Effects of sudden change in cycle length on human atrial, atrioventricular nodal and ventricular refractory periods.
Author(s) -
Isaac Wiener,
Steven H. Kunkes,
David Rubin,
Joel Kupersmith,
Milton Packer,
Roberta Pitchon,
Paul Schweitzer
Publication year - 1981
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.64.2.245
Subject(s) - medicine , cardiology , atrial flutter , effective refractory period , refractory period , atrial fibrillation
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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom