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Anesth Analg 2004;98:790-795
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000096259.89137.00


CRITICAL CARE AND TRAUMA

The Effect of Bupivacaine on Myocardial Tissue Hypoxia and Acidosis During Ventricular Fibrillation

Guy Weinberg, MD, Chanannait Paisanthasan, MD, Douglas Feinstein, PhD, and William Hoffman, PhD

From the Department of Anesthesiology, University of Illinois at Chicago College of Medicine and the Chicago VA Hospital Westside Division, Chicago, Illinois

Address correspondence and reprint requests to Guy Weinberg, MD, Department of Anesthesiology, M/C 515, University of Illinois at Chicago, 1740 West Taylor Street, Chicago, IL 60612. Address email to guyw{at}uic.edu

Previously we observed that during bupivacaine-induced circulatory collapse, myocardial tissue pH declined more slowly than expected. Here we evaluated the effect of bupivacaine on myocardial acidosis induced by ventricular fibrillation. Sixteen dogs were anesthetized with 1.5% end-tidal isoflurane, the chest was opened, and a probe that measured oxygen pressure (PmO2), carbon dioxide pressure, pH, and temperature was inserted into myocardial tissue. After baseline measures, each dog received either 10 mg/kg bupivacaine (n = 8) or a sham saline treatment (n = 8). Three minutes later ventricular fibrillation was initiated electrically, and the rate of change in PmO2 and pH during ventricular fibrillation was measured. Baseline physiological measures were similar in the two groups of dogs. During ventricular fibrillation there was a rapid decrease in PmO2, and the rate of decrease was not different between sham- and bupivacaine-treated dogs. Tissue pH decreased during ventricular fibrillation, and the rate of decrease was 4 times faster in sham- compared with bupivacaine-treated dogs (P < 0.05). These results show that bupivacaine attenuated myocardial tissue acidosis during ventricular fibrillation. This potentially beneficial effect may be a result of bupivacaine’s ability to inhibit myocardial lactate and carbon dioxide production. This suggests a potential clinical application of bupivacaine for myocardial preservation.

IMPLICATIONS: In this animal study pretreatment with bupivacaine attenuated the progression of myocardial acidosis during ventricular fibrillation. The dogs regained normal hemodynamic variables after lipid infusion. The findings suggest such that bupivacaine may protect the heart against ischemic acidosis.




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Anesth. Analg.Home page
L. S. Coleman, G. Weinberg, W. Hoffman, D. Feinstein, and C. Paisanthasan
Bupivacaine and Ventricular Fibrillation * Response
Anesth. Analg., October 1, 2004; 99(4): 1269 - 1269.
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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2004 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2004 by the International Anesthesia Research Society.