Chapter 18. Syncope

Cardiac Arrest

See also Chapter 9.

Clinical Findings

Loss of consciousness due to cardiac arrest (ventricular fibrillation or asystole) from any cause occurs in 3–5 seconds if the patient is standing or within 15 seconds if the patient is recumbent. The patient usually rapidly regains consciousness if adequate cardiac output is restored promptly; most patients who regain consciousness within 12 hours will recover without neurologic sequelae.

Treatment and Disposition

Initiate cardiopulmonary resuscitation; see Chapter 9 for further details. Immediate hospitalization in an intensive care unit for evaluation and treatment is required.

Cardiac Arrhythmias

See also Chapter 34.

Clinical Findings

See Table 18–1 for common causes of cardiac and neurologic related syncope. Palpitations, fatigue, dyspnea, or chest pain may precede loss of consciousness. Atypical chest pain (mainly nonexertional, left precordial, sharp, and of variable duration) suggests mitral valve prolapse.

Rapid (≥160 beats/min), slow (≤50 beats/min), or irregular pulse must be carefully investigated. Tachycardia of 180–200 beats/min will produce syncope in half of healthy persons. In patients with underlying heart disease or atherosclerosis, tachycardia as fast as 135 beats/min or bradycardia as slow as 60 beats/min may result in loss of consciousness.

Chest auscultation with the patient in various positions (eg, sitting, left lateral decubitus, squatting) may disclose abnormal murmurs and clicks in the case of mitral valve prolapse. The electrocardiogram (ECG) may confirm the diagnosis of arrhythmia, heart block, sick sinus, or prolonged QT interval. However, a single ECG, obtained when the patient is asymptomatic, is frequently normal or nondiagnostic. A diagnosis can be firmly established only by demonstrating arrhythmias during symptomatic periods.

Treatment and Disposition

Patients with syncopal attacks thought to be due to structural cardiac disease or an arrhythmia should be hospitalized for further evaluation.

The emergency department evaluation of the patient presenting with syncope consists of a careful history, a physical examination that includes orthostatic blood pressure measurements, and a 12-lead ECG. The initial goal should be to identify life-threatening causes of syncope.

Confirm that Loss of Consciousness Was Caused by Syncope

Syncope is a symptom characterized by transient, self-limited loss of consciousness. It is associated with a loss of postural tone, usually resulting in falling. Syncope must be differentiated from other symptoms such as dizziness, presyncope, and vertigo, all of which do not result in loss of consciousness. Typically syncopal episodes are brief, lasting no longer than 20 seconds. Recovery from syncope is usually characterized by almost immediate restoration of appropriate behavior and orientation. Syncope should not be confused with other causes of loss of consciousness such as seizure hypoxia, hyperventilation, hypoglycemia, and intoxications.

Rule Out Blood Loss

In the awake patient with a history of one or more episodes of loss of consciousness, rule out blood loss due to various causes such as aortic aneurysm rupture, vaginal or gastrointestinal bleeding.

Measure Blood Pressure and Pulse

Supine hypotension (systolic blood pressure < 90 mm Hg) or severe peripheral vasoconstriction should be considered evidence of hemorrhagic shock until proven otherwise (Chapter 11).

Orthostatic vital signs should be obtained, though they may be contraindicated in patients who have supine hypotension; those in shock; and those with severe altered mental status, spinal injuries, or pelvic and lower extremity injuries. Measure blood pressure and pulse after the patient has been lying down for 3 minutes. Record blood pressure, pulse, and symptoms again after the patient has been standing for 1 minute. A positive test for orthostatic hypotension is an increase of pulse of 30 beats/min or more, or a decrease in systolic blood pressure of 20 mm Hg or less than 90 mm Hg. The presence of symptoms such as dizziness or syncope should also be noted as a positive test. Many conditions can produce postural hypotension in the absence of hypovolemia (Table 18–2). The utility of orthostatic vital signs in children is questionable.

Gain Venous Access

Use an intravenous catheter (≥18 gauge), and administer a crystallized solution (eg, normal saline) as needed. If blood loss is suspected and the hematocrit or hemoglobin is normal, a repeat determination after volume repletion may confirm blood loss. Serial CBCs may be helpful in detecting active bleeding, and a dextrose test may be helpful if the history or physical examination suggests hypoglycemia.

