This study provides a review of the contemporary literature for the effects of most commonly used anesthetic drugs for sedation and anesthesia during adult electrophysiologic (EP) studies where supraventricular tachycardias (SVT) need to be induced for diagnostic purposes and/or catheter ablation. Some medications may affect cardiac electrophysiology and conduction, altering the ability to induce the arrhythmia, and may have negative impact on mapping and ablation treatment. The objective of the study is to determine the best sedative choice during SVT ablations. The authors searched MEDLINE, PubMed, and Google Scholar databases for published articles within the past 20 years (1998‐2018) that have evaluated the effects of common anesthetic drugs during SVT ablations. Further articles were identified through crossreferencing, discussion with electrophysiologists, and hand‐searching key electrophysiology and anesthesia journals. Eight review articles, two randomized control trials, six prospective observational studies, one retrospective observational study, and two case reports were included in this review. Seven of the studies focused on the pediatric population. The findings about the effects of the commonly used anesthetics are discussed further in detail. Sevoflurane had no clinically important effects on sinoatrial (SA) node activity, or the normal atrioventricular (AV), or accessory pathway. Midazolam and fentanyl, alone or in combination, neither alter the inducibility of reentrant tachycardia nor have they shown to affect the SA node, refractory periods of AV conduction, or accessory pathways. Similar findings were reported by investigators with propofol, except for ectopic atrial tachycardia in children, which remained un‐inducible in one of the studies. Remifentanil and dexmedetomidine lengthened both sinus cycle and AV conduction. Dexmedetomidine increased the atrial refractory period and diminished atrial excitability. Ketamine shortened atrial conduction and successfully returned prolongation of sinus node conduction due to dexmedetomidine. In conclusion, the current literature regarding sedation for SVT studies in the adult population is sparse. Midazolam, propofol, fentanyl, and remifentanil can be used safely in patients undergoing EP studies without significant interference with electrophysiological variables or the inducibility of reentrant tachycardias in usual clinical doses. Low‐dose ketamine has potential use as an adjunctive medication in the EP lab and additional studies would be beneficial. The effects of dexmedetomidine on conduction and arrhythmia inducibility during SVT ablation is not as clear as studies have yielded conflicting results, and may not be the best choice for sedation in this patient population.

Cerebral oxygen saturation (rSO2) is a non-invasive monitor used to monitor cerebral oxygen balance and perfusion. Decreases in rSO2 >20 % from baseline have been associated with cerebral ischemia and increased perioperative morbidity. During transcatheter aortic valve replacement (TAVR), hemodynamic manipulation with ventricular pacing up to 180 beats per minute is necessary for valve deployment. The magnitude and duration of rSO2 change during this manipulation is unclear. In this small case series, changes in rSO2 in patients undergoing TAVR are investigated. Ten ASA IV patients undergoing TAVR with general anesthesia at a university hospital were prospectively observed. Cerebral oximetry values were analyzed at four points: pre-procedure (baseline), after tracheal intubation, during valve deployment, and at procedure end. Baseline rSO2 values were 54.5 ± 6.9 %. After induction of general anesthesia, rSO2 increased to a mean of 66.0 ± 6.7 %. During valve deployment, the mean rSO2 decreased <20 % below baseline to 48.5 ± 13.4 %. In two patients, rSO2 decreased >20 % of baseline. Cerebral oxygenation returned to post-induction values in all patients 13 ± 10 min after valve deployment. At procedure end, the mean rSO2 was 67.6 ± 8.1 %. As expected, rapid ventricular pacing resulting in the desired decrease in cardiac output during valve deployment was associated with a significant decrease in rSO2 compared to post-induction values. However, despite increased post-induction values in all patients, whether related to increased inspired oxygen fraction or reduced cerebral oxygen consumption under anesthesia, two patients experienced a significant decrease in rSO2 compared to baseline. Recovery to baseline was not immediate, and took up to 20 min in three patients. Furthermore, baseline rSO2 in this population was at the lower limit of the published normal range. Significant cerebral desaturation during valve deployment may potentially be limited by maximizing rSO2 after anesthetic induction. Future studies should attempt to correlate recovery in rSO2 with recovery of hemodynamics and cardiac function, provide detailed neurological assessments pre and post procedure, determine the most effective method of maximizing rSO2 prior to hemodynamic manipulation, and provide the most rapid method of recovery of rSO2 following valve deployment.