonary medicine 20.6 (2014): 618-622.

Kallet, Richard H., and Janet V. Diaz. "The physiologic effects of noninvasive ventilation." Respiratory care 54.1 (2009): 102-115.

Jones, Shirley F., Veronica Brito, and Shekhar Ghamande. "Obesity Hypoventilation Syndrome in the Critically Ill." Critical care clinics 31.3 (2015): 419-434.

Razlaf, Peter, et al. "Non-invasive ventilation in immunosuppressed patients with pneumonia and extrapulmonary sepsis." Respiratory medicine 106.11 (2012): 1509-1516.

Lemiale, Virginie, et al. "Effect of noninvasive ventilation vs oxygen therapy on mortality among immunocompromised patients with acute respiratory failure: A randomized clinical trial." JAMA 314.16 (2015): 1711-1719.

Barbas, Carmen Sílvia Valente, and Ary Serpa Neto. "New puzzles for the use of non-invasive ventilation for immunosuppressed patients." Journal of thoracic disease 8.1 (2016): E100.

Antonelli, Massimo, et al. "Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial." Jama 283.2 (2000): 235-241.

Keenan, Sean P., et al. "Clinical practice guidelines for the use of noninvasive positive-pressure ventilation and noninvasive continuous positive airway pressure in the acute care setting." Canadian Medical Association Journal 183.3 (2011): E195-E214.

Murad, A., et al. "The role of noninvasive positive pressure ventilation in community-acquired pneumonia." Journal of critical care 30.1 (2015): 49-54.

Sidhom, Samy, et al. "PREDICTORS OF NONINVASIVE VENTILATION FAILURE." Chest 136.4 (2009): 32S.

Nicolini, Antonello, et al. "Predictors of non-invasive ventilation failure in severe respiratory failure due to community acquired pneumonia." Tanaffos 13.4 (2014): 20.

Question 30 - 2021, Paper 2

A 25-year-old female is brought into the Emergency Department with acute severe asthma. She is intubated and ventilated and transferred to the ICU.

a)    Discuss your assessment and management to prevent the potential of the patient developing dynamic hyperinflation.    (60% marks)

The patient becomes hypotensive.

b)    Excluding worsening dynamic hyperinflation, list four likely differential diagnoses. (10% marks)

c)    Outline one diagnostic investigation and one management strategy for each differential diagnosis.
(30% marks)
 

College answer

Not available.

Discussion

a)

Specific strategies to assess for, and to prevent dynamic hyperinflation in status asthmaticus, include:

  • Minimise interference from chest wall movement
    • Sedation, analgesia
    • Neuromuscular junction blockers
  • Minimise airway airflow resistance
    • Bronchodilator continuous nebs +/- intravenous infusion
    • Ketamine for sedation
    • Heliox is an option if oxygenation is satisfactory
  • Maximise expiratory air flow: two schools of thought:
    • Keep PEEP minimal, i.e. use ZEEP - this maximises the gradient for 
    • Keep some low PEEP, eg 5-8, to prevent small airways from closing during expiration, thereby worsening gas trapping
  • Maximise expiratory time
    • ​​​​​​​Use I:E ratio with a prolonged expiratory phase, eg. 1:4, up to 1:6 or even 1:10
  • Monitor for dynamic hyperinflation
    • ​​​​​​​Observe ventilator flow and volume waveforms: it needs to reach zero before the next breath
    • Watch for pulsus paradoxus or increasing pulse pressure variation: this could be a signal that the intrinsic PEEP is increasing
    • Perform serial expiratory hold manoeuvres to assess intrinsic PEEP

b)

Different possible reasons this patient is becoming hypotensive:

  • Hypovolemia (common in asthma; too breathless to eat and drink)
  • Anaphylaxis to intubation drugs
  • Tension pneumothorax
  • Tachyarrhythmia due to excessive bronchodilators
  • Effect of the sedative drugs

c)

  • Hypovolemia: bedside TTE; fluid bolus
  • Anaphylaxis: mast cell tryptase (though this would be a clinical diagnosis); adrenaline IM, followed by an infusion
  • Tension pneumothorax: CXR/bedside lung ultrasound, though again this is usually a clinical diagnosis
  • Tachyarrhythmia: ECG; management could consist of DC cardioversion, a calcium channel blocker or amiodarone.

References

Oddo, Mauro, et al. "Management of mechanical ventilation in acute severe asthma: practical aspects." Intensive care medicine 32.4 (2006): 501-510.

Golchin, A., K. Hachey, and A. Khan. "Is There a Role of Applied PEEP (PEEPe) in Controlled Mechanically Ventilated Severe Asthma Exacerbations?." C52. CRITICAL CARE CASE REPORTS: GOOD VIBRATIONS-MECHANICAL VENTILATION FROM NIV TO ECMO. American Thoracic Society, 2018. A5270-A5270.

Smith, THOMAS C., and JOHN J. Marini. "Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction." Journal of Applied Physiology 65.4 (1988): 1488-1499.

Kondili, Eumorfia, et al. "Pattern of lung emptying and expiratory resistance in mechanically ventilated patients with chronic obstructive pulmonary disease." Intensive care medicine 30.7 (2004): 1311-1318.