Viva 3

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

1) What are the differential diagnoses for her presentation?

The rest of the viva focussed on the assessment and management of bronchial asthma

What are the differential diagnoses for her presentation?

Most likely:

  • Asthma
  • Anaphylaxis / allergy
  • Angioedema
  • Bronchitis or bronchiolitis
  • Anxiety with hyperventilation
  • COPD

Less likely:

  • Cardiac causes, eg. pulmonary oedema
  • Foreign body in the airway
  • Acute pulmonary embolism
  • Airway distortion due to mechanical causes, eg. bronchial mass, bronchiectasis, pneumothorax
  • Sepsis with metabolic acidosis
  • Ketoacidosis (with wheeze due to dynamic collapse of the airways)

This is a variant of Question 2 from the second paper of 2001, which was a question about the differential diagnosis of wheeze.  Causes of widespread wheeze may include:

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 tracheomalacia
  • 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
This lady is a known asthmatic. Which details of history and examination might suggest that she has severe asthma?

Historical features:

  • Previous intubation
  • Frequent admissions

Examination findings:

  • Agitation or delirium
  • Use of accessory muscles
  • Intercostal recession
  • Tracheal tug
  • Silent chest
  • Cyanosis
  • Inability to speak
  • Pulsus paradoxus in excess of 15mmHg
  • Heart rate in escess of 120

Pulmonary function test data:

  • FEV1 less than 1L
  • PEFR less than 100L/min (or less than 60% predicted)

ABG data:

  • Hypercapnea and respiratory acidosis (PaCO2more than 45mmHg) is a good reliable marker.

ED staff have commenced continuous salbutamol nebs. This ABG was collected after 30 minutes of your immediate management (FiO2 = 30%) . How do you interpret this result in context of this situation?
  • Acidaemia
  • Respiratory acidosis
  • Hypoxia
  • Metabolic acid-base balance is undisturbed
  • Lactate is normal

The presence of respiratory acidosis suggests that the patient is tiring
The absence of raised lactate suggests that nebulised salbutamol is ineffective
(air entry is too poor).

A trial of NIV is suggested. What are the advantages and disadvantages of NIV in asthma?

Theoretical benefits in asthma:

  • Decreased work of breathing
  • Increased tidal volume
  • Improved delivery of nebulised drug
  • Prevention of intubation


  • May delay intubation
  • Inappropriate settings may increase the effort of breathing
  • Increased positive airway pressure increases risk of pneumothorax
  • Addition of extrinsic PEEP which is higher than intrinsic PEEP will exacerbate dynamic hyperinflation
  • NIV makes it more difficult to clear secretions if there is a strong infective component.
What is the evidence for the use of NIV in asthma?
  • Much of the support for NIV in asthma is extrapolated from COPD
  • Small randomized trials
  • No clear mortality benefit from meta-analysis
  • Small size and differences in methodology makes the data difficult to analyse
  • Patients in these trials generally have had a very low prtality
  • Data is too heterogeneous to make any firm recommendations

Lim et al, (2012) ended up scraping together five studies - which only had n=206 in total. Of the 90-or so patients in two RCTs analysed by Lim et al, only two required intubation. There were no deaths in either group. How can you demonstrate a mortality benefit if nobody is dying?..

What are the predictors of failure for NIV in asthma?
  • Persistent high respiratory rate after 1 hour of NIV
  • Persistent tachycardia  after 1 hours of NIV
  • Persistently high CO (> 60 mmHg) after 1 hour of NIV

Alternatively, the candidate interpret see this question as "when would you intubate the asthmatic?" That will be the next question:

What are the indications for intubation in asthma?
  • Progressive respiratory exhaustion (rising PaCO2)
  • Decreasing level of consciousness, altered sensorium
  • Severe hypoxemia
  • Silent chest
  • Respiratory arrest (or cardiac arrest)

These are the consensus indications for intubation quoted by Brenner et al (2009).

The ED staff decided to go ahead with intubation. Immediately following the intubation, the patient has a PEA arrest. What might be the potential causes of this cardiac arrest?

Most likely

  • Dynamic hyperinflation
  • Hypoxia
  • Tension pneumothorax
  • Hypovolemia 

Less likely:

  • Acidosis
  • Anaphylactic reaction to the induction drugs
  • Hypokalemia
  • Primary cardiac problem, eg. MI
  • Massive PE

The candidates need to mention something about dynamic hyperinflation here.

With fluid resuscitation, ETT disconnection and 2 cycles of CPR, spontaneous circulation is restored. 
Peak inspiratory pressure is high and the chest is virtually silent. Describe what ventilator settings you will initially set.
  • Use lowest FiO2 to achieve SpO2 of 90-92%
  • Use a small tidal volume, 5-7ml/kg
  • Use a slow respiratory rate, 10-12 breaths per minute (or even less!)
  • Use a long expiratory time, with I:E ratio 1:3 or 1:4
  • Increase inspiratory flow rate to maximum. .
  • Reset the pressure limits (i.e. ignore high peak airway pressures).  .
  • Use a volume-control mode of ventilation.
  • Use minimal PEEP.
  • Keep the Pplat below 25cmH2o to prevent dynamic hyperinflation. 
  • Titrate PEEP to work of triggering once the patient is breathing spontaneously.

(this is based on the college answer to Question 1 from the first  paper of 2015)

Bedside nurses are complaining about tenaceous sputum plugs. What is your practice regarding the use of mucolytic agents in  acute severe asthma?

The options for mucolytic choice are

  • Recombinant human DNase (rhDNase)
  • Hypertonic saline
  • N-acetylcysteine

Evidence in support of this practice is lacking:

  • No RCT-level data for asthma
  • RCT-level data for CF and COPD has not demonstrated any benefit
  • Consensus guidelines (eg. Expert Panel Report 3, 2007) do not recommend this therapy

Selected patients may still benefit, but:

  • Mucolytics may worsen bronchospasm
  • Frequent post-mucolytic suctioning may worsen bronchospasm
  • Bronchoscopic delivery may not be practical, as bronchoscopy may be poorly tolerated
  • Difficult to assure the delivery of the nebulised drug to the site of activity (eg. if salbutamol penetration is poor because of ventilatory failure, what makes you think rhDNAse will get in there?)
Air entry remains poor and PaCO2 remains raised (to around 70-80 mm Hg). What additional strategies could you use to improve gas exchange?
  • Use heavy sedation.
  • Use neuromuscular blockade.
  • Intravenous beta-agonist bronchodilators 
  • Methylxanthines
  • Nebulised adrenaline
  • Magnesium sulfate
  • Helium-oxygen mixture
  • Ketamine
  • Volatile anaesthetics

At this late stage in the viva, anything goes - if they had made it this far in 10 minutes they can go on about ECMO as much a they like.

Disclaimer: the viva stem above may be an original CICM stem, acquired from their publicly available past papers. Or, perhaps it is a slightly altered version of the original CICM stem. Or, it is a completely original viva stem, concocted by the monstrously amoral author of Deranged Physiology for nothing more than his own personal amusement. In either case, because the college do not make the main viva text or marking criteria available, almost everything here has been confabulated. It might sound like a plausible viva and it could be used for the purpose of practice, but all should be aware that it does not represent the "true" canonical CICM viva station. 


Oh's Intensive Care manual: Chapter 35   (pp. 401) Acute  severe  asthma by David  V  Tuxen  and  Matthew  T  Naughton.

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