Syncope

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[edit] Syncope

Wishwa N. Kapoor

[edit] EPIDEMIOLOGY AND ETIOLOGY

Syncope is defined as a sudden transient loss of consciousness associated with loss of postural tone with spontaneous recovery not requiring cardioversion. Syncope must be separated from seizures and other states of altered consciousness such as dizziness, vertigo, coma, and narcolepsy (see Chapter 50 ).

Syncope is a common problem. Loss of consciousness is reported by 12% to 30% of young adults. This symptom accounts for 1% to 6% of hospital admissions and up to 3% of emergency department visits. Syncope is also common in the elderly. In one study of residents of a long-term care institution (older than 75 years of age), the annual incidence was 6%, and 23% had previous lifetime episodes.

Syncope can be a prelude to sudden death in certain subgroups. Patients with cardiac causes of syncope have higher 1-year mortality and sudden death rates than patients with noncardiac or unknown causes. Patients with underlying structural heart disease also have higher mortality regardless of the cause of syncope.

Syncope has a large differential diagnosis from benign problems to life-threatening illnesses (Box 62-1). A detailed description of these entities is beyond the scope of this review; see Additional Readings for further sources.

In studies that evaluated patients presenting with syncope, there has been a wide variation in the proportion of patients diagnosed with various etiologies. This variation is largely due to patient selection (differences ranging from emergency room to intensive care unit [ICU] patients) and lack of uniform criteria for assigning causes of syncope. The most common etiologies include vasovagal syncope diagnosed clinically and orthostatic hypotension. In approximately one third of patients a cause could not be determined. Since that time, tilt testing has become more widely used. Additionally, greater attention has been paid to psychiatric illnesses as causes of syncope. Comorbid illness and medications may be responsible for syncope in the elderly without the ability to assign a single etiology as the cause. Taking this recent information into account, it appears that unexplained syncope is much less frequent, constituting less than 10% of the cases. More specifically, studies noted above diagnosed vasovagal syncope on a clinical basis (e.g., syncope in the setting of various precipitating factors such as pain and instrumentation) or using associated autonomic symptoms. Recent studies using upright tilt testing to provoke vasovagal syncope have shown that symptoms can be induced on tilt testing in 26% to 87% of selected patients with unexplained syncope, suggesting that vasovagal syncope may be a very common cause of syncope.

A subgroup of patients with unexplained syncope may have psychiatric diseases (15% to 20%) that are not recognized as a possible cause of syncope. These illnesses include generalized anxiety disorder, panic disorder, major depression, and somatization disorder.

A third group of patients are those in whom new diagnoses, which caused their initial syncopal episode, become apparent in follow-up. This group composes less than 5% of patients with unexplained syncope and includes patients with dysrhythmias (e.g., supraventricular tachycardia) and seizures.

[edit] PATHOPHYSIOLOGY

The vast majority of causes of syncope result from transient reduction of cerebral blood flow to those parts of the brain subserving consciousness (brainstem, reticular activating system). There are four broad categories of mechanisms that may result in a sudden decrease in cerebral blood flow (see Box 62-1): (1) vasomotor instability associated with disorders that decrease systemic vascular resistance, venous return, or both; (2) severe reduction of cardiac output owing to obstruction of blood flow within the heart or pulmonary circulation; (3) cardiac dysrhythmias leading to a transient decline in cardiac output; and (4) transient ischemia due to cerebrovascular disease with focal or generalized decreased cerebral perfusion.

Rarely, normal or even increased cerebral blood flow may be associated with loss or alteration of consciousness because of a lack of essential nutrients necessary for cerebral metabolism. These states include hypoglycemia and hypoxemia; however, these disorders more frequently lead to somnolence and coma than syncope. Additionally, seizures may present as syncope; in this instance cerebral blood flow is generally normal.

[edit] PATIENT EVALUATION

[edit] History

The evaluation of syncope begins with defining the episode and associated symptoms. Once the patient is found to have had syncope, a workup can be initiated to determine the etiology.

