Syncope is defined as sudden, self-terminating loss of consciousness. Syncope is a common problem, accounting for 1% to 2% of ED visits in the U.S. The primary objective for evaluation
is identification of individuals at increased risk of death due to associated conditions, especially cardiac conditions.
by P.L. Wander, MD, Jennifer Best, MD, FACP, FHM
A 71-year-old woman is admitted after losing consciousness and falling at home. Her history is significant for hypertension, bilateral internal carotid artery stenoses, chronic kidney disease, and diabetes. Resting vital signs are normal. Cardiac, pulmonary, and neurologic exams are unremarkable, as is an electrocardiogram (ECG). She was noted to have a small scalp laceration. Noncontrast CT of the head demonstrates a small occipital subdural bleed thought to be a result of her fall.
What is the most cost-effective evaluation for this patient admitted with suspected first syncopal episode?
Syncope is defined as sudden, self-terminating loss of consciousness. The final common pathway of all causes of syncope is global cerebral hypoperfusion—specifically, hypoperfusion of the reticular activating system. The differential diagnosis of syncopal loss of consciousness includes neurally mediated (e.g., vasovagal) syncope, orthostatic hypotension, cardiac arrhythmias, structural heart disease, and cerebrovascular disease.
Among young, otherwise healthy people, neurally mediated syncope, which has a relatively benign prognosis, is by far the most common etiology, while in older patients, primary cardiac causes are more common. Nonsyncopal mechanisms, such as seizure and hypoglycemia, should also be considered in the differential diagnosis of transient loss of consciousness (see Table 1, p. 19).1
Syncope is a common problem, accounting for 1% to 2% of ED visits in the U.S.2 The primary objective for evaluation is identification of individuals at increased risk of death due to associated conditions, especially cardiac conditions such as structural heart disease; myocardial ischemia and infarction (MI); Wolff-Parkinson-White, Brugada, or long QT syndromes; and polymorphic ventricular tachycardia.3 True syncope can be associated with other concerning causes, such as aortic stenosis, aortic dissection, and massive pulmonary embolus, as well as arrhythmias from underlying cardiac disease.4
History: A detailed history and physical examination reveals the cause in 50% of syncopal episodes. Key factors include the account of third-party observers, although it is important to note that tonic-clonic movements can be associated with the global cerebral hypoperfusion of syncope as well as with seizure.4 History of dyspnea, chest pain, or palpitations argue for a primary cardiac or pulmonary cause.
Among patients who endorse a history of palpitations, the sensation of rapid and regular pulsations in the neck points very strongly toward an AV-nodal re-entrant tachycardia, because the carotid pulse and cannon A wave arrive simultaneously in the neck.5 Postictal confusion and focal neurologic exam findings suggest a neurologic rather than syncopal cause, although there are exceptions, and the relationship between seizure and impaired myocardial perfusion is complex.
One factor shown to be significantly associated with a cardiac cause for episodic syncope is family history of sudden cardiac death.4
Physical exam: A thorough general and neurologic exam is critical in evaluation of a first syncopal episode. Supine and standing blood pressure and heart rate should be measured, waiting at least one minute (and by some protocols up to three minutes) after the patient stands up to record standing vitals. Measurement of sitting vitals is not necessary. Neither postural hypotension nor tachycardia are sensitive for hypovolemia in normal volunteers, but a 30-point increase in heart rate is more than 99% specific; a 20-point drop in systolic blood pressure (SBP) is less so.5 A difference of more than 20 mmHg between systolic arm pressures in an individual with chest pain suggests aortic dissection.
Other findings useful in diagnosis of syncope include signs of aortic stenosis, pulmonary hypertension, and myxoma. Absent aortic component of S2, a late-peaking or prolonged murmur, sustained apical impulse, and delayed carotid upstroke (“pulsus tardus”) strongly support the presence of severe aortic stenosis. Absence of a palpable pulmonic component of S2 argues strongly against significant pulmonary hypertension.
