Shortening of the QT interval of the EKG is associated primarily with increased ventricular contractility rather than heart rate.

The objective of this study was to gather direct evidence on whether the duration of the QT interval relates primarily to heart rate or to ventricular contractility. The electrocardiographic and cardiodynamic consequences of electrical stimulation (15 V, 5 ms, 10Hz) of various intrathoracic sympathetic efferent neuronal structures were studied in 10 anesthetized mongrel dogs. Stimulation of efferent sympathetic axons in the right intraganglionic nerve, which innervates the sinoatrial node, induced tachycardia (110 +/- 5 - 133 +/- 6 bpm; p < 0.01) without significantly altering right or left ventricular intramyocardial ventricular chamber pressures. The QT interval, as determined by leads I, II and III of the EKG and a transthoracic lead, was not affected by this intervention 310 +/- 8 - 302 +/- ms). Increasing heart rate to a similar degree (111 +/- 3 - 131 +/- 3 bpm) by right atrial pacing did not induce changes in the QT interval. When right (23 +/- 3 - 49 +/- 8 mm Hg; p < 0.01) and left (81 +/- 10 - 127 +/- 19 mm Hg; p < 0.01) ventricular forces were augmented without concomitant increases in heart rate by stimulating efferent sympathetic axons in the left caudal pole cardiopulmonary nerve the QT interval shortened (322 +/- 11 - 290 +/- 12 ms; p < 0.01). Only when an efferent sympathetic nerve, that contains fibers destined for both the sinoatrial node and the ventricles was stimulated did both heart rate and ventricular contractility augment and QT shorten (318 +/- 10 - 290 +/- 11 ms; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)