ICU Fellowship Snippet – Asthma Management

Dr Swapnil Pawar May 8, 2024 22

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    ICU Fellowship Snippet – Asthma Management
    Dr Swapnil Pawar


As the duty locum intensivist you have been called to urgently review a patient on the medical ward of a small private hospital. The patient, Jane, is a 32 year old female who was admitted to the ward yesterday with shortness of breath.

She presents with shortness of breath often, and has recently been started on a bronchodilator. A local GP registrar was on the ward reviewing another patient and noticed that Jane was working very hard to breathe. The registrar emergently intubated her prior to your arrival.

You arrive on the ward 10 minutes post intubation. The registrar and a ward nurse are hand-ventilating Jane, who is hypoxic – sats 85% and hypotensive BP 75/50mmHg. Outline your management.

Written by Dr Madhuri Anupindi


This is an emergency situation requiring simultaneous urgent evaluation and resuscitation to identify and treat the cause and contributors to her deterioration. My approach would be to activate the emergency response team if available in the hospital for extra personnel, and rapidly assess whether this is an issue with the ETT, a peri-intubation event or a deterioration in the patient’s underlying pathology.

  • Call for help, allocate roles, ensure maximum oxygen via BVM, resus and airway trolley present, good IV access and small boluses of metaraminol aiming SBP 90mmHg
  • Initial priority is to confirm ETT is in position and not obstructed
    • End tidal co2
    • Fogging/misting
    • Equal air entry
  • If concerns that obstructed ETT/oesophageal intubation:
    • Remove ETT, hand bag with guedel, obtain emergency airway equipment
    • LMA if difficulties hand bagging
    • Aim re-intubate with most experienced operator
  • If ETT in place not obstructed: patient pathology or peri-intubation event
    • Quick assessment of patient: vital signs, etco2 trace ?obstructed, observe chest wall movement, auscultate, feel compliance of lungs with bagging, look for rash, assess circulation
    • Brief history from staff surrounding medications given (?adequate paralysis), grade of intubation, aspiration and Jane’s history and progress on the ward
    • Investigations: Bedside: ABG, ECG, Imaging: CXR
    • Specific treatment depends on finding
      • Dynamic hyperinflation: stop bagging à disconnect, allow adequate expiration
      • Hypovolemia: fluid bolus of crystalloid
      • Vasodilation secondary to induction drugs: vasopressors
      • Anaphylaxis: rash à adrenaline
      • Pneumothorax à decompress
      • Aspiration during intubation: optimise ventilation settings, may need bronch
      • Endobronchial intubation à withdraw ETT
      • De-recruitment post intubation
      • Worsening community acquired pneumonia: vasopressors for hypotension, ensure appropriate antimicrobial therapy, optimise ventilation settings – may need therapies such as inhaled pulmonary vasodilator
      • Decreased cardiac output due to myocardial depression or arrhythmia: may need inotropes, electrolytes, anti-arrhythmics
      • Dyssynchrony (less likely as just been intubated) à sedation/paralysis
    • Logistics
      • Bring ventilator, monitor from ICU – aim to stabilise/improving trajectory then transfer to ICU
      • Depending on trajectory and resources in this hospital may need early call to a larger unit/retrieval


On further assessment you confirm appropriate ETT position, however Jane has an obstructed etco2 trace with global wheeze and a CXR that shows no pneumothorax or consolidation. Her saturations have increased to 92% and you have been able to transfer her to the hospital’s ICU and place her on the ventilator. What initial settings would you use?

Settings aim to avoid dynamic hyperinflation, optimise oxygenation and ventilation with likely tolerating a degree of hypercapnoea, and minimising barotrauma.

Volume control mode: able to assess plateau pressure – aim < 25 cm h20

  • PEEP of 0 initially while paralysed and not triggering breaths
  • I:E ratio of 1:4 and assess flow time and volume time waveform to ensure that it returns to baseline during expiration otherwise prolong the expiratory time or reduce respiratory rate à high flow rate 60 – 80L/min to reduce inspiratory time
  • RR of 10 but may change depending on I:E ratio and flow/time waveform as just outlined
  • Volume of 6ml/kg but may need to decrease if plateau pressures > 25cm h20
  • Fio2 of 100% to begin with and then decrease titrating to sats > 92%
  • May need to increase peak inspiratory pressure alarm – tolerate high peak pressures as long as plateau pressure < 25 cmh20

Ensure humidified circuit

You’ve mentioned using 0 PEEP for this patient. Briefly outline the rationale for zero PEEP versus low PEEP in asthma?  

The amount of PEEP to use in the intubated asthmatic patient is not clear.


  • Small amount of external PEEP may decrease end-expiratory alveolar collapse
  • When patients are triggering the ventilator, a high intrinsic PEEP can make it difficult for patients to initiate a breath. Adding external PEEP of 60 – 80% of the intrinsic PEEP can help reduce the effort required to trigger the ventilator

Zero PEEP:

  • Patients often are generating auto-PEEP so theoretically already are splinting their airways open
  • Extrinsic PEEP may then just contribute to dynamic hyperinflation
  • In the fully sedated mechanically ventilated patient who is not triggering their own breaths, they do not have work of breathing to overcome so adding extrinsic PEEP risks exacerbating dynamic hyperinflation

What is dynamic hyperinflation and outline two methods to assess for it in the intubated asthmatic patient?

