F. A. Kralios

Unipolar electrograms from ventricular epicardium in dogs were analyzed for the timing of local excitation and repolarization with computer assistance. The most rapid decrease in voltage in the QRS (dV/dt min) was used to determine local excitation time, and the maximum rate of voltage increase (dV/dt max) near the peak of the T wave was used to time local repolarization. The difference between dV/dt min and dV/dt max, the activation-recovery interval, is theoretically related to the net effect of the durations of the action potentials at that site. Paired data for refractory periods and activation-recovery intervals obtained from the same electrodes during fixed activation orders were obtained before and during repolarization changes induced by changes in cycle length, infusion of norepinephrine, and cardiac sympathetic nerve stimulation. Correlation coefficients were close to 1.00 and standard errors were 2.0 to 4.3 msec for changes at individual sites. Pooling of data from multiple sites increased standard errors and reduced correlation coefficients. Results provide quantification of errors in the use of unipolar electrograms to time local repolarization changes induced by variations in rate and adrenergic tone. They should increase the practical usefulness of the unipolar electrogram as a tool for assessing the time course and spatial distribution of repolarization changes.

Functional distributions of individual cardiac nerves distal to the stellate ganglia were determined in 30 open-chest, anesthetized dogs by mapping sites of refractory-period shortening during stimulation of the nerves. On the right, recurrent cardiac nerve stimulation produced marked shortening of refractory periods in the interventricular septum, and lesser changes on the anterior heart surface. On the left, ventromedial cardiac nerve stimulation shortened refractory periods in a similar distribution, but changes were not marked as with the recurrent cardiac nerve. The other left-side nerve that produced repolarization changes, the ventrolateral cardiac nerve, produced marked refractory-period changes on the posterior heart surface. Its distribution showed little overlap with that of the ventromedial or recurrent cardiac nerves. T waves inverted in an electrocardiographic Y lead during recurrent cardiac and ventromedial cardiac nerve stimulation, while ventrolateral cardiac nerve stimulation increased the positivity of T waves in that lead. The cardiac distributions of individual nerves documented in this study provide an anatomical basis for localized alterations in ventricular electrophysiologic properties.

The functional distribution of the cardiac sympathetic nerves to the atria and their arrhythmiogenic effects were determined in 16 open-chest pentobarbital-anesthetized dogs. Shortening of refractory periods at four right and two left atrial sites during stimulation of the nerves was taken as a criterion of their distribution. Stimulation of right stellate ganglion, craniovagal, and right stellate cardiac nerves produced localized shortening on the right atrium, particularly at the sinus node area, and invariably induced sinus tachycardia. The recurrent cardiac nerve produced little shortening at all sites and less arrhythmiogenic effect. The left stellate ganglion and ventrolateral cardiac nerve affected only left atrial sites and induced atrioventricular junctional rhythm. The ventromedial cardiac nerve affected all sites and had no consistent arrhythmiogenic effect. The innominate nerve had no substantial effect. We concluded that the functional distribution of the cardiac sympathetic nerves is localized, and that rate, rhythm, and refractory period changes induced by stimulation of these nerves are characteristic of the area of distribution.