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Modulation of the Q‐T Interval by the Autonomic Nervous System
Author(s) -
BROWNE KEVIN F.,
PRYSTOWSKY ERIC,
HEGER JAMES J.,
ZIPES DOUGLAS P.
Publication year - 1983
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1983.tb04443.x
Subject(s) - medicine , propranolol , atropine , autonomic nervous system , refractory period , heart rate , cardiology , electrocardiography , sinus rhythm , pr interval , anesthesia , rhythm , prolongation , effective refractory period , interval (graph theory) , atrial fibrillation , blood pressure , mathematics , combinatorics
Recent investigations have clarified some of the effects of the autonomic nervous system on duration and spatial distribution of the Q‐T interval in humans. The use of atrial pacing to fix heart rate or 24‐hour continuous electrocardiographic recording to develop a regression formula for individual patients has provided a means to interpret the effects of an intervention that alters both the heart rate and the Q‐T interval. Drugs that affect Ihe autonomic nervous system can influence Q‐T interval directly or by changing rate. Bazett's formula to correct for rate may be misleading after certain drug interventions. For example, the Q‐T interval during sinus rhythm or afrial pacing and the ventricular effective refractory period shorten after atropine plus propranolol, but corrected Q‐T interval using Bazetf's formula does not change. No change occurs in the Q‐T interval during sinus rhythm or atrial pacing, or in ventricular effective refractory period after administration of propranolol although corrected Q‐T interval using Bazett's formula markedly shortens. Q‐T interval during sinus rhythm and atrial pacing and ventricular effective refractory period decrease after atropine but correct Q‐T interval lengthens. To define further the relationship of the autonomic nervous system on the duration of the Q‐T interval we studied the effects of sleep. Fifteen patients receiving no drugs underwent 3–6 days of continuous electrocardiography recordings. The duration of the Q‐T interval was longer during sleep in all 15 patients independent of heart rate change. This prolongation of the Q‐T interval during sleep may reflect increased parasympathetic tone or decreased sympathetic tone on the ventricle. Further investigation of the relation of the autonomic nervous system to ventricular depolarization and repolarization may delineate some of Ihe trigger mechanisms for the development of lethal ventricular arrhythmias in humans.