The Prolongation of QRS-Duration Resulting from Delayed Recovery of Ventricular Excitability : A New Mechanism for Intraventricular Conduction Disturbance A Preliminary Note

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Chlorpromazine (1, 5, and 20mg/Kg) was injected intravenously to anesthetized and open-chest dogs under artificial respiration. Using right atrial pacing, the heart rate was increased stepwise from intrinsic sinus rate to higher rate where the A-V block first developed. ECG (II) was recorded simultaneously with arterial blood pressure, ventricular monophasic action potentials and left atrial electrogram. In the control, QRS-duration was constant (46.9±0.8 msec) irrespective of heart rate. After the drug injection, however, the duration increased significantly with increasing heart rate, the effect depending on the injected dosage (r=0.283, P<0.1 in 1mg/Kg ; r=0.406, P<0.01 in 5mg/Kg ; r=0.631, P<0.001 in 20mg/Kg). During the drug action, QRS-duration of atrial premature beats was also longer than that of sinus beats, and the lengthening increased with shortening of preceding cycle length. The observed QRS-prolongations were due to neither incomplete ventricular repolarization nor bundle branch block. The mechanism of prolongation was attributed to delayed or time-dependent recovery of ventricular excitability, i.e., slowed removal of inactivation in rapid sodium system in the ventricular muscle fibers.
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