Effects of sudden change in cycle length on human atrial, atrioventricular nodal and ventricular refractory periods.

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Abstract
In the steady state, the refractory periods of the human atrium, atrioventricular (AV) node, and ventricle are a function of cycle length. The change in refractoriness that occurred when these refractory periods were measured after 8 beats at a shorter cycle length were compared to the change that occurred when these refractory periods were measured after a single beat at the shorter cycle length. For a decrease in cycle length of 235 .+-. 63 ms, the atrial effective refractory period shortened 31 .+-. 24 ms (P < 0.01) when measured after 8 beats at the shorter cycle length, and 26 .+-. 24 ms (P < 0.01) when measured after a single beat at the shorter cycle length. Similar changes were seen in atrial functional refractory period. For a decrease in cycle length of 214 .+-. 63 ms, the AV nodal effective refractory period increased 30 .+-. 39 ms (P < 0.05) when measured after 8 beats, and 31 .+-. 34 ms (P < 0.05) when measured after a single beat. The AV nodal functional refractory period showed moderate shortening with decreases in cycle length when measured after both 8 beats and a single beat (P = NS [not significant]). For both the atrium and AV node, there was no significant difference the change in refractoriness after a single beat or after 8 beats at the shorter cycle length. For a decrease in cycle length of 175 .+-. 52 ms, the ventricular effective refractory period shortened 26 .+-. 10 ms (P < 0.01) when measured after 8 beats, and 16 .+-. 12 ms (P < 0.01) when measured after a single beat at the shorter cycle length. Thus a single beat at the shorter interval produced 60% of the shortening of refractoriness produced by 8 beats at the shorter interval (P < 0.01). These findings may provide insight into the mechanism of initiation of tachycardia by premature beats.