Syncope
Salim H. Ahmed
I. INTRODUCTION
A. Syncope is a common medical problem that accounts for approximately 6% of medical admissions and 3% of emergency room visits. Syncope is defined as a sudden transient loss of consciousness with associated loss of postural tone. Recovery is spontaneous, without neurologic deficit and without requiring electrical or chemical cardioversion. Generally, a fall in systolic blood pressure below 70 mm Hg or a mean arterial pressure of 40 mm Hg results in loss of consciousness. Cerebral blood flow usually decreases with aging, making the elderly at higher risk for syncope.
B. Syncope as a symptom can be caused by a variety of medical diseases that produce a transient interruption of cerebral blood flow.
1. A genuine effort should be made to determine a specific cause of syncope. Identifying a specific cause can help in the selection of therapy, prevent recurrences, minimize expensive evaluations, and decrease morbidity.
2. Patients with cardiac syncope have higher rates of mortality and sudden death at follow-up. Identifying and treating cardiac syncope can improve outcome.
II. CLINICAL PRESENTATION.
Although a variety of diagnostic tests are available for evaluation of syncope, a thorough history and physical examination are crucial to determine the cause and the best diagnostic approach. A good history and physical examination can provide a clue to the diagnosis in up to 50% of cases.
A. Signs and symptoms.
Accurately described symptoms can lead to specific diagnostic considerations, as illustrated in Tables 33.1 and 33.2. Table 33.3 lists the prevalence of various causes of syncope as seen in the Evaluation of Guidelines in Syncope Study 2 (EGSYS-2) trial, a prospective systemic evaluation of consecutive patients referred to various emergency rooms for syncope.
1. The most important aspect of history taking is to determine the circumstances before syncope (i.e., the prodrome); whether there is association with any particular activity, exertion, or change in position; and the frequency of occurrence.
2. The initial approach to any patient with syncope should include a search for the presence of structural heart disease such as valvular stenosis, cardiomyopathy, or myocardial infarction. The presence of any of these may suggest more malignant causes such as ventricular tachycardia.
3. Symptoms of vasovagal syncope. Calkins et al. (1) reported that a careful history could diagnose vasovagal syncope. They reported that women (< 55 years) with a postsyncopal recovery period that included fatigue and patients with clear precipitating factors, diaphoresis, palpitations preceding syncope, and severe fatigue after syncope were more likely to have vasovagal syncope than ventricular tachycardia or complete heart block.
4. Convulsive syncope. Occasionally, a syncopal episode is accompanied by mild muscular jerking as a result of cerebral anoxia. This phenomenon is not true epilepsy, and the physician must make every effort to distinguish between
syncope and a seizure. Syncope typically occurs without an aura and has a more deliberate onset. Seizures are characterized by severe jerking motions, longer periods of unconsciousness, and severe fatigue after the event (i.e., postictal state). Seizures may occur without regard to patient positioning. In contrast, syncope rarely happens when a person is recumbent.
syncope and a seizure. Syncope typically occurs without an aura and has a more deliberate onset. Seizures are characterized by severe jerking motions, longer periods of unconsciousness, and severe fatigue after the event (i.e., postictal state). Seizures may occur without regard to patient positioning. In contrast, syncope rarely happens when a person is recumbent.
TABLE 33.1 Cardiovascular Causes of Syncope | ||||||||||||||||||||||
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5. Other entities that make diagnosis difficult are vertigo, transient ischemic events, somatization disorders (e.g., conversion and hysteria), cataplexy, epilepsy, and drop attacks.
TABLE 33.2 Clinical Features Suggesting Specific Causes | ||||||||||||||||||||||||||||||
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TABLE 33.3 Causes of Syncope in the Evaluation of Guidelines in Syncope Study 2 Trial | ||||||||||||||||||||
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6. The examiner should always carefully review the medications of a patient with syncope for their potential role, directly or by interaction with other medications.
B. Physical findings
1. The physical examination is especially important when the patient is unable to describe the event and no witnesses are available, as certain findings on examination can direct the physician in the diagnostic evaluation.
2. The comprehensive evaluation should include a funduscopic examination of the eye for evidence of embolism. The evaluation should also search for the presence of carotid bruit and assessment of the carotid upstroke; subtle neurologic deficits that may result from a stroke or neuropathy; cardiac murmurs with attention given to valvular findings and extra heart sounds (such as tumor plop); peripheral pulses for evidence of peripheral vascular disease and entities such as subclavian steal; and dermatologic clues that may suggest collagen vascular disease or vasculitis.
3. In examining a patient with syncope, it is important to check blood pressure in both arms as well as orthostatic blood pressure. Repeated orthostatic blood pressure measurements may be needed when there is a high level of clinical suspicion for orthostatic syncope (see Section II.C.1.c).
4. Syncope in the absence of underlying heart disease is not associated with increased mortality. The morbidity of such episodes is related to harm that may occur in association with a syncopal event.
C. Etiology and pathophysiology
1. Neurally mediated syncope. Vasovagal or neurally mediated syncope is the most common cause of syncope. Many situations can lead to vasovagal