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      Deep Sedation and Atrioventricular Nodal Reentry Tachycardia Ablation

      editorial
      1 , *
      Research in Cardiovascular Medicine
      Kowsar
      AVNRT ablation, Arrhythmias, Cardiac

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          Abstract

          Cardiac ablation is an invasive procedure requiring conscious and deep sedation for immobility and analgesia. AVNRT ablation generates acute pain during the radiofrequency application. Although the success rate is high, the procedure is uncomfortable for patients who must remain motionless. Sedation in EP lab is needed for several purposes such as providing anaesthesia and airway management for cardio version during EP study and induction of atrial fibrillation, pain management, and haemodynamic monitoring. The best anaesthetic agent should not alter Electrophysiological properties including SA node, AV node functions, conduction velocities, and refractoriness. Most anaesthetic agents have not been studied in the context of EPS and most of our data were based on animal and laboratory experiments. A few investigators reported that anesthetic agents have no significant clinical effects on conduction system (1, 2). There are some reports concerning non-inducibility of AVNRT after intravenous sedation in pediatrics (3). Fazelifar et al. investigated inducibility of AVNRT and electrophysiological properties after deep sedation (4). Anesthesia with benzodiazepines and opiates used in a repeated bolus fashion can easily be provided without influencing accurate EP testing and/or arrhythmia induction. There are no known specific side-effects of benzodiazepines on cardiac conduction (1). Propofol and benzodiazepine may change heart rate via baroreflex regulatory mechanisms (5, 6). The authors demonstrated that AVNRT induction is not related to anesthetic agents and it could be performed safely in all patients who undergo slow pathway induction. Induction and ablation of reentrant arrhythmias such as AVNRT can be performed safely after deep sedation. Ablation after sedation in other supra-ventricular tachy-arrhythmias requires another well-designed randomized trial.

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          Most cited references6

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          Sympathetic responses to induction of anesthesia in humans with propofol or etomidate.

          Anesthetic induction with propofol commonly results in hypotension. This study explored potential mechanisms contributing to hypotension by recording cardiovascular responses including sympathetic neural activity from patients during induction of anesthesia with propofol (2.5 mg.kg-1 plus 200 micrograms.kg-1.min-1) or, for comparison, etomidate (0.3 mg.kg-1 plus 15 micrograms.kg-1.min-1). Twenty-five consenting, nonpremedicated, ASA physical status 1 and 2, surgical patients were evaluated. Measurements of R-R intervals (ECG), blood pressure (radial artery), forearm vascular resistance (plethysmography), and efferent muscle sympathetic nerve activity ([MSNA] microneurography: peroneal nerve) were obtained at rest and during induction of anesthesia. In addition, a sequential bolus of nitroprusside (100 micrograms) followed by phenylephrine (150 micrograms) was used to obtain data to quantitate the baroreflex regulation of cardiac function (R-R interval) and sympathetic outflow (MSNA) in the awake and anesthetized states. Etomidate induction preserved MSNA, forearm vascular resistance, and blood pressure, whereas propofol reduced MSNA by 76 +/- 5% (mean +/- SEM), leading to a reduction in forearm vascular resistance and a significant hypotension. Both cardiac and sympathetic baroslopes were maintained with etomidate but were significantly reduced with propofol, especially in response to hypotension. These findings suggest that propofol-induced hypotension is mediated by an inhibition of the sympathetic nervous system and impairment of baroreflex regulatory mechanisms. Etomidate, conversely, maintains hemodynamic stability through preservation of both sympathetic outflow and autonomic reflexes.
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            Electrophysiological Effects of Propofol on the Normal Cardiac Conduction System

            To determine the electrophysiological effects of propofol and to explain the potential mechanism(s) whereby it causes bradyarrhythmias, 10 closed-chest pigs weighing 20-25 kg were studied. Each animal was premedicated by intramuscular administration of ketamine hydrochloride, intubated, and mechanically ventilated. Femoral arterial and venous catheters were placed, and a comprehensive electrophysiologic evaluation was performed at baseline and after two doses (1 mg/kg i.v. bolus and 0.1 mg/kg/min infusion and an extra 1-mg/kg i.v. bolus and 0.2 mg/kg/min infusion) of propofol. The electrophysiological effects obtained on low- and high-dose propofol were compared to baseline values. Propofol caused a dose-related decrease in sinus cycle length (baseline 565 ± 36 ms, low-dose propofol 541 ± 28, high-dose propofol 527 ± 26 ms; p < 0.05), a prolongation of the corrected sinus node recovery time (baseline 119 ± 35 ms, low-dose propofol 126 ± 32, high-dose propofol 130 ± 30 ms; p < 0.01), and an increase in the His-ventricular interval (baseline 33 ± 4 ms, low-dose propofol 36 ± 4, high-dose propofol 40 ± 3 ms; p < 0.005). All other electrophysiological parameters remained unchanged, and there were no cases of spontaneous atrioventricular block or sinus pauses. We conclude that propofol causes dose-related depression of sinus node and His-Purkinje system functions, but has no effect on the atrioventricular node function and on the conduction properties of atrial and ventricular tissues in normal pig hearts.
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              Effects of propofol or isoflurane anesthesia on cardiac conduction in children undergoing radiofrequency catheter ablation for tachydysrhythmias.

              To determine suitability for ablation procedures in children, two commonly used anesthetic agents were studied: propofol and isoflurane. Twenty patients presenting for a radiofrequency catheter ablation procedure were included and randomly assigned to two groups. A baseline electrophysiology study was performed during anesthesia with thiopental, alfentanil, nitrous oxide, and pancuronium in all patients. At the completion of the baseline electrophysiology study (EPS), 0.8-1.2% isoflurane was administered to patients in group 1 and 2 mg/kg propofol bolus plus an infusion of 150 micrograms.kg-1.min-1 was administered to patients in group 2. Nitrous oxide and pancuronium were used throughout the procedure. After 30 min of equilibration, both groups underwent a repeat EPS. The following parameters were measured during the EPS: cycle length, atrial-His interval, His-ventricle interval, corrected sinus node recovery time, AV node effective refractory period, and atrial effective refractory period. Using paired t tests, the electrophysiologic parameters described above measured during propofol or isoflurane anesthesia were compared to those measured during baseline anesthesia. Statistical significance was accepted as P < 0.05. There was no statistically significant difference in the results obtained during baseline anesthesia when compared with those measured during propofol or isoflurane anesthesia. Neither propofol nor isoflurane anesthesia alter sinoatrial or atrioventricular node function in pediatric patients undergoing radiofrequency catheter ablation, compared to values obtained during baseline anesthesia with alfentanil and midazolam.
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                Author and article information

                Journal
                Res Cardiovasc Med
                Res Cardiovasc Med
                10.5812/cardiovascmed
                Kowsar
                Research in Cardiovascular Medicine
                Kowsar
                2251-9572
                2251-9580
                28 October 2013
                November 2013
                : 2
                : 4
                : 180
                Affiliations
                [1 ]Cardiac Electrophysiology Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, IR Iran
                Author notes
                [* ]Corresponding author: Abolfath Alizadeh-Diz, Department of Cardiology, Rajaie Cardiovascular Medical and Research Center, Vali-Asr Ave, Niayesh Blvd, Tehran, IR Iran. Tel: +98-2123922164, E-mail: alizadeh_73@ 123456yahoo.com
                Article
                10.5812/cardiovascmed.15032
                4253780
                25478519
                47f92e85-b0d2-41d1-808e-445dcd49e5fa
                Copyright © 2013, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran; Published by Kowsar Corp.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 24 September 2013
                : 24 September 2013
                Categories
                Editorial

                avnrt ablation,arrhythmias, cardiac
                avnrt ablation, arrhythmias, cardiac

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