There are few physical exam findings reliably seen in pulmonary embolism, but the presence of tachycardia is reliably seen about 80% of the time.4 Although atrial myxoma is associated with a characteristic “tumor plop” heard in early diastole, the finding is not common.5
Diagnostic studies: In a recent observational study of more than 2,000 adults older than 65 hospitalized after a syncopal episode, cardiac enzymes, electroencephalography, CT scan of the head, and carotid ultrasonography determined the etiology of syncope in less than 1% of cases. Inpatient monitoring on telemetry was helpful about 5% of the time. On the other hand, postural vital signs contributed to the diagnosis more than 20% of the time, at a fraction of the cost of these other diagnostics (see Table 2, above).6
The role of transthoracic echocardiogram (echo) is more controversial. It does seem clear, however, that echo is more likely to be diagnostic in adults older than 60, in the presence of a heart murmur on physical exam or with an abnormal ECG.7 Although it demonstrated an arrhythmia that determined the etiology of syncope in only 3% of cases in this study, ECG is still routinely recommended; it is relatively inexpensive, risk-free, and can reveal abnormalities, including bundle-branch block, prior MI, and nonsustained ventricular tachycardia, which may be associated with cardiovascular comorbidities.4
Although the diagnostic tests above are of limited utility in uncovering the cause of syncopal episodes, they may be helpful when history or physical examination suggests a specific cause. For example, in individuals presenting with syncope who have lateralizing neurologic signs or symptoms or carotid bruits, carotid ultrasound is an appropriate diagnostic tool. In a retrospective analysis of 140 older adults who underwent carotid ultrasonography as part of a syncope evaluation, carotid lesions were identified in just 2% of subjects.8 These lesions were not thought to have been the primary etiology of syncope but did prompt additional evaluation or intervention.
Among older individuals or individuals with known heart disease, longer-term cardiac monitoring might be appropriate. The method of cardiac monitoring should be guided by the frequency of episodes. For events occurring daily, Holter monitoring is appropriate. For events occurring at least monthly, an event monitor is appropriate.
For less frequent events, the clinician can consider an implantable loop recorder (ILR).3 In a study of 167 individuals without a clear cause of syncope after initial evaluation, diagnosis was achieved in 90% of patients after one year of monitoring by ILR.9
Among individuals in whom the etiology remains unclear, tilt-table testing is often considered. This modality remains controversial and is unlikely to establish a diagnosis in individuals with an otherwise normal evaluation.3 Electrophysiologic testing is of similarly low yield in individuals with otherwise normal evaluation and is generally not recommended, except in individuals with known heart disease, including history of MI, congestive heart failure (CHF), and pre-excitation.10
Diagnostic algorithms: Algorithm-driven diagnostic protocols for evaluation of syncope do exist, but they are generally based on expert consensus opinion rather than large-scale studies. There are evidence-based syncope risk scores under development, but definitive validation is forthcoming. Examination of two such protocols is provided here.
The San Francisco Syncope Rule is among the most well-known algorithms, and predicts adverse outcomes at seven days. The study cohort included 684 patients presenting with syncope to an academic ED. Adverse outcomes, including death, myocardial infarction, arrhythmia, pulmonary embolus, stroke, subarachnoid hemorrhage, ED return, or hospitalization at seven days, were identified. History of CHF, hematocrit less than 30%, ECG abnormality, shortness of breath, and SBP less than 90 mmHg at presentation were associated with increased risk of an adverse outcome. If any of these findings is present, a patient is considered at high risk for adverse outcome at one week.2 The rule is simple to use; however, external validation has been controversial.
In another risk-prediction study—a large multicenter study of patients older than 60—age greater than 90 years, male sex, history of arrhythmia, SBP greater than 160 mm Hg, ECG abnormality, and elevated troponin I were used to construct a score for risk stratification.11 Specific ECG abnormalities included nonsinus rhythm, heart rate less than 40 beats per minute, evidence of acute or chronic ischemic heart disease, prolonged QRS or QT, left or right ventricular hypertrophy, left-axis deviation, and bundle-branch block. Notably, in this older cohort, CHF (specifically, systolic dysfunction with ejection fraction less than 40%) was not significantly associated with risk of adverse event at 30 days. Study authors stratified participants into low- (score ≤0), intermediate- (score 1-2), and high-risk groups (score >2), with 30-day risk of an adverse event ranging from 2.5% to 20%.
One caveat to the interpretation of these data is the fact that even in the “low risk” group, risk of adverse event was still 2.5%, a figure that many clinicians might consider intolerably high.11 This risk score has not been externally validated.
Our patient was admitted to the inpatient medicine service. She was monitored overnight on telemetry without evidence of arrhythmia. Collateral history revealed new use of multiple antihypertensives prescribed by outside providers, including both atenolol and propranolol. Her subdural hematoma was managed conservatively and she remained free of neurologic deficits. On discharge, her hypertension regimen was simplified. She was referred for outpatient stress echocardiogram.
Detailed history and physical exam, including postural vital signs, should form the backbone of the routine evaluation of syncope. An ECG is a critical—and inexpensive—initial diagnostic test, while inpatient telemetry, although a routine component of inpatient evaluation, is expensive and relatively low-yield. Risk prediction rules might ultimately help guide admission decisions and inpatient workup, but definitive external validation of these rules has yet to be accomplished. TH
Dr. Wander is a resident in the Department of Medicine at the University of Washington School of Medicine in Seattle. Dr. Best is an assistant professor of medicine in the Division of General Internal Medicine at the University of Washington School of Medicine.
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