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Section 2. Falls, Fractures, and Injury
Chapter 18. Syncope
Topic:    Syncope

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Syncope

Syncope is sudden, transient loss of consciousness characterized by unresponsiveness and loss of postural control, followed by spontaneous and typically complete recovery. Syncope is a symptom--not a disease

Geriatric Essentials

  • Syncope in elderly people often results from several interacting abnormalities or disorders rather than from a single abnormality or disorder.
  • Cardiac causes, some of which are life threatening, are more common among the elderly.
  • The cause of syncope is unknown in about 33% of cases in the elderly.
  • Syncope must always be differentiated from a fall with head trauma that results in brief unconsciousness.
  • Up to 33% of elderly patients who experience syncope are injured during the episode.

About 0.5% of community-dwelling people in their 60s experience syncope each year; this rate is only slightly higher than the frequency in young and middle-aged adults. However, the rate increases to about 1% for people in their 70s and to 1.7% for men and 2.0% for women in their 80s. Syncope is recurrent in about 33% of patients. About 3% of emergency department visits and 2 to 6% of hospital admissions are for syncope; 80% of these visits involve patients > 65. About 25% of elderly patients in long-term care settings have experienced syncope during the past 10 yr, and 6 to 7% experience it each year.

Although syncope by itself does not increase the risk of death in the elderly, some of its causes are life threatening. Notably, in patients who experience an episode of unconsciousness that ultimately requires resuscitation, sudden cardiac death is the diagnosis, rather than syncope. About 33% of syncopal episodes result in injuries, and syncope may lead to physical disability and subsequent functional decline.

Etiology

Syncope in the elderly often results from several interacting abnormalities or disorders rather than from a single abnormality or disorder. Any disorder that can cause an abrupt decrease in cerebral blood flow can cause syncope (see Table 18-1). A cause is neither immediately obvious nor ultimately discovered in about 33% of cases.

Primary cardiac disorders: Primary cardiac disorders account for only about 10% of cases. Previous diagnosis of coronary artery disease or a cardiac arrhythmia strongly predicts a primary cardiac disorder as the cause of a subsequent syncopal episode. Among patients with syncope attributed to a cardiac cause, the incidence of subsequent sudden cardiac death is about 25%. Abrupt reduction in cardiac output can cause syncope. This reduction may be caused by a number of cardiac disorders; most of them are more common among elderly than among younger patients.

Arrhythmias are the most common cardiac cause of syncope. Tachyarrhythmias (eg, atrial fibrillation, ventricular tachycardia) cause syncope when heart rate is too fast to allow adequate ventricular filling. Bradyarrhythmias (eg, sick sinus syndrome, atrioventricular block) cause syncope when heart rate is too slow to provide adequate cardiac output. MI accounts for 2 to 6% of syncopal episodes among elderly patients. Aortic stenosis, mitral regurgitation, mitral stenosis, and hypertrophic cardiomyopathy are also common causes.

Orthostatic hypotension: Orthostatic hypotension is usually asymptomatic, but it can cause syncope. Among elderly people in long-term care settings, orthostatic hypotension causes 6% of syncopal episodes. It has many causes, including age-related physiologic changes, drugs, dehydration, and autonomic insufficiency syndromes (eg, pure autonomic failure, multiple system atrophy, parkinsonism, multiple cerebral infarctions). Diabetes is the most common cause of autonomic insufficiency involving the peripheral nervous system.

Postprandial hypotension: Postprandial hypotension, which is common among elderly people, can cause syncope. Nearly all elderly nursing home residents and 33% of community-dwelling elderly people experience some postprandial decrease in BP. Small decreases (< 20 mm Hg) in systolic BP are common within 75 min of eating a meal and usually cause no symptoms. Large decreases (> 20 mm Hg) may cause syncope. Patients with hypertension may experience the largest decreases in postprandial BP.

Reflex-mediated syncope: Examples are syncope due to straining while defecating (defecation syncope) or urinating (micturition syncope) or due to strenuous coughing (cough syncope). These movements can cause syncope by increasing intrathoracic pressure, increasing vagal tone, reducing venous return to the heart, and decreasing cardiac output, thereby reducing BP.

Carotid sinus hypersensitivitycan cause syncope when neck movement, a tight collar, or a tumor or other lesion at the carotid bifurcation stimulates baroreceptors in the carotid sinus, resulting in excessive slowing of the heart, vasodilation, or both. Carotid sinus syndrome refers to symptomatic carotid sinus hypersensitivity and is defined by a sinus pause that lasts > 3 sec (cardioinhibitory response) or a drop in systolic BP of > 50 mm Hg (vasodepressor response) during carotid sinus massage. Risk factors for carotid sinus hypersensitivity include older age, cardiovascular disorders, and use of drugs that affect the sinus node (eg, beta-blockers, digoxin, methyldopa, Ca channel blockers).

Vasovagal (neurocardiogenic) syncope, which is caused by stimulation of the vagus nerve, is more common among younger than elderly people. Causes include the simple act of swallowing (called swallow syncope), GI disorders (eg, fecal impaction, diarrhea), fright, and pain. Hunger, fatigue, or emotional stress commonly predisposes patients to vasovagal syncope, and a typical autonomic prodrome (eg, light-headedness, pallor, cold sweat) usually precedes it. However, elderly patients are more likely to present without the typical prodromal symptoms.

Other causes: Cerebrovascular insufficiency is considered the cause of syncope only if accompanied by transient focal neurologic deficits. Rarely, in patients with osteoarthritis, vertebrobasilar insufficiency due to compression of vertebral arteries by cervical osteophytes causes syncope when patients move their head in certain positions.

Drugs (eg, OTC drugs with anticholinergic properties) may cause tachyarrhythmias, which can precipitate syncope. Prescription drugs that may cause syncope include anticholinergic drugs (eg, phenothiazines, tricyclic antidepressants), sympatholytic drugs (eg, guanethidine, prazosin, reserpine, terazosin), volume-contracting drugs (eg, diuretics), and vasodilators (eg, ACE inhibitors, Ca channel blockers, nitrates, phosphodiesterase inhibitors). Syncope may also result from ingestion of alcohol, which has vasodilatory properties, or from use of ophthalmic drugs that have systemic effects (eg, topical beta-blockers, which can cause bronchospasm, bradycardia, or heart failure). Many other drugs have also been implicated.

A seizure can be considered a cause of syncope if it manifests solely as transient loss of consciousness and loss of postural control. However, such episodes are rare because most seizures also cause motor activity and a prolonged postictal depression, which are not technically part of the syncope definition. Conversely, seizure activity can occur during a true syncopal event when cerebral perfusion is inadequate. Therefore, determining whether a seizure is a cause or result of syncope is often difficult.

Hypoglycemia, including that induced by antihyperglycemic drugs, occasionally causes syncope but more often causes light-headedness without loss of consciousness.

Pathophysiology

Syncope results from inadequate delivery of O2 or metabolic substrate to the brain or from disorganized electrical activity in the brain during seizures. Elderly people are subject to many age- and disease-related conditions that threaten cerebral blood flow or blood O2 content. In most elderly people, particularly those who already have some degree of ongoing compromise in cerebral perfusion, any acute insult that further reduces O2 delivery to the brain (eg, pneumonia, cardiac arrhythmia, a hypotensive drug, situational stress that reduces BP) may cause syncope.

Many cardiovascular and neuroendocrine homeostatic mechanisms that normally maintain BP (eg, baroreflex sensitivity to hypertensive and hypotensive stimuli, heart rate response to postural change) become impaired with aging. Thus, the ability to maintain adequate cerebral perfusion during hypotensive stress is reduced. Hyperventilation associated with heart failure and dyspnea can further decrease cerebral blood flow by as much as 40%. Other common disorders (eg, COPD, anemia) can reduce cerebral O2 delivery even further.

Age-related decreases in basal and stimulated renin levels and in aldosterone production and increases in atrial natriuretic peptide levels predispose the elderly to syncope by impairing renal Na conservation and intravascular volume maintenance. The elderly are less likely to experience thirst in response to hypertonic dehydration. Therefore, they are more likely to become dehydrated and experience hypotension in response to diuretics, acute febrile illness, or limited salt and water intake.

Diagnosis

Syncope must always be differentiated from a fall with head trauma that results in brief unconsciousness. Because syncope often results in head trauma, and head trauma may cause loss of consciousness, both syncope and head trauma should be considered in most elderly patients with loss of consciousness who have hit their head. Identifying the cause or causes of syncope is important for determining both prognosis and treatment. The evaluation should begin with a thorough history and a physical examination, which, in most cases, are sufficient to identify the cause. See also the European Society of Cardiology's Guidelines on Management (Diagnosis and Treatment) of Syncope--Update 2004.

History: The patient and any witnesses should be asked to describe what the patient was doing just before the syncopal episode. In particular, a physician should note whether the episode occurred after a change in posture from lying down or sitting to standing or after a long period of standing; either event suggests orthostatic hypotension as a cause. If syncope occurred during exercise, tachyarrhythmias such as ventricular tachycardia and reduced cardiac output due to aortic stenosis should be considered possible causes.

The patient and family members or other people close to the patient should be asked about recent changes in the patient's condition that may suggest causes. The physician ascertains whether any prescription or OTC drugs, including ophthalmic drugs, are being used.

A seizure disorder is suggested when syncope is preceded by an olfactory or a gustatory aura or is accompanied by tongue biting, tonic-clonic movements, or incontinence, followed by postictal confusion.

The nature of recovery from syncope can also provide important clues. For example, slow recovery suggests a seizure disorder, focal neurologic abnormalities suggest a stroke or transient ischemic attack, cardiac symptoms and ECG changes suggest MI, nausea or abdominal discomfort suggests a vasovagal mechanism, and a rapid return to baseline suggests an arrhythmia. Multiple episodes of syncope over a relatively short period of time suggest a cardiac cause such as an arrhythmia.

Physical examination: To rule out orthostatic hypotension, a physician should measure BP and heart rate with the patient supine after resting for 5 min; then with the patient upright after standing (preferably, but sitting is acceptable) for 1 min and 3 min. Orthostatic hypotension is diagnosed if systolic BP decreases by at least 20 mm Hg or diastolic BP decreases by 10 mm Hg. A small (< 10 beats/min) or no increase in heart rate with standing or sitting may indicate baroreflex impairment or a drug effect; tachycardia (heart rate > 100 beats/min), which is rare in response to postural change in elderly people, may indicate volume depletion.

The carotid arteries are auscultated for bruits to rule out flow abnormalities contraindicating carotid sinus massage. The carotid arteries should also be palpated to determine the quality of the carotid upstroke. With normal aging, the upstroke usually becomes brisker because vascular rigidity increases. In elderly people with aortic stenosis, amplitude of the upstroke may be reduced to a level that is considered normal for younger people but abnormal for elderly people.

The heart is auscultated for murmurs of aortic stenosis, mitral regurgitation, mitral stenosis, or hypertrophic cardiomyopathy. An apical heave, an aortic systolic murmur that is loud or peaks late, and a diminished 2nd aortic sound suggest hemodynamically significant aortic stenosis. A holosystolic murmur at the apex is characteristic of mitral regurgitation but may also occur with aortic stenosis or hypertrophic cardiomyopathy. Accentuation of the systolic murmur during the Valsalva maneuver helps distinguish hypertrophic cardiomyopathy from aortic stenosis or mitral regurgitation.

A neurologic examination is essential for detecting the rigidity, bradykinesia, and abnormal gait of parkinsonism or multiple system atrophy; focal abnormalities that may indicate cerebrovascular insufficiency or space-occupying lesions; and signs of a peripheral neuropathy that may affect autonomic fibers.

Testing: Certain tests should be done in all elderly patients with syncope because disorders that can cause syncope often manifest atypically in elderly patients. A resting ECG should be done to detect evidence of arrhythmia, a conduction abnormality, ischemia, or infarction. Pulse oximetry should be done if patients are evaluated immediately after a syncopal episode. Other routine tests should include WBC count to detect occult infection and Hct to detect anemia. Electrolytes, BUN, and creatinine should be measured to help assess hydration status and rule out electrolyte disorders. Measuring plasma glucose helps exclude hypoglycemia or hyperglycemia; the first sign of hyperosmolar dehydration with hyperglycemia may be syncope.