A detailed history of the episode (from the patient and a witness, if present) is needed to separate syncope from other states of altered consciousness such as dizziness, vertigo, drop attacks, coma, and seizure. A particularly difficult distinction is between syncope and seizure. One study comparing the symptoms of syncope and seizure showed that seizures were associated with blue face (or not pale), frothing at the mouth, tongue biting, disorientation, aching muscles, sleepiness after the event, and duration of unconsciousness of more than 5 minutes. By contrast, symptoms associated with syncope were sweating or nausea before the event and being oriented after the event. The best discriminatory symptom is disorientation after the episode, which often signifies a seizure.

Once it has been determined that the patient had syncope, a history is crucial in choosing diagnostic tests selectively to arrive at an etiology. Emphasis is placed on the details of the events leading to the episode, the characteristics of the loss of consciousness, and symptoms immediately after the patient regains consciousness (Table 62-1). For example, in diagnosing vasovagal syncope a history of a particular precipitating factor or the presence of autonomic symptoms is useful. Micturition, cough, defecation, and swallowing may be associated with sudden loss of consciousness. These disorders, termed situational syncope, are diagnosed by history from the patient. Brainstem ischemia due to transient ischemic attacks, basilar artery migraines, and subclavian steal syndrome may lead to drop attacks or syncope, but loss of consciousness is generally associated with other neurologic symptoms and signs referable to the brainstem. A detailed drug history may uncover a potential etiology for syncope. The most common drugs causing syncope include nitrates, vasodilators, and β-blockers (Box 62-2).

Table 62-1 Clinical Features Suggestive of Specific Causes

History may suggest specific entities that can be further evaluated by directed testing (see Table 62-1). For example, syncope with arm exercise suggests subclavian steal syndrome; loss of consciousness in a deaf child with effort or emotional distress may be due to ventricular tachydysrhythmias associated with congenital long QT syndromes; and fainting in a patient with flushing and itching may be a manifestation of systemic mastocytosis. Box 62-1 shows specific features from the history that suggest various diagnoses.

[edit] Physical Examination

A detailed physical examination may provide information needed to establish specific entities as a cause of syncope and exclude others. Findings on examination of particular importance are orthostatic hypotension, cardiovascular abnormalities, and neurologic signs.

Syncope due to orthostatic hypotension can be difficult to diagnose, since 5% to 55% of patients with other etiologies of syncope have orthostatic hypotension (defined as a systolic blood pressure decline of 20 mm Hg or more), and postural hypotension is reported in up to 24% of the elderly. Thus the development of syncope or presyncope upon standing, in association with orthostatic blood pressure decline, is important in the diagnosis of the etiology of loss of consciousness. Blood pressure measurements should be performed upon standing after a supine period of 5 to 10 minutes. Lack of a blood pressure drop upon sitting does not exclude orthostatic hypotension. Several blood pressure determinations upon standing during a 2-minute period are sufficient to detect orthostatic hypotension in most patients. Repeated orthostatic blood pressure measurements are needed when there is high clinical suspicion for orthostatic hypotension, since postural hypotension can be episodic. Orthostatic hypotension may be worse upon arising in the morning or after meals.

Cardiovascular findings may be important clues to the etiology of syncope. For example, aortic dissection and subclavian steal syndrome are associated with differences in the pulse intensity and blood pressure (generally less than 20 mm Hg) in the two arms. Many organic heart diseases that cause syncope have specific cardiovascular findings. These entities include aortic stenosis, idiopathic hypertrophic subaortic stenosis, pulmonary hypertension, myxomas, and aortic dissection.

When a cause of syncope can be found, the history and physical examination lead to the etiology in approximately 45% of patients. Furthermore, organic cardiac diseases and neurologic diseases (e.g., subclavian steal syndrome) are strongly suspected by the history and physical examination. Testing for these diseases should be selective and based on findings from the history and physical examination. Suggestive findings on the history and physical examination are helpful in assigning the ultimate cause of syncope by directed testing in approximately 8% of additional patients.

[edit] DIAGNOSIS

[edit] Diagnostic Testing

Results of blood tests are generally not helpful in assigning an etiology for syncope. Hypoglycemia, hyponatremia, hypocalcemia, and renal failure have been found in 2% to 3% of patients, but primarily in those with seizures. These disorders were often clinically suspected; in one study only one unexpected finding was discovered (hyponatremia with seizures). Syncope due to bleeding has been diagnosed clinically with confirmation by Hemoccult tests or complete blood counts.

When the history and physical examination do not lead to an etiology or provide clues for directed testing, further evaluation focuses on dysrhythmia detection, search for vasovagal syncope, and, less commonly, psychiatric illnesses.

[edit] Dysrhythmia Detection.

Dysrhythmias are primarily of concern in patients with structural heart disease or abnormal electrocardiogram (ECG). If symptoms are consistent with dysrhythmic syncope, efforts should be directed first to rule out dysrhythmias as the cause of syncope. The following means are available for diagnosis of dysrhythmias.

[edit] ECG/Rhythm Strip.

An ECG or a rhythm strip is useful in three ways. First, an ECG may show severe abnormalities that are diagnostic of the cause of syncope (2% to 11% of patients). Examples include complete heart block, symptomatic supraventricular tachydysrhythmias, and ventricular tachycardias. Second, an ECG may show abnormalities that increase the likelihood of dysrhythmic syncope but are not diagnostic of the cause of syncope (e.g., bundle branch block, Wolff-Parkinson-White syndrome). Third, an ECG may be normal, which markedly decreases the probability of dysrhythmias as the cause of syncope.

Treadmill testing can be used to provoke exercise-induced tachydysrhythmias when they are suspected clinically (e.g., patients with exertional syncope) or to look for ischemia. However, this test is rarely useful in establishing a cause of syncope.

[edit] Carotid Massage.

Less than 1% of patients presenting with syncope are assigned the diagnosis of carotid sinus syncope. Carotid sinus hypersensitivity is found in 5% to 25% of asymptomatic populations, but only 5% to 20% of these individuals have spontaneous symptoms consistent with carotid sinus syncope. Consider carotid sinus syncope in (1) those who have spontaneous symptoms suggestive of carotid sinus syncope (e.g., syncope while shaving, wearing tight collars, or turning the head), and (2) in elderly patients with recurrent syncope with a negative diagnostic evaluation. Carotid sinus syncope is diagnosed when carotid massage reproduces the patient's spontaneous symptoms. To diagnose carotid hypersensitivity, carotid massage can be performed for 5 to 15 seconds on each side with concurrent ECG and blood pressure monitoring. A cardioinhibitory response is defined as cardiac asystole of greater than 3 seconds. A vasodepressor response is diagnosed when there is a systolic blood pressure decline of 50 mm Hg or more that is not associated with bradycardia or occurs after bradycardia has been abolished with atropine or atrioventricular sequential pacing.

[edit] Prolonged ECG Monitoring.

The sensitivity and specificity of ECG monitoring for diagnosis of dysrhythmic syncope are not known because of the lack of criteria for abnormal results or a gold standard that is independent of dysrhythmias diagnosed by monitoring. The only certain means of diagnosing dysrhythmias as a cause of syncope is to document dysrhythmias at the time of symptoms. The results of ambulatory monitoring have been disappointing, since symptom correlation is found in only 4% of patients. In an additional 17% no dysrhythmias are found during symptoms, thus potentially excluding dysrhythmias as the etiology. In the remaining patients (approximately 80%) either asymptomatic dysrhythmias or no dysrhythmias are found. Since dysrhythmias may be episodic, finding asymptomatic brief dysrhythmias or no dysrhythmias does not exclude a rhythm disturbance as a cause of syncope.

Monitoring longer than 24 hours is not likely to increase the yield of symptomatic dysrhythmias. In one study, although there was an increased yield of brief dysrhythmias after the first 24 hours (14.7% were abnormal during the first 24 hours, 11% during the second 24 hours, and 4.2% during the third 24 hours), none of the dysrhythmias during the second and third 24 hours were associated with symptoms.

