Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1998;97:2245-2251

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Skanes, A. C.
Right arrow Articles by Tang, A. S. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Skanes, A. C.
Right arrow Articles by Tang, A. S. L.

(Circulation. 1998;97:2245-2251.)
© 1998 American Heart Association, Inc.


Clinical Investigation and Reports

Ventriculophasic Modulation of Atrioventricular Nodal Conduction in Humans

Allan C. Skanes, MD, FRCPC; ; Anthony S. L. Tang, MD, FRCPC

From the Department of Medicine, University of Ottawa, Ontario, Canada.

Correspondence to Dr A.S.L. Tang, University of Ottawa Heart Institute, 1053 Carling Ave, Ottawa, Ontario K1Y 4E9, Canada. E-mail ttang{at}heartinst.on.ca

Background—Baroreceptor-mediated phasic changes in vagal tone have been hypothesized to cause ventriculophasic sinus arrhythmia (VPSA). The objectives of this study were to demonstrate ventriculophasic modulation of AV nodal conduction and to substantiate the role of the baroreflex on ventriculophasic AV nodal conduction (VPAVN) by pharmacological perturbation of parasympathetic tone.

Methods and Results—Twelve patients with infra-Hisian second-degree heart block and VPSA were studied. Incremental atrial pacing was performed until AV nodal Wenckebach block at baseline, after phenylephrine infusion, and after atropine. AV nodal conduction curves were constructed for each phase and compared. At baseline, VPAVN was present in 9 of 12 patients on the steep portion of the AV nodal conduction curves. Phenylephrine increased systolic blood pressure from 149±33 to 177±22 mm Hg (P<0.001) and sinus cycle length from 844±169 to 1010±190 ms (P<0.001) and shifted the AV nodal conduction curves up and to the right. Phenylephrine induced VPAVN in 2 of 3 patients in whom it was not present at baseline and in 11 of 12 total. Atropine abolished both VPSA and VPAVN in all patients.

Conclusions—VPAVN was demonstrated in patients with infra-Hisian second-degree AV block. It was accentuated by phenylephrine and abolished by atropine, suggesting a baroreflex mechanism for VPSA and VPAVN.


Key Words: arrhythmia • baroreceptors • vagus nerve • atrioventricular node • phenylephrine