Sympathetic neural responses to induced ventricular tachycardia

Michael L. Smith, Kenneth A. Ellenbogen, Larry A. Beightol, Dwain L. Eckberg

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


Although sympathetic mechanisms play a major role in buffering abrupt arterial pressure reductions, including those that occur during tachyarrhythmias, human sympathetic nervous system responses to ventricular tachycardia have not been measured. Muscle sympathetic nerve activity was recorded directly from the peroneal nerve in 16 patients during diagnostic induction of 19 episodes of sustained monomorphic ventricular tachycardia (average rate 189 beats/min, range 130 to 250). Average systolic and diastolic pressures decreased from 149 78 to 61 49 mm Hg by 10 s and increased toward baseline levels to 88 64 mm Hg by 1 min of ventricular tachycardia. Average sympathetic nerve activity increased by 92% at 10 s in direct proportion to arterial pressure reductions and in inverse proportion to ventricular rate and remained 83% above baseline levels at 1 min. The late recovery of arterial pressure during ventricular tachycardia was related significantly to the magnitude of early sympathetic responses. Sympathetic activity tended to lose its discrete bursting pattern during ventricular tachycardia, and power spectral analysis showed that the large sympathetic peaks at the heart rate frequency present during sinus rhythm are absent during ventricular tachycardia. This study is the first to delineate human sympathetic nervous system responses to ventricular tachycardia. The results suggest that in the patients studied, large early sympathetic surges differed from those that occur during sinus rhythm and contributed to hemodynamic stability during ventricular tachycardia.

Original languageEnglish
Pages (from-to)1015-1024
Number of pages10
JournalJournal of the American College of Cardiology
Issue number4
StatePublished - Oct 1991


Dive into the research topics of 'Sympathetic neural responses to induced ventricular tachycardia'. Together they form a unique fingerprint.

Cite this