Evaluation of Ketamine's Impact on Vasopressor Requirements in Critically Ill Patients: A Retrospective Cohort Study.

Background: Ketamine is a commonly used sedative agent for procedural sedation and rapid sequence intubation. Ketamine can also be administered via continuous infusion as an adjunct agent for sedation and analgesia in mechanically ventilated patients requiring high levels of sedation. In individuals who are not catecholamine-depleted, ketamine induces the release of norepinephrine, epinephrine, and dopamine, leading to transient increases in cardiovascular function. This mechanism suggests that ketamine, when used as a sedative agent, could potentially reduce vasopressor requirements in patients undergoing vasopressor therapy to maintain stable hemodynamics while needing high levels of sedation. The existing literature on continuous infusion ketamine's effect on vasopressor requirements is conflicting, with some studies reporting potential benefit and others showing no clinical difference. Methods: This retrospective cohort study was conducted at Saint Joseph Hospital, a 433 bed community hospital located in Lexington, KY. The study included mechanically ventilated patients admitted between August 7, 2018, and December 31, 2024 who received a vasopressor agent for at least 3 hours for hemodynamic support prior to the initiation of continuous infusion ketamine, and received both ketamine and vasopressors concomitantly for at least 3 hours. To be included, patients must have also been receiving vasopressors at a dose ≥0.1 mcg/kg/min norepinephrine equivalents (NEE). The primary outcome was change in vasopressor requirements in critically ill patients at 6, 12, 24 hours after initiation of a continuous ketamine infusion as an adjunct sedative. Purpose: The purpose of this research is to investigate whether the use of ketamine as an adjunct sedative and analgesic agent can decrease vasopressor requirements in critically ill patients. Results: Forty-one patients met inclusion criteria. There was a difference in mean vasopressor requirements from baseline to 6, 12, 24, hours after continuous ketamine infusion initiation (P = .035). Mean vasopressor requirements decreased from 0.218 NEE at baseline to 0.186 NEE at 6 hours (P = .002), 0.145 NEE at 24 hours (P = .022). Conclusion: Based on the results of this study, continuous infusion ketamine can reduce mean vasopressor requirements when used as an adjunct sedative in mechanically ventilated patients.