Syncope
Ragavendra R. Baliga
Michael H. Lehmann
DEFINITION
Syncope (from the Greek Syn with koptein, meaning to cut off) is the sudden, transient loss of consciousness and postural tone with subsequent spontaneous recovery. Before syncope, the patient may experience a variety of prodromal symptoms, typically including the awareness of an impending faint. The latter “near-syncopal” or “presyncopal” state may not progress to frank loss of consciousness, if the underlying pathophysiologic disturbances that would otherwise culminate in syncope are aborted (either spontaneously or via countermaneuvers, such as assuming the recumbent position). Hypotension with cerebral hypoperfusion distinguishes true syncope from other syndromes with which it may be confused.
Most individuals with the “common faint” (vasovagal syncope, described later) do not consult a doctor, and hence the prevalence of syncope is difficult to determine. About one third of adults experience at least one episode of syncope in their life-time, and syncope accounts for about 3% of emergency department visits and up to 6% of general hospital admissions in the United States (1). The recurrence rate is as high as 34% on 3-year follow-up (2).
The range of prognoses in syncope is wide, and the main task of the clinician, therefore, is to determine whether the patient has a benign or a life-threatening cause for syncope (3,4). One must be concerned about the possibility that the syncopal event actually represents a self-aborted cardiac arrest, with a potentially catastrophic outcome the next time around. Yet even when syncope is not a harbinger of sudden death, it may incur serious secondary morbidity consequent to trauma.
An important caveat to bear in mind for a patient with syncope is recognition that that the actual event has come and gone, leaving the physician to, in effect, “reconstruct” what transpired. Even when abnormalities are uncovered in the course of various diagnostic procedures, it is not immediately evident that the physician has determined the true cause. The physician must integrate all available information, with focused use of diagnostic tests, and then apply sound clinical judgment to arrive at the most reasonable working diagnosis, which will guide therapy selection. Often, only with the passage of time is the accuracy of the hypothesized cause borne out (suppression of further events) or refuted (syncope recurrence)—in which case, diagnostic reevaluation is required.
PRINCIPAL CAUSES
Neurally Mediated Syncope
Patients with these conditions have in common the paroxysmal occurrence of peripheral vasodilatation, bradycardia, or both, which reflects sympathetic withdrawal and hypervagotonia (5) (Table 5.1).
Vasovagal, vasodepressor, or neurocardiogenic syncope—also called the “common faint”—is often caused by a precipitating event such as prolonged standing, hypovolemia (commonly dehydration), fear, severe pain, the sight of blood, strong emotion, or instrumentation; however, it can also occur without
obvious cause. In a typical episode of the common faint, a prodrome exists in which the patient may feel unsteady, “feel bad,” be confused, yawn, or experience ringing in the ears or visual disturbances (dimming, blurring, or seeing spots). Often associated warmth and nausea are found, sometimes with vomiting; facial pallor and diaphoresis are common. These presyncopal features (typically lasting from 30 to 60 seconds) are not seen in all patients; the faint may occur suddenly without warning, not allowing time for protection against injury. At the onset of syncope, hypotension occurs, often (but not necessarily) accompanied by bradycardia. With protracted hypotension, attendant seizure-like activity (involuntary muscle jerking) may be present. On recovery, along with return of consciousness, color returns to the face, blood pressure increases, and bradycardia resolves. Characteristically, consciousness is regained rapidly after the individual is in the supine position, although commonly a feeling of postevent fatigue is found. In patients who have minimal presyncopal warning, telltale symptoms and signs of vasovagal syncope—nausea, warmth, diaphoresis, and pallor—sometimes become apparent only during the recovery phase. The long-term prognosis in neurocardiogenic syncope is generally excellent; however, in some patients, recurrences are frequent and are a major cause for seeking medical attention.
obvious cause. In a typical episode of the common faint, a prodrome exists in which the patient may feel unsteady, “feel bad,” be confused, yawn, or experience ringing in the ears or visual disturbances (dimming, blurring, or seeing spots). Often associated warmth and nausea are found, sometimes with vomiting; facial pallor and diaphoresis are common. These presyncopal features (typically lasting from 30 to 60 seconds) are not seen in all patients; the faint may occur suddenly without warning, not allowing time for protection against injury. At the onset of syncope, hypotension occurs, often (but not necessarily) accompanied by bradycardia. With protracted hypotension, attendant seizure-like activity (involuntary muscle jerking) may be present. On recovery, along with return of consciousness, color returns to the face, blood pressure increases, and bradycardia resolves. Characteristically, consciousness is regained rapidly after the individual is in the supine position, although commonly a feeling of postevent fatigue is found. In patients who have minimal presyncopal warning, telltale symptoms and signs of vasovagal syncope—nausea, warmth, diaphoresis, and pallor—sometimes become apparent only during the recovery phase. The long-term prognosis in neurocardiogenic syncope is generally excellent; however, in some patients, recurrences are frequent and are a major cause for seeking medical attention.
TABLE 5.1. Principal causes of syncope | ||||||||||||||||||||||
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Situational or reflex syncope is loss of consciousness during or immediately after coughing, micturition, swallowing, or defecation. Alcohol has been implicated in micturition-related syncope.
Carotid sinus syncope is induced by carotid sinus stimulation, resulting in hypotension, bradycardia, or both. In sensitive individuals, typically elderly men, carotid sinus syncope may develop with tight shirt collars or while shaving the neck.
Orthostatic Syncope
This type of syncope results from orthostatic hypotension, diagnosed by documentation of a 20 mm Hg or more decrease in systolic blood pressure during the initial 5 minutes after the patient is in upright position; the associated heart rate either remains unchanged or increases (in contrast to vasovagal syncope). Orthostatic hypotension is a common cause of syncope in the elderly and is exacerbated by medications (as discussed later). Detection of orthostatic hypotension should trigger an investigation for fluid depletion and blood loss, particularly with syncope of new onset. A major intraabdominal hemorrhage (e.g., gastrointestinal or from ectopic pregnancy) can precipitate syncope before overt signs of bleeding are apparent. Autonomic insufficiency is a cause of orthostatic hypotension in diabetic patients, patients with Parkinson disease, and the elderly.
Cardiac Syncope
A cardiac cause of syncope is seen in about one fifth of patients. Syncope associated with cardiovascular disease portends a much higher risk of mortality than is the case in the absence of underlying structural heart disease. Patients with cardiac syncope are at highest risk of dying within 1 to 6 months (6). The 1-year mortality rate is 18% to 33%, in comparison with that of syncope with noncardiac causes (0 to 12%) or syncope in patients with no known etiology (6%) (7). The incidence of sudden death in patients with a cardiac cause is substantially higher than in the other two groups. Cardiac causes of syncope include the following.
Arrhythmic syncope results from tachyarrhythmias (ventricular or supraventricular) and bradyarrhythmias. Specific examples include sinus arrest; atrial fibrillation with very rapid conduction over an accessory pathway in patients with Wolff-Parkinson-White syndrome; and sustained monomorphic ventricular tachycardia (VT). Patients with complete heart block may develop self-limiting syncopal episodes in which no effective cardiac output exists as a result of transient asystole or ventricular tachyarrhythmias (Stokes-Adams attacks).
Torsades de pointes is a polymorphic VT that occurs in patients with prolonged ventricular repolarization [long-QT syndrome (LQTS)]. LQTS may occur on either a congenital or acquired basis (e.g., hypokalemia or exposure to certain drugs, as described later). Torsades de pointes can readily progress to ventricular fibrillation (Fig. 5.1). Thus, individuals with LQTS are at risk not only for syncope but also for “seizures” (from transient cerebral hypoxia) and sudden death. Other congenital, potentially lethal arrhythmic disorders include Brugada syndrome (ST-segment elevation in precordial leads V1, V2, and V3, often with incomplete or complete right bundle-branch block) (8), familial catecholaminergic polymorphic VT (9), and arrhythmogenic right ventricular dysplasia with associated ventricular arrhythmias (10). In some variants of hypertrophic cardiomyopathy, patients may exhibit minimal, if any, cardiac hypertrophy, and yet affected individuals may be predisposed to sudden death, presumably from sustained ventricular tachyarrhythmias. Another explanation for syncope in hypertrophic cardiomyopathy is the obstructive type, in which an intraventricular gradient is found (see Chapter 15).
Pacemaker and implantable cardiac defibrillator (ICD) malfunction may be a cause of syncope in patients with these devices. With ICDs, however, it should be appreciated that even when a rapid ventricular tachyarrhythmia is successfully treated with the device, syncope may nonetheless occur, depending on the duration of hypotension preceding the termination of tachyarrhythmia. ICD interrogation can provide information about possible tachyarrhythmia occurrence and therapy delivery/outcome coincident with the syncopal event in question.