Other, more specialized laboratory tests are done only if indicated by the history and physical examination. If the patient was exercising or experiencing chest pain or dyspnea just before the syncopal episode or if ECG abnormalities are present, cardiac enzymes and isoenzymes should be measured to rule out MI. If the patient is taking an antiarrhythmic, an anticonvulsant, or digoxin, measuring drug concentration levels may help determine whether the drug level is subtherapeutic, therapeutic, or toxic. If the drug level is subtherapeutic, syncope may have resulted from inadequate treatment of a known predisposing disorder, such as a seizure disorder. If the drug level is toxic (sometimes even if within the usual therapeutic range), syncope may have resulted from a drug-induced proarrhythmia.

Ambulatory (24-h) ECG monitoring (with a Holter monitor) should be done only when the history strongly suggests arrhythmia as the cause. Even in such circumstances, results can be difficult to interpret because monitoring usually detects no arrhythmias or so many asymptomatic arrhythmias that their relationship to syncope is uncertain. Ambulatory ECG is helpful only for patients who, if arrhythmias are detected, will be treated with antiarrhythmic drugs despite the risk of severe toxic effects (eg, patients who have underlying cardiovascular disorders, patients who have had a recent MI and are at high risk of sudden death). Some patients with arrhythmias are not candidates for these drugs because of the toxic effects.

Continuous-loop event recorders can be worn continuously for 1 mo or implanted for longer periods and activated when symptoms occur. A memory function records several minutes of cardiac rhythm before the recorder is activated; thus, patients can document an arrhythmia by activating the recorder after recovering from syncope. Because symptomatic arrhythmias occur sporadically and are often missed during ambulatory ECG monitoring, continuous-loop recording should be done when 24-h monitoring is unrevealing and serious arrhythmias are suspected or syncope is recurrent and unexplained.

Cardiac electrophysiologic studies can detect occult sinus node disorders, conduction abnormalities, and inducible ventricular arrhythmias in > 50% of patients with unexplained syncope. However, the value of these studies is difficult to determine because elderly patients who do not have syncope are likely to have electrophysiologic abnormalities and because those who have syncope often spontaneously stop having episodes. Thus, electrophysiologic studies should be reserved for elderly patients who have recurrent unexplained syncope and who have ECG or other clinical evidence of coronary artery disease or a structural cardiac disorder.

Ambulatory BP monitoring should be done to detect hypotension if syncope occurs soon after activities that potentially predispose to hypotension (eg, eating meals, taking drugs, postural changes). Because BP monitors are often heavy and cumbersome, patients may prefer to use a portable automated device and diary to record BP at certain times of day, including early morning after arising from bed, 1 h after taking drugs or eating, and at the time the syncopal episode occurred.

Carotid sinus massage should be done to detect carotid sinus hypersensitivity when no other cause of syncope is apparent, but only in patients who have no evidence of cerebrovascular disease (eg, carotid bruit, previous stroke, transient ischemic attacks) or cardiac conduction abnormalities. The technique consists of a circular 5-sec massage of one carotid sinus at a time while the patient is monitored with ECG. BP is measured before and immediately after each massage. Carotid sinus massage is usually safe when done for 5 sec in carefully screened patients. Serious complications (eg, stroke) can occur in patients with underlying cerebrovascular disease or during vigorous, prolonged massage.

Doppler echocardiography should be done in patients with exercise-induced syncope or with previously undetected murmurs to check for hemodynamically significant valvular heart disease and hypertrophic cardiomyopathy.

Tilt-table testing (with and without isoproterenol infusions) should be reserved for certain patients whose history and physical examination suggest reflex-mediated syncope or for patients with exercise-induced syncope if ECG and echocardiography results are negative. A head-up tilt at 60 to 80° for up to 45 min can precipitate vasovagal syncope with associated bradycardia and hypotension. One mechanism for this response is probably the Bezold-Jarisch reflex, which is provoked by vigorous cardiac contraction around a relatively empty ventricular chamber. Using isoproterenol to strengthen cardiac contraction can increase the test's sensitivity. However, isoproterenol is often contraindicated in elderly patients with known or suspected coronary artery disease. The development of vasovagal syncope during the tilt-table test suggests that vasovagal syncope caused the unexplained episode. Usually, vasovagal syncope can be readily diagnosed without the tilt-table test based on a history of typical vagal prodromes (eg, nausea; light-headedness; pale, cold, clammy skin). The tilt-table test may also help identify delayed orthostatic hypotension as the cause of syncope.

