a) Describe your initial ventilator settings for a patient just intubated for acute severe asthma. Explain the rationale for each of your choices. (50% marks)

b) Hypotension commonly occurs after intubation in an asthmatic. What are the potential aetiologies and what steps would you take to prevent and/or treat them? (50% marks)

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College answer

Either volume controlled or pressure controlled modes are acceptable.

Generally spontaneous modes are avoided early and when unstable, needs deep sedation +/- paralysis to facilitate non injurious mode of ventilation

FiO2 1.0 – newly intubated – titrate down asap as risk of O2 toxicity and Aa gradient not usually a


PEEP: – controversial – Conventional teaching advocates a PEEP 0 to minimise high Paw, but there will already be some dynamic hyperinflation with intrinsic PEEP – set PEEP in or around this. Acceptable to mention PEEP titration to pressure/volume curves, but not required.(a discussion around what PEEP would be set with a reasonable justification was required for marks)

VT 4-6ml per kg – limited by plateau pressure < 30 – note PIPs will be high and need to be tolerated,

e.g. up to 50 cmH2O), ventilator alarms will need to be adjusted

RR / T insp. to be minimised to avoid dynamic hyper-inflation (or prolong exp. time) Generally aim Pplat <30cm/H20 and PEEPi <10

Dehydration – unwell by days, inadequate PO intake and then positive intrathoracic pressure – decreasing preload further, minimised by IV fluids loading prior to intubation, and volume loading afterwards to treat.

Afterload reduction/obliteration of sympathetic stimulation – drugs (sedatives and bronchodilators), use vasoconstrictors (titrated metaraminol or noradrenaline), may alter induction drugs or doses used

Dynamic hyperinflation exacerbating the preload reduction. Prevention is with settings targeting lower RR, and shorter insp time, Pplat <30 cmH2O and PEEPi<10. Treat by disconnection of patient from the ventilator and transiently ceasing ventilation. Occasionally manual compression of chest required to aid expiration.

Tension pneumothorax. Prevention is by avoiding high tidal volumes/ mean airway pressures, and accepting high pCO2 if necessary. Paralysis to prevent coughing. Tension pneumothorax is treated with immediate decompression (e.g. with 14 G needle, then early intercostal chest drain).

*If dynamic hyperinflation as a cause of hypotension was not mentioned, a candidate could only score a maximum of 4/10)

Examiners Comments:

Generally, well answered other than the justification for PEEP use.



  • FiO2: lowest possible to achieve SpO2 of 90-92% (this improves V/Q matching)
  • Tidal volume: small, 5-7ml/kg (as there is no reason to use larger volumes; moreover larger volumes may give rise to dynamic hyperinflation)
  • Respiratory rate: slow, 10-12 breaths per minute (or even less - depending on the degree of dynamic hyperinflation; the extra expiratory time should promote lung emptying and CO2 clearance)
  • Long expiratory time, with I:E ratio 1:3 or 1:4 (for the same reason as the decreased resp rate)
  • Use a volume-controlled mode, or any other mode with a square flow waveform (i.e. constant flow) - this decreases the peak airway pressure
  • Reset the pressure limits (i.e. ignore high peak airway pressures) as the peak airway pressure during inspiration is almost completely the product of the increased airway resistance
  • Use minimal PEEP (some PEEP may be beneficial, but a high PEEP will be harmful)
  • Keep the Pplat below 25cmH2o to prevent dynamic hyperinflation. 
  • Titrate PEEP to work of triggering once the patient is breathing spontaneously.


The asthmatic patient, upon intubation, has the tendency to arrest. There are several possible reasons for this. They are presented here in the format of [problem]:[solution], though in all honesty a table would probably work better. 

Preload problems

  • Obstructive shock could result from:
    • Dynamic hyperinflation
    • Tension pneumothorax
  • These are exacerbated by hypovolaemia.
  • The solution would be:
    • Avoid excessive bag-mask ventilation, and use a slow manual respiratory rate
    • Look actively for pneumothorax
    • Volume-load the patient prior to intubation, i.e. give a fluid bolus

Contractility problems

  • Cardiotoxic drugs given during intubation can give rise to haemodynamic instability, as you take away the patient's sympathetic drive by anaesthetising them. 
  • The solution would be to use agents such as ketamine, which are more "cardiostable" in sane induction doses.

Rate and rhythm problems

  • The patient, approaching intubation, will have been recently filled with proarrhythmic medications such as salbutamol, adrenaline or aminophylline
  • The same drugs lower the threshold for arrhythmia by decreasing serum potassium and by promoting metabolic (lactic) acidosis.
  • The additional proarrhythmic effect of post-intubation hypotension could push the patient over into fatal arrhythmias (eg. VF) or merely haemodynamically unproductive ones (SVT).
  • One possible protective strategy would be to ensure the biochemistry and electrolytes are well-corrected, and have sticky defib pads on the patient's chest before the intubation takes place.

Afterload problems

  • Though completely unrelated to asthma, one needs to consider the possibility that the patient is haemodynamically unstable after intubation because they are having an anaphylactic reaction to the induction agents. 


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