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.

No abstract

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.

No abstract

IntroductionThe opiate antagonist, naloxone, which is associated with prolonged survival in animal models of shock, has been demonstrated to increase arterial pressure and cardiac output. It is possible that the increase in cardiac output is due to a decrease in volume in the total capacitance vasculature and a subsequent increase in venous return. Because the influence of naloxone on the capacitance vasculature is unknown, the present study was undertaken to determine the influence of naloxone on intravascular volume in the total capacitance circulation. Other investigators have observed prolonged survival with naloxone administration in various hypotensive experimental conditions including endotoxin shock (1) and hypovolemic shock (2-4). The prolonged survival may be related to increases in cardiac contractility, cardiac output, and mean arterial pressure, which have been observed after administration in hypotensive animals (1-9) or patients (10, 11). It is also possible that the increases in cardiac output and arterial pressure are due, in part, to a decrease in capacitance volume; however, capacitance volume changes have not been previously examined.Hence, the present study was undertaken in order to assess the influence of naloxone administration on the total capacitance vasculature. A venous bypass preparation was employed to determine regional and total intravascular volume changes and the extent to which these changes are mediated by direct, neurogenic, and hormonal influences. MethodsVenous bypass preparation. 31 mongrel dogs of either sex, weighing between 11 and 18 kg (mean 14±0 kg) were anesthetized with chloralose (60-80 mg/kg iv) and urethan (600-800 mg/kg iv), intubated, and ventilated with a mixture of room air and 100% oxygen. A median sternotomy was performed and 3,000 U of sodium heparin was administered iv. The experimental preparation utilized in dogs 1-10 is illustrated in Fig. 1. The azygos vein was ligated and the superior and inferior vena cavae were cannulated with no. 32 or 34 French catheters. The total systemic venous return was drained to an overflow column and central venous pressure was adjusted by setting the height of the column at 5 cm H20 with the right atrium as a reference point. The venous return was drained from the overflow column into a 2-liter no. 2022 graduated cylinder (Corning Glass Works, Corning, NY), which had 20-ml graduations. The draihage from the overflow column into the reservoir was sufficiently rapid to prevent accumulation of blood in the overflow column. From the 2-liter graduated cylinder, blood was pumped (Travenol perfusion pump, Travenol Laboratories, Inc., Morton Grove, IL) to the right atrium via a no. 26 French catheter in the right atrial appendage at a constant rate of 350-800 ml/min (mean 579±26 ml/min, 89% of the perfusion rates were between 500 and 800 ml/min). Because blood was returned to the animal at a constant rate, it was possible to record changes in volume in the total capacitance vasculature as reciprocal changes in volume in...