Effect of atropine on escape mechanism of the subsidiary pacemakers in patients with dysfunction of the sinus node.
Effects of intravenous atropine on postpacing impulse recovery time of the subsidiary pacemakers were studied by incremental atrial pacing in 9 patients with sinus nodal (SN) dysfunction. Patients having either or both of the following anomalies are used: 1) persistent sinus bradycardia (sinus cycle length greater than 1000 msec), or documented episodes of sinoatrial block or arrest and/or 2) maximum corrected SN recovery time of longer than 525 msec before and after atropine. Seven patients had a history of cerebral ischemic symptoms. The mean +/- SEM of the maximum A-V junctional recovery times (MJRTs) before and after atropine, measured in 5 patients, were 2,485 +/- 825 msec and 1,164 +/- 281 msec, respectively (p less than 0.01). The average percent reduction of the junctional escape times in these 5 patients was 53.2%. In all 9 patients MJRT shortened to less than 1,610 msec after atropine. Moreover, a low atrial pacemaker also was the escape mechanism following pacing in 2 patients after atropine; the maximum atrial recovery times were 2,500 msec and 1,220 msec, respectively. We conclude that atropine can markedly enhance escape mechanism of the subsidiary pacemakers in patients with SN dysfunction.
D000328:Adult; D001285:Atropine / Q000008:administration & dosage / Q000494:pharmacology*; D001919:Bradycardia / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004562:Electrocardiography; D005260:Female; D006327:Heart Block / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012848:Sinoatrial Block / Q000503:physiopathology*; D012849:Sinoatrial Node / Q000503:physiopathology
D001285:Atropine