Printable list of al respiratory Medicine SAQs

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

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

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

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

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 V_T patients (Petersen et al, 1999 - the mean V_T 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-V_T patient does not become hypocarbic and lose their respiratory drive.
• Low or zero PEEP: provided the V_T 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:

• Consider tracheostomy
• Consider NAVA
• Extubate on to NIV

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.

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

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

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

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.

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

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:

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.

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.

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%)

• Decrease inspiratory work of breathing, by:
  • Counteracting autoPEEP and improving inspiratory effort
  • Counteracting airway resistance with driving IPAP pressure
• Alter expiratory work of breathing, as the result of:
  • Splinting airways in expiration
  • Opposing dynamic airway compression
• Assuring FiO2 delivery (tight-fitting mask)
• Decrease the need for intubation
• Enhance the delivery of inhaled bronchodilator into distal bronchi
• Practically speaking, NIV in asthma reduces ICU stay and decreases bronchodilator requirements. However, the evidence is pretty weak.

(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.

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

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

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 V_T 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.

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

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

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

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

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.

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

• Mainly case series and case reports
• Not strongly supported by evidence
  • Some support for difficult wounds
  • Some support for diabetic foot disease
  • Some support for severe soft tissue infections
  • Not much support for carbon monoxide poisoning

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.

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

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

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

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.
  • a 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.

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).

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.

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.

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.

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.

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".

References

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.

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.

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.

College Answer

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

Discussion

An alternative tabulated answer would resemble the following:

References

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

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

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.
  • a 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).

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.

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).

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.

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.

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.

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

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

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)

College Answer

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.

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.

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:

• Use a Pressure Control mode (it may be safer, though the evidence is not strong)
• Lung-protective ventilation: use low tidal volumes (6ml/kg)
• Open-lung ventilation: avoid derecruitment by using a high PEEP
  • The ideal PEEP can be found either by finding the lower inflection point or the pressure-volume curve or by observing a stepwise decrease in PEEP after a recruitment manoeuvre.
  • As the ARDS severity increases, consider using a higher PEEP. 
• Use a lower driving pressure (ΔP) -Amato et al, 2015. That means, using a higher PEEP and aiming for a lower plateau pressure
• Accept a level of "permissive hypercapnea"

Additional ventilator manoeuvres to improve oxygenation:

• Use an I:E ratio of 1:1, even though manipulating the I:E ratio does not seem to improve survival, even though it may improve oxygenation.
• One might attempt some recruitment manoeuvres if hemodynamics permit. Again, these offer a transient improvement in oxygenation, but do not influence survival.

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

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.

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 and decrease the I:E ratio.  This would have the effect of increasing the peak inspiratory flow, as the same volume would have to be pushed into the patient over a shorter period of time, and in the state of bronchospasm this would likely produce higher peak airway pressures, but the college did not ask for this.

References

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

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:

• Ventilation strategies for ARDS
• Supportive non-ventilation strategies for ARDS

In summary:

Initial ventilator strategy:

• Use a Pressure Control mode (it may be safer, though the evidence is not strong)
• Lung-protective ventilation: use low tidal volumes (6ml/kg)
• Open-lung ventilation: avoid derecruitment by using a high PEEP
  • The ideal PEEP can be found either by finding the lower inflection point or the pressure-volume curve or by observing a stepwise decrease in PEEP after a recruitment manoeuvre.
  • As the ARDS severity increases, consider using a higher PEEP. 
• Use a lower driving pressure (ΔP) -Amato et al, 2015. That means, using a higher PEEP and aiming for a lower plateau pressure
• Accept a level of "permissive hypercapnea"

Additional ventilator manoeuvres to improve oxygenation:

• Use an I:E ratio of 1:1, even though manipulating the I:E ratio does not seem to improve survival, even though it may improve oxygenation.
• One might attempt some recruitment manoeuvres if hemodynamics permit. Again, these offer a transient improvement in oxygenation, but do not influence survival.

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

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 

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.

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 

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

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

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:

• Intrinsic PEEP and the expiratory hold manoeuvre
• Alveolar pressure and the inspiratory hold manoeuvre
• Interpreting the shape of the pressure waveform

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

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.

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.

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.

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.

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

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

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

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.
  • P_aw 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:

• Physiology of gas exchange in HFOV
• Principles of high frequency oscillatory ventilation (HFOV)

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.

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.

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:

• Use a Pressure Control mode (it may be safer, though the evidence is not strong)
• Lung-protective ventilation: use low tidal volumes (6ml/kg)
• Open-lung ventilation: avoid derecruitment by using a high PEEP
  • The ideal PEEP can be found either by finding the lower inflection point or the pressure-volume curve or by observing a stepwise decrease in PEEP after a recruitment manoeuvre.
  • As the ARDS severity increases, consider using a higher PEEP. 
• Use a lower driving pressure (ΔP) -Amato et al, 2015. That means, using a higher PEEP and aiming for a lower plateau pressure
• Accept a level of "permissive hypercapnea"

Additional ventilator manoeuvres to improve oxygenation:

• Use an I:E ratio of 1:1, even though manipulating the I:E ratio does not seem to improve survival, even though it may improve oxygenation.
• One might attempt some recruitment manoeuvres if hemodynamics permit. Again, these offer a transient improvement in oxygenation, but do not influence survival.

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

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.

(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

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 capnometry waveform interpretation
• Analysis of ventilator waveforms
• Pressure-volume and flow-volume loops

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

References

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).

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.

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

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:

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.

College Answer

a) Either of the following answers acceptable 
• Water in circuit 
• Secretions in trachea or circuit 

 

Discussion

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.

College Answer

Discussion

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.

A 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.

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.

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

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

• As the college has mentioned, the evidence for this practice is dodgy.
• The first randomised trial for this thrombolysis in massive PE comes from 1995, and was performed in a group of only 8 patients.
• All 4 patients receiving thrombolysis had survived without pulmonary hypertension at 2 years follow-up; whereas all the heparin-treated patients had died.
• Ten years later, thrombolysis is seen as a mandatory first-line step in the treatment of massive PE. It appears to reduce mortality by 55% according to a 2004 meta-analysis (including data from 748 patients).

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.

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

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.

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

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
  • in fact, in neonates this may lead to pneumothorax
• 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.

• Nasal fracture, or any other sort of nasal injury
• Recent nasal surgery
• Base of skull fracture - you might induce a pneumocephalus and god knows what else
• Decreased level of consciousness (or for that matter, anything else which might mandate intubation)

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.

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.

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.

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 P_plat 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

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
  • Acidosis
  • Increased PaCO₂ (the Bohr Effect)
  • Increased temperature
  • Increased 2,3-DPG (eg. in pregnancy) 
  • Sulfhaemoglobin
• 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

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

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.

References

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:

References

College Answer

a) Shift of the pressure volume loop to the left suggestive of increased lung compliance.

b) Emphysema (COPD).

References

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

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

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

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

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

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.

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, Chlamydia, Coxiella, etc.