Experimental alteration of A-V nodal function provides insight into the physiological mechanisms of ventricular aberration.
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Does not inform clinical management of ventricular aberration; leaves open mechanistic translation from animal models.
The auriculoventricular node usually performs the important function of delaying the auricular impulse in its passage to the ventricles. Direct proof that the site of the delay is at the A-V node has been provided experimentally in this laboratory by Osborne and co-workers.¹Without this delay the auricles and ventricles would contract practically at the same time, with the resulting decrease in ventricular filling, and the auricles would become functionally useless. When the delaying function of the node is altered, various degrees of block occur, or, on the contrary, conduction through the node becomes accelerated. At the same time, aberrant ventricular complexes of widely varying configuration and timing frequently appear.² Since a knowledge of the relationship between A-V nodal disturbances and various ventricular aberrations appeared important clinically as well as physiologically, experiments were designed to study this relationship more fully. As noted in previous reports,* alteration of nodal
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Louis Rakita (1956) studied this question.
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