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Integration of heart rate and sympathetic neural effects on AV conduction
1Department of Surgery and Physiology, Northwestern University Medical School, Chicago, Illinois 60611.
Insights
Sympathetic stimulation
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Function
Background:
- Sympathetic activation typically increases heart rate (HR) and decreases atrioventricular interval (AVI).
- Atrial pacing alone, however, increases AVI.
- Differentiating direct sympathetic effects on AV conduction from indirect HR-mediated changes is crucial.
Purpose of the Study:
- To isolate and quantify the direct impact of sympathetic activation on atrioventricular (AV) conduction time.
- To compare AV conduction during sympathetic stimulation versus artificial pacing at similar heart rates.
- To understand the interplay between heart rate and sympathetic tone in modulating AV nodal function.
Main Methods:
- Utilized chloralose-anesthetized, autonomically decentralized dogs for electrophysiological recordings.
- Continuously monitored beat-by-beat electrocardiograms, blood pressure, and intracardiac electrograms.
- Administered propranolol via the sinoatrial node artery to assess direct sympathetic effects.
Main Results:
- Sympathetic stimulation increased HR by 60 bpm and decreased AVI by 22 ms.
- Atrial pacing to match sympathetic HR increase resulted in a 10 ms AVI increase.
- Direct sympathetic stimulation (post-propranolol) caused a 14.8 ms AVI decrease without HR change.
- AV conduction differed significantly when identical HRs were achieved via sympathetic stimulation versus atrial pacing.
Conclusions:
- Sympathetic activity directly influences AV conduction, but its effect is modulated by concurrent heart rate changes.
- The direct effect of sympathetic stimulation on the AV node is less potent in altering AV conduction compared to when heart rate increases simultaneously.
- The relationship between heart rate and sympathetic tone on AV conduction is complex and not strictly linear.
Abstract:
Sympathetic activation increases heart rate (HR) and reduces atrioventricular interval (AVI), whereas atrial pacing alone increases AVI. We sought to differentiate the direct effects of sympathetic activation on atrioventricular (AV) conduction time from the indirect changes associated with concurrent alterations in HR. We recorded electrocardiograms, blood pressure (BP), and intracardiac electrograms from chloralose-anesthetized autonomically decentralized dogs. Beat-by-beat HR and AVI data were collected continuously. Sympathetic stimulation (0.25-2.5 Hz; mean 0.81 Hz) resulted in a HR change of +60 beats/min after 60 s. This tachycardia was associated with a mean decrease in AVI of 22 ms. Computer-driven atrial pacing to reproduce the HR associated with control sympathetic stimulation caused a mean AVI increase of 10 ms. Propranolol (200 micrograms) was then administered via the sinoatrial node artery and sympathetic stimulation repeated. Although HR remained constant, AVI decreased by 14.8 ms. The AVIs associated with an identical HR achieved by two different mechanisms (sympathetic stimulation and atrial pacing) were significantly different. Although removal of the contribution of sympathetically induced HR changes on AV conduction might be expected to result in potentiation of neural effects at the AV node, none was evident. Thus sympathetic activity restricted to the AV node is less effective in influencing AV conduction than the response that occurs when HR changes occur concurrently. Therefore, the opposing actions of HR and sympathetic tone on AV conduction may not be predicted by a simple linear relationship.