As with any disease process, classification of etiology aids in diagnosis, treatment, and prognosis for patients. Understanding the patient’s prognosis helps 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, neurological, vascular (or reflex mediated), and idiopathic (Table 19.1).

Cardiac syncope is due to a transient lack of adequate cardiac output, causing inadequate cerebral perfusion and subsequent loss of consciousness. 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). These occurrences are seen most frequently in patients with histories of congestive heart failure and low ejection fraction and portend a poor prognosis (1-year mortality up to 40%). Other culprit dysrhythmias include severe sinus bradycardia or transient high-grade heart blocks, supraventricular tachycardias, sick sinus syndrome, 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 dysrhythmia related). Although these pathologies can cause transient reductions in cardiac output sufficient to create a syncopal episode, their overall occurrence is rare. One population of young patients who have dangerous syncope is those with congenital prolonged QT syndrome. This is why it is important to check a rhythm strip on every syncope patient.

Reflex-mediated syncope is the most common cause and (barring secondary trauma, as from a subsequent fall or automobile collision) poses the best prognosis. Although listed as 35% here, some studies have attributed up to 58% of syncope to this etiology [5]. Reflex-mediated syncope 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 [6]. 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.

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

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

Assessment

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