THE PATHOPHYSIOLOGY OF BARIUM: HYPOKALEMIC AND CARDIOVASCULAR EFFECTS

¹ Department of Nephrology, Division of Medicine, The Mt. Sinai Hospital of Cleveland, Cleveland, Ohio

The ingestion of absorbable barium salts, e.g., carbonate or chloride, produces a combination of ectopic ventricular contractions, ventricular tachycardia, skeletal muscle paralysis, salivation, diarrhea, hypertension and finally, respiratory paralysis and ventricular fibrillation. Infusion of barium chloride into anesthetized dogs produced all of the above, plus a prompt and substantial hypokalemia. The data suggest that the hypokalemia is due to a transfer of potassium from extracellular to intracellular compartments rather than to urinary or gastrointestinal losses. Potassium administration prevented or reversed all of the clinical effects except the hypertension. Arterial hypertension was a constant feature of BaCI₃ infusion and was not affected by simultaneous potassium infusion, by the injection of phentolamine or by bilateral nephrectomy. Barium and potassium were each found to be powerful antagonists of the other's cardiac toxicity. The intracellular accumulation of potassium induced by barium together with the reported ability of barium to stimulate myocardial adenosine triphosphatase suggests the possibility of a role for barium in the management of digitalis poisoning.

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