John L. Atlee

Mechanisms for cardiac dysrhythmias during anesthesia.

The review has two major sections. The first considers normal and abnormal electrical activity of the heart, and the second discusses anesthetic and adjunct drug effects on these

Practice advisory for the perioperative management of patients with cardiac rhythm management devices: Pacemakers and implantable cardioverter- defibrillators - A report by the American Society of Anesthesiologists Task Force on perioperative management of patients with cardiac rhythm management devices

PRACTICE advisories are systematically developed reports that are intended to assist decision making in areas of patient care. Advisories provide a synthesis and analysis of expert opinion, clinical feasibility data, open forum commentary, and consensus surveys. Advisories are not intended as standards, guidelines, or absolute requirements. They may be adopted, modified, or rejected according to clinical needs and constraints. The use of practice advisories cannot guarantee any specific outcome. Practice advisories summarize the state of the literature and report opinions derived from a synthesis of task force members, expert consultants, open forums, and public commentary. Practice advisories are not supported by scientific literature to the same degree as standards or guidelines because of the lack of sufficient numbers of adequately controlled studies. Practice advisories are subject to periodic revision as warranted by the evolution of medical knowledge, technology, and practice. Methodology

Prolongation of the QT interval by enflurane, isoflurane, and halothane in humans.

&NA; Previous investigations in laboratory animals have documented the ability of the volatile anesthetics to prolong the QT interval and the QT interval corrected for level of heart rate, QTc. The purpose of the present investigation was to evaluate the direct electrocardiographic and hemodynamic effects of enflurane, isoflurane, and halothane in healthy, unpremedicated patients using an inhalation induction to avoid the confounding effects of other anesthetic agents. Experiments were conducted in 22 adult male patients, (ASA physical status I or II) divided into three groups given either enflurane (n = 6), isoflurane (n = 8), or halothane (n = 8) anesthesia. Twenty‐four‐hour preoperative, preinduction, and postinduction hemodynamic and electrocardiographic measurements were obtained. Anesthetic blood concentrations, levels of plasma electrolytes, and arterial blood gas tensions were also quantitated. Halothane administration (0.81 ± 0.06 mM) did not significantly alter the PR interval or QRS duration but significantly increased the QT (0.38 ± 0.01 to 0.45 ± 0.01 s) and QTc intervals (0.39 ± 0.01 to 0.44 ± 0.02 s). Isoflurane anesthesia (1.04 ± 0.11 mM) did not significantly change QRS duration or PR and QT intervals but significantly prolonged the QTc interval (0.42 ± 0.01 to 0.47 ± 0.14 s). Similarly, enflurane anesthesia (2.16 ± 0.13 mM) significantly prolonged the QTc (0.40 ± 0.01 to 0.46 ± 0.14 s) without change in QRS duration or PR and QT intervals. Plasma electrolyte levels and arterial gas tensions remained within normal limits in all patients. All patients maintained a normal sinus rhythm during the study despite prolongation of the QTc induced by the volatile anesthetics. These results extend previous observations in experimental animals to humans and suggest that ventricular repolarization is directly altered by the volatile anesthetics. Despite the absence of cardiac arrhythmias in this study, prolongation of the QTc interval by volatile inhalation anesthetics suggests that caution should be used during administration of volatile anesthetics to patients with congenital, acquired, or pharmacologically induced prolongation of the QTc.

Perioperative cardiac dysrhythmias : diagnosis and management

Professor of Anesthesiology. Received from the Medical College of Wisconsin, Milwaukee, Wisconsin. Submitted for publication March 6, 1996. Accepted for publication January 2, 1997. Address reprint requests to Dr. Atlee: Department of Anesthesiology, Froedert Memorial Lutheran Hospital (East), 9200 West Wisconsin Avenue, Milwaukee, Wisconsin 53226. Address electronic mail to: jatlee@post.its. mcw.edu.

Perioperative ventricular dysrhythmias in patients with structural heart disease undergoing noncardiac surgery.