Dynamic hyperinflation is an increase in end-expiratory lung volume due to incomplete expiratory emptying of the lungs in patients with airflow obstruction. It is failure of the lung to return to its functional residual capacity or relaxed volume at the end of expiration.

Expiratory hold manoeuvre:

  • End expiratory pause:
    • Occlusion of circuit at end expiration allows alveolar pressure to equilibrate with airway pressure
    • This number minus any extrinsic PEEP applied is the intrinsic PEEP
    • Requires patient to be sedated and paralysed for accuracy
    • This method often underestimates intrinsic PEEP as dynamic airway closure prevents the alveoli with the highest pressure equilibrating with the circuit
  • Plateau pressure
    • Measure with an inspiratory hold manoeuvre à pressure falls from the peak (resistance + compliance) to the plateau (static compliance only) which is at no flow and therefore theoretically is equilibrated with alveolar pressure
    • For accurate measurement patient needs to be sedated and paralysed and the circuit should not have significant leak
    • As lung volume increases in dynamic hyperinflation the plateau pressure will also increase


Despite being sedated and paralysed with appropriate ventilator settings, inhaled bronchodilators and IV steroids, she fails to improve. What other treatments are available for severe asthma exacerbations and their mechanism of action?


Treatment Mechanism of Action Comments
Magnesium Blocks calcium channels smooth muscle cells of the airway, inhibits histamine release from mast cell and acetylcholine release from cholinergic nerve terminals à bronchodilation and decreases airway excitability

Membrane stabilising effect in atria à may help attenuate tachyarrhythmias from beta-agonist therapy

Can be given intravenously or inhaled – IV has increased bioavailability but more side effects

Recommended in multiple guidelines e.g. Australian Asthma Handbook but poor  evidence base


3Mg trial: IV or nebulised magnesium sulphate versus standard therapy for severe acute asthma – no significant different in admission rates or secondary outcomes

Cochrane review 2014: single infusion of IV MgSo4 reduced hospital admissions and improves lung function in adults with acute asthma



IV Salbutamol Beta 2 adrenoceptor agonist à activation of adenyl cyclase àincreased cAMP à activation of protein kinase A à inhibits phosphorylation of myosin and decrease in intracellular calcium à bronchodilation

Increased cAMP à inhibits mast cell degranulation

Increased risk of systemic adverse effects

Inhaled salbutamol may not reach severely obstructed airways whereas IV salbutamol is systemic

Adrenaline Beta 2-adrenoreceptor agonism à bronchodilation

Inhibits mast cell degranulation

Alpha-adrenoreceptor à vasoconstriction – decreasing airway oedema and improving haemodynamics

Can be given IV as infusion, IM or nebulised

Generally, not recommended by guidelines unless associated with anaphylaxis or in cases of severe life-threatening asthma

Methylxanthines: Aminophylline, Theophylline Inhibits III and IV phosphodiesterase which is the enzyme responsible for breaking down cAMP in smooth muscle cells à increased cAMP à bronchodilation

Binds to adenosine A2B receptor à blocks adenosine mediated bronchoconstriction

Narrow therapeutic range and variable clearance

Requires monitoring of levels

Less familiarity amongst clinicians

Used more in paediatric population


Several guidelines overseas e.g. Global initiative for asthma do not recommend

Cochrane review 2012: use of IV aminophylline did not result in significant additional bronchodilation

IV Ketamine Blocks NMDA receptors à prevent bronchoconstriction

Inhibits catecholamine reuptake à increased catecholamines causing bronchodilation

Inhibition of vagal outflow

Reduction of calcium influx à direct smooth muscle relaxation

Minimal evidence of benefit from ketamine in severe asthma

Useful induction agent for the severe asthmatic

Inhaled volatile agents Block voltage gated calcium channels and reduction in calcium stores in sarcoplasmic reticulum à smooth muscle relaxation Requires anaesthetic machine

Difficulties with scavenging

Side effects include myocardial depression, arrhythmias, hypotension, intrapulmonary shunting and cerebral vasodilation


Extracorporeal support

VV ECMO or extracorporeal CO2 removal (ECCO2R)

Venous blood extracted, pumped through artificial membrane lung and  oxygenated then returned to the patient (for VV ECMO)

CO2 cleared via diffusion as a flowing or ‘sweep’ gas containing no co2 runs along other side of the membrane resulting in a diffusion gradient. of the membrane

Bridge to recovery

Requires specialised centre and expertise

Allows for minimisation of ventilator induced lung injury whilst waiting for bronchospasm to break

ECCO2R allows for smaller cannulas and lower blood flow rates



List the signs of salbutamol toxicity


  • Tremors
  • Tachycardia
  • Tachypnoea
  • Agitation


  • Hypokalaemia
  • Hyperglycaemia
  • Lactic acidosis
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