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Before discussing the assessment and management of syncope, it is important to understand the multiple etiologies that lead to the final pathway of a transient loss of consciousness. Any process that results in a loss of consciousness must affect both cerebral hemispheres simultaneously or involve the reticular activating system in the brainstem. In the case of syncope, the pathologic process is transient, resulting from a loss of needed substrate to the brain (be it oxygen or other nutrients) that corrects without external therapeutic intervention (such as the administration of IV dextrose). Typically, the impairment of substrate delivery is caused in part by upright posture. Thus, assuming a supine position after consciousness is lost improves substrate delivery and typically leads to spontaneous recovery.

As with any disease process, classification of etiology aids in diagnosis, treatment, and prognosis for patients. Understanding the patient’s prognosis aids in ensuring a safe disposition. Unfortunately, the classification schemes for etiologies of syncope are broad, vary by author, are to some degree subjective, and frequently overlap. For the purpose of this discussion, syncope will be classified into four broad categories: cardiac, neurologic, vascular (or reflex‐mediated), and idiopathic (Table 16.1).

Cardiac syncope is due to a transient lack of adequate cardiac output, causing inadequate cerebral perfusion and subsequent loss of consciousness. Vascular processes causing syncope are included in this group. Dysrhythmia is a common cardiac etiology and is one of great clinical importance. The most common dysrhythmia associated with syncope is transient ventricular tachycardia (VT). Such patients frequently have a history of congestive heart failure with low ejection fraction, which portends a poor prognosis (1‐year mortality up to 40%). Other culprit dysrhythmias include severe sinus bradycardia or transient high‐grade heart blocks, sick sinus syndrome, supraventricular tachycardias, and atrial fibrillation with rapid ventricular response. As a rule, all of the aforementioned dysrhythmias must be paroxysmal in nature to cause a syncope episode because there must be a return of cerebral perfusion for the patient to regain consciousness.

Other cardiac causes of syncope include restrictive cardiomyopathies, valvular heart disease (especially severe aortic stenosis and mitral regurgitation), pulmonary embolus, and rarely, cardiac ischemia (although syncope from such is most likely related to dysrhythmia). Although these pathologies can cause transient reductions in cardiac output sufficient to create a syncopal episode, their overall occurrence is rare. One rare population of young patients who have dangerous syncope is the patient population that has congenital prolonged QT syndrome. This is why it is important to check the QT interval on a rhythm strip or 12‐lead ECG on every syncope patient.

Reflex‐mediated syncope is the most common type (up to 58% [6]) and offers the best prognosis. It occurs when the body has an inappropriate autonomic response to a change in posture. Under normal circumstances, when a person moves from recumbent to upright, a significant amount of blood (300–800 mL) will pool in the lower extremities [7]. In response, the sympathetic nervous system causes peripheral vasoconstriction, stimulates increased cardiac contractility, and increases the heart rate. These processes counteract the transient “distributive shock” experienced by the central nervous system, thus preventing syncope.

Table 16.1 Classification of syncope

Cardiac (~20%)	Neurological (~10%)	Reflex‐mediated (~35%)	Idiopathic (~35%)
Dysrhythmia	Migraine	Vasovagal
Ventricular fibrillation	Subclavian steal	Orthostatic
Ventricular tachycardia	Transient ischemia	Hyperventilation
Supraventricular tachycardia	Subarachnoid hemorrhage	Carotid sinus syndrome
Atrial fibrillation with rapid ventricular response	Psychogenic
Outflow obstruction
Aortic stenosis
Atrial myxoma
Mitral stenosis
Restrictive cardiomyopathy
Pericardial tamponade
Cardiac ischemia
Pulmonary embolism
Aortic dissection
Congenital heart disease
Congenital prolonged
QT syndrome

For patients experiencing reflex‐mediated syncope, there is an inappropriate stimulation of the parasympathetic nervous system. It offsets or overwhelms the appropriate sympathetic response. These patients experience hypotension, with or without bradycardia. The resultant lack of cerebral perfusion results in a syncopal episode.

An additional etiology of syncope is hemorrhage. Common causes include gastrointestinal bleeding, ectopic pregnancy, and hemorrhagic ovarian cysts. These are in essence a “distributive shock” cause from the perspective of the central nervous system.

Neurogenic syncope, as a pure cause of transient loss of consciousness, is actually a rare event. Many of the neurologic events that result in syncope have poorly explained mechanisms. Additionally, many neurologic events that involve loss of consciousness are incorrectly labeled as syncope. It is important to note, however, that some neurologic causes of syncope represent serious pathologic processes, such as subarachnoid hemorrhage and transient ischemic attack. It is rare that such diseases manifest as a syncopal episode, but these potential diagnoses should be considered.