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Cardiac Parasympathetic Stimulation via QRS‐Synchronous Low‐Energy Shocks In Humans
Author(s) -
FRIEDMAN PAUL A.,
HILL MICHAEL R.S.,
STANTON MARSHALL S.
Publication year - 1999
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1999.tb00636.x
Subject(s) - medicine , qrs complex , atropine , cardiology , coronary sinus , shock (circulatory) , anesthesia , stimulation , intracardiac injection , prolongation
Parasympathetic Stimulation via Intracardiac Shocks. Introduction: In patients receiving test shocks to verify lead connections at implantation, we anecdotally have observed postshock delay. The purpose of this study was to determine whether QRS‐synchronous low‐energy shocks delivered by implantable defibrillators result in postshock cycle length prolongation, and to determine the mechanism of this phenomenon. Methods and Results: Twenty‐five patients undergoing defibrillator testing were studied, three with epicardial patches and 22 with transvenous leads. Each patient received QRSsynchronous shocks of 0.2, 0.4, 0.6, and 2.0 J in random order. Patients were further randomized to receive either saline or 2.0 mg atropine intravenously, and then given a second sequence of shocks. At baseline, the postshock cycle length (1, 035 ± 245 msec) was significantly longer than the preshock cycle length (968 ± 177 msec, P = 0.01). In patients with a coronary sinus (CS) or superior vena cava (SVC) lead, the mean prolongation was 91 ± 160 msec, compared with 12 ± 106 msec for patients without such a lead (P < 0.0001). All energy levels resulted in significant postshock prolongation compared with preshock cycle lengths (P < 0.05). Postshock prolongation before atropine was 76 ± 162 msec, compared with −13 ± 52 msec afterward (P < 0.00001). Biphasic shocks resulted in greater postshock prolongation than monophasic shocks of equal energy. Conclusion: Low‐energy shocks delivered during the QRS complex cause postshock cycle length prolongation in man. This effect required the presence of a CS or SVC lead. Atropine inhibited this effect, suggesting the phenomenon was mediated by direct cardiac parasympathetic nerve stimulation by the intracardiac shock.