Postintubation hypotension in the critically ill: An (un)necessary evil?
We read with great interest the article published by Green et al. demonstrating an important association between postintubation hypotension and increased mortality in the critically ill trauma population.1 We are eager to raise an important issue to further the discussion: the danger of administering drugs to facilitate intubation in hypoxemic and hypotensive patients, which may induce apnea and exacerbate hypotension. Indeed, control of the airway is of prime importance, but this may be achieved without adverse hemodynamic consequences if pharmacology is limited. We advocate for an awake intubation attempt in the critically ill.
Endotracheal intubation in the operating room and acute care settings are very different procedures, but this is not always recognized. The critically ill patient should be evaluated as having a physiologically difficult airway,2 in contrast to the traditional difficult airway evaluated in the operating room. These intubations usually occur in an unstable patient, often with a short period of time to allow for evaluation and planning, and in an environment not always ideally suited to airway management.
As demonstrated in the current analysis, even at reduced doses, traditional use of induction agents is associated with a significant risk of postintubation hypotension. This association underscores the importance of peri-intubation fluid resuscitation, suggesting that postintubation hypotension is a marker of inadequate volume loading before the administration of drugs and positive pressure, which reduce preload and exacerbate hypotension.
Compounding drug-induced hypotension, we must not forget that inducing apnea for intubating the critically ill patient is of major concern for several reasons. Unlike the elective patient who can withstand 6 to 8 minutes of apnea if preoxygenated, the arterial saturation rarely rises with preoxygenation and apnea induces rapid desaturation.3 Compensatory hyperventilation is lost, and acidosis worsens during apnea; this acidosis may reduce peripheral vascular resistance and cardiac contractility and significantly exacerbates hypotension.
The patients of Green et al.1 were severely ill (78% of patients with injury severity scores >12), yet most patients received general anesthetic inductions with hypnotic agents (e.g., mean propofol dose of approximately 100 mg) and neuromuscular blockers. The classical “hemodynamically stable” agents such as ketamine and etomidate still induce hypotension with very deep sedation, and indeed a significant number of patients in the postintubation hypotension group received ketamine for induction. Furthermore, the administration of rapidly acting paralytics may still be fraught with danger, especially when used by nonexperienced intubators. In this analysis, 85% of intubations were performed by non–airway experts, and it is unclear if any of the 15% “staff” intubations were performed by anesthesiologists.
Intubating the critically ill patient while maintaining spontaneous respiration reduces the risk of worsening hypotension and hypoxemia and allows time for expert personnel to assist if initial attempts fail. This is in contrast to the current practice, where the initial approach is almost always induction of deep sedation (with significant risk of hypotension) with or without paralysis (inducing apnea). It is commonly rationalized that the use of sedation and neuromuscular blockade during intubation in the critically ill is that paralysis improves the rate of successful first or second attempt, and that the complication rate of intubation increases with multiple attempts. This rationale, however, fails to acknowledge that drug-induced hypotension and hypoxemia are the catalysts for such complications.
In some agitated patients, the awake approach will not be possible. The critically ill patient, due to hypotension, hypoxemia, sepsis, or hypercapnia, will have a reduced level of awareness and usually can be intubated with minimal sedation and topicalization. In healthy patients, direct laryngoscopy is usually possible with minimal sedation.