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Anesth Analg 1981; 60:481-491
© 1981 International Anesthesia Research Society
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Comparison of Cardiopulmonary Responses to Graded Hemorrhage during Enflurane, Halothane, Isoflurane, and Ketamine Anesthesia

Richard B. Weiskopf, MD*, Mary I. Townsley, BA, Kathryn K. Riordan, BS{ddagger}, Karen Chadwick, BS{ddagger}, Mark Baysingery, BS{ddagger}, and Eileen Mahoney, BA{ddagger}

*Associate Professor of Anesthesia, Department of Anesthesia, University of California, San Francisco {ddagger}Biological Science Assistant, Department of Surgery, Letter-man Army Institute of Research, Presidio of San Francisco, California.

Abstract

To assess the influence of anesthetic agents during mild to moderate hemorrhage, the cardiopulmonary function of five awake, unmedicated dogs was compared with that during anesthesia with enflurane, halothane, isoflurane, and ketamine. Each dog was evaluated during anesthesia with each agent during normovolemia and after blood losses of 10%, 20%, and 30%. Before blood loss, in comparison with the awake state, ketamine increased heart rate (118 ± 11 beats/min, awake, vs 168 ± 17) and cardiac output (5.3 ± 0.4 L/min, awake, vs 6.0 ± 0.2). Halothane and isoflurane did not alter these variables. Enflurane decreased mean arterial blood pressure (110 ± 2 torr, awake, vs 72 ± 3), cardiac output (3.5 ± 0.1 L/min), and stroke volume (46 ± 4 ml, awake, vs 29 ± 2) to a greater extent than did the other anesthetics. Blood loss decreased cardiac output more with ketamine than with the inhalation anesthetics (ketamine, 0.120 L/min/percentage of blood loss; halothane, 0.077; isoflurane, 0.071; enflurane, 0.058; determined by least-squares linear regression, 0–30% blood loss), so that after 30% hemorrhage cardiac output was essentially the same during halothane (2.45 ± 0.19 L/min), isoflurane (2.83 ± 0.19 L/min), and ketamine (2.48 ± 0.15 L/min) anesthesia. Also, during hemorrhage, systemic vascular resistance increased most with ketamine; thus, after 30% blood loss, mean arterial blood pressure was highest with ketamine (ketamine, 94 ± 7 torr; enflurane, 48 ± 5 torr; halothane, 81 ± 4 torr; isoflurane, 58 ± 4 torr). Rate-pressure product and minute work were highest with ketamime throughout hemorrhage, except for minute work after 30% blood loss. These cardiovascular changes were reflected in the measurements of metabolism. Total body oxygen consumption (o2) was highest with ketamine after 0% to 20% blood loss (e.g., after 0% blood loss: ketamine, 8.6 ± 1.2 ml of O2/min/kg; enflurane, 4.5 ± 0.5; halothane, 4.0 ± 0.3; isoflurane, 4.9 ± 0.6). During blood loss, Vo2 did not change with any inhalation anesthetic, but decreased with ketamine (6.0 ± 0.5 ml of O2min/kg after 30% blood loss); this decrease was associated with an increase in arterial blood lactate concentration and base deficit (ketamine, BE –8.0 ± 0.5 meq/L after 30% blood loss), suggesting that oxygen demand was not met during hypovolemia with ketamine anesthesia. In contrast, lack of change in blood lactate, base deficit, or oxygen consumption during hemorrhage with the inhalation anesthetics suggests that oxygen demand was satisfied when the dogs were bled during enflurane, halothane, or isoflurane anesthesia.

Key Words: ACID-BASE EQUILIBRIUM • ANESTHETICS, Intravenous: ketamine • ANESTHETICS, Volatile: enflurane, halothane, isoflurane • HEMORRHAGE: anesthetics, effects of • METABOLISM: lactate







Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 1981 by the International Anesthesia Research Society.