PubMed1982
The possible role of the atrioventricular nodal (AVN) function curve during tachycardia as a cause of cycle length alternation was investigated using a computer model of circus movement tachycardia utilizing an atrioventricular accessory pathway. Two types of AVN function curves during tachycardia were entered into the computer: straight lines of various gradients and representative examples of patient-based AVN function curves obtained during clinical electrophysiologic studies. Perturbations of the tachycardia model were induced by introducing a short cycle, by suddenly prolonging a conduction interval, or by moving the AVN function curve relative to that in stable tachycardia. Using the straight line AVN function curves, stable, sustained cycle length alternation could be induced by perturbation of the tachycardia cycle if the gradient of the line was -1 (slope = 45 degrees). If the gradient was more than -1 (slope less than 45 degrees), the perturbation was damped. If the gradient was less than -1 (slope greater than 45 degrees), the perturbation was amplified, leading to termination of tachycardia by block in the AVN. Similar but more complex responses to perturbation of tachycardia were found using patient-based AVN function curves. Thus, sustained cycle length alternation and amplification or damping of perturbation could be produced. Using physiologic AVN function curves, the response to perturbation of tachycardia depended on the interrelationship of the shape of the AVN function curve, the location of the cycle length of tachycardia on the curve, the magnitude and direction of the perturbation, and the AVN effective refractory period. We conclude that cycle length alternation during tachycardia may be explained by the characteristics of a single antegrade AVN function curve without postulating the presence of additional AVN pathways. The stability of circus movement tachycardias depends on the interaction of several variables.