Syncope or fainting is a symptom complex consisting of a brief loss of consciousness associated with an inability to maintain postural tone that spontaneously resolves without medical intervention. Syncope accounts for approximately 1% to 2% of ED visits each year and up to 6% of hospital admissions.^1,2,3 In the Framingham Heart Study, 7814 patients were followed for 17 years, and 10.5% reported syncope.⁴ Syncope in the preceding year is the best predictor of recurrence.⁵ It can affect the young and the old, with the elderly having the greatest morbidity.⁶ Near-syncope, a premonition of fainting without loss of consciousness, shares the same basic pathophysiologic process as syncope and may carry the same risks.^7,8

The final common pathway of syncope is the same regardless of the underlying cause: about 10 seconds of complete disruption of blood flow or nutrient delivery to both cerebral cortices or to the brainstem reticular activating system, or reduction of cerebral perfusion by 35% to 50%. Most commonly, an inciting event causes a drop in cardiac output, which decreases oxygen and substrate delivery to the brain. Less commonly, vasospasm reduces CNS blood flow. Cerebral perfusion and consciousness are restored by the supine position, the response of autonomic autoregulatory centers, or restoration of a perfusing cardiac rhythm.

The causes of syncope are numerous (Table 52-1). The major causes of syncope identified in the Framingham Heart Study were vasovagal (reflex mediated, 21%), cardiac (10%), orthostatic (9%), medication related (7%), neurologic (4%), and unknown (37%).⁴ In most studies, even with exhaustive patient evaluation, the cause remains unknown in about 40% of individuals.^9,10 After ED investigation, the unknown proportion may be 50% to 60%. Diagnosis is important, because each diagnostic classification carries with it prognostic risk. In the Framingham study, cardiac syncope doubled the risk of death, neurologic syncope increased the risk of death by 50%, and syncope of unknown cause increased the risk of death by 30%, compared to the general population cohort of the study. Individuals with neurally/reflex-mediated or vasovagal syncope had no increased risk of death compared with the general population cohort.⁴

CARDIAC-RELATED SYNCOPE

Cardiac-related syncope is the most dangerous type and is a risk for sudden death. Because patients with documented cardiac syncope have a 6-month mortality rate that exceeds 10%, timely and thorough evaluation is warranted.^4,10 Well-appearing patients with undiagnosed cardiac disease are the most challenging group. The causes of cardiac syncope are divided into two categories: structural disease and dysrhythmias (Table 52-1). In both settings, the heart is unable to provide adequate cardiac output to maintain cerebral perfusion.

Syncope can occur if structural disease limits the heart’s ability to increase cardiac output to meet demand. Examples of structural cardiac disease associated with syncope include aortic stenosis, hypertrophic cardiomyopathy, pulmonary embolism, and myocardial infarction. Consider aortic stenosis as a structural cardiac cause of syncope in the elderly. The classic symptom constellation of aortic stenosis is chest pain, dyspnea on exertion, and syncope. Hypertrophic cardiomyopathy is characterized by a stiff noncompliant left ventricle, diastolic dysfunction, and outflow tract obstruction. It is the most common cause of sudden cardiac death in young adults, but the disorder may be first recognized in those >60 years old.¹¹ Massive acute pulmonary embolism may cause syncope due to obstruction of the pulmonary vascular bed and reduction in cardiac output.¹² Acute myocardial infarction may cause syncope if myocardial dyskinesia reduces cardiac output. Individual chapters in the Cardiovascular Disease section of this text provide more discussion on structural cardiopulmonary disorders that may cause syncope.

Although both brady- and tachydysrhythmias may lead to transient cerebral hypoperfusion (Table 52-1), there is no absolute high or low heart rate that will predictably produce syncope. Symptoms depend on both the autonomic nervous system’s ability to compensate for a decrease in cardiac output and the degree of underlying cerebrovascular disease. Dysrhythmias may also result from of a primary electrolyte imbalance, as in hypomagnesemia (e.g., torsade de pointes). Dysrhythmias can occasionally occur in structurally normal hearts, such as in the familial disorders of Brugada syndrome, long or short QT syndromes, and catecholamine-associated polymorphic ventricular tachycardia. Syncope from dysrhythmias is typically sudden and usually without prodromal symptoms.

VASOVAGAL AND NEURALLY/REFLEX-MEDIATED SYNCOPE

Vasovagal syncope, a form of reflex-mediated or neurally mediated syncope, is associated with inappropriate vasodilatation, bradycardia, or both, as a result of inappropriate vagal or sympathetic tone.^13,14 A prodrome of lightheadedness, with or without nausea, pallor, and/or sweating, and an associated feeling of warmth may accompany vasovagal syncope. A slow, progressive onset with associated prodrome suggests vasovagal syncope. Vasovagal syncope may occur after exposure to an unexpected or unpleasant sight, sound, or smell; fear; severe pain; emotional distress; or instrumentation. It may also occur in association with prolonged standing or kneeling in a crowded or warm place. Situational syncope occurs during or immediately after coughing, micturition, defecation, or swallowing.

