Peri-intubation hypotension is bad. We must look for predictors and work to prevent this from happening.
Mitigating Peri-intubation Hypotension
Peri-intubation hypotension carries significant morbidity and mortality in emergency airway management of the critically ill. Several studies have shown that hypotension before intubation carries significant risk of cardiac arrest (OR 3.4), and post-intubation hypotension is fairly common (as high as 22%) with in-hospital mortality up to 35%. Furthermore, and arguably the most specific marker for risk of cardiac arrest is the shock index. The shock index is defined as the heart rate divided by the systolic blood pressure and is known to be associated with poor outcomes in many clinical scenarios. In the context of airway management, a shock index of >0.8 has been repeatedly demonstrated to carry a risk of post-intubation hypotension with odds ratio as high as 55.
Why do patients become hypotensive? Several factors have been identified and theorized to contribute to peri-intubation as potential mechanisms:
- Sedative medications
- Loss of adrenergic tone
- Vasoplegia as a direct effect of induction medications
- Transition to positive pressure ventilation
- Worsening acidosis due to the apneic period
What interventions exist to prevent cardiovascular collapse during intubation?
Correct reversible causes of hypotension
A thorough workup and identification of reversible causes of shock should always precede an intubation that is not truly emergent. Different clinical scenarios will dictate the amount of clinical investigation that can occur prior to intubation however identifying a massive PE or tamponade could drastically change your intubation strategy and pre-intubation optimization.
Although an IV fluid bolus is a common maneuver to mitigate peri-intubation hypotension, there’s a lack of substantial evidence to promote its practice in the critically ill. The only study to date, a pragmatic trial, was recently published and demonstrated no significant difference in a composite of new hypotension, new or increased vasopressor use, cardiac arrest or death. This study also demonstrated that when providers “hang fluids for intubation,” only a median of 200cc of fluids is received by the patient. While perhaps not entirely definitive, looking elsewhere to prevent hemodynamic collapse is probably the pragmatic choice.
Avoid induction agents known to cause hypotension
Propofol is well known to cause peri-intubation hypotension due to its effect on systemic vascular resistance and myocardial contractility. While many studies have demonstrated this point, one of such demonstrated a drop in systolic blood pressure from a median of 126 to 93mmHg, representing a >25% reduction. Similarly, midazolam is also well known to induce hypotension, with one comparison trial between midazolam and etomidate finding 19.5% of patients receiving midazolam had hypotension and an average of 10% reduction in MAP.
Etomidate is hemodynamically neutral, making it a strong choice for emergent intubations. Perhaps even more favorable, ketamine increases blood pressure and heart rate by blocking the reuptake of catecholamines. Ketamine has repeatedly been shown to increase heart rate (20-34%), systolic blood pressure (22-26%) and MAP (23-30%). While ketamine receives scrutiny for induction in the intubation of hypertensive emergencies, its profile is ideal for the critically ill.
Alternatively, a combination of 0.5mg/kg propofol and 0.5mg/kg ketamine, “ketofol”, was recently shown to have no significant difference in mean arterial pressure when compared to etomidate in a prospective, randomized trial of 152 patients. While hemodynamically neutral, the additional step of combining medications may be less desirable.
The most reliable method of correcting hypotension prior to induction is with the use of vasopressors. In emergent intubations with risk of cardiovascular collapse, vasopressors can be safely administered via peripheral IV or IO if central access is not available. While norepinephrine remains the first line vasopressor for most states of shock, phenylephrine and epinephrine are reasonable choices. Push-dose epi and epinephrine drips have been popularized and many guides are available for bedside concoction. Alternatively, starting a drip of norepinephrine may be equally as rapid in a well-prepared ED or ICU. In patients at risk of decompensation, starting with a safe buffer, such as MAP of >80 may be prudent.
Knowing that peri-intubation hypotension carries a substantial risk for morbidity and mortality, having a strong strategy for mitigating a hypotensive intubation should always be part of your airway strategy.
- Consider the pathophysiology specific to your patient, choose an intubation strategy to protect your patient from hemodynamic collapse
- Choose ideal induction agent that fits your intubation and hemodynamic needs
- Consider early and aggressive use of vasopressors to mitigate hypotension
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