Correlation between effects of ouabain on the canine electrocardiogram and transmembrane potentials of isolated Purkinje fibers.

Isolated canine Purkinje fiber bundles (PF) were perfused with the blood of intact donor dogs to correlate changes induced by ouabain (0) in the PF transmembrane potential (TP) and the donor ECG. 0 was administered intravenously to the donor, and standard microelectrode technics were used to record the TP. The only significant 0 effect prior to occurrence of toxic arrhythmias was induction of ST-T wave changes in the ECG and prolongation of action potential duration (APD). Early 0 toxicity was defined as the onset of junctional or ventricular premature contractions or junctional tachycardia. Simultaneous with early toxicity there were decreases in AP amplitude, resting membrane potential, maximal slope of phase 0 depolarization, APD, and plateau, and slowing of conduction, which often varied in extent from cycle to cycle. With increased duration of early toxicity or onset of late toxicity (ventricular tachycardia), TP changes were accentuated. Increased automaticity occurred at the time of early toxicity when plasma potassium concentration ([K + JO) <4 mEq/liter. In three of seven instances in which [K + ] > 4.0 mEq/liter, low amplitude potentials were recorded during phase 4. The possible role of these potentials in relation to the generation of toxic arrhythmias is discussed.