Vasovagal syncope often has a prodrome of vasodepressor premonitory symptoms, such as nausea, diaphoresis, tachycardia, and pallor. Episodes can be aborted by lying down or removing the inciting stimulus. Cardiogenic syncope by contrast is characteristically abrupt in onset, often resulting in injury, transient (lasting for seconds to a few minutes), and followed by prompt recovery of full consciousness. In orthostatic (postural) hypotension, a greater than normal decline (20 mm Hg) in BP immediately upon arising from the supine to the standing position is observed, with or without tachycardia depending on the status of autonomic (baroreceptor) function.
The evaluation for syncope depends on findings from the history and physical examination (especially orthostatic BP evaluation, auscultation of carotid arteries, and cardiac examination).
A resting ECG is recommended for all patients undergoing evaluation for syncope. High-risk findings on ECG include non-sinus rhythm, complete or partial left bundle branch block, and voltage criteria indicating left ventricular hypertrophy. Patients with a normal initial evaluation, including unremarkable history and physical, absence of cardiac disease or significant comorbidities and normal baseline ECG may not need further testing. When initial evaluation suggests a possible cardiac arrhythmia, continuous ambulatory ECG monitoring, event recorder (for infrequent episodes), or an implantable cardiac monitor can be considered. Caution is required before attributing a patient’s syncopal event to rhythm or conduction abnormalities observed during monitoring without concomitant symptoms. For instance, dizziness or syncope in older patients may be unrelated to incidentally observed bradycardia, sinus node abnormalities, or ventricular ectopy.
Tilt-table testing may be useful in patients with suspected vasovagal syncope where the diagnosis is unclear after initial evaluation, especially when syncope is recurrent. The hemodynamic response to tilting determines whether there is a cardioinhibitory, vasodepressor, or mixed response. The overall utility of the test is improved when there is a high pretest probability of neurally mediated syncope, since the sensitivity and specificity of the test in the general population is only moderate. Although different testing protocols are used, passive tilting to at least 70 degrees for 10–40 minutes—in conjunction with isoproterenol infusion or sublingual nitroglycerin, if necessary—is typical. Syncope due to bradycardia, hypotension, or both will occur in approximately one-third of patients with recurrent syncope. With more aggressive protocols, false-positive responses may occur.
3. Electrophysiologic studies
Electrophysiologic study has limited role in the evaluation of syncope, particularly in patients without structural heart disease or when there is a low suspicion for arrhythmic etiology. In patients with ischemic heart disease, LV dysfunction, known conduction disease, or arrhythmia, electrophysiologic study may help elucidate the mechanism of syncope and guide treatment decisions. The diagnostic yield in patients with structural heart disease is approximately 50%.
When the symptoms are associated with exertion or stress, exercise testing may be helpful.