Mechanism of Autonomic Mediated Syncope (Neurocardiogenic).
The exact mechanism of Autonomic Mediated syncope is not completely understood. One popular theory is that syncopal episodes may be due to inappropriate activation of stretch receptors (detectors) in the left ventricle (largest chamber of the heart). Normally, on standing upright about 500-1000 mls of blood is displaced by gravity from the chest to the lower limbs. Most of this change occurs in the first 10 seconds. In addition, with prolonged standing, about 700 ml of plasma leaks out off capillaries. As a consequence of the gravitational pooling and reduction in plasma volume the return of venous blood to the heart is reduced and blood pressure drops. Corrective mechanisms are triggered. The heart begins to beat more rapidly, the heart muscle contracts more vigorously and the blood vessels around the body constrict. These changes help restore the blood pressure to normal.
However, in patients with Autonomic Mediated Syncope, it is thought that the vigorous muscle contractions may inappropriately activate over sensitive stretch receptors in the left ventricular wall.
Normally these receptors are activated only if the pressure in the heart is too high. Activation triggers corrective mechanisms that act to increase vagal tone, thus slowing the heart rate, and reduce sympathetic tone, thus lowering the blood pressure. Unfortunately, in Autonomic Mediated Syncope the blood pressure is already too low and the corrective mechanisms triggered by the stretch receptors simply exacerbate the situation creating a vicious cycle which leads to a dramatic slowing of the heart rate and a precipitous fall in the blood pressure with syncope ensuing. (See Flow diagram)
Although this theory sounds very plausible, there is no hard evidence to support it. In fact, recent evidence appears to refute it. Increasingly it is thought that the problem lies with the control centres in the brain, rather than with the stretch receptors in heart muscle.