Look for Possible Gastrointestinal Tract Bleeding

Nasogastric intubation may be indicated in suspected gastrointestinal tract bleeding or in syncope with unexplained postural hypotension. Check stool specimens for blood (gross and microscopic).

Consider Other Possible Causes of Bleeding

Consider pelvic bleeding (eg, ruptured ectopic pregnancy) or trauma, especially that is not visually obvious, such as splenic, hepatic, retroperitoneal, or pelvic injury. Look for a history of anticoagulant use.

Determine Presence or Absence of Related Symptoms

Syncope Associated with Cardiac Arrhythmias or Conduction Abnormalities

Obtain an ECG. This quick, easy, noninvasive test is indicated in all cases of syncope except for those with an otherwise clear cause. ECG abnormalities suggesting an arrhythmic cause of syncope are listed in Table 18–1.

Syncope Associated with Prominent Abdominal or Pelvic Pain

Patients with abdominal or pelvic pain may have hypovolemic syncope secondary to gastrointestinal hemorrhage, leaking aortic aneurysm, or ruptured ectopic pregnancy. Aortic dissection and rupture of a viscus into the peritoneal cavity may also produce syncope initially by vagal stimulation or later as a result of blood loss.

Syncope Associated with Chest Pain or Dyspnea

Consider myocardial infarction, pulmonary embolism (PE), tension pneumothorax, or dissecting aortic aneurysm.

Syncope Associated with Neurologic Symptoms (Eg, Headache, Vertigo, Diplopia)

Consider possible neurologic cause such as basilar artery insufficiency, migraine, and subclavian steal syndrome. Loss of consciousness as an isolated symptom is rarely if ever caused by basilar artery ischemia.

Further Evaluation of Syncope

A detailed, accurate history from the patient, family, observers, or ambulance attendants is the most important factor in making the diagnosis. A head computed tomography (CT) scan must be obtained in the emergency department if the patient has focal neurologic findings or a history suggestive of subarachnoid hemorrhage as the etiology of syncope. The most helpful features are the following.

Epileptic Aura

History of an epileptic aura preceding the loss of consciousness or a period of confusion (postictal state) upon regaining consciousness strongly suggests seizures as the diagnosis (see Chapter 19). This aura must be differentiated from symptoms of decreased cerebral blood flow (eg, those occurring before a syncopal episode or as a result of orthostatic hypotension or cardiac arrhythmia).

Position of the Patient at Time of Loss of Consciousness

Episodes beginning when the patient is lying down suggest seizure or cardiac arrhythmia, whereas orthostatic hypotension and vasovagal syncope occur when the patient is standing or sitting up.

Syncope Related to Active Physical Exertion

Syncope following active physical exertion is frequently noted in cardiac outflow obstruction (eg, aortic stenosis, hypertrophic obstructive cardiomyopathy, myxoma) and is elicited occasionally in patients with cardiac arrhythmias or pulmonary vascular disease.

Other Causes of Syncope

Micturition and coughing are associated with distinctive syncopal syndromes. Simple fainting may occur during the first trimester of pregnancy and must be differentiated from syncope due to blood loss from ectopic pregnancy. Rare causes of syncope include glossopharyngeal neuralgia, hyperventilation, psychiatric causes, and Meniere's disease (look for associated hearing loss and vertigo).

Disposition

Deciding whether to admit the patient with syncope is based on two different objectives: admission for diagnosis or for treatment. When the cause of syncope remains unknown, a risk assessment can be used for the admission decision. The following risk factors warrant consideration for hospitalization: (1) suspected or known heart disease, (2) ECG abnormalities suspicious for arrhythmic syncope, (3) syncope with onset during exercise, (4) family history of sudden death, (5) syncope causing severe injury, and (6) older age and associated comormidities. Reasons for admission/of patients who require treatment include the following: (1) syncope due to cardiac arrhythmia, ischemia, or structural cardiac disease; (2) cerebrovascular accident or focal neurologic deficits; and (3) severe orthostatic hypotension.

Neurally Mediated Syncope

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.

Vasovagal Syncope

Essentials of Diagnosis

• 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

General Considerations

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.

Clinical Findings

Vasovagal episodes begin in a standing or sitting position and only rarely in a supine position.

Prodrome

The prodrome lasts from 10 seconds to a few minutes and includes weakness, lightheadedness, nausea, pallor, sweating, salivation, blurred vision, and tachycardia.

