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Myocardial Function during Halothane and Enflurane Anesthesia in Patients with Coronary Artery Disease

Thomas J. Delaney, MD^*, James R. Kistner, MD, Carol L. Lake, MD, and Edward D. Miller, Jr., MD

*Fellow. Department of Anesthesiology, University of Virginia Medical Center, Charlottesville, Virginia 22908. Assistant Professor. Department of Anesthesiology, University of Virginia Medical Center, Charlottesville, Virginia 22908. Associate Professor. Department of Anesthesiology, University of Virginia Medical Center, Charlottesville, Virginia 22908.

Abstract

Halothane and enflurane are known myocardial depressants in healthy individuals. Whether these two agents produce the same degree of myocardial depression in patients with coronary artery disease has not been studied. Informed consent was obtained from 16 adults with ischemic heart disease undergoing coronary artery bypass grafting. Patients with significant ventricular dysfunction were excluded from the study. Control measurements were made while the patient breathed 100% oxygen. The patients were divided into two groups, anesthetized with either halothane or enflurane, and repeat measurements made at 1/2 and 3/4 MAC for each agent. The last series of measurements (3/4 MAC) was made approximately 1 hour after the induction of anesthesia but before intubation, surgical skin preparation or surgical incision. Our data indicate that at 1/2 and 3/4 MAC for halothane, mean arterial blood pressure (MAP) decreased from 92 ± 2 torr to 73 ± 3 torr and 67 ± 2 torr, respectively (p < 0.05). Pulmonary capillary wedge pressure (PCWP) increased from 6.2 ± 0.7 torr to 9.1 ± 1.6 torr and 9.4 ± 1.7 torr at 1/2 and 3/4 MAC halothane (p < 0.05). Cardiac index decreased from the control values of 2.67 ± 0.08 L/min/m² to 2.19 ± 0.06 L/min/m² for 1/2 MAC and to 2.24 ± 0.08 L/min/m² at 3/4 MAC halothane (p < 0.05). Assisted ventilation was maintained throughout and arterial P_co2 was unchanged from control. Enflurane likewise resulted in a decrease in MAP from 99 ± 6 torr to 75 ± 4 torr at 1/2 MAC and 68 ± 5 torr at 3/4 MAC (p < 0.05). PCWP did not increase. In contrast, however, cardiac index was unchanged from control value of 2.65 ± 0.16 L/min/m² at both 1/2 and 3/4 MAC. Arterial P_co2 was unchanged from the awake control value. Our data indicate that while both halothane and enflurane decrease mean arterial blood pressure, the mechanisms responsible differ. The primary afterload-reducing effect of enflurane may be beneficial to some patients with ischemic heart disease whereas other patients may benefit from the greater myocardial depression seen with halothane.

Key Words: ANESTHETICS • Volatile: halothane • ANESTHETICS • Volatile: enflurane • HEART: myocardial function • ANESTHESIA: cardiovascular