Mechanism of Vasovagal Syncope
The correct answer is that vasovagal syncope occurs through an abnormal decrease in sympathetic vasoconstriction (leading to vasodilation) combined with increased parasympathetic activity (causing bradycardia), not through sudden sympathetic activation—making none of the provided options entirely accurate, though option D comes closest by describing reduced sympathetic activity, vasodilation, and bradycardia. 1
Pathophysiological Mechanism
The European Society of Cardiology guidelines clearly establish that vasovagal syncope is a reflex-mediated phenomenon with distinct afferent and efferent pathways 1:
Afferent Pathway (Trigger Phase)
- Information transfers from circulatory and visceral receptors (arterial baroreceptors in the aortic arch and carotid sinus) through the glossopharyngeal (IX) and vagus (X) nerves to the vasomotor centers in the brainstem 1
- Triggers include hemodynamic instability (central hypovolemia, hypotension, tachycardia), emotional stress, pain, or gastrointestinal symptoms 1
- Higher brain functions (emotional triggers like fear or blood phobia) can directly activate or facilitate the reflex 1, 2
Efferent Pathway (Response Phase)
The reflex produces two main effector mechanisms 1, 3:
1. Vasodepressor Component (Sympathetic Withdrawal):
- Abnormal decrease in sympathetic vasoconstriction causes vasodilation, particularly in splanchnic and lower limb capacitance vessels 1
- This is NOT sympathetic activation but rather sympathetic inhibition or withdrawal 1
- Direct measurements show complete disappearance of muscle sympathetic nerve activity at the moment of syncope 4, 5
2. Cardioinhibitory Component (Parasympathetic Activation):
- Increased vagal (parasympathetic) activity causes bradycardia or even asystole 1
- The vagus nerve mediates this cardiac slowing 1
Why the Answer Options Are Problematic
Option A is incorrect: Vasovagal syncope does not involve abnormal electrical brain activity or seizures—it is a cardiovascular reflex causing cerebral hypoperfusion 1
Option B is incorrect: This describes the opposite of what occurs. Vasovagal syncope involves withdrawal or reduction of sympathetic activity, not sudden activation 1, 4
Option C is incorrect: While transient arrhythmias (bradycardia/asystole) can occur, they are secondary to the reflex mechanism, not the primary cause 1
Option D is closest but imprecise: It correctly identifies vasodilation and bradycardia, but the phrase "reduction in sympathetic and parasympathetic activity" is misleading—parasympathetic activity actually increases (causing bradycardia) while sympathetic activity decreases 1, 6, 4
Clinical Sequence
Research demonstrates the temporal progression 1, 4:
- Initial phase: Venous pooling below the diaphragm reduces central blood volume and cardiac output 1
- Compensatory phase: Initially, sympathetic activity may increase to maintain blood pressure 4, 5
- Trigger phase: Progressive circulatory changes with baroreceptor dysfunction lead to disorganized sympathetic discharge 1
- Syncope phase: Abrupt and complete withdrawal of sympathetic activity combined with vagal activation causes precipitous blood pressure drop and bradycardia/asystole 4, 5
Key Clinical Pitfall
The most common misconception is that vasovagal syncope involves sympathetic "overactivity" or "activation"—the exact opposite is true. The hallmark is sympathetic withdrawal leading to loss of vasoconstrictor tone 1, 4.