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Autonomic control of vasovagal syncope
D L Jardine1, H Ikram, C M Frampton
1Department of Cardiology, Christchurch Hospital, Christchurch, New Zealand.
The American Journal of Physiology
|June 25, 1998
Summary
Baroreceptor sensitivity (BS) may contribute to vasovagal syncope by influencing sympathetic withdrawal during orthostasis. This study investigated the interplay between BS, sympathetic, and parasympathetic activity in syncope initiation.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Function
Background:
- The precise interaction between baroreceptor sensitivity (BS), sympathetic withdrawal, and parasympathetic activity in vasovagal syncope remains unclear.
- Altered BS may predispose individuals to abnormal autonomic responses during orthostasis, potentially leading to hypotension and syncope.
Purpose of the Study:
- To investigate the hypothesis that altered baroreceptor sensitivity (BS) contributes to abnormal sympathetic and parasympathetic responses during orthostasis, precipitating vasovagal syncope.
Main Methods:
- Continuous monitoring of blood pressure (BP), heart rate (HR), BS, forearm blood flow, and muscle nerve sympathetic activity (MNSA).
- Measurements were taken in 18 vasovagal syncope patients during head-up tilt, syncope, and recovery, compared to 17 healthy controls.
Main Results:
- During early tilt, BP was maintained by increased HR and MNSA, but BS decreased more in the syncopal group.
- At presyncope, falling BP correlated with increased sympathetic activity, while BS increased to baseline.
- At syncope, BP, HR, and sympathetic activity decreased, with no increase in BS. Vasodilatation and bradycardia were linked to sympathetic withdrawal.
Conclusions:
- The exact mechanism initiating hypotension during presyncope is unknown, but baroreceptor sensitivity (BS) may play a role.
- Vasodilatation and bradycardia in presyncope appear more related to sympathetic withdrawal than increased parasympathetic activity.