More prolonged monitoring for weeks to months is also possible using patient-activated intermittent loop recorders. This type of recorder can capture dysrhythmias during a syncopal episode if the patient activates it after regaining consciousness. Studies of loop monitoring have included patients referred because of frequent recurrences (median events exceeding 10 per patient). In these highly selected patients, true-positive results (dysrhythmias detected during syncope) were found in 8% to 20% and true-negative results (no dysrhythmias during syncope) in 12% to 27%.

[edit] Electrophysiologic Studies.

In patients with structural heart disease or abnormal ECG (e.g., bundle branch block, accessory pathway, old myocardial infarction), electrophysiologic studies (EPS) should be considered if dysrhythmias are not excluded by noninvasive tests (ECG and ambulatory or loop monitoring). These tests are generally not indicated in patients without heart disease and normal ECG. The diagnostic yield of EPS is approximately 50% (ventricular tachycardia and bradycardias) in patients with organic heart disease and 10% in patients with a normal heart.

Some centers have used the detection of low-amplitude signals in the terminal portion of QRS complex by signal-averaged ECG as a screening test for selecting patients for EPS. The sensitivity of low-amplitude signals (late potentials) is reported to be 73% to 89%, with a specificity of 89% to 100% for detection of inducible sustained ventricular tachycardia in patients with syncope. However, this test is not generally useful to eliminate further consideration of EPS; complete studies are often needed in patients with organic heart disease and syncope because other abnormalities (conduction system disease and supraventricular tachycardia) are relatively common findings on these tests.

[edit] Upright Tilt Testing.

Vasovagal syncope (also known as neurally mediated or neurocardiogenic syncope) can be induced by keeping susceptible individuals upright on a tilt table with or without stimulation with adrenergic agents such as isoproterenol. The mechanism of tilt-induced syncope is not entirely understood (Fig. 62-1). Inhibitory reflexes originating from the heart are widely believed to be responsible for this type of syncope. This reflex originates in the cardiac sensory receptors (mechanoreceptors) located primarily in the inferior and posterior wall of the left ventricle. These receptors may be stimulated by stretch; cardiac distention; forceful, rapid systolic contraction; or chemical substances. The stimulation of receptors leads to increased neural discharges through unmyelinated C fibers to the medulla (vasomotor center), leading to enhanced parasympathetic and decreased sympathetic activity. The result is sudden hypotension and/or bradycardia.

Figure 62-1 Pathophysiologic mechanism for induction of vasovagal syncope during upright tilt testing.

Upright posture leads to pooling of blood in the lower limbs, resulting in decreased venous return (see Fig. 62-1). Normal compensatory response to orthostatic stress is reflex tachycardia, more forceful contraction of the ventricles, and vasoconstriction. However, in individuals susceptible to vasovagal syncope, this forceful ventricular contraction, in the setting of a relatively empty ventricle, may activate the cardiac mechanoreceptors, triggering reflex hypotension and/or bradycardia. Catecholamine release (as may occur with anxiety, fear, and panic), by increasing ventricular contraction, may also activate the nerve endings responsible for triggering this reflex.

A large number of studies have been reported using many different tilt testing protocols. Most of the protocols in the United States use isoproterenol after a period of drug-free tilt testing. Table 62-2 summarizes some of the performance characteristics of tilt testing without considering the heterogeneity in testing protocols.

Table 62-2 Tilt Testing in Syncope

What is the role of tilt table testing in evaluating syncope? In patients without heart disease in whom the history, physical examination, and initial ECG do not lead to an etiology of syncope, upright tilt testing may define a potential diagnosis. Furthermore, in patients who have underlying heart disease and do not have evidence of dysrhythmias based on ECG monitoring and EPS, this test may provide a specific diagnosis. However, because of problems with the specificity of the test, only symptom reproduction during testing should be considered a positive response. Furthermore, tilt testing should generally be limited to patients who have had multiple recurrences of syncope, since treatment is the major issue in this group.

