Syncope

31 Syncope



Syncope is a transient loss of consciousness with an inability to maintain postural tone. Typically, it is quickly followed by a spontaneous recovery of consciousness and the ability to resume the initial upright position. Syncope does not include other conditions of altered consciousness such as seizure or shock, but can be difficult to distinguish from them. Syncope is very common and is responsible for 1% to 5% of visits to emergency departments and approximately 5% of hospital admissions. This translates into almost a million syncope evaluations in the United States each year. The various etiologies of syncope can be divided into five broad categories including neurally mediated (i.e., vasovagal), orthostatic (most common), cardiac arrhythmia (both tachycardia and bradycardia), cardiac lesions obstructing outflow (i.e., aortic stenosis), and cerebrovascular ischemic attacks such as a vertebrobasilar attack (which is a rare cause of syncope) (Table 31-1). The dilemma is to differentiate benign neurally mediated syncope (NMS) from less common but more harmful etiologies.



These various etiologies all cause inadequate cerebral perfusion that ultimately results in syncope. After a careful history and physical examination and ECG, further diagnostic tests are often warranted to rule out the various causes. Regardless of the diagnosis, however, the treatment for syncope is always directed toward the underlying cause.



Etiology and Pathogenesis



Neurally Mediated Syncope


NMS, also referred to as “vasovagal syncope,” is the most common cause of syncope. Typical fainting is not a pathologic cardiac condition, but most likely a remnant defense mechanism in response to stress that dates back to the origins of humans and is also seen in other vertebrate animals in response to stress. Several types of situational syncope are also neurally mediated, such as micturition, postprandial, and post-exercise syncope. The pathophysiology of NMS remains to be fully elucidated. Several theories involve baroreceptor reflex abnormalities that cause disconnection between the autonomic nervous system and the cardiovascular system. Another theory is that venous pooling that occurs with the upright position leads to reduced cardiac filling, which then leads to activating mechanoreceptors that cause a paradoxical withdrawal of sympathetic tone (Fig. 31-1). The triad of apnea, bradycardia, and hypotension was first termed the Bezold-Jarisch reflex in the 1940s when it was appreciated that afferent and efferent pathways in the vagus nerve control heart rate and vasomotor tone by increasing or decreasing parasympathetic discharge to the heart. Several cardiac receptors are part of the intricate network including various baroreceptors and chemoreceptors.



In truth there probably is no single unifying syndrome that occurs in all NMS patients. In general, there seems to be an initial trigger that increases sympathetic activity followed by a withdrawal of sympathetic outflow and an increase in vagal activity. This results in tachycardia and vasoconstriction followed by bradycardia and vasodilation, which result in hypotension and ultimately unconsciousness.







Clinical Presentation


The symptoms that surround a syncopal event can often aid in determining the underlying etiology (Box 31-1).The quality and duration of symptoms preceding the loss of consciousness can vary considerably depending on the etiology. Observations of witnesses are also very important and can help recreate the events and timeline from prodrome to duration of unconsciousness and mental status upon arousal. Typically, NMS patients have a prodrome before losing consciousness that lasts from several seconds to minutes. The prodrome may consist of nausea, diaphoresis, anxiety, or palpitations. These symptoms are followed by a very brief period of unconsciousness (usually less than 1 minute) and then a rapid recovery within a few minutes. After the event, the patient may feel fatigued but should be oriented and coherent. These episodes generally occur when the person is in the upright position, similar to orthostatic hypotension events. Occasionally, patients will have little or no warning before passing out. A lack of prodrome is more frequently associated with an arrhythmic etiology. Traditionally, Stokes-Adams syndrome has been used to describe this abrupt loss of consciousness due to a marked decrease in heart rate, although it has come to represent abrupt loss of consciousness from both tachyarrhythmias and bradyarrhythmias. If syncope occurs during exertion it is imperative that cardiac etiologies be considered. Chest pain may also accompany a tachycardic arrhythmia such as VT due to coronary disease.



It is important to note that tonic-clonic movements can be seen in both syncope and seizure activity, and it is often difficult to distinguish the two. Confusion present after arousal is more consistent with seizure activity. Strokes rarely cause syncope but can do so when either severe bilateral carotid artery disease or basilar artery insufficiency is present. Syncope due to these neurovascular causes are often in conjunction with focal neurologic findings.


Jun 12, 2016 | Posted by in CARDIOLOGY | Comments Off on Syncope

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