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Neurally Mediated Syncope
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Neurally mediated syncope is a broad category involving an inappropriate vasodilation or bradycardia in response to a stimulus that results in a loss of postural tone. Common precipitating factors are shown in Table 18–3. It is often used synonymously with vasovagal syncope, also this is but one subtype. It may have a visceral (eg, micturition and defecation) or emotional component. Carotid sinus syncope is classified as a form of neurally mediated syncope.
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Essentials of Diagnosis
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- Usually occurs when patient is standing or sitting
- Lasts 10 seconds to a few minutes
- Associated with lightheadedness, nausea, pallor, sweating, and blurred vision
- No postictal period
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General Considerations
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Vasovagal disorders account for most episodes of syncope. Physiologic decreases in both arterial pressure and heart rate mediated by parasympathetic tone combine to produce central nervous system hypoperfusion and subsequent syncope. Prolonged cerebral hypoxia with resultant tonic–clonic movements is more likely to occur if the patient remains upright.
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Vasovagal episodes begin in a standing or sitting position and only rarely in a supine position.
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The prodrome lasts from 10 seconds to a few minutes and includes weakness, lightheadedness, nausea, pallor, sweating, salivation, blurred vision, and tachycardia.
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Brain hypoperfusion causes dimming of vision; the patient then loses consciousness and sinks to the ground. Examination reveals an unconscious individual who is pale and is sweating and who has dilated pupils and a slow, weak pulse. With loss of consciousness, bradycardia replaces tachycardia.
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Abnormal movements may be noted during the period of unconsciousness. These are mainly tonic or opisthotonic. These may be accentuated by prolonged periods of decreased cerebral blood flow or hypoxia, as may occur if the patient remains seated or is held up by others.
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Postsyncopal Findings
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The patient is lucid and awake seconds to less than a minute after sinking to a recumbent position; a postictal confusional state is absent unless a seizure has occurred. However, nervousness, dizziness, headache, nausea and vomiting, pallor, and perspiration may persist for hours.
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Syncope may recur, especially if the patient stands up within 30 minutes after the attack. Syncope due to a specific precipitating factor (eg, cough) may be reproduced in the emergency department.
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After ruling out more serious causes of syncope and addressing concomitant issues such as trauma from a fall, reassurance and a recommendation to avoid precipitating factors are usually all that is necessary. Cough suppression and sitting down to urinate are helpful in posttussive and micturitional syncope. Adequate nutrition and hydration should be encouraged.
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Refer the patient to an outpatient clinic or primary care physician after a period of observation and confirmation of the diagnosis in the emergency department.
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Carotid Sinus Syncope
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Carotid sinus syncope classically results from pressure on an abnormally sensitive carotid sinus by a tight collar, neck mass, enlarged cervical nodes, or tumor. This pressure causes vagal stimulation that slows the sinoatrial and atrioventricular nodes and inhibits sympathetic vascular tone. The resulting bradycardia and systemic hypotension then produce syncope. The syndrome may be reproduced in the emergency department by pressure on the carotid sinus for 5–10 seconds while the patient is both supine and erect: cardiac monitoring or ECG documents the induced bradyarrhythmia. Such pressure may also produce syncope resulting from cerebral ischemia if the examiner compresses the artery contralateral to an occluded carotid. Syncope is then due to cerebral hypoperfusion secondary to cerebrovascular disease and not to carotid sinus hypersensitivity.
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Treatment and Disposition
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The patient with syncope should be placed supine and pressure on the carotid sinus relieved (eg, loosening a tight collar). Refer the patient to an outpatient clinic or primary care physician for evaluation.
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Cardiopulmonary Syncope
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General Considerations
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A cardiovascular origin for syncope is suggested when it occurs during recumbency, during or following physical exertion, or in a patient with known heart disease. Loss of consciousness in cardiac disease is most often due to an abrupt decrease in cardiac output, with subsequent cerebral hypoperfusion producing symptoms identical to those of fainting. Such cardiac dysfunction may result from rhythm disturbances (bradyarrhythmias or tachyarrhythmias), cardiac inflow or outflow obstruction, acute myocardial infarction, intracardiac right-to-left shunts, leaking or dissecting aortic aneurysms, or acute pulmonary embolus. Table 18–1 lists some of the more common cardiopulmonary causes of syncope.