Noncardiac surgical patients with preoperative ventricular dysrhythmias and structural heart disease may be at increased risk of adverse cardiac outcome.We evaluated how anesthesia and surgery affect the course of ventricular dysrhythmias (premature ventricular beats [PVB] and repetitive forms of ventricular beats [RFVB]: couplets and nonsustained ventricular tachycardia) noted preoperatively in patients with structural heart disease and whether the frequency of ventricular dysrhythmias affects cardiac outcome. In a prospective study, 70 patients scheduled for noncardiac surgery with structural heart disease and RFVB on preoperative Holter electrocardiogram were continuously monitored intraoperatively and for 3 days postoperatively. Holter tracings were analyzed for rhythm, medians of total PVB and RFVB per hour. Preoperative RFVB recurred intraoperatively in 35% and postoperatively in 87% of patients. There was a significant intra- and postoperative decrease of total PVB per hour (P < 0.05) and RFVB per hour (P < 0.01). Frequency of ventricular dysrhythmias in the five patients suffering adverse outcome (unstable angina, n = 1; congestive heart failure, n = 4) did not significantly differ from those with good outcome. We conclude that in noncardiac surgical patients with structural heart disease and RFVB, the frequency of ventricular dysrhythmias is not associated with adverse cardiac outcome. Implications: Using continuous electrocardiogram monitoring, we investigated whether the frequency of perioperative ventricular dysrhythmias independently affects outcome in patients with structural heart disease undergoing noncardiac surgery. The incidence of perioperative dysrhythmia in patients with an adverse outcome (8%) did not differ from those with a good outcome.

The use of esmolol, nicardipine, or their combination to blunt hemodynamic changes after laryngoscopy and tracheal intubation

Laryngoscopy and tracheal intubation (LTI) often provoke an undesirable increase in blood pressure (BP) and/or heart rate (HR). We tested the premise that nicardipine (NIC) and esmolol (ESM) in combination (COMB) would oppose both. Adult surgical patients received pretreatment (randomized) with IV bolus NIC 30 &mgr;g/kg (n = 31), ESM 1.0 mg/kg (n = 34), or COMB (one-half dose each, n = 32). Peak BP and HR after LTI were compared with controls (CONT;n = 35) with no pretreatment. Anesthetic induction was standardized: IV thiopental (5–7 mg/kg), fentanyl (1–2 &mgr;g/kg), and succinylcholine (1.5 mg/kg). Systolic (S), diastolic (D), and mean (M) BP and HR awake before pretreatment (baseline) were similar in all test groups. No patient was treated for hypotension, bradycardia, or tachycardia after pretreatment or anesthetic induction. Peak HR after LTI was increased versus baseline in CONT and all test groups, but did not differ from CONT among the test groups. Peak SBP and DBP increased versus baseline in CONT, and with ESM and NIC, but not COMB. Peak SBP, DBP, and MBP were increased with ESM versus COMB, and peak DBP with ESM versus NIC. Compared with no pretreatment before the IV induction of general anesthesia, the peak increase in BP after LTI is best blunted by the combination of nicardipine and ESM, compared with either drug alone. No single drug or combination in the doses tested opposed increased HR. Implications Compared with no pretreatment before the IV induction of general anesthesia, the peak increase in blood pressure after laryngoscopy and tracheal intubation is best blunted by the combination of nicardipine and esmolol, compared with either drug alone. No single drug or combination in the doses tested opposed increased heart rate.

Cardiac Rhythm Management Devices (Part II)Perioperative Management

IN the first installment of this two-part communication, we reviewed the indications for an implanted pacemaker or internal cardioverter–defibrillator (ICD), provided a brief overview of how a device is selected, and described the basics of pacemaker and ICD design and function. Here we discuss specific device malfunction, electromagnetic and mechanical interference, and management for patients with a device or undergoing system implantation or revision. As in part I, the NASPE-BPEG (for North American Society for Pacing and Electrophysiology–British Pacing and Electrophysiology Group; sometimes abbreviated as NBG) generic pacemaker code is used to designate pacing modes.

Atrioventricular Conduction Times and Atrioventricular Nodal Conductivity during Enflurane Anesthesia in Dogs

Because alterations in conduction may be important as a cause of arrhythmias during anesthesia, the authors used His-bundle electrocardiography to evaluate the effects of enflurane on atrioventricular (AV) nodal, His–Purkinje, and ventricular conduction times in dogs. Evaluations were made in hearts beating spontaneously and during atrial pacing at rates between 120 and 200 beats/min. To test the effects of enflurane on the atrial effective refractory period, functional refractory period of the AV node, and AV nodal conductivity, atrial extrastimuli (test beats) were delivered at various cycle lengths (500 msec or less) after the last of a series of paced beats at 120 or 200 beats/min. AV nodal conductivity was evaluated by measurements of minimum conduction time, fatigue (the relation of minimum conduction time to change in heart rate), and interval-related conductivity (the prolongation of AV nodal conduction time beyond minimum conduction time related to prematurity of test response). Increasing concentrations of enflurane from 1.0 to 2.0 MAC prolonged AV nodal, but not His–Purkinje or ventricular, conduction times. AV nodal conduction time increased as heart rate was increased, and this rate-dependency was enhanced by enflurane. His–Purkinje and ventricular conduction times were not affected by rate or enflurane. The atrial effective refractory period, functional refractory period of the AV node, and AV nodal conductivity were depressed by enflurane. For the His–Purkinje and ventricular conduction system, the present results are in contrast to those previously reported for halothane. Conduction changes are necessary for ventricular arrhythmias caused by re-entry of excitation. These findings may in part explain the clinical impression that ventricular arrhythmias appear less likely to occur with enflurane than with halothane.

Halothane Depression of A-V Conduction Studied by Electrograms of the Bundle of His in Dogs

Catheter electrocardiography was used to obtain electrograms from the bundle of His in the dog to quantify and localize the effects of halothane on the specialized conducting system of the heart. The time from atrial depolarization to His-bundle deflection (P–H interval) and the time from His-bundle deflection to the beginning of ventricular depolarization (H–V interval) were measured. Fast rates of atrial pacing were used to slow A-V conduction. Change in P–H interval was plotted as a function of change in pacing rate, and change in slope measured depression of A-V conduction. Halothane exerted its greatest effect by slowing conduction between the atria and the bundle of His; there was also some slowing of conduction in the ventricle (prolonged H–V interval). Blocking doses of atropine did not improve halothane-depressed conduction. Blocking doses of propranolol significantly depressed conduction, as measured by both P–H and H–V intervals. These data suggest that arrhythmias seen with halothane may be due in part to impaired conduction.

Conscious-state comparisons of the effects of inhalation anesthetics on specialized atrioventricular conduction times in dogs

The effects of 1.2, 1.7, and 2.3 MAC enflurane (ENF), halothane (HAL), and isoflurane (ISO) on specialized atrioventricular (AV) conduction times were compared with awake (control) in 23 dogs that were chronically instrumented for His bundle studies. Compared with awake, 1.2 MAC ENF and HAL produced 17% and 18% increases in AV nodal conduction time, respectively. There was little added prolongation related to depth of ENF or HAL. ISO did not prolong AV nodal conduction time at 1.2 MAC compared with awake, but it did prolong conduction compared with awake at 1.7 (9%) and 2.3 MAC (12%). All agents produced an approximate 5% increase in His-Purkinje and ventricular conduction times compared with awake, with little additional effect related to depth of anesthesia. In separate experiments in ten of these dogs, anesthetic effects on conduction were determined following combined autonomic blockade with atropine and propranolol. During autonomic blockade, there was no effect of any anesthetic compared with awake, or to increased level of anesthesia, on specialized AV conduction times. The authors conclude that of the major inhalation anesthetics in current clinical use, ISO is least depressant of and ENF and HAL about equally depressant of AV nodal and His-Purkinje conduction times. Furthermore, depression of AV nodal conduction appears to be an indirect rather than direct effect of anesthesia. Finally, most depression of conduction occurs with light anesthesia, with little added depression related to depth of anesthesia over levels likely to be encountered clinically.