Baroreflex Failure Syndrome: Pathophysiology and Clinical Implications

Immediate Cardiovascular Consequences

The European Society of Cardiology notes that cutting the nerves to the baroreceptors results in loss of baroreceptor reflex control, leading to severe blood pressure lability with volatile hypertension, orthostatic hypotension, inadequate vasoconstriction, and chronotropic incompetence 1, 2
Loss of buffering capacity against blood pressure fluctuations occurs because arterial baroreceptors in the carotid sinus and aortic arch can no longer transfer information via the glossopharyngeal (IX) and vagus (X) nerves to the vasomotor centers in the brainstem 3, 1
Inadequate vasoconstriction develops because the efferent sympathetic pathway cannot receive appropriate feedback to regulate vascular tone, particularly in the splanchnic region and lower limbs 1, 2
Chronotropic incompetence manifests as the inability to appropriately increase heart rate in response to postural changes or other stressors 1, 2

Severe orthostatic hypotension results from the inability to increase peripheral vascular resistance upon standing 1, 2
Venous pooling below the diaphragm occurs without compensatory vasoconstriction, leading to decreased venous return and cardiac output 2, 4
The key deficit is failure of vascular tone adjustment, as vasoconstriction is the critical factor in maintaining arterial pressure in the upright posture 5, 4

Control of vasomotor function by the arterial baroreflex is the key mechanism for rapid hemodynamic adjustments to postural changes 3, 1
Baroreceptor malfunctioning disorganizes the discharge activity of vascular sympathetic fibers, leading to ineffective vasoconstrictor activity 1
The loss of baroreceptor reflex control is multifactorial and can be exacerbated by other factors such as fluid depletion or medications 6
Reduction in systemic vascular resistance becomes unregulated, particularly problematic during situations requiring rapid cardiovascular adjustment 7, 6

The condition produces labile hemodynamics similar to but more severe than those seen in hypertensive patients undergoing anesthesia 7, 6