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Cardiac Inflow Obstruction
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Essentials of Diagnosis
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- Suspect with syncope due to change in position
- Look for physical examination findings—cardiac findings, engorged neck veins, weak pulse, or hypotension
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Patients with atrial or ventricular myxomas and atrial thrombi usually present with embolization but may also have sudden loss of cardiac output and syncope; syncope occurring with change in position is classic but uncommon. A left atrial myxoma often mimics mitral stenosis but is occasionally manifested by mitral regurgitation murmur. Mitral valve prolapse may also cause syncope.
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Constrictive pericarditis or cardiac tamponade causes reduced cardiac output and may result in syncope. Any maneuver or drug that decreases heart rate or venous return will further impair cardiac output. The diagnosis is suggested by the presence of engorged neck veins, clear lung fields on chest X-ray, weak pulse, and hypotension. Tension pneumothorax reduces cardiac output by decreasing venous return and may produce syncope. There is usually a history of chest trauma or chronic pulmonary disease with bullae. Chest X-ray and physical examination confirm the diagnosis.
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Treatment and Disposition
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Patients with syncope thought to be due to cardiac inflow obstruction require hospitalization.
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Cardiac Outflow Obstruction
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Essentials of Diagnosis
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- Consider with syncope related to exertion
- Look for cardiac physical findings
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Loss of consciousness secondary to congenital or acquired severe stenosis may occur in all age groups. Exertional syncope occurs as a result of cerebral hypoperfusion due to exercise-induced vasodilation in the presence of a fixed cardiac output. Two other pathophysiologic events are recognized: (1) acute transient left ventricular failure with normal sinus rhythm and (2) transient arrhythmia or cardiac standstill, causing an acute drop in cardiac output. Sudden death may result. Autonomic insufficiency also has been reported in these patients. Reflex peripheral vascular vasodilation (presumably due to left ventricular baroreceptor activity) has been demonstrated in the absence of cardiac arrhythmia.
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Syncope usually follows exercise and is often associated with dyspnea, anginal chest pain, and sweating. Physical findings that occur with hemodynamically severe aortic stenosis include the following:
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- Characteristic midsystolic ejection murmur (often associated with a palpable thrill).
- Sustained and prolonged left ventricular lift.
- Paradoxically split second sound.
- Delayed upstroke and reduced amplitude (pulsus parvus et tardus) on the carotid pulse.
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Treatment and Disposition
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Promptly hospitalize all patients with symptomatic aortic stenosis (angina, congestive heart failure, or syncope) to evaluate them for possible valve replacement. Median survival time following the initial episode of syncope due to aortic stenosis in the patient who does not receive a prosthesis is 1.5–3 years.
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Severe pulmonary stenosis may produce syncope, especially following exertion. A hemodynamic process similar to that of aortic stenosis is responsible. Physical findings include right parasternal lift, systolic ejection murmur at the upper left sternal border, a prominent S4, and a conspicuous wave in the jugular venous pulse.
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Treatment and Disposition
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Immediate hospitalization is required, because the patho-physiology and prognosis of this condition are similar to those of aortic stenosis.
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Hypertrophic Cardiomyopathy
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Essentials of Diagnosis
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- Syncope with exercise, dyspnea on exertion, and chest pain
- Cardiac findings including systolic ejection murmur, S4, and perhaps a thrill
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Symptoms include syncope with exercise, dyspnea on exertion, and chest pain. Physical findings include a prominent fourth heart sound, ventricular lift, transient arrhythmias, and systolic ejection murmur and perhaps a thrill, both of which increase with exertion and with decreased left ventricular chamber size (eg, as produced during the Valsalva maneuver). Echocardiography confirms the diagnosis.
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Treatment and Disposition
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Hospitalize the patient for further evaluation and treatment.
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Pulmonary Vascular Disease
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Pulmonary Hypertension
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Syncope or near syncope may be found in patients with pulmonary hypertension. Progressive dyspnea and chest pain, palpitations with a loud P2, tricuspid regurgitation, and right ventricular heave are often found.
