Steady state and time-dependent slowing of conduction in canine hearts. Effects of potassium and lidocaine.

Abstract

Studies of single cardiac fibers predict that intraventricular conduction should exhibit time-, as well as voltage-dependent changes when the myocardium is depolarized with K and/or is exposed to lidocaine. To test this hypothesis, H-V intervals and QRS durations for nonpremature responses (voltage-dependent conduction) and premature responses (time-dependent conduction) were measured in intact dog hearts paced from the right atrium or His bundle at a basic rate of 1.5-2.0/s. Hyperkalemia to a maximum plasma level of 9.6 mM was induced by infusing KCl. Lidocaine was administered to achieve plasma levels of 2-4 .mu.g/ml. Premature stimuli were applied to the His bundle no earlier than the end of the T wave to avoid stimulating incompletely repolarized fibers. For the nonpremature responses, prolongation of the H-V interval and QRS duration did not routinely occur until K+ = 8.0 mM, even in the presence of lidocaine. At higher K+ levels this voltage-dependent slowing of conduction became more pronounced and was exaggerated by lidocaine. For the premature responses, prolongation of H-V intervals and QRS durations occurred before voltage-dependent conduction slowing appeared. This time-dependent slowing of conduction became more pronounced at higher K+ levels and after lidocaine administration. These results validate the results of single fiber studies and are pertinent to an understanding of arrhythmias associated with hyperkalemia and myocardial ischemia and the antiarrhythmic effects of lidocaine.