Carotid sinus hypersensitivity, characterized by bradycardia or hypotension, is another type of reflex-mediated syncope. The carotid body, located at the carotid bifurcation, contains pressure-sensitive receptors. The stimulation of an abnormally sensitive carotid body by external pressure may lead to two autonomic responses. Most commonly, there is an abnormal vagal response, leading to bradycardia and asystole of >3 seconds. Less commonly, there is a vasodepressor response, leading to a decrease in blood pressure of >50 mm Hg without a significant change in heart rate. Both responses may occur simultaneously. Carotid sinus hypersensitivity is more common in men, the elderly, and among those with ischemic heart disease, hypertension, and certain head and neck malignancies. Although some patients may demonstrate a hypersensitive carotid sinus response on provocative testing, unless this response culminates in syncope or recurrence of prodromal symptoms, and unless it is associated with an inciting event, such as shaving or turning of the head, it cannot be definitely diagnosed as the cause of syncope. About 25% of patients with carotid sinus hypersensitivity have true carotid sinus syndrome with spontaneous symptoms.⁵ Consider carotid sinus hypersensitivity in older patients with recurrent syncope and negative cardiac evaluations.

ORTHOSTATIC SYNCOPE

Orthostatic syncope is suggested when postural hypotension is associated with syncope or presyncope.¹⁵ When a person assumes an upright posture, gravity shifts blood to the lower part of the body, and cardiac output drops. This change triggers the healthy autonomic nervous system to increase sympathetic output and decrease parasympathetic output, increasing heart rate and peripheral vascular resistance, and thus increasing cardiac output and blood pressure.^16,17 If the autonomic response is insufficient to counter the drop in cardiac output upon standing, decreased cerebral perfusion and syncope may follow. Symptom onset is usually within the first 3 minutes after assuming the upright posture, but may be more delayed in some patients. However, positive orthostatic changes have been documented in up to 40% of asymptomatic patients >70 years old and in about a quarter of those <60 years old, so orthostasis does not always result in syncope.^14,18 Causes of orthostatic syncope include intravascular volume loss and poor vascular tone caused by α-receptor disorders or medications. Many serious causes of syncope may be associated with orthostatic changes, so consider other life-threatening causes before attributing syncope to orthostasis, especially in the elderly.

PSYCHIATRIC DISORDERS

Psychiatric disorders are found in a modest percentage of patients with syncope¹⁹—up to 40% of those with vasovagal syncope and up to 62% of those with unexplained syncope.²⁰ In one study, the most frequent psychiatric diagnoses associated with syncope were generalized anxiety disorder and major depressive disorder.²¹ Hyperventilation has been used as a provocative maneuver in diagnosing panic disorder and generalized anxiety disorders and can lead to hypocarbia, cerebral vasoconstriction, and syncope.²² Hyperventilation may not be obvious to the observer but can be documented by end-tidal carbon dioxide monitoring. In general, a patient with syncope and a psychiatric disorder is likely to be young, with repeated episodes of syncope and multiple prodromal symptoms.²¹ A psychiatric cause for syncope should be one of exclusion, assigned only after organic causes have been excluded.

NEUROLOGIC SYNCOPE

Neurologic causes of syncope are rare. To meet the definition of syncope, symptoms must be transient and with no persistent neurologic deficits. Thus, patients with loss of consciousness with persistent neurologic deficits or altered mental status do not have true syncope. Brainstem ischemia, vertebrobasilar atherosclerotic disease, or basilar artery migraine may result in a decrease in blood flow to the reticular activating system, leading to sudden, brief episodes of loss of consciousness. Loss of consciousness is typically preceded by other signs or symptoms, such as diplopia, vertigo, focal neurologic deficits, or nausea. Subclavian steal syndrome is a rare cause of brainstem ischemia. It is characterized by an abnormal narrowing of the subclavian artery proximal to the origin of the vertebral artery, so that with exercise of the ipsilateral arm, blood is shunted, or “stolen,” from the vertebrobasilar system to the subclavian artery supplying the arm muscles. Anatomically, narrowing is more common on the left. Physical examination may identify decreased pulse volume and diminished blood pressure in the affected arm.

Subarachnoid hemorrhage may present with syncope but is usually accompanied by other symptoms such as focal neurologic deficits, headache, or persistent altered mental status. The mechanism for syncope is thought to be an increase in intracranial pressure with a decrease in cerebral perfusion pressure. Subarachnoid hemorrhage can also follow a fall and head injury from syncope secondary to another cause. See chapter 166, Spontaneous Subarachnoid and Intracerebral Hemorrhage, for further discussion.

Seizure may be confused with syncope, because brief tonic-clonic movements are often associated with syncope. However, confusion (postictal state) lasting several minutes, tongue biting, incontinence, or an epileptic aura suggests a seizure.

MEDICATION-INDUCED SYNCOPE

Medications may contribute to syncope by a variety of means (Table 52-2), but the most common is orthostasis.²³ β-Blockers or calcium channel blockers may lead to a blunted heart rate response after orthostatic stress. Diuretics may produce volume depletion, and some medications have proarrhythmic properties, increasing the concern for dysrhythmia as the cause of syncope.

The goal of ED evaluation is to identify those at risk for immediate and future morbidity or sudden death. For patients with a specific diagnosis, the diagnosis directs the disposition plan. For patients without a specific diagnosis, risk stratification is based on a careful history, thorough physical examination, and electrocardiogram interpretation, with additional testing as needed.

HISTORY

Obtain clinical history from the patient and any witnesses of the event. Begin with a detailed description of the events preceding the loss of consciousness, including patient position, environmental stimuli, strenuous activity, or arm exercise. Record premonitory symptoms such as headache, diplopia, vertigo, or focal weakness. Ask about chest pain and palpitations. Clarify the duration of loss of consciousness and symptoms occurring after regaining consciousness. Symptoms associated with syncope that should raise concern of an immediately life-threatening diagnosis include chest pain

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