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(Chest. 1973;63:986-994.)
© 1973 American College of Chest Physicians

Vulnerability of Canine Ventricle to Fibrillation During Hypoxia and Respiratory Acidosis

R. M. Rogers M.D., F.C.C.P.1; J. F. Spear Ph.D.1; E. N. Moore D.V.M.1; L. H. Horowitz M.D.1; and J. E. Sonne M.S.1

1 Cardiopulmonary Division, Department of Medicine and Department of Physiology, University of Pennsylvania School of Medicine; and Comparative Cardiovascular Studies Unit, Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia

Ventricular arrhythmias, including ventricular fibrillation (VF), have been reported to be associated with respiratory failwe; however, the etiologic mechanism is poorly understood. In order to investigate the genesis of these arrhythmias, the effects of hypercarbia (secondary to alveolar hypoventilation) with and without hypoxia and metabolic acidosis and alkalosis on the ventricular fibrillation threshold (VFT) were studied in anesthetized, open-chest dogs. The current (in milliamperes) required to induce VF was determined by passing a train of 10 to 12 constant current pulses through the ventricular myocardium during the vulnerable period of the cardiac cycle. Neither respiratory acidosis (pH 6.97 to 7.27, Pco2 55 to 120 mm Hg) nor hypoxia (Po2 28.5 to 66.0 mm Hg with normal Pco2) significantly changed the VFT. Respiratory acidosis coincident with hypoxia, however, increased the VFT to 170 percent ± 25 percent of the control. This result was observed regardless of whether hypoxia or hypercapnia was induced initially or if they were induced simultaneously. Our experimental results during metabolic acidosis agreed with previous studies, with an observed decrease in VFT of approximately 50 percent from control. During metabolic alkalosis, we observed increases in the VFT ranging from 125 percent to 560 percent of control. These experimental studies suggest that respiratory failure per se decreases the probability of VF as measwed by the VFT technique. Other factors such as metabolic acidosis, coronary artery disease, cardiotonic drugs and therapeutic measures might singly or in concert play a more important role.




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