Syncop:
It is helpful to think about the pathophysiology of vasovagal syncope as a reflex arc, with an afferent limb and an efferent limb. Although the autonomic nervous system mediates vasovagal syncope, pathophysiological mechanisms are not completely understood. The afferent limb of the reflex arc begins with a trigger. Although this trigger may be emotional stress or pain, it is often unidentifiable. It is believed that this trigger, usually in combination with central hypovolemia (from upright posture or dehydration) results in increased cardiac contractility in the setting of a relatively underfilled left ventricle. This may trigger mechanoreceptors in the ventricle that signal via vagal afferents to the central nervous system.
The efferent limb of the reflex arc is better understood. Increased vagal firing (increased parasympathetic activity) at the sinus node and the atrioventricular node causes a decrease in heart rate. This decrease in heart rate can be profound, with asystole that can be several seconds long. At the same time, decreased sympathetic activity results in decreased vascular tone in both arterioles and venules. The results in decreased preload, venous return, and ventricular volume. Since cardiac output is the product of stroke volume and heart rate, this reflex arc affects both factors in the equation: slowing the heart rate and decreasing the amount of volume. This results in a drop in the patient's mean arterial pressure. Cerebral autoregulation results in constant cerebral blood flow over a wide range of mean arterial pressures, but when the mean arterial pressure falls below the body's ability to autoregulate, the patient loses consciousness. Typically, if the patient falls or is laid supine, the increase in circulating blood volume from the lower extremities combined with the decreased work necessary to get blood to the brain (i.e., the heart does not have to pump "uphill" against gravity) will cause the patient to regain consciousness rapidly.
@studentnote1
It is helpful to think about the pathophysiology of vasovagal syncope as a reflex arc, with an afferent limb and an efferent limb. Although the autonomic nervous system mediates vasovagal syncope, pathophysiological mechanisms are not completely understood. The afferent limb of the reflex arc begins with a trigger. Although this trigger may be emotional stress or pain, it is often unidentifiable. It is believed that this trigger, usually in combination with central hypovolemia (from upright posture or dehydration) results in increased cardiac contractility in the setting of a relatively underfilled left ventricle. This may trigger mechanoreceptors in the ventricle that signal via vagal afferents to the central nervous system.
The efferent limb of the reflex arc is better understood. Increased vagal firing (increased parasympathetic activity) at the sinus node and the atrioventricular node causes a decrease in heart rate. This decrease in heart rate can be profound, with asystole that can be several seconds long. At the same time, decreased sympathetic activity results in decreased vascular tone in both arterioles and venules. The results in decreased preload, venous return, and ventricular volume. Since cardiac output is the product of stroke volume and heart rate, this reflex arc affects both factors in the equation: slowing the heart rate and decreasing the amount of volume. This results in a drop in the patient's mean arterial pressure. Cerebral autoregulation results in constant cerebral blood flow over a wide range of mean arterial pressures, but when the mean arterial pressure falls below the body's ability to autoregulate, the patient loses consciousness. Typically, if the patient falls or is laid supine, the increase in circulating blood volume from the lower extremities combined with the decreased work necessary to get blood to the brain (i.e., the heart does not have to pump "uphill" against gravity) will cause the patient to regain consciousness rapidly.
@studentnote1