Ketamine is not associated with more post-intubation hypotension than etomidate in patients undergoing endotracheal...

Emergency department (ED) patients undergoing emergent tracheal intubation often have multiple physiologic derangements putting them at risk for post-intubation hypotension. Prior work has shown that post-intubation hypotension is independently associated with increased morbidity and mortality. The choice of induction agent may be associated with post-intubation hypotension. Etomidate and ketamine are two of the most commonly used agents in the ED, however, there is controversy regarding whether either agent is superior in the setting of hemodynamic instability. The goal of this study is to determine whether there is a difference in the rate of post-intubation hypotension who received either ketamine or etomidate for induction. Additionally, we provide a subgroup analysis of patients at pre-existing risk of cardiovascular collapse (identified by pre-intubation shock index (SI) > 0.9) to determine if differences in rates of post-intubation hypotension exist as a function of sedative choice administered during tracheal intubation in these high-risk patients. We hypothesize that there is no difference in the incidence of post-intubation hypotension in patients who receive ketamine versus etomidate.

A retrospective cohort study was conducted on a database of 469 patients having undergone emergent intubation with either etomidate or ketamine induction at a large academic health system. Patients were identified by automatic query of the electronic health records from 1/1/2016-6/30/2019. Exclusion criteria were patients <18-years-old, tracheal intubation performed outside of the ED, incomplete peri-intubation vital signs, or cardiac arrest prior to intubation. Patients at high risk for hemodynamic collapse in the post-intubation period were identified by a pre-intubation SI > 0.9. The primary outcome was the incidence of post-intubation hypotension (systolic blood pressure < 90 mmHg or mean arterial pressure < 65 mmHg). Secondary outcomes included post-intubation vasopressor use and mortality. These analyses were performed on the full cohort and an exploratory analysis in patients with SI > 0.9. We also report adjusted odds ratios (aOR) from a multivariable logistic regression model of the entire cohort controlling for plausible confounding variables to determine independent factors associated with post-intubation hypotension.

A total of 358 patients were included (etomidate: 272; ketamine: 86). The mean pre-intubation SI was higher in the group that received ketamine than etomidate, (0.97 vs. 0.83, difference: -0.14 (95%, CI -0.2 to -0.1). The incidence of post-intubation hypotension was greater in the ketamine group prior to SI stratification (difference: -10%, 95% CI -20.9% to -0.1%). Emergency physicians were more likely to use ketamine in patients with SI > 0.9. In our multivariate logistic regression analysis, choice of induction agent was not associated with post-intubation hypotension (aOR 1.45, 95% CI 0.79 to 2.65). We found that pre-intubation shock index was the strongest predictor of post-intubation hypotension.

In our cohort of patients undergoing emergent tracheal intubation, ketamine was used more often for patients with an elevated shock index. We did not identify an association between the incidence of post-intubation hypotension and induction agent between ketamine and etomidate. Patients with an elevated shock index were at higher risk of cardiovascular collapse regardless of the choice of ketamine or etomidate.