EEG and brain CT or MRI should be done only when seizures, cerebrovascular insufficiency, or stroke is suspected. Research studies suggest that these tests have little value unless the history yields evidence of a seizure or underlying focal neurologic abnormalities are identified during the examination.

Treatment

Optimal treatment requires an interdisciplinary approach. First, all likely causes and predisposing conditions should be identified and corrected. If a primary cardiac disorder is suspected as the cause, patients should be admitted to the hospital for cardiac monitoring and evaluation.

Even major interventions (eg, aortic valve repair) are relatively well tolerated in otherwise healthy elderly people and can greatly improve quality of life. Similarly, pacemaker insertion, coronary artery revascularization, and carotid endarterectomy can be considered when appropriate. The patient's coexisting disorders, not age, are the deciding factors in determining treatment.

When no primary cause of syncope is identified, potential predisposing conditions are corrected. For example, patients with anemia may benefit from vitamins, iron supplements, erythropoietin, or transfusions, depending on the cause of anemia.

For patients with postprandial hypotension, adjusting the time a hypotensive drug is taken to avoid a peak effect after a meal may help. Patients with angina, who often are treated with hypotensive drugs (eg, beta-blockers, nitrates), should be treated as long as treatment does not reduce BP excessively. Drug regimens of patients with carotid sinus hypersensitivity or a cardiac conduction abnormality should be evaluated to check for cardioinhibitory or hypotensive drugs that may be contributing to syncope.

Patients with orthostatic hypotension may benefit from increasing salt intake, wearing compression stockings, and elevating the head of the bed. If orthostatic hypotension persists despite these measures, drug therapy can be tried.

For patients with carotid sinus syndrome, stopping cardioinhibitory or hypotensive drugs (eg, beta-blockers, Ca channel blockers, digoxin) usually helps. If stopping drugs is not effective or if these drugs are not implicated, patients with a cardioinhibitory response can be treated with cardiac pacing, and patients with associated hypotension may benefit from vasopressors (eg, midodrine).

Because syncope is often recurrent, measures to prevent serious injury or accidents during an episode should be taken. Patients should not drive for at least 6 mo after the last episode if syncope is unexplained and untreated. Patients should be taught to recognize premonitory symptoms and lie down immediately when they occur.

Prevention

Syncope often can be prevented by identifying precipitating factors and teaching patients how to avoid them. For example, elderly men with micturition syncope can learn to urinate while sitting down, and patients with nitrate-induced syncope can be given a different antianginal drug or learn to sit or lie down after taking a nitroglycerin tablet. Patients with postprandial syncope can eat small, frequent meals and lie down after eating. Walking after a meal may prevent postprandial hypotension but should be done only with supervision. Patients with orthostatic hypotension should not rise from bed quickly, particularly in the middle of the night. They should sit on the edge of the bed and flex their feet before standing. If patients are able, crossing the legs while standing may help prevent orthostatic hypotension. Patients can learn to avoid straining (ie, Valsalva maneuver) during defecation; using stool softeners and altering the diet helps. Drinking ample fluids may help prevent syncope, particularly during hot weather or acute illness; diuretics should be avoided during these situations.

Physicians and nurses should avoid prescribing potentially hypotensive drugs to elderly patients who may not need them, and patients who need these drugs should be monitored for orthostatic and postprandial hypotension. Excessive alcohol use should be discouraged. To minimize orthostatic and postprandial hypotension, patients with hypertension should be cautiously treated while BP is monitored. Physical therapists can help patients maintain sufficient muscle tone in the lower extremities to ensure adequate venous blood return to the heart. Nutritionists can advise patients with orthostatic hypotension how to maintain adequate salt and fluid intake.

This topic was last updated February 2006.

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