History
History and physical examination are the most specific and sensitive ways to evaluate syncope. [1] The diagnosis is achieved with a thorough history and physical examination in 50-85% of patients. No single laboratory test has greater diagnostic efficacy. The 2007 American College of Emergency Physicians (ACEP) Clinical Policy on Syncope listed history, physical examination, and 12-lead electrocardiography (ECG) as their only current level A recommendations. [2]
A detailed account of the event must be obtained from the patient. The account must include the circumstances surrounding the episode: the precipitant factors, the activity the patient was involved with prior to the event, and the patient's position when it occurred.
Precipitating factors can include fatigue, sleep or food deprivation, warm ambient environment, alcohol consumption, pain, and strong emotions such as fear or apprehension.
Activity prior to syncope may give a clue as to the etiology of symptoms. Syncope may occur at rest; with change of posture; on exertion; after exertion; or with specific situations such as shaving, coughing, voiding, or prolonged standing. Syncope occurring within 2 minutes of standing suggests orthostatic hypotension. [28]
Assess whether the patient was standing, sitting, or lying when the syncope occurred. Syncope while seated or lying is more likely to be cardiac. [29]
The following questions should be answered:
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Was loss of consciousness complete?
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Was loss of consciousness with rapid onset and short duration?
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Was recovery spontaneous, complete, and without sequelae?
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Was postural tone lost?
If the answers to these questions are positive, the episode has a high likelihood of being syncope. If one or more answers are negative, consider other forms of loss of consciousness prior to proceeding with syncope evaluation. [3] The clinician should attempt to gather all information with respect to symptoms preceding the syncope.
Prior faintness, dizziness, or light-headedness occurs in 70% of patients experiencing true syncope. Other symptoms, such as vertigo, weakness, diaphoresis, epigastric discomfort, nausea, blurred or faded vision, pallor, or paresthesias, may also occur in the presyncopal period.
Symptoms of nausea or diaphoresis prior to the event may suggest syncope rather than seizure when the episode was not witnessed, whereas an aura may suggest seizure.
Patients with true syncope do not remember actually falling to the ground. Presyncope involves the same symptoms and pathophysiology but terminates prior to loss of consciousness and can occasionally include loss of postural tone.
The duration of symptoms preceding a syncopal episode has been reported to be an average of 2.5 minutes in vasovagal syncope and an average of only 3 seconds in arrhythmia-related cardiac syncope.
Clinicians should specifically inquire as to red-flag symptoms, such as exertional onset, chest pain, dyspnea, low back pain, palpitations, severe headache, focal neurologic deficits, diplopia, ataxia, or dysarthria prior to the syncopal event.
Patients should be asked to estimate the duration of their loss of consciousness. Syncope is associated with patient estimates ranging from seconds up to 1 minute in most cases. To discriminate from seizures, patients should also be asked if they remember being confused about their surroundings after the event or whether they have oral trauma, incontinence, or myalgias.
A detailed account of the event must also be obtained from any available witnesses. Witnesses can aid the clinician in differentiating among syncope, altered mental status, and seizure.
Convulsive activity, automatisms, or attempts to elicit focality can indicate seizure. Witnesses may be able to estimate the duration of unconsciousness and to assist in ascertaining whether the patient experienced postevent confusion.
Postevent confusion is the most powerful tool for discriminating between syncope and seizure. A postictal phase suggests that a seizure has occurred. Postevent confusion has been described with syncope, but the confusion should not last more than 30 seconds. Seizurelike activity can occur with syncope if the patient is held in an upright posture.
A medication history must be obtained in all patients with syncope with special emphasis placed on cardiac and antihypertensive medications. Drugs commonly implicated in syncope include the following:
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Agents that reduce blood pressure (eg, antihypertensive drugs, diuretics, nitrates)
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Agents that affect cardiac output (eg, beta blockers, digitalis, antiarrhythmics)
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Agents that prolong the QT interval (eg, tricyclic antidepressants, phenothiazines, quinidine, amiodarone)
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Agents that alter sensorium (including alcohol, cocaine, analgesics with sedative properties)
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Agents that alter serum electrolytes (especially diuretics)
Inquiry must be made into any personal or familial past medical history of cardiac disease. Patients with a history of myocardial infarction (MI), arrhythmia, structural cardiac defects, cardiomyopathies, or congestive heart failure (CHF) have a uniformly worse prognosis than other patient groups.
Remember to consider the broad differential diagnosis of syncope. Assess whether the patient has a history of seizure disorder, diabetes, stroke (cerebrovascular accident [CVA]), deep vein thrombosis (DVT), or abdominal aortic aneurysm (AAA) or if pregnancy is a possibility.
Physical Examination
A complete physical examination is requisite for all patients who present to the emergency department (ED). Special attention must be paid to certain aspects of the physical examination in patients who present with syncope.
Always analyze the vital signs. Fever may point to a precipitant of syncope, such as a urinary tract infection (UTI) or pneumonia. Postural changes in blood pressure (BP) and heart rate may point toward an orthostatic cause of syncope but are generally unreliable. Tachycardia may be an indicator of pulmonary embolism, hypovolemia, tachyarrhythmia, or acute coronary syndrome. Bradycardia may point toward a vasodepressor cause of syncope, a cardiac conduction defect, or acute coronary syndrome.
A glucose level, checked by rapid fingerstick (eg, Accu-Chek), should be evaluated in any patient with syncope. Hypoglycemia can produce a clinical picture identical to syncope, including the prodromal symptoms, absence of memory for the event, and spontaneous resolution.
A detailed cardiopulmonary examination is essential. Irregular rhythms, ectopy, bradyarrhythmias, and tachyarrhythmias should be detected. Auscultation of heart sounds may reveal murmurs indicating high-grade valvular defects. Search for objective evidence of congestive heart failure, including jugular venous distension, lung rales, hepatomegaly, and pitting-dependent edema. Examine the abdomen for the presence of a pulsatile abdominal mass.
A detailed neurologic examination assists in establishing a baseline as well as defining new or worsening deficits. Patients with syncope should have a normal baseline mental status. Confusion, abnormal behavior, headache, fatigue, and somnolence must not be attributed to syncope; a toxic, metabolic, or central nervous system cause must be considered. The patient should have a detailed neurologic examination, including evaluation for carotid bruits, cranial nerve deficits, motor deficits, deep tendon reflex lateralization, and sensory deficits. Severe neuropathies may correlate with vasodepressor syncope.
The patient must be examined for signs of trauma. Trauma may be sustained secondary to syncope with resultant head injury, lacerations, and extremity fractures. Tongue trauma is thought to be more specific for seizures. Remember to consider antecedent head trauma resulting in loss of consciousness as opposed to syncope with resultant trauma if the history or findings are unclear.
Patients with syncope may require a stool guaiac examination, as appropriate based on their history. In one study, all patients with anemia contributing to syncope were guaiac-positive.
A few bedside examinations may help to elucidate the origin of a patient's syncope. The Hallpike maneuver may be performed in patients who describe short, intermittent prodromes with primarily vertiginous components to assess for benign paroxysmal positional vertigo.
Orthostatic changes marked by a decrease in systolic BP by 20 mm Hg, a decrease in diastolic BP by 10 mm Hg, or an increase in heart rate by 20 beats/min (bpm) with positional changes or systolic BP less than 90 mm Hg with the presence of symptoms may indicate postural hypotension. Bradycardia coinciding with the examination indicates vasodepressor syncope. Be aware that this examination is notoriously insensitive and has limited use.
Carotid sinus massage has been used with some success to diagnose carotid sinus syncope but can prompt prolonged sinus pauses and hypotension.
