Bronchospasm on the Table: Deepen the Gas, Reach for the IV, or Reach for Epinephrine
Airway pressures climb the moment the surgeon starts working near his diaphragm. Under general anesthesia, with no patient to ask about their breathing, the usual asthma-attack escalation ladder doesn't apply the same way.
P.G., a 34-year-old man with a history of moderate persistent asthma, last well-controlled on his home inhaled corticosteroid/long-acting beta-agonist combination, is under general anesthesia for a laparoscopic cholecystectomy when peak inspiratory pressures climb from a baseline 18 to 34 cmH2O within two minutes of the surgeon beginning subdiaphragmatic dissection — a recognized bronchospasm trigger from vagal stimulation near the diaphragm. His end-tidal CO2 waveform shows the classic upsloping "shark-fin" pattern of expiratory airflow obstruction, and his oxygen saturation, which had been a comfortable 98%, is drifting down through 93%.
Managing bronchospasm under general anesthesia is genuinely different from managing an awake asthma exacerbation, and not simply because the drugs available differ: there is no patient to report worsening dyspnea, no accessory-muscle use to watch develop over minutes, and no reliable auscultatory exam once positive-pressure ventilation and surgical draping are both in the way — the usual clinical signals an awake escalation ladder relies on to calibrate pace simply aren't available. Sevoflurane, already running, has real bronchial smooth-muscle relaxant activity of its own — Rooke's comparison of the volatile agents measured respiratory system resistance directly after intubation and found sevoflurane reduced it, which is why deepening the agent already in the circuit is a genuine first move rather than a stalling one. Worth marking where that evidence stops: Rooke studied 1.1 MAC, and P.G. is already running at 1.2, so going deeper is extrapolation past the concentration actually tested, in a man whose blood pressure has to absorb it; inhaled albuterol delivered through the circuit targets the beta-2 receptor mechanism more specifically, but its actual delivery to a bronchospastic airway under positive-pressure ventilation is less certain than in a spontaneously breathing patient, since much of a nebulized or MDI dose can be lost to the circuit and ETT rather than reaching distal airways efficiently.
He'd told the pre-operative team, almost as a joke, that laparoscopic surgery "tickles his asthma a little" based on a prior unrelated procedure years earlier — a detail buried in the pre-anesthesia note that turns out, in hindsight, to have been the single most useful line in his entire chart. It's exactly the kind of patient-reported pattern that an awake history can capture and a purely objective monitor cannot, which is part of why the team had already flagged him as bronchospasm-risk before the case started rather than being caught entirely by surprise when the pressures climbed.
Intraoperatively, two minutes into the event
Deepen the sevoflurane first — it's already running and has real direct bronchial smooth-muscle relaxant activity of its own, so this is the fastest available step with no new drug or delivery route needed. I'm going to 1.5 MAC now, and higher only if the pressures don't answer — Rooke's data stop at 1.1, and I'd rather not buy airway resistance with blood pressure in a man who currently has plenty of the second.
I'd add inhaled albuterol through the circuit in parallel, not wait to see if volatile alone resolves it — the two work through genuinely different mechanisms, and delivery through a bronchospastic airway under positive-pressure ventilation is less reliable than it would be in a spontaneously breathing patient, so starting it now rather than as a second step doesn't cost us anything if volatile alone turns out to be enough.
Both reasonable as first moves — but I'd flag the threshold for the next step explicitly, because we have none of the usual signals an awake asthma escalation relies on to calibrate pace. If his saturation or airway pressures haven't clearly turned around within the next two to three minutes, move to IV epinephrine without further delay rather than working slowly up the ladder the way we would with an awake, communicative patient telling us how they feel.
Agreed: sevoflurane deepened to 2.0 MAC and albuterol given through the circuit simultaneously rather than sequentially. Airway pressures and oxygenation began improving within ninety seconds and normalized over the following four minutes; epinephrine was never required. Surgery proceeded to completion without further bronchospastic events.
The team flagged for his post-operative record that a lower threshold for epinephrine had been explicitly agreed in advance rather than improvised in the moment — noted as the specific practice worth carrying into future cases with his asthma history, regardless of whether epinephrine was ultimately needed this time.