Structural syncope is caused by valvular stenosis (aortic, mitral, pulmonic), prosthetic valve dysfunction or thrombosis, hypertrophic cardiomyopathy, pulmonary embolism, pulmonary hypertension, cardiac tamponade, and anomalous origin of the coronary arteries. Syncope in aortic stenosis occurs during exertion when the fixed valvular obstruction prevents an increase in cardiac output into the dilated vascular bed of the exercising skeletal muscles. The syncope can occur during exertion or immediately afterward. Syncope can also occur at rest in aortic stenosis when paroxysmal tachyarrhythmias or bradyarrhythmias accompany this valvular abnormality. Aortic dissection, subclavian steal, severe left ventricular dysfunction, and myocardial infarction are other important causes of cardiac syncope. In elderly patients, syncope may be the presenting feature in acute myocardial infarction (11). Left atrial myxomas or ballvalve thrombi that fall into the mitral valve during diastole can result in the obstruction of ventricular filling and in syncope.
Metabolic Disturbance
Syncope due to hypoglycemia is the loss of consciousness that accompanies a blood glucose level of less than 40 mg per deciliter and is preceded by tremors, confusion, salivation, hyperadrenergic state, and hunger. Hypoglycemic syncope should be suspected in diabetic patients who take insulin or oral hypoglycemic agents. In contrast to true syncope, the loss of consciousness caused by hypoglycemia is not associated with hypotension, persists even when the patient is in the supine position, and usually does not resolve until the blood glucose level is restored to normal. Hypoadrenalism, which can cause postural hypotension as a result of inadequate cortisol secretion, is an important and treatable, albeit uncommon, cause for syncope and should be suspected when long-term steroid therapy is suddenly discontinued
or when other stigmata of adrenal insufficiency are present.
or when other stigmata of adrenal insufficiency are present.
 FIGURE 5.1. A 25-year-old woman who had had a single syncopal episode 2 years earlier was hospitalized after a 2-min episode of syncope during an argument with a police officer over a traffic ticket. A 12-lead electrocardiogram obtained on admission showed sinus rhythm, 52 beats/min, with a markedly prolonged QT interval of 0.68 sec. Twenty-four-hour Holter monitoring in the hospital revealed recurrent asymptomatic, mostly short, episodes of torsade de pointes. One such episode, beginning with bradycardia-related further QT prolongation, occurred during sleep and degenerated into ventricular fibrillation that lasted 1.5 min and terminated spontaneously. [From: Benhorin J, Medina A. Congenital long QT syndrome (images in medicine). N Engl J Med 1997;336:1568, with permission.] |
Neurologic Disease
Neurologic conditions can mimic syncope by causing impairment or loss of consciousness; these conditions include transient cerebral ischemia (usually in the vertebrobasilar territory), migraines (basilar artery territory), temporal lobe epilepsy, atonic seizures, and unwitnessed grand mal seizures. Disorders resembling syncope, but without loss of consciousness, include drop attacks (sudden loss of postural tone), cataplexy, and transient ischemic attacks of carotid origin. In
neurologic conditions associated with severe pain, such as trigeminal or glossopharyngeal neuralgia, the loss of consciousness is usually caused by vasovagal syncope.
neurologic conditions associated with severe pain, such as trigeminal or glossopharyngeal neuralgia, the loss of consciousness is usually caused by vasovagal syncope.
Psychiatric Disorder
Syncope or syncope-like syndromes associated with psychiatric conditions are not associated with increased rates of mortality but have high 1-year recurrence rates (up to 50%) (12). The association between syncope and psychiatric disorders may be complicated. First, psychiatric disorders may represent comorbidity in a patient with syncope and have no role in syncope occurrence. Second, psychiatric disorders may cause syncope-like states, often involving a conversion reaction. Psychiatric conditions associated with syncope include generalized anxiety and panic disorders (in which hyperventilation leads to cerebral vasoconstriction and possible loss of consciousness), major depression, alcohol and substance abuse, and somatization disorders. Third, a complex interaction may occur between syncope and the psychiatric condition. Stress, depression, and psychosocial disorders are capable of provoking arrhythmias and myocardial infarction. It is possible that all these factors may, in turn, precipitate syncope, although the magnitude of this problem is unclear. Finally, it is possible that recurrent syncope itself may secondarily give rise to psychiatric conditions such anxiety and panic attacks. A diagnosis of syncope resulting from psychiatric disorders is usually made after organic causes have been excluded. Diagnosis may be difficult when patients have both organic and psychogenic seizures.
Unexplained Etiology
Earlier studies reported that, in about half of the patients with syncope, no cause could be determined. However, with the wider use of tilt testing, event monitoring, electrophysiologic studies, and more aggressive investigation of elderly patients and those with suspected psychiatric causes, the proportion of syncope cases in which the cause can be determined has increased.