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Syncope is found in a subset of patients with a pulmonary embolism. The syncope may be recurrent and is more often found in women. PE patients with syncope may have a higher incidence of angiographic obstruction, new right incomplete bundle branch block, and cardiac arrest when compared to patients without syncope.
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Treatment and Disposition
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Provide supplemental O2 via face mask or assisted ventilation. Treat with heparin by continuous infusion or subcutaneous low molecular heparin. Consider thromboembolic agents in patients who are hemodynamically unstable or have massive PE. Admission of unstable patients to an ICU is appropriate. See Chapter 33 for further details.
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Cerebrovascular Syncope
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Although syncope resulting from cerebrovascular disease is often diagnosed, such an association is uncommon because both cerebral hemispheres and the brain-stem reticular formation must be compromised before consciousness is lost.
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Basilar Artery Insufficiency
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Atherosclerotic occlusive disease of the extracranial vertebral artery is usually insidious with disabling or fatal consequences. Symptoms of vertebrobasilar insufficiency are often not well recognized by physicians, leading to delays in treatment. Vertebrobasilar ischemic symptoms are often positional and may be associated with stereotypical movement such as extension of the neck or rotational movement of the head in a particular direction. Basilar artery insufficiency manifests as a cluster of symptoms with the most common being vertigo and visual dysfunction. Episodic perioral numbness or paraesthesia, ataxia, dysarthria, syncope, headache, nausea, vomiting, tinnitus, and cranial nerve dysfunction can also be found.
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Treatment and Disposition
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Accurate diagnosis is often difficult. Neurological consultation is recommended. Hospitalization is recommended and treatment with aspirin should be started although the effective dose has not yet been clarified.
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Subclavian Steal Syndrome
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Subclavian artery steal is caused by stenosis of the subclavian artery proximal to the takeoff of the vertebral artery. This causes a retrograde flow in the ipsilateral internal mammary artery and the vertebral arteries. Symptoms of subclavian artery steal may include vertigo and syncope with left arm exertion, angina, or ulcerated or gangrenous fingers.
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Blood pressures measured in the upper extremities are nearly always unequal. The average difference is a 45-mm Hg decrease in systolic pressure in the arm supplied by the stenotic vessel.
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Treatment and Disposition
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If subclavian steal is suspected, vascular consult is warranted. Elective hospitalization should be considered.
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(See also Chapter 20.) Syncope occurs in a minority of patients with migraines. It usually manifests as a gradual loss of consciousness in the context of other migraine symptoms and is typically associated with familial hemiplegic migraine. Basilar artery migraine presents with syncope typically proceeded by visual blackening, vertigo, or diplopia.
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Orthostatic Hypotension
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Orthostatic hypotension is a physical finding, not a disease. Multiple medical conditions can cause an abnormal response to positional change. Maintenance of blood pressure during position change is complex, and neurohumoral, cardiac, vascular, neurologic, and muscular responses must occur quickly. If response is abnormal, blood pressure and organ perfusion can be reduced with resultant symptoms of CNS hypoperfusion. This includes weakness, nausea, headache, lightheadedness, dizziness, blurred vision, fatigue, tremulousness, palpitation, vertigo, and impaired cognition. Orthostatic hypotension may result from multiple disorders; the more common causes are listed in Table 18–2.
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Syncope often occurs following rapid change in the upright position, that is, from lying to sitting or from sitting to standing. Prolonged motionless standing, especially after exercise, or standing after prolonged bed rest, may also cause syncope. Patients usually describe lightheadedness, dimming of vision, weakness, and a fainting sensation. True vertigo does not occur.
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Blood pressure that is significantly lower (>20 mm Hg systolic difference) when the patient is standing than when he or she is supine is diagnostic. Orthostatic tachycardia may be present as well.
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A stool sample should be evaluated for the presence of blood. CBC may reveal anemia or hemoconcentration due to blood loss or dehydration, respectively. Electrolyte determinations should be made to detect abnormalities produced by dehydration or drugs. Serum drug levels should be obtained as indicated.
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Hospitalize the patient if postural hypotension is currently producing symptoms and cannot be easily corrected in the emergency department or if an acute underlying cause of hypotension is discovered. If postural hypotension is corrected and no acute pathology persists, the patient may be discharged to an outpatient clinic or their primary care physician.