Cardiac parasympathetic stimulation via QRS-synchronous low-energy shocks in humans

Paul Andrew Friedman, M. R S Hill, Marshall S. Stanton

Research output: Contribution to journalArticle

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Abstract

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 QRS-synchronous 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.

Original languageEnglish (US)
Pages (from-to)10-16
Number of pages7
JournalJournal of Cardiovascular Electrophysiology
Volume10
Issue number1
StatePublished - 1999

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Shock
Atropine
Superior Vena Cava
Coronary Sinus
Defibrillators
Implantable Defibrillators

Keywords

  • Implantable defibrillator
  • Intracardiac shock
  • Parasympathetic nervous system

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Cardiac parasympathetic stimulation via QRS-synchronous low-energy shocks in humans. / Friedman, Paul Andrew; Hill, M. R S; Stanton, Marshall S.

In: Journal of Cardiovascular Electrophysiology, Vol. 10, No. 1, 1999, p. 10-16.

Research output: Contribution to journalArticle

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AB - 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 QRS-synchronous 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.

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