Syncope: Etiology and diagnostic approach

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ABSTRACTThere are three major types of syncope: neurally mediated (the most common), orthostatic hypotensive, and cardiac (the most worrisome). Several studies have shown a normal long-term survival rate in patients with syncope who have no structural heart disease, which is the most important predictor of death and ventricular arrhythmia. The workup of unexplained syncope depends on the presence or absence of heart disease: electrophysiologic study if the patient has heart disease, tilt-table testing in those without heart disease, and prolonged rhythm monitoring in both cases if syncope remains unexplained.


  • Neurally mediated forms of syncope, such as vasovagal, result from autonomic reflexes that respond inappropriately, leading to vasodilation and relative bradycardia.
  • Orthostatic hypotension is the most common cause of syncope in the elderly and may be due to autonomic dysfunction, volume depletion, or drugs that block autonomic effects or cause hypovolemia, such as vasodilators, beta-blockers, diuretics, neuropsychiatric medications, and alcohol.
  • The likelihood of cardiac syncope is low in patients with normal electrocardiographic and echocardiographic findings.
  • Hospitalization is indicated in patients with syncope who have or are suspected of having structural heart disease.



Syncope is a transient loss of consciousness and postural tone with spontaneous, complete recovery. There are three major types: neurally mediated, orthostatic, and cardiac (Table 1).


Neurally mediated (reflex) syncope is the most common type, accounting for two-thirds of cases.1–3 It results from autonomic reflexes that respond inappropriately, leading to vasodilation and bradycardia.

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Neurally mediated syncope is usually preceded by premonitory symptoms such as lightheadedness, diaphoresis, nausea, malaise, abdominal discomfort, and tunnel vision. However, this may not be the case in one-third of patients, especially in elderly patients, who may not recognize or remember the warning symptoms. Palpitations are frequently reported with neurally mediated syncope and do not necessarily imply that the syncope is due to an arrhythmia.4,5 Neurally mediated syncope does not usually occur in the supine position4,5 but can occur in the seated position.6

Subtypes of neurally mediated syncope are as follows:

Vasovagal syncope

Vasovagal syncope is usually triggered by sudden emotional stress, prolonged sitting or standing, dehydration, or a warm environment, but it can also occur without a trigger. It is the most common type of syncope in young patients (more so in females than in males), but contrary to a common misconception, it can also occur in the elderly.7 Usually, it is not only preceded by but also followed by nausea, malaise, fatigue, and diaphoresis4,5,8; full recovery may be slow. If the syncope lasts longer than 30 to 60 seconds, clonic movements and loss of bladder control are common.9

Mechanism. Vasovagal syncope is initiated by anything that leads to strong myocardial contractions in an "empty" heart. Emotional stress, reduced venous return (from dehydration or prolonged standing), or vasodilation (caused by a hot environment) stimulates the sympathetic nervous system and reduces the left ventricular cavity size, which leads to strong hyperdynamic contractions in a relatively empty heart. This hyperdynamic cavity obliteration activates myocardial mechanoreceptors, initiating a paradoxical vagal reflex with vasodilation and relative bradycardia.10 Vasodilation is usually the predominant mechanism (vasodepressor response), particularly in older patients, but severe bradycardia is also possible (cardioinhibitory response), particularly in younger patients.7 Diuretic and vasodilator therapies increase the predisposition to vasovagal syncope, particularly in the elderly.

On tilt-table testing, vasovagal syncope is characterized by hypotension and relative bradycardia, sometimes severe (see Note on Tilt-Table Testing).10–12

Situational syncope

Situational syncope is caused by a reflex triggered in specific circumstances such as micturition, defecation, coughing, weight-lifting, laughing, or deglutition. The reflex may be initiated by a receptor on the visceral wall (eg, the bladder wall) or by straining that reduces venous return.

Carotid sinus hypersensitivity

Carotid sinus hypersensitivity is an abnormal response to carotid massage, predominantly occurring in patients over the age of 50. In spontaneous carotid sinus syndrome, syncope clearly occurs in a situation that stimulates the carotid sinus, such as head rotation, head extension, shaving, or wearing a tight collar. It is a rare cause of syncope, responsible for about 1% of cases. Conversely, induced carotid sinus syndrome is much more common and represents carotid sinus hypersensitivity in a patient with unexplained syncope and without obvious triggers; the abnormal response is mainly induced during carotid massage rather than spontaneously. In the latter case, carotid sinus hypersensitivity is a marker of a diseased sinus node or atrioventricular node that cannot withstand any inhibition. This diseased node is the true cause of syncope rather than carotid sinus hypersensitivity per se, and carotid massage is a "stress test" that unveils conduction disease.

Palpitations do not necessarily imply that syncope is due to an arrhythmia

Thus, carotid massage is indicated in cases of unexplained syncope regardless of circumstantial triggers. This test consists of applying firm pressure over each carotid bifurcation (just below the angle of the jaw) consecutively for 10 seconds. It is performed at the bedside, and may be performed with the patient in both supine and erect positions during tilt-table testing; erect positioning of the patient increases the sensitivity of this test.

An abnormal response to carotid sinus massage is defined as any of the following13–15:

  • Vasodepressor response: the systolic blood pressure decreases by at least 50 mm Hg
  • Cardioinhibitory response: sinus or atrioventricular block causes the heartbeat to pause for 3 or more seconds
  • Mixed vasodepressor and cardioinhibitory response.

Overall, a cardioinhibitory component is present in about two-thirds of cases of carotid sinus hypersensitivity.

Carotid sinus hypersensitivity is found in 25% to 50% of patients over age 50 who have had unexplained syncope or a fall, and it is seen almost equally in men and women.13

One study correlated carotid sinus hypersensitivity with the later occurrence of asystolic syncope during prolonged internal loop monitoring; subsequent pacemaker therapy reduced the burden of syncope.14 Another study, in patients over 50 years old with unexplained falls, found that 16% had cardioinhibitory carotid sinus hypersensitivity. Pacemaker placement reduced falls and syncope by 70% compared with no pacemaker therapy in these patients.15

On the other hand, carotid sinus hypersensitivity can be found in 39% of elderly patients who do not have a history of fainting or falling, so it is important to rule out other causes of syncope before attributing it to carotid sinus hypersensitivity.

Postexertional syncope

While syncope on exertion raises the worrisome possibility of a cardiac cause, postexertional syncope is usually a form of vasovagal syncope. When exercise ceases, venous blood stops getting pumped back to the heart by peripheral muscular contraction. Yet the heart is still exposed to the catecholamine surge induced by exercising, and it hypercontracts on an empty cavity. This triggers a vagal reflex.

Postexertional syncope may also be seen in hypertrophic obstructive cardiomyopathy or aortic stenosis, in which the small left ventricular cavity is less likely to tolerate the reduced preload after exercise and is more likely to obliterate.


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