Emergency Medical Services. Группа авторов

CHAPTER 16 Syncope

       David J. Schoenwetter

Introduction

      Syncope is defined as a “loss of consciousness and postural tone caused by diminished cerebral blood flow” [1]. Also, by definition the condition must be self‐corrected as to cause a return to normal state of consciousness. Syncope is a common complaint in both the emergency department (ED) and in prehospital medicine and is the sixth leading cause of hospital admission in people over the age of 65 [2, 3]. Of course, estimates are limited by the accuracy of determining true syncope versus other transient causes of loss of consciousness. Transient loss of consciousness has a cumulative lifetime incidence of approximately 35% to 41%, with recurrent syncope occurring in 13.5% of patients [4, 5].

Pathophysiology

      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