Syncope

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.

Associated Symptoms

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.

Postsyncopal Findings

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.

Recurrence

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.

Treatment

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.

Disposition

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.

Carotid Sinus Syncope

Clinical Findings

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.

Treatment and Disposition

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.

Cardiopulmonary Syncope

General Considerations

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.

Cardiac Inflow Obstruction

Essentials of Diagnosis

• Suspect with syncope due to change in position
• Look for physical examination findings—cardiac findings, engorged neck veins, weak pulse, or hypotension

Clinical Findings

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.

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.

Treatment and Disposition

Patients with syncope thought to be due to cardiac inflow obstruction require hospitalization.

Cardiac Outflow Obstruction

Essentials of Diagnosis

• Consider with syncope related to exertion
• Look for cardiac physical findings

Aortic Stenosis

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.

Clinical Findings

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:

• 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.

Treatment and Disposition

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.

Pulmonary Stenosis

Clinical Findings

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.

Treatment and Disposition

Immediate hospitalization is required, because the patho-physiology and prognosis of this condition are similar to those of aortic stenosis.

Hypertrophic Cardiomyopathy

Essentials of Diagnosis

• Syncope with exercise, dyspnea on exertion, and chest pain
• Cardiac findings including systolic ejection murmur, S4, and perhaps a thrill

Clinical Findings

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.

Treatment and Disposition

Hospitalize the patient for further evaluation and treatment.

Pulmonary Vascular Disease

Clinical Findings

Pulmonary Hypertension

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.

Pulmonary Embolism

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.

Treatment and Disposition

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.

Cerebrovascular Syncope

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.

Basilar Artery Insufficiency

Clinical Findings

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.

Treatment and Disposition

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.

Subclavian Steal Syndrome

Clinical Findings

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.

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.

Treatment and Disposition

If subclavian steal is suspected, vascular consult is warranted. Elective hospitalization should be considered.

Migraine

(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.

Orthostatic Hypotension

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.

Clinical Findings

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.

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.

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.

Disposition

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.

Hyperventilation

Essentials of Diagnosis

• Diagnosis of exclusion
• Numbness and tingling (especially circumoral)
• Muscle twitching and carpal pedal spasm

General Considerations

Psychogenic hyperventilation is a frequent cause of altered consciousness (eg, faintness, lightheadedness) but rarely culminates in syncope. Acute anxiety is the usual cause. The disorder is usually benign, but serious cardiopulmonary causes of hyperventilation or subjective dyspnea must be ruled out (Chapter 13).

Clinical Findings

Common symptoms include lightheadedness, shortness of breath, numbness and tingling (especially circumoral or acral), muscular twitching, and in severe cases, carpal pedal spasm. Positive Chvostek and Trousseau tests are noted during the acute stage. Respiratory alkalosis without other abnormalities (eg, metabolic acidosis) is noted on arterial blood gas analysis. Symptoms are reproduced by hyperventilating in a controlled setting (eg, emergency department).

Treatment and Disposition

Reassure the patient, and alleviate underlying anxiety. If the patient is acutely hyperventilating, ask the patient to count to 3 slowly between breaths. Patients experiencing a panic attack may benefit from alprazolam, 0.25–0.5 mg orally. Rebreathing from a paper bag is no longer recommended because of the potential risk of hypoxia.

Psychiatric Causes

Essentials of Diagnosis

• Diagnosis can be made only after careful exclusion of other causes
• Presence of bizarre postures or movements

General Considerations

Psychiatric causes of syncope include major depression, general anxiety disorder, and panic disorder. Fainting is also a known manifestation of somatization disorder. Alcohol and drug abuse can lead to syncopal episodes. Malingering may be a factor; patients may use the episodes of feigned unconsciousness to manipulate other people for secondary gain. Patients with factitious disorder also may fake unconsciousness, but they do so for psychological reasons.

Clinical Findings

Features that suggest psychiatric causes of syncope are lack of any prodrome, presence of bizarre postures or movements, lack of pallor, and prolonged unconsciousness. Many patients will have a well-documented history of psychiatric responses to stress. Without such a history, a psychogenic cause can be made only after thorough evaluation has excluded other causes of syncope.

Treatment and Disposition

Refer the patient to an outpatient clinic or primary care physician for follow-up.