KEYS TO THE HISTORY
A meticulously documented history is critical in the assessment of syncope. For new-onset syncope, the examiner focuses primarily on ruling out underlying structural heart disease and other life-threatening conditions such as acute myocardial infarction and upper gastrointestinal hemorrhage, which necessitates evaluation in the emergency department. In contrast, the diagnostic assessment of recurrent syncope involves a broader consideration of causes and is often undertaken in an ambulatory setting. The history and physical examination should identify a cause of syncope in about 45% of patients (13). These basic elements of a medical evaluation can lead to recognition of ischemic heart disease, heart failure, aortic stenosis, hypertrophic cardiomyopathy, and pulmonary embolism; neurologic causes such as seizure disorder and subclavian steal syndrome; and familial conditions such as long-QT syndrome. Emphasis should be placed on the circumstances surrounding the syncopal event, the nature of prodromal and associated symptoms, characterization of the recovery period, medications and drugs, the presence of known cardiac disease, family history (e.g., cardiomyopathy or LQTS), and psychiatric history. Observations from witnesses or a family member may be helpful. In documenting the history, the examiner should focus on the relation of syncopal events to posture, exertion, and palpitations. The examiner should determine the number and chronicity of prior syncopal and near-syncopal episodes; the latter may be more frequent (albeit of shorter duration) than full-blown syncopal events and may provide an opportunity for diagnostic electrocardiographic monitoring to capture a clinically relevant event. Inquiry also should be made into whether the patient has sustained any trauma in association with the symptoms; serious secondary injury warrants a more aggressive diagnostic and treatment strategy aimed at preventing subsequent morbidity.
Circumstances Surrounding Onset
Painstaking attention should be paid to the chronology of symptoms: sudden onset without a prodrome may suggest arrhythmias, whereas protracted autonomic symptoms (pallor, diaphoresis, nausea) in association with a precipitating factor such as pain, extreme heat or emotion, viewing an unpleasant sight, or prolonged standing suggest vasovagal syncope. Loss of consciousness after prolonged standing at attention suggests vasovagal syncope, whereas that which occurs immediately on standing is caused by orthostatic hypotension. Situational syncope occurs during or immediately after swallowing, coughing, defecation, and micturition. Alcohol ingestion may be the most important predisposing factor in micturition syncope. Alcohol ingestion has also been implicated in about 10% of syncope cases in young adults, and the syncope in those cases has been attributed to orthostatic stress because of impaired vasoconstriction (14). Carotid syncope occurs with head rotation while the person is wearing tight collars. Exertional syncope suggests possible structural heart disease such as aortic stenosis, hypertrophic cardiomyopathy, or exercise-induced tachycardias. In highly competitive athletes, vasovagal syncope documented by history and head-up tilt testing has been shown to occur during as well as after exertion (15). Syncope associated with arm exercise is a feature of subclavian steal syndrome. A history of exertional chest pain, as well as exertional syncope, in an adolescent or young adult, raises the possibility of anomalous origin of a coronary artery (16). Syncope in patients with LQTS may occur in association with physical exertion (particularly swimming), during emotional stress, or in response to sudden, unexpected acoustic stimuli (e.g., sound of an alarm clock or telephone) (17).
Posture at the Onset of Attack
Vasodepressor syncope typically occurs in the upright position; once the patient is horizontal, the autonomic derangements begin to reverse. In some instances, if the patient returns to the upright position too soon, a recurrent faint may occur. Syncope resulting from arrhythmias and other causes of loss of consciousness that resemble syncope, such as hypoglycemia and hyperventilation, can occur independent of posture. Moreover, syncope caused by pain or emotion-related vasovagal syncope (e.g., after a needlestick or on the sight of blood or injury) need not occur while the patient is upright. By definition, syncope caused by orthostatic hypotension occurs soon (within seconds to minutes) after the patient assumes an upright posture from the recumbent or sitting position.
Associated Symptoms
Associated symptoms are not always present and depend on the cause of syncope. The peri-event symptoms typically associated with neurally mediated syncope have been discussed. Of note, recovery from cardiac syncope is often rapid (within 30 seconds). Palpitations preceding syncope, especially an awareness of rapid heart beating, suggest an arrhythmic origin (see Chapter 3)—although tachyarrhythmic syncope need not be accompanied by such prodromal symptoms. Features of neurologic syncope include brainstem findings (vertigo, dysarthria, ataxia, visual disturbances), whereas postevent confusion is more likely to be caused by seizures. Loss of consciousness associated with headache indicates migraine or seizures, whereas that associated with throat or facial pain suggests glossopharyngeal or trigeminal neuralgia.
