Monophasic action potentials (MAPs) were utilized to examine the basis for
cesium-induced
arrhythmia in the dog.
Cesium chloride (1 mmol/kg i.v.) produced an immediate prolongation of MAP (250 +/- 11 to 396 +/- 34 ms, p less than 0.05). Coupled
premature ventricular beats (345 +/- 46 ms) and polymorphic
ventricular tachycardia developed in association with early afterdepolarizations during the first 1-3 min after
cesium administration. A slowing of the sinus heart rate with
vagus nerve stimulation exacerbated the
arrhythmia. During the subsequent 7 min, the MAP duration decreased from 396 +/- 34 to 316 +/- 19 ms. At 8-10 min, the
premature ventricular beats were associated with delayed afterdepolarizations in the MAP recordings. However, there was no change in the coupling intervals of the
premature ventricular beats (351 +/- 29 ms). Ventricular arrhythmias and delayed afterdepolarizations during this phase were exacerbated by increasing the heart rate with atrial pacing. T wave alternans and U wave formation in the ECG were associated with early or delayed afterdepolarizations in MAP.
Cesium chloride (1 mmol) injected into the left anterior descending coronary artery produced local MAP prolongation and ventricular bigeminy. Although the MAP duration returned to predrug values after intracoronary
cesium injection, the severity of ventricular
arrhythmia increased with succeeding doses. These data suggest that early and delayed afterdepolarizations, T wave alterations, and ventricular beats can be dissociated from the initial action potential prolongation with
cesium and closely resemble altered
calcium transients observed in vitro.