Ventricular arrest occurs in isolated heart perfused with potassium-deficient solution when the extracellular potassium concentration is suddenly raised to a physiological concentration. This is known as a paradoxical phenomenon of Zwaardemaker and Libbrecht. Records of electrocardiograms, and ventricular and atrial transmembrane potentials from perfused rabbit hearts before, during and after this type of arrest revealed that its mechanism differs from the mechanism of cardiac arrest produced by an increase of external [K] above physiological concentration. The Zwaardemaker-Libbrecht phenomenon is associated with a striking increase in the velocity of repolarization while the typical effects of high-K concentration on the resting membrane potential and amplitude and upstroke velocity of the action potential are either very slight or absent. Conduction in the atria, ventricles and between the atria and the ventricles apparently is not disturbed during the Zwaardemaker-Libbrecht phenomenon; therefore, we attribute the cardiac arrest to a selective inhibition of the pacemaker activity. This might be due to an inhibition of the diastolic depolarization of the pacemaker fibers. A speculation is made that the type of imbalance between the intra- and extracellular K concentration in the myocardium which causes the Zwaardemaker-Libbrecht effect in the isolated heart could occur in situ and cause sudden death.