Differentiating Syncope from Seizures
This distinction can be clinically challenging (Table 5.2), and eyewitness accounts are often helpful in discriminating between the two conditions. Both phenomena involve loss of consciousness. As a further confounding factor, myoclonic jerking may occur during the course of true syncope secondary to transient cerebral hypoxia (18). The best discriminatory features between syncope and seizures are the sensorium of the patient after the
episode and the patient’s age. When a patient older than 45 years is disorientated after an episode, seizures are 5 times more likely than syncope to have occurred (19). Older individuals with prolonged disorientation after an episode of loss of consciousness are therefore more likely to have had a seizure. An exception would be arrhythmic syncope with a prolonged hypotensive episode, which may secondarily cause transient cerebral hypoxic injury and postevent disorientation. Other clinical features suggestive of a seizure include cyanotic facial appearance, as opposed to pallor, during the episode; frothing at the mouth; unconsciousness lasting more than 5 minutes; feeling sleepy after the episode; aching muscles; and tongue biting along the lateral aspect of the tongue.
episode and the patient’s age. When a patient older than 45 years is disorientated after an episode, seizures are 5 times more likely than syncope to have occurred (19). Older individuals with prolonged disorientation after an episode of loss of consciousness are therefore more likely to have had a seizure. An exception would be arrhythmic syncope with a prolonged hypotensive episode, which may secondarily cause transient cerebral hypoxic injury and postevent disorientation. Other clinical features suggestive of a seizure include cyanotic facial appearance, as opposed to pallor, during the episode; frothing at the mouth; unconsciousness lasting more than 5 minutes; feeling sleepy after the episode; aching muscles; and tongue biting along the lateral aspect of the tongue.
TABLE 5.2. Characteristics of syncope versus seizures | |||||||||||||||||||||||||||
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Seizures are also suggested by an aura before the event, horizontal eye movement during the event, and a headache after the episode. Fecal and urinary incontinence can occur in both syncope and seizures but are far more common with seizures. Tonic-clonic movements suggest grand mal seizures. Syncope caused by cerebral ischemia can be accompanied by rigidity and clonic movements of the arms and legs. In petit mal epilepsy, the lack of responsiveness is associated with preserved postural tone. Temporal lobe seizures can easily be mistaken for syncope because they usually lack tonic-clonic movements and are associated with autonomic changes such as flushing and fluctuating changes in the level of consciousness. Vertebrobasilar insufficiency should be suspected when the patient has features of brainstem ischemia such as tinnitus, diplopia, vertigo, dysarthria, and focal sensory loss or weakness.
Age at Onset
In younger individuals (younger than 30 years), common causes (Table 5.3) include neurally mediated syncope, undiagnosed seizures, Wolff-Parkinson-White syndrome
and other supraventricular tachycardias, hypertrophic cardiomyopathy, LQTS and other inherited arrhythmic disorders, and congenital coronary anomalies (16).
and other supraventricular tachycardias, hypertrophic cardiomyopathy, LQTS and other inherited arrhythmic disorders, and congenital coronary anomalies (16).
TABLE 5.3. Causes of syncope by age | ||||||||||||||||||||||||||||||||||||||||||||||||
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In middle-aged individuals, typical causes of syncope are neurally mediated and cardiac (arrhythmic, mechanical/obstructive) in origin.
Syncope in the elderly (older than 65 years) may be overlooked when the episode is described by the patient simply as a “fall,” owing to postsyncope retrograde amnesia (4). In the elderly, the cause of syncope is often multifactorial, and older patients tend to have serious arrhythmias (sustained VT in the setting of cardiomyopathy), orthostatic hypotension, or neurologic disorders that are contributory (3). Elderly patients are also prone to neurally mediated syncope related to known triggers, such as micturition, defecation, coughing, laughing, swallowing, and eating. Postprandial hypotension (secondary to splanchnic vascular volume shifts) can result in syncope during or after a meal. Another confounding factor in this age group is polypharmacy: Many medications at therapeutic doses cause postural hypotension. Aortic stenosis, myocardial infarction, and carotid sinus hypersensitivity are other conditions that predispose to syncope in the elderly. Carotid sinus hypersensitivity has been suggested to be responsible for syncope or “falls” in the elderly, and the bradycardia documented in these patients has been successfully managed by dual-chamber pacing (4). The multifactorial nature of syncope in older patients often necessitates a management approach aimed at correcting many of these factors simultaneously.
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