An imbalance in electrolyte concentration during separation from cardiopulmonary bypass (CPB) may lead to a disruption in excitation-contraction coupling resulting in a failure to wean. The etiology of myocardial dysfunction is multifactorial, and includes alterations in acid-base balance, glucose metabolism, and cellular function. The purpose of this study was to assess the effect of hyperkalemia on myocardial function during separation from CPB. A porcine model (n = 5) of hypothermic (32 degrees C) CPB was used where hyperkalemia [K+ (6.5 +/- 1.0)] was created before weaning. A 3-minute weaning process was initiated once normothermia was achieved. Mixed venous and arterial samples were obtained during CPB, weaning, and 10 minutes postbypass. Samples were assayed for [K+], [Ca++], glucose, pH, CPK-MB, and lactic acid levels. Hyperkalemia resulted in the generation of severe arrhythmias in all animals. During the immediate prewean period, there was a significant correlation between venous [K+] and pH (p < .01, r2 =.891). Arterial pH did not change during the weaning or post-CPB period, while venous pH declined significantly throughout the same period (7.35 +/- 0.75 to 7.20 +/- 0.17, p < .05). No other measured variables correlated with hyperkalemia. In summary, hyperkalemia caused a significant decline in venous pH evidenced in the early separation period, but had no effect on other variables. Therefore, measurement of venous pH may be an early marker indicating myocardial dysfunction and dysrhythmia.