Vasovagal Episode

Etiology

The etiology of vasovagal syncope is unclear. Some believe that the vasovagal reaction is an exaggeration of an adaptive response meant to assist in hemostasis in times of trauma. In other words, in the setting of physical trauma, the body reflexively lowers blood pressure and heart rate to reduce the amount of bleeding. Others have sought a genetic link for the syndrome. [5]Research elucidating a genetic predisposition for vasovagal syncope is challenging due to the high background incidence of the disease, but genomic analysis demonstrates some differences in copy number variations in families with a high burden of reflex syncope. More research in this area is warranted.

Epidemiology

Vasovagal syncope is the most common form of syncope in adults. More than 85% of syncopal events in people younger than 40 years are attributable to vasovagal syncope. Even in geriatric patients, more than 50% of syncopal episodes are due to vasovagal syncope. Vasovagal syncope requires an intact and functioning autonomic nervous system, and therefore, its incidence is low in populations with autonomic nervous system dysfunction, such as patients with Parkinson disease. The lifetime incidence of an episode of vasovagal syncope is more than 33%.

Pathophysiology

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.

Toxicokinetics

Although vasovagal syncope occurs secondary to a reflex arc with an unclear trigger, in patients who are susceptible, medications that cause alterations in heart rate or vascular tone may exacerbate symptoms.

History and Physical

The differential diagnosis for syncope is broad and includes cardiac arrhythmia, acute blood loss, seizure, orthostasis, dehydration, dissection, subarachnoid hemorrhage, pulmonary embolus, ruptured ectopic pregnancy, trauma (concussion, epidural hematoma), toxins, and many other pathologies. History and physical exam should focus on ruling out life-threatening entities before a diagnosis of vasovagal syncope. Patients should be asked specifically about family and personal history of cardiovascular diseases, the potential for gastrointestinal blood loss, the potential for genitourinary blood loss, and medications that could be complicating the presentation (i.e., antihypertensives, antihistamines, anticholinergics, anticoagulants). Patients with syncope also frequently require a trauma evaluation to assess for injuries sustained during the syncopal event.

Most patients with vasovagal syncope present with a history of a syncopal prodrome. Patients will classically describe a feeling of lightheadedness. Feelings of warmth and nausea are common. Many patients describe tunnel vision, ringing in their ears, and profuse sweating. Patients should return to consciousness spontaneously. During the event, the patient will usually be bradycardic, hypotensive, pale, and diaphoretic. After the event, the patient should have an entirely normal physical exam. Abnormalities on physical exam (such as tongue biting, which suggests seizure, or ongoing pallor, which suggests symptomatic anemia) or atypical history should prompt a more thorough evaluation into the underlying cause of syncope.

Evaluation

Every patient with a complaint of syncope should have a complete history and physical exam, with attention to the presence or absence of pallor, cardiac abnormalities (murmurs, tachy/bradydysrhythmias, and irregular heartbeat), pulmonary abnormalities, and signs of trauma. Patients may require radiographic studies of trauma sustained during the vasovagal event.[6][7][8][6]

Every person undergoing evaluation for syncope including presumed vasovagal syncope should have an ECG to look for evidence of underlying arrhythmogenic cardiac abnormalities, such as Wolff-Parkinson-White syndrome, prolonged QT syndrome, Brugada syndrome, or heart blocks. It is also wise to check for pregnancy in women of childbearing potential. Strong consideration should be given to fecal blood testing in patients in whom blood loss anemia is suspected, as hemoglobin may be normal in patients with acute hemorrhage.

Further emergency evaluation for syncope is tailored based on the presentation of the patient and existing comorbid conditions. In healthy patients with a classic history of vasovagal syncope, a normal exam, and a normal ECG, no further testing is indicated, and laboratory testing is low yield. When a diagnosis is not certain, or when patients have multiple potential causes of syncope, serum electrolyte testing, complete blood count, and cardiac enzymes may be indicated.

In patients with recurrent syncope or when a diagnosis remains elusive, Holter monitoring, event monitoring, and tilt table testing may be used in an outpatient setting to define the etiology of syncope better.

Treatment / Management

Typically, vasovagal syncope is treated conservatively. When known and avoidable, patients are instructed to avoid triggers. Patients are also instructed to drink more fluids to improve their volume status (and therefore their preload) and to change positions slowly. Patients are educated as to the "warning signs" of a vasovagal event and instructed to place themselves in a supine position should they feel an event coming. This often prevents actual syncope and reduces traumatic risk from falling. In refractory or disabling cases and cases of prolonged asystole, cardiac pacing is a therapeutic option.[9][10][11][12](B2)

Differential Diagnosis

• Dehydration

• Diabetic neuropathy

• Diuresis

• Drug-induced orthostasis

• Dysautonomia

• Ectopic pregnancy

• Haemorrhage

• Hypotension

• Hypovolemia

• Multisystem atrophy

• Peripheral polyneuropathy

• Postural hypotension

• Subclavian steal

• Vasomotor insufficiency