Dexmedetomidine (Dex) is an attractive agent for procedural sedation due to its unique pharmacodynamic profile, specifically affording predictable sedation without concurrent respiratory depression. However, Dex has previously been reported to prevent or terminate arrhythmias. The purpose of this study was to investigate paroxysmal supraventricular tachycardia (PSVT) inducibility and homeostatic stability during electrophysiology studies (EPSs) and ablation when a standardized Dex protocol was used as the primary sedation agent.
We performed a retrospective review of 163 consecutive procedures for PSVT ablation that received Dex as the primary sedative with adjunct fentanyl and midazolam boluses (DEX-FENT-MIDAZ). This cohort was compared to 163 consecutive control procedures wherein strictly fentanyl and midazolam were used for sedation. The primary outcome reviewed was PSVT inducibility assessed before ablation. Reviewed secondary outcomes included level of sedation and intraprocedure hemodynamics and oxygenation.
The arrhythmia profiles of the DEX-FENT-MIDAZ and control cohorts were very similar. The overall incidence of a “negative” EPSs in which arrhythmia was not induced was 24% in the DEX-FENT-MIDAZ group and 26% in the control group (P = .7). Unintended deep sedation was significantly less with DEX-FENT-MIDAZ (4.3% vs 27%; P ≤ .0001). However, DEX-FENT-MIDAZ use was associated with a higher incidence of intraprocedure hypotension.
Dex sedation during EPSs is not associated with a reduction in PSVT inducibility. The therapeutic utility of Dex during EPS arises from the predictable sedation Dex affords but is associated with an increased incidence of intraprocedure hypotension.
From the *Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University (OHSU), Portland, Oregon
†Division of Biostatistics, OHSU-Portland State University (PSU) School of Public Health, Portland, Oregon
‡Division of Cardiology, Veterans Affairs Portland Health Care System, Portland, Oregon
§Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon.
Published ahead of print 11 April 2018.
Accepted for publication February 5, 2018.
The authors declare no conflicts of interest.
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This material is the result of the work supported with resources and the use of facilities at the Veterans Affairs Portland Health Care System. The contents do not represent the views of the US Department of Veterans Affairs or the US Government. The STrengthening the Reporting of OBservational studies in Epidemiology (STROBE) guidelines for reporting observational studies were followed while conducting this study and for preparation of this manuscript.
Reprints will not be available from the authors.
Address correspondence to Peter M. Jessel, MD, Division of Cardiology, Veterans Affairs Portland Health Care System, 3710 SW US Veterans Hospital Rd, Portland, OR 97239. Address e-mail to JesselP@ohsu.edu.