Serum potassium, calcium and magnesium after resuscitation from ventricular fibrillation: A canine study

Serum electrolytes were measured before and sequentially for 3 hours after resuscitation from ventricular fibrillation in a canine model that was designed to approximate the human cardiac arrest and resuscitation process. Twenty anesthetized dogs were resuscitated from ventricular fibrillation; 7 required epinephrine during resuscitation and 13 did not. To control for the effects of anesthesia, 10 dogs were anesthetized and instrumented, but ventricular fibrillation was not induced.Serum potassium decreased from 3.7 ± 0.3 mmol/liter at baseline to 3.2 ± 0.4 mmol/liter 45 minutes after resuscitation in the experimental dogs resuscitated without epinephrine, as compared with 3.6 ± 0.3 to 3.4 ± 0.2 mmol/liter in control dogs (p = 0.07 versus control dogs by two-way analysis of variance) and returned toward baseline at the end of 3 hours. Serum calcium decreased from 9.6 ± 0.6 mg/dl at baseline to 8.9 ± 0.9 mg/dl at 5 minutes after resuscitation as compared with 9.4 ± 0.7 to 9.5 ± 0.7 mg/dl in control dogs (p < 0.05 versus control dogs) and returned to baseline by 3 hours. Serum magnesium decreased from 1.5 ± 0.1 to 1.3 ± 0.2 mEq/dl by 3 hours in resuscitated dogs as compared with 1.6 ± 0.2 to 1.5 ± 0.2 mEq/dl in control dogs (p = 0.06 versus control dogs). These changes in serum potassium, calcium and magnesium were independent of the administration of epinephrine during the resuscitation process. Changes in potassium were independent of arterial pH or bicarbonate therapy. Serum glucose increased after ventricular fibrillation but not in control dogs (p < 0.0005 versus control). No changes in other electrolytes were observed.Thus, serum potassium, calcium and magnesium decreased after resuscitation from ventricular fibrillation in this canine model. These data suggest that, although the hypokalemia seen after ventricular fibrillation in humans may in some cases precede the event, a decrease in potassium may develop after resuscitation

Left Ventricular Thrombosis after Myocardial Infarction

To the Editor: Asinger et al. have made a solid contribution to our understanding of left ventricular thrombosis after acute myocardial infarction (August 6 issue).1 Yet, one is astonished to note that the authors and the Journal's usually Olympian reviewers permit misleading use of the word “transmural.“ A large body of work performed from 1951 to 1980 has demonstrated that infarcts producing Q-waves and those with only ST-T changes cannot reliably identify transmural and nontransmural infarcts.2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Recent work also shows that the two echocardiographic patterns indicate comparable five-year survival17 and do not discriminate between single-vessel and multivessel disease.18 The report. . . © 1981, Massachusetts Medical Society. All rights reserved.SCOPUS: le.jinfo:eu-repo/semantics/publishe