TY - JOUR
T1 - Effects of sudden change in cycle length on human atrial, atrioventricular nodal and ventricular refractory periods
AU - Wiener, I.
AU - Kunkes, S.
AU - Rubin, D.
AU - Kupersmith, J.
AU - Packer, M.
AU - Pitchon, R.
AU - Schweitzer, P.
PY - 1981
Y1 - 1981
N2 - In the steady state, the refractory periods of the human atrium, atrioventricular (AV) node, and ventricle are a function of cycle length. We compared the change in refractoriness that occurred when these refractory periods were measured after eight beats at a shorter cycle length with 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 msec, the atrial effective refractory period shortened 31 ± 24 msec (p < 0.01) when measured after eight beats at the shorter cycle length and 26 ± 24 msec (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 msec, the AV nodal effective refractory period increased 30 ± 39 msec (p < 0.05) when measured after eight beats and 31 ± 34 msec (p < 0.05) when measured after a single beat. The AV nodal functional refractory period showed moderate shortening with decreases in cycle length, both when measured after eight beats and when measured after a single beat (p = NS). For both the atrium and AV node, there was no significant difference between the change in refractoriness after a single beat at the shorter cycle length and after eight beats at the shorter cycle length. For a decrease in cycle length of 175 ± 52 msec, the ventricular effective refractory period shortened 26 ± 10 msec (p < 0.01) when measured after eight beats and 16 ± 12 msec (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 eight beats at the shorter interval (p < 0.01). These findings have implications for the performance and interpretation of stimulation studies and provide insight into the mechanism of initiation of tachycardia by premature beats.
AB - In the steady state, the refractory periods of the human atrium, atrioventricular (AV) node, and ventricle are a function of cycle length. We compared the change in refractoriness that occurred when these refractory periods were measured after eight beats at a shorter cycle length with 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 msec, the atrial effective refractory period shortened 31 ± 24 msec (p < 0.01) when measured after eight beats at the shorter cycle length and 26 ± 24 msec (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 msec, the AV nodal effective refractory period increased 30 ± 39 msec (p < 0.05) when measured after eight beats and 31 ± 34 msec (p < 0.05) when measured after a single beat. The AV nodal functional refractory period showed moderate shortening with decreases in cycle length, both when measured after eight beats and when measured after a single beat (p = NS). For both the atrium and AV node, there was no significant difference between the change in refractoriness after a single beat at the shorter cycle length and after eight beats at the shorter cycle length. For a decrease in cycle length of 175 ± 52 msec, the ventricular effective refractory period shortened 26 ± 10 msec (p < 0.01) when measured after eight beats and 16 ± 12 msec (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 eight beats at the shorter interval (p < 0.01). These findings have implications for the performance and interpretation of stimulation studies and provide insight into the mechanism of initiation of tachycardia by premature beats.
UR - http://www.scopus.com/inward/record.url?scp=0019461582&partnerID=8YFLogxK
U2 - 10.1161/01.CIR.64.2.245
DO - 10.1161/01.CIR.64.2.245
M3 - Article
AN - SCOPUS:0019461582
VL - 64
SP - 245
EP - 248
JO - Unknown Journal
JF - Unknown Journal
IS - 2
ER -