[edit] Psychiatric Assessment.

Several psychiatric illnesses can result in syncope. Generalized anxiety disorder may produce hyperventilation and vasodepressor reaction. In panic disorder, up to 9% of the patients have faintness as a somatic complaint. Patients with somatization disorders have multiple physical symptoms including loss of consciousness, which is reported in 4.5% of patients with this disorder. Medical patients with major depression often have nonspecific physical complaints, and syncope may be one of the manifestations. Patients with syncope due to psychiatric disorders are generally younger and have multiple episodes. They have lower prevalence of heart disease and may have other nonspecific complaints associated with syncope such as headache, fatigue, dizziness, and palpitations.

[edit] Low-yield Tests.

Other tests are rarely helpful in assigning an etiology for syncope. Skull films, lumbar puncture, radionuclide brain scan, and cerebral angiography have not yielded diagnostic information for a cause of syncope in the absence of clinical findings suggestive of a specific neurologic process. Glucose tolerance testing has not led to a diagnosis of hypoglycemia in patients with syncope. Electroencephalogram (EEG) and head computed tomography (CT) scans have shown diagnostic abnormalities in 2% to 4% of patients when these tests are performed. These abnormalities are almost always suspected clinically (history of seizure, symptoms suggestive of seizure or abnormal neurologic examination). Head CT scan is needed if subdural bleeding due to head injury is suspected.

[edit] Summary of Diagnostic Approach.

Fig. 62-2 is a flow diagram that summarizes the diagnostic approach to syncope. A detailed clinical assessment (by history and physical examination) of patients with syncope is crucial and leads to the assignment of the vast majority of the causes of syncope. Additionally, in a smaller proportion of patients, clinical assessment suggests specific entities such as aortic stenosis or neurologic signs and symptoms suggestive of a seizure disorder. These findings should be used to guide further testing to arrive at a diagnosis and initiate treatment.

Figure 62-2 Algorithm summarizing the diagnostic approach to syncope.

An ECG is needed in most patients with syncope, except when the etiology by the history and physical examination is clearly not cardiac. As noted previously, a normal ECG may help decrease the probability of cardiac etiologies.

When a cause of syncope is not established by the history, physical examination, and initial ECG, the following approach can be used to proceed with the diagnostic evaluation.

[edit] Tests for Dysrhythmia Detection.

Dysrhythmic syncope is a major concern in patients with structural heart disease or abnormal ECG. The first step in the evaluation of these patients is prolonged ECG monitoring, since this is a noninvasive test. If a diagnosis is made by finding dysrhythmias and correlating symptoms, invasive tests such as EPS may be avoided. In patients with negative or unclear findings on ECG monitoring (e.g., asymptomatic brief nonsustained ventricular tachycardia) who have recurrent syncope, event recorders are recommended. If ambulatory and event recorders are nondiagnostic, EPS should be considered for selection of therapy. In patients with structural heart disease who have one episode of syncope suggestive of cardiac etiology, EPS is recommended for evaluation of dysrhythmic syncope.

Since the prognosis of patients with negative EPS is favorable, empiric therapy (with a pacemaker or antidysrhythmic drugs) is not justified. Upright tilt testing is recommended in patients with recurrent or disabling symptoms who have negative EPS to define a potential etiology and initiate treatment.

In patients with structural heart disease and syncope, evaluation of the extent and severity of heart disease is needed in order to plan treatment. Thus stress testing and echocardiography may allow better definition of the extent of coronary artery disease and ventricular function in patients with possible ischemic heart disease. These tests are recommended prior to the consideration of EPS and tilt testing, which can result in hypotension that is best avoided in patients with coronary artery disease.

[edit] Patients Without Heart Disease.

Prognosis of syncope patients without heart disease is excellent with regard to the outcome of mortality. In young patients with a normal ECG, the likelihood of dysrhythmias is low. In this group, prolonged ECG monitoring or EPS is generally negative and not needed. Vasovagal syncope and psychiatric disorders are the major diagnostic considerations and should be pursued as the initial step in the evaluation. A similar diagnostic approach can be taken with older patients without heart disease and a normal ECG, but further studies are needed to define better the role of prolonged ECG monitoring in these patients. The yield of EPS is low in this group, and so it is not justified in the vast majority of the patients.

[edit] Recurrent Syncope.

In patients with recurrent syncope, the diagnostic considerations are large, but these patients are less likely to have dysrhythmias and are more likely to have psychiatric illnesses and vasovagal syncope. The initial approach to diagnostic testing should be based on the presence or absence of heart disease (as noted above). In this group of patients, if a cause of syncope is not established, patient-activated intermittent ECG loop recorders may be useful for the evaluation of brief episodic dysrhythmias.

Although studies in the 1980s have shown that a cause of syncope was not established in up to 45% of patients, by using the approach outlined here with the availability of newer diagnostic modalities a cause of syncope can be assigned in the vast majority of patients presenting with this symptom. Patients without a diagnosis have a low incidence of mortality and sudden death but should be followed closely and reevaluated on recurrence.

[edit] MANAGEMENT

Treatment decisions are based on the etiology of syncope. A detailed discussion of the treatments of all of the etiologies is covered in specific chapters. General considerations for treatments are as follows.

[edit] Vasovagal Syncope

The severity and natural history of vasovagal syncope are variable. Patients may have a large number of events at one time that diminish or resolve spontaneously. There are rare patients who continue to have episodes over many years. Thus the frequency and severity of events are important in devising treatment plans for the patient. Because treatments may have potential side effects, they should be reserved for patients who have frequent or disabling symptoms. Treatment should be avoided in those with one or rare lifetime episodes.

Many patients with vasovagal syncope have precipitating factors or situations. These situations should be identified by a careful history, and the patient instructed to avoid them. Common triggers include prolonged standing, venipuncture, large meals, and heat (such as hot baths or sunbathing). Additionally, fasting, lack of sleep, and alcohol intake may predispose to vasovagal syncope and should be avoided. Since psychiatric illnesses probably lead to vasovagal reactions, screening for the psychiatric illnesses noted above should be performed. Treatment of the psychiatric illness often resolves the recurrent syncope.

Several types of drug therapies have been tried for patients with vasovagal syncope (Table 62-3). β-Blockers (e.g., metoprolol, atenolol) are the most commonly used drugs. The mechanism of action of β-blockers is not fully understood, but they can diminish cardiac contractility, inhibiting the activation of cardiac mechanoreceptors. Anticholinergic agents such as transdermal scopolamine (one patch every 3 days) are particularly useful in patients with profound bradycardia during upright tilt testing. Disopyramide has also been reported to decrease recurrence of syncope. This drug has anticholinergic and negative inotropic effects, which may inhibit activation of cardiac mechanoreceptors. Theophylline has rarely been used at doses as low as 6 to 12 mg/kg/day. The mechanism of action of theophylline in the treatment of vasovagal syncope is not known, but a blockade of the effects of adenosine, which has vasodilatory effects, is postulated. Measures to expand volume have been used and include increased salt intake, custom-fitted counterpressure support garments from ankle to waist, and fludrocortisone acetate. Potential side effects include recumbent hypertension, hypokalemia, fluid retention, and congestive heart failure. Finally, atrioventricular pacing may be considered in patients with significant bradycardia in response to upright tilt testing. Even in these patients, the initial treatment of choice is pharmacologic. Pacemaker therapy should be reserved for those who have disabling symptoms and fail drug therapy.

Table 62-3 Commonly Used Therapies for Recurrent Vasovagal Syncope

[edit] Orthostatic Hypotension

The initial approach to treatment of orthostatic hypotension is to ensure adequate salt and volume intake and to avoid or discontinue drugs that cause orthostatic hypotension. Patients with orthostatic hypotension should be advised to raise the head of the bed at night, to rise from bed or chair slowly, and to avoid prolonged standing. Compressive stockings applied up to thigh levels may help decrease venous pooling. Frequent small feedings may be helpful in patients with marked postprandial orthostatic hypotension.

Pharmacologic agents of potential benefit include fludrocortisone (0.1 to 1 mg/day) in conjunction with increased salt intake. Various adrenergic agents have been used, including ephedrine, phenylephrine, and others. A more detailed discussion of pharmacologic treatment of orthostatic hypotension is found elsewhere.

[edit] SYNCOPE IN THE ELDERLY

The elderly often have multiple chronic diseases and physiologic impairments that can predispose to syncope. Thus in the elderly, several seemingly mild abnormalities may contribute to a sudden reduction of cerebral blood flow and syncope. As an example, mild volume depletion with upper respiratory tract infection in a patient with chronic renal insufficiency and systolic hypertension may be sufficient to cause syncope, whereas any one problem alone is not severe enough to cause loss of consciousness.

The initial approach to the management of the elderly should be to search for a single disease as a cause of syncope. If a single disease is found (such as severe aortic stenosis, symptomatic bradycardia, or symptomatic orthostatic hypotension), treatment of that disease can be planned. However, a single disease as the cause of syncope is often not apparent. In these patients, inability to compensate for common situational stresses may be a factor in the setting of multiple medical problems, medications, and physiologic impairments. A careful assessment of the effect of underlying pathologic conditions and medications is important to determine whether multiple pathologic processes could have led to syncope. Once these potential processes are identified, treatment should be directed to correcting these factors. As an example, consider an elderly patient presenting with syncope, who has taken enalapril, 10 mg/day, and has anemia (hemoglobin 9.0), mild orthostatic hypotension, and a recent upper respiratory tract infection. In this patient, if no other etiology of syncope is apparent based on clinical findings and selective use of laboratory tests, volume repletion, treatment of anemia, and adjustment or change of antihypertensive medication may help prevent further episodes of syncope.

[edit] ADDITIONAL READINGS

• FM Abboud: Neurocardiogenic syncope. N Engl J Med 1993; 328:1117.
• DG Benditt, DW Ferguson, BP Grubb,et al.: Tilt table testing for assessing syncope. J Am Coll Cardiol 1996; 28:263 - 275.
• DG Benditt, S Remole, S Bailin,et al.: Tilt table testing for evaluations of neurally-mediated (cardioneurogenic) syncope: rational and proposed protocols. Pacing Clin Electrophysiol 1991; 14:1528 - 1537.
• JP DiMarco, JT Philbrick: Use of ambulatory electrocardiographic (Holter) monitoring. Ann Intern Med 1990; 113:53.
• Guidelines for clinical intracardiac electrophysiological and catheter ablation procedures: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. (Committee on clinical intracardiac electrophysiologic and catheter ablation procedures). Developed in collaboration with the North American Society of Pacing and Electrophysiology. Circulation 1995; 92:673 - 691.
• WN Kapoor: Evaluation and outcome of patients with syncope. Medicine 1990; 69:160.
• WN Kapoor, NL Brant: Evaluation of syncope by upright tilt testing with isoproterenol: a nonspecific test. Ann Intern Med 1992; 116:358.
• WN Kapoor, M Fortunato, BH Hanusa,et al.: Psychiatric illnesses in patients with syncope. Am J Med 1995; 99:505 - 512.
• WN Kapoor, MA Smith, NL Miller: Upright tilt testing in evaluating syncope: a comprehensive literature review. Am J Med 1994; 97:78 - 88.
• L Lipsitz: Orthostatic hypotension in the elderly. N Engl J Med 1989; 321:952.
• M Linzer, EH Yang, NA Estes,et al.: Diagnosing syncope: Part 1: Value of history, physical examination, and electrocardiography: the clinical efficacy assessment project of the American College of Physicians. Ann Intern Med 1997; 126:989 - 996.
• M Linzer, EH Yang, NA Estes,et al.: Diagnosing syncope: Part 2: Unexplained syncope. Ann Intern Med 1997; 127:76 - 86.