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Ann Thorac Surg 1988;46:556-562
© 1988 The Society of Thoracic Surgeons

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Articles

Effects of Simulated Intraoperative Electrophysiological Testing on Function of the Canine Left Ventricle

Cardiovascular Surgery Research Laboratory, Department of Surgery, and the Department of Anesthesiology, Columbia University College of Physicians & Surgeons, New York, NY

Accepted for publication June 22, 1988.

^* Address reprint requests to Dr. Spotnitz, Columbia University College of Physicians & Surgeons, 630 W 168th St, New York, NY 10032

With the increasing application of arrhythmia surgery, intraoperative electrophysiological study is done frequently, although its potential to cause acute depression of cardiac function remains unresolved. This study examines the acute effects of simulated electrophysiological testing on left ventricular function. Seven dogs were anesthetized with sodium pentobarbital and instrumented for measurement of heart rate, mean aortic pressure, cardiac output (CO), and systemic vascular resistance (SVR). Systolic pressure-dimension work loops were analyzed over varying preloads. Contractility was assessed from the end-systolic pressure-dimension relationship (E_es) and from preload recruitable stroke work (PRSW). After the collection of control data, electrophysiological testing was simulated by pacing at 200 beats per minute for 30 seconds, fibrillating for 15 seconds, and finally defibrillating with a 10-J countershock. Data were recorded after 3 and 6 simulations of ventricular fibrillation (VF3, VF6). Mean heart rate and mean aortic pressure did not vary significantly during the course of the experiment. CO decreased from a control value of 2.7 ± 0.2 L/min (± the standard error of the mean) to 2.0 ± 0.1 (p > 0.05) after VF3 and remained significantly depressed after VF6. SVR increased from a control value of 3,231 ± 211 dyne sec cm^–5 to 3,976 ± 305 dyne sec cm^–5 after VF3 (p = not significant) and increased further to 4,774 ± 442 dyne sec cm^–5 after VF6 (p > 0.05). Neither E_es nor PRSW varied significantly even after 6 EP simulations, thereby indicating that contractility was unchanged during the experiment. We conclude that CO decreases in simulated electrophysiological studies but the decrease appears to be due to reflex vasoconstriction rather than direct myocardial depression.

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