(981) Risk Factors for Hemodynamic Changes in Critically Ill Adult Patients Receiving Intravenous Ketamine

Introduction: Ketamine is a rapid-acting anesthetic used in critically ill patients due to its favorable sympathomimetic effects. Hypotension (HOTN) with ketamine administration has been described in patients with presumed depletion of endogenous catecholamines, but other risk factors related to ketamine-induced hemodynamic (HD) derangements remain unclear. The purpose of this study is to identify risk factors (RF) associated with HD changes following intravenous ketamine administration.

Methods: This retrospective, single-center, cohort study included patients admitted to the ICU or ED that received ketamine. Patients were grouped in either high (HSI) or low (LSI) shock index cohorts. Shock index was calculated by dividing maximum HR by lowest SBP [HSI ≥0.9 BPM/mmHg and LSI < 0.9 BPM/mmHg]. The primary outcome assessed rates of clinically significant HOTN. Secondary outcomes compared rates of hypertension (HTN), tachycardia, bradycardia, and vasopressor use between cohorts as a time dependent analysis up to 24 hours after ketamine administration. A multivariate regression was performed to identify independent RF for HD changes after ketamine administration.

Results: A total of 111 patients (HSI n=66 vs LSI n=45) were included. HSI patients were older (HSI 55.9±14.6 vs LSI 48.1±18.7 years; p=0.02) and had higher Simplified Acute Physiology Scores (SAPS) II (HSI 61.1±16.1 vs LSI 50.4±17.9; p=0.002). The HSI cohort had a higher percentage of vasopressor use at baseline and required higher rates of initiation or increased doses of existing vasopressors after ketamine administration compared to LSI. HSI patients were more likely to experience HTN up to 24 hours after ketamine (p < 0.05), but there were no significant differences in tachycardia, bradycardia, or HOTN between cohorts. SAPS II, history of HTN, and weight were associated with ketamine-induced HTN. A history of HTN was an independent RF for ketamine-induced HTN (OR 2.65 [95% CI 1.10-6.38]). There were no independent RFs identified for ketamine-induced HOTN.

Conclusions: Changes in HD were common after ketamine administration, however assessing the true contribution of ketamine-induced effects is difficult. Having a history of HTN was an independent RF for developing HTN after ketamine administration.