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.
Assessment
The first task in assessing and managing syncope is to separate syncope from the other potential reasons for a loss of consciousness. First, any nontransient loss of consciousness, by definition, is not syncope. A patient who has a loss of consciousness from hypoglycemia, requires IV dextrose, and then awakens to a normal level of consciousness has not had a syncopal episode. Likewise, if the patient has a complex, nonmotor seizure and then recovers from a postictal state to a normal mental status, this, too, is not syncope. However, for the EMS clinician, all of these situations can be dispatched as “altered mental status,” “unconscious,” or “syncope,” depending on local dispatch protocols and the information provided by the 9‐1‐1 caller. This can incorrectly prejudice EMS clinicians to presume or discount syncope as the diagnosis.
Patients frequently present with “presyncope” or “near syncope.” These patients did not lose consciousness
