Pathophysiology and management of neurocardiogenic syncope

Objective: To discuss the physiologic mechanisms underlying neurocardiogenic syncope in the context of several different management strategies. Pathophysiology: Neurocardiogenic syncope or the "common faint" is variously called neurally mediated hypotension, vasovagal syncope, or vasodepressor syncope. It is the most common type of syncope. The pathophysiology of neurocardiogenic syncope is complex and not completely elucidated. Individuals susceptible to neurocardiogenic syncope are unable to maintain the adaptive neurocardiovascular responses to upright posture for prolonged periods. These patients tend to have a modest reduction in central blood volume, which is aggravated by upright posture. It is often noted in individuals receiving sympathetic blocking agents and vasodilator drugs for hypertension, elderly patients receiving tranquilizers, patients with anemia, and individuals with transient reductions in blood volume such as those that occur after a brisk diuresis or blood donation. The classic syncopal episode often is preceded by a constellation of prodromal symptoms several seconds before the event that may include nausea, headache, diaphoresis, dizziness, chest pain, palpitations, dyspnea, and paresthesia. Management: Head-up tilt testing has become the diagnostic study of choice for the identification of patients with neurocardiogenic syncope. Therapeutic options include general measures such as volume expansion; pharmacologic approaches such as beta-adrenergic receptor blockade, anticholinergic agents, selective, serotonin reuptake inhibitors, methylxanthines, and alpha agonists; and invasive methods such as placement of a dual-chamber cardiac pacemaker.