Suppression of ventricular arrhythmias by volatile anesthetics in a canine model of chronic myocardial infarction

• Published in: Anesthesiology (Philadelphia) 1990-06, Vol.72 (6), p.1012-1021
• Main Authors: DEUTSCH, N, HANTLER, C. B, TAIT, A. R, UPRICHARD, A, SCHORK, M. A, KNIGHT, P. R
• Format: Article
• Language: English
• Subjects: Anesthetics - pharmacology; Anesthetics. Neuromuscular blocking agents; Animals; Biological and medical sciences; Blood Pressure - drug effects; Cardiac Pacing, Artificial; Dogs; Electrocardiography - drug effects; Enflurane - pharmacology; Female; Halothane - pharmacology; Heart Rate - drug effects; Heart Ventricles; Isoflurane - pharmacology; Male; Medical sciences; Myocardial Infarction - complications; Myocardial Infarction - physiopathology; Neuropharmacology; Pharmacology. Drug treatments; Tachycardia - etiology; Tachycardia - physiopathology
• ISSN: 0003-3022; 1528-1175
• DOI: 10.1097/00000542-199006000-00011

Ventricular tachycardia likely secondary to a reentrant mechanism may be reliably induced by programmed electrical stimulation in dogs 4-6 days after creating a 2-h experimental, occlusion-reperfusion myocardial infarction. The effects of 1.1 and 1.8 MAC halothane, isoflurane, and enflurane on pacing-induced arrhythmias were studied in this model. The ease of initiation of ventricular tachycardia was measured in both awake and anesthetized dogs (n = 18). Excitation thresholds, conduction times, and refractory periods in both normal and infarcted myocardium were also determined to understand changes in the ease of induction of the arrhythmias secondary to anesthetic exposure. Halothane and enflurane administration suppressed the induction of ventricular tachycardia compared with the unanesthetized control (P less than 0.01 for both). During isoflurane anesthesia, there was a trend that was not statistically significant for pacing-induced ventricular tachycardia to be less frequent than during the conscious state (P = 0.11). Halothane and enflurane prolonged refractory periods in both normal and infarcted myocardium, whereas isoflurane had that effect only in normal myocardium. In addition, halothane and enflurane tended to increase refractory periods more than isoflurane in both regions. Conduction times and excitation thresholds were not altered by anesthetic administration. It is concluded that halothane and enflurane suppress inducible ventricular arrhythmias secondary to a prior myocardial infarction. In addition, the increased efficacy of halothane and enflurane as antiarrhythmic agents compared with isoflurane in this model may be related to their greater prolongation of refractory periods.