Chapter 21. Syncope

Syncope accounts for up to 2% of all ED visits and 6% of hospital admissions. Syncope is defined as a transient loss of consciousness accompanied by loss of postural tone, followed by complete resolution without intervention. Although syncope typically is a benign vasovagal event, it may represent a life-threatening dysrhythmia/condition, particularly in the elderly. In up to half of syncope cases presenting to the ED, there is no definite etiology established for the syncopal episode.

Syncope is most commonly reflex mediated. A sympathetic response to stress is suddenly withdrawn, leading to pronounced vagal tone with hypotension or bradycardia. The hallmark of vasovagal syncope is the occurrence, in a standing patient, of a prodrome of dizziness, nausea, pallor, diaphoresis, and diminished vision. The history should include a search for stimuli (eg, phlebotomy, injury, fear) known to be associated with vasovagal syncope. Carotid sinus hypersensitivity, which is more common in the elderly, is suggested by a history of presyncopal shaving, head-turning, or wearing of a constricting collar. Carotid sinus hypersensitivity should be a considered in patients with syncope that is recurrent despite a negative cardiac workup. In situational syncope, the autonomic reflexive response may result from a specific physical stimulus such as micturition, defecation, or extreme coughing.

Orthostatic syncope occurs when a sudden change in posture after prolonged recumbence is associated with inadequate compensatory increases in heart rate and peripheral vascular resistance. Orthostatic syncope is often due to autonomic dysfunction, which has a myriad of potential causes(eg, peripheral neuropathy, spinal cord injury, Shy-Drager syndrome). Any disorder causing volume depletion may also cause orthostatic syncope.

Cardiac syncope is due to a dysrhythmia or a structural cardiopulmonary lesion. Tachydysrhythmias (eg, ventricular tachycardia, torsades des pointes, supraventricular tachycardia) are common causes of syncope, but the most likely finding on ED evaluation is incidental bradycardia. Syncope from dysrhythmias is typically sudden and without prodrome. Drug- or exercise-induced vasodilation may cause syncope as underlying cardiac structural abnormalities are unmasked. In the elderly, this scenario is most commonly due to aortic stenosis, a diagnosis which must be rigorously investigated as a cause of syncope. In the young patient, the cardiac structural abnormality is most commonly hypertrophic cardiomyopathy. Approximately 10% of patients with pulmonary embolism will havepulmonary outflow obstruction that leads to syncope.

Cerebrovascular disorders are rare as a cause of syncope. If brainstem ischemia is the cause, the patient usually reports other posterior circulation deficits (eg, diplopia, vertigo, nausea) associated with the “drop attack.” If patients report that upper extremity exercise preceded the event, there may be intermittent obstruction of the brachiocephalic or subclavian artery (ie, subclavian steal syndrome). Subarachnoid hemorrhage may also present with syncope, which is likely due to a transient rise in intracranial pressure.

Because of poor autonomic responses and multiple medications, the elderly are particularly prone to syncope, which is usually due to cardiac causes. Cardiovascular responses to orthostatic or vasodilatory challenges may be blunted by antihypertensive agents such as β-blockers and calcium channel antagonists. Cardiovascular medications may also cause conduction abnormalities or life-threatening dysrhythmias. Diuretics also contribute to the risk of orthostatic hypotension, due to their volume-depleting effect. Syncope is a dual threat to the elderly, in that causes are more serious and injury risks are higher.

Analysis of the San Francisco syncope cohort of 1418 consecutive patients led to generation of a decision rule that is may contribute to risk stratification decision-making in syncope patients. Presence of any one of five variables identified a patient at risk for serious outcome, with 89% sensitivity and 52% specificity for death at 1 year: an abnormal ECG, a complaint of shortness of breath, hematocrit less than 30%, systolic blood pressure <90 mm Hg on arrival, or a history of congestive heart failure.

Although an etiology for the syncopal episode may be difficult to establish, the most important tools in the syncope workup are a comprehensivehistory, physical examination, and ECG. From there, risk stratification is the most practical approach. The history should be directed to high-risk factors, including age, medications, and prodromal events. Sudden events that occur without warning suggest dysrhythmias; exertion may implya structural cardiopulmonary lesion. Associated symptoms are helpful for indicating a syncopal episode's etiology as cardiac (eg, palpitations and chest pain) or neurologic (eg, vertigo and focal weakness). Back or abdominal pain may suggest a leaking abdominal aortic aneurysm or ruptured ectopic pregnancy. Single-vehicle crashes or trauma in the absence of defensive injuries should prompt an investigation for syncope as a precipitating event. The medical history is useful in revealing likely cardiac or psychiatric (eg, hyperventilation) causes for syncope. When present, family history of cardiac disease or sudden death may also be informative.

Physical examination may occasionally reveal the cause of syncope. The cardiac examination may uncover a ventricular flow obstruction. A cardiac murmur may represent aortic stenosis or hypertrophic cardiomyopathy. An accentuated pulmonary gallop can suggest pulmonary embolism. A complete neurologic assessment and rectal examination (with Hemoccult testing) may yield further secondary causes for syncope.

An ECG should be obtained to assess for signs of ischemia or dysrhythmia. Suggestive ECG findings include prolonged QT interval (indicating propensity for torsades des pointes) or PR interval shortening with delta wave (ie, Wolf-Parkinson-White syndrome). Prolonged monitoring may show a transient, but recurring, dysrhythmia.

Laboratory testing should be selective. A hematocrit may explain orthostatic syncope and direct further workup (eg, for occult gastrointestinal bleeding). Women of childbearing potential warrant a pregnancy test. Although not recommended routinely, electrolytes may show a decreased bicarbonate after a seizure. Electrolytes are also indicated in patients with weakness or irritable myocardium (eg, as can occur with hypomagnesemia).

There are a variety of bedside tests that may provide clues in selected cases. A significant (>20 mm Hg) blood differential between upper extremities suggests subclavian steal syndrome. Carotid sinus massage can be performed in selected patients (without bruits) if one suspects carotid sinus hypersensitivity; a positive test requires reproduction of symptoms as well as bradycardic or hypotensive response. Orthostatic hypotension (autonomic instability from drugs or disease) is defined as a systolic blood pressure drop of at least 20 mm Hg upon standing; this diagnosis should only be made if postural hemodynamic changes are associated with reproduction of symptoms.

Seizure is the most common disorder mistaken for syncope. Some hallmarks of seizure (eg, tongue biting and incontinence) may also be seen with convulsive syncope, which occurs when cerebral anoxia causes briefclonus. The most helpful factor in differentiating syncope from seizures is the latter's postictal confusion and slow return to normal consciousness.

By definition, syncope results in spontaneous recovery of consciousness. Therefore, the main goal of ED care is to identify those patients at risk for further medical problems. Patients can be categorized into 1 of 3 classes after a careful history, physical examination, and ECG:

1. If the diagnosis is established (eg, pulmonary embolus, ectopic pregnancy, GI bleed) then the patient can be appropriately managed by directing attention to the underlying cause of the syncopal event. Patients for whom a life-threatening etiology is identified, including those withneurologic or cardiac causes, warrant admission.

2. Patients with unclear diagnosis who are high-risk are those for whom there is concern about sudden cardiac death or ventricular dysrhythmia. As suggested by the San Francisco Syncope Rule, concerning findings placing patients in the high-risk category include: abnormal ECG, complaint of shortness of breath, systolic blood pressure of <90 mm Hg on arrival, hematocrit less than 30%, age older than 45 years, or a history of ventricular dysrhythmia or congestive heart failure. Admission of these patients is warranted, for observation and to facilitate expedited workup (usually focused on cardiac etiologies).

3. Patients with unclear diagnosis who are low-risk are unlikely to have a cardiac etiology for their syncope. These patients lack the high-riskcriteria noted above. They are young (<45 years), have few comorbidities, and have a normal physical examination and ECG. In this group, syncope is usually vasovagal and no further workup is required if the episode is isolated. Low-risk patients can be safely discharged home with instructions to return for any recurrence of presyncopal symptoms. Worrisome or recurrent cases may benefit from further outpatient workup including Holter or loop-event monitoring. These patients should also be advised that, pending further outpatient workup, they are considered at-risk for syncope and should modify behavior accordingly (eg, avoid driving).