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Research Snapshot Theater: Cardiovascular, Adult VII

Dexmedetomidine on the Incidence of Supraventricular Tachycardia in Critical Illness

Monday, March 23, 2026
11:30 AM - 12:30 PM Central Time
Location: Connections Central - RST 02
Introduction: Supraventricular tachycardia (SVT) in critically ill patients is linked with poor outcomes. Dexmedetomidine (DEX) is a sedative with potential anti-arrhythmic properties. Prior studies have shown inconsistent results of DEX on postoperative SVT. Furthermore, DEX’s role on SVT is underexplored in the mixed ICU setting. This study evaluates the effect of DEX on SVT in a broad, critically ill, mechanically ventilated (MV) population.


Methods: This retrospective study used data from electronic health records of MV adults admitted to ICUs in a US Midwest center from 7/1/2018 to 10/30/2022. Patients were divided into DEX and no DEX exposure cohorts. Time-dependent propensity scores were calculated hourly with time-variant covariates (vitals, labs, sedation level, Sequential Organ Failure Assessment [SOFA] scores) and time-invariant covariates (demographics, comorbidity indices). Using time-dependent propensity scores, we paired cohorts with a risk-set, greedy matching algorithm. Risk of clinically significant SVT (defined as a heart rate > 100 bpm and administration of intravenous anti-arrhythmic drugs) was assessed using Cox proportional hazard ratio.


Results: After 1:1 matching of 17,939 total patients, 7281 patients in the DEX cohort were compared to 7281 patients in the no DEX cohort. Covariates of matched pairs were similar, including SOFA scores (median [IQR], DEX: 8.0 [5.5-10.0] vs no DEX: 9.0 [6.0-11.0]) and time of propensity matching (DEX: 0.7 [0.1-2.0] days from ICU admission vs no DEX: 0.7 [0.2-2.0]). The DEX cohort received the drug 0.56 [0.07-1.94] days post-intubation with a cumulative dose of 0.55 [0.14-2.13] mg over a duration of 0.64 [0.18-1.86] days. The DEX group was associated with increased risk of clinically significant SVT (1617 patients [22.2%] vs 1187 patients [16.3%], hazard ratio 1.39 [95% CI, 1.29-1.50]. Time to clinically significant SVT after DEX cessation was 0.34 [0.03-1.41] days.


Conclusions: DEX exposure was associated with increased risk of SVT in a heterogeneous population of critically ill MV patients. Increased risk of SVT may be due to removal of nodal activity blockade or rebound effect of DEX. To our knowledge, this is the largest study to date assessing the impact of DEX on SVT and highlights the need to further elucidate this relationship.