The Cardiac Electrophysiology of Postresuscitation Hypokalemia in Dogs
- 1 March 1990
- journal article
- Published by Wiley in Pacing and Clinical Electrophysiology
- Vol. 13 (3) , 256-263
- https://doi.org/10.1111/j.1540-8159.1990.tb02038.x
Abstract
Hypokalemia has been observed in man after out‐of‐hospital ventricular fibrillation and after cardiover‐sion from ventricular tachycardia in the electrophysiology laboratory, and also in dogs following ventricular fibrillation (maximal effect 45–60 minutes after resuscitation). Since the electrophysiological effects of postresuscitation hypokalemia are unknown, we evaluated the effects of this hypokalemia on ventricular fibrillation thresholds (group 1) and on right ventricular effective refractory periods (group 2). In both groups, anesthetized dogs with normal hearts were divided into experimental animals that had 2 minutes of ventricular fibrillation followed by cardioversion without medications and control animals without ventricular fibrillation. In group 1, we measured serum potassium before ventricular fibrillation (or time 0 in control dogs) and then measured potassium and ventricular fibrillation threshold at 45, 60, 75, and 90 minutes after baseline. In group 2 animals we measured right ventricular effective refractory periods and serum potassium at baseline and sequentially from 7 to 180 minutes after resuscitation. In group 1, the maximum change in potassium from baseline was ‐0.8 ± 0.3 mEq/L at 60 minutes after resuscitation as compared to ‐0.1 ± 0.3 mEq/L in control animals at 60 minutes (P < 0.01). At 60 minutes, ventricular fibrillation threshold was 8 ± 3 mA in ventricuJar fibrillation animals and 7 ± 3 mA in control animals (P = NS). In group 2 animals, the maximum change in serum potassium also occurred 60 minutes after resuscitation and was ‐0.8 ± 0.3 mEq/L as compared to ‐0.2 ± 0.2 mEq/L in control animals (P < 0.001). Right ventricular effective refractory periods after an 8‐beat drive at 200 msec were 121 ± 35 msec in the resuscitated animals versus 123 ± 19 msec in control animals 60 minutes after baseline (P = NS). In conclusion, postresuscitation hypokalemia had no effect on the ventricular fibrillation threshold or right ventricular effective refractory period in anesthetized dogs with structurally normal hearts prior to arrest.Keywords
This publication has 15 references indexed in Scilit:
- Hypokalemia after cardioversion from ventricular tachycardia induced in the electrophysiology laboratoryAmerican Heart Journal, 1987
- Serum potassium, calcium and magnesium after resuscitation from ventricular fibrillation: A canine studyJournal of the American College of Cardiology, 1987
- Influence of beta2-adrenoceptor stimulation and blockade on cardiac electrophysiologic properties and serum potassium concentration in the anesthetized dogAmerican Heart Journal, 1987
- Frequency of hypokalemia after successfully resuscitated out-of-hospital cardiac arrest compared with that in transmural acute myocardial infarctionThe American Journal of Cardiology, 1987
- Effects of calcium antagonists on infarcting myocardiumThe American Journal of Cardiology, 1987
- Effect of hypokalemia on susceptibility to ventricular fibrillation in the normal and ischemic canine heartAmerican Heart Journal, 1986
- Effects of Selective and Nonselective ??-Agonists on Plasma Potassium and NorepinephrineJournal of Cardiovascular Pharmacology, 1984
- Hypokalemia from Beta2-Receptor Stimulation by Circulating EpinephrineNew England Journal of Medicine, 1983
- Hypokalemia after resuscitation from out-of-hospital ventricular fibrillationJAMA, 1982
- Ventricular vulnerability during acute coronary occlusionThe American Journal of Cardiology, 1969