A silent chest, a rising CO2 and a request for non-invasive ventilation
A 27-year-old woman with asthma since childhood is brought by her sister after three days of a viral illness. She has taken six salbutamol puffs in the last two hours and can no longer complete a sentence. She is agitated and intermittently drowsy, sitting bolt upright and using accessory muscles. RR 34, HR 138, SpO2 88% on a 15 L non-rebreather mask, peak expiratory flow unrecordable, chest quiet with minimal wheeze. In the resuscitation bay she has received three back-to-back salbutamol 5 mg nebulisers with ipratropium, IV hydrocortisone 200 mg and magnesium sulfate 2 g over 20 minutes. Arterial blood gas on 15 L: pH 7.21, pCO2 58 mmHg, pO2 61 mmHg, bicarbonate 22 mmol/L. She is becoming harder to rouse. The registrar suggests another round of nebulisers and a trial of non-invasive ventilation before calling anaesthesia.
1. Explain why the pCO2 of 58 mmHg is the decisive finding, and why non-invasive ventilation is the wrong next step.
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Why the CO2 matters. A patient with acute severe asthma hyperventilates; the pCO2 should be low. A pCO2 that is normal (35–45) already signals failing respiratory effort, and a pCO2 of 58 with pH 7.21 marks a life-threatening, peri-arrest attack - the respiratory muscles can no longer sustain the work of breathing. It is not an improvement, and it is not a reason to wait.
Supporting signs in this patient. Silent chest (too little air moving to generate wheeze), SpO2 88% on 15 L, exhaustion, agitation alternating with drowsiness, and unrecordable peak flow. Every one of these is a criterion for imminent respiratory arrest.
Why not non-invasive ventilation.
- There is no evidence of benefit in acute asthma, and guidelines advise against it outside trials; it is used in COPD, not asthma.
- It does not stent open bronchospastic airways, and it does not solve expiratory flow limitation, so dynamic hyperinflation continues.
- It requires a cooperative patient. This woman is drowsy - gastric insufflation, aspiration and delay are the likely outcomes.
- Most importantly, each extra nebuliser cycle is time lost. The correct next step is immediate, senior-led intubation with anaesthesia and critical care present, in a resuscitation area with equipment and drugs prepared for a difficult airway.
2. State your induction plan and the first ventilator settings with numbers, and explain what each choice is protecting against.
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Before induction. Preoxygenate with a tight-fitting mask; have a 500 mL crystalloid bolus running, because these patients become profoundly hypotensive after induction and positive pressure; prepare suction, a bougie, and a second operator; consider an arterial line and a nasogastric tube afterwards.
Induction. Ketamine 1–2 mg/kg IV (bronchodilator, preserves blood pressure) with rocuronium 1.2 mg/kg for rapid sequence intubation. Avoid a high-dose propofol induction in a hypovolaemic, exhausted patient.
Ventilator settings (volume-controlled, predicted body weight ~60 kg → ~420–480 mL):
- Tidal volume 6–8 mL/kg predicted body weight.
- Respiratory rate 8–10/min - deliberately low; the expiratory time, not the minute volume, is what prevents harm.
- PEEP 0–5 cmH2O; high PEEP worsens air trapping.
- Inspiratory:expiratory ratio 1:4 to 1:5, achieved with an inspiratory flow of 60–80 L/min and a square waveform to shorten inspiratory time.
- FiO2 1.0 initially, titrated to SpO2 92–96%.
- Plateau pressure <30 cmH2O, peak pressure accepted up to ~50 if the plateau is acceptable.
Accept permissive hypercapnia down to a pH of about 7.15–7.20. Chasing a normal pCO2 means increasing the rate, which shortens expiration, increases auto-PEEP and causes hypotension and barotrauma. Continue inhaled salbutamol through the circuit, deepen sedation, and consider paralysis for the first 24 hours.
3. Ten minutes after intubation the blood pressure is 70/40 mmHg, peak airway pressure 55 cmH2O and plateau pressure 34 cmH2O. Give your ordered actions.
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Working diagnosis: dynamic hyperinflation (auto-PEEP) with sedation-related vasodilation. The plateau of 34 indicates a high alveolar pressure, and the high peak–plateau gradient reflects airway resistance. In this setting, the blood pressure should be restored by emptying the lungs, not by flooding the patient with fluid.
Order of actions.
- FiO2 1.0, then disconnect the endotracheal tube from the circuit for 30–60 seconds to let trapped gas escape. A rapid rise in blood pressure confirms the diagnosis.
- Reduce respiratory rate to 6–8/min, shorten inspiratory time and lengthen expiration, reduce tidal volume towards 6 mL/kg, and keep PEEP at 0–5.
- Check for asymmetry or sudden change in compliance - if a tension pneumothorax is suspected, needle-decompress immediately before any imaging.
- Deepen sedation; add neuromuscular blockade if dyssynchrony persists. Small fluid bolus and a vasopressor (noradrenaline) if pressure remains low after decompression.
- Continue bronchodilators through the circuit, IV magnesium, and consider a ketamine infusion.
If it remains refractory: volatile anaesthetic (sevoflurane) via the ventilator circuit, or extracorporeal support, in a critical care unit. A chest radiograph and arterial blood gas follow the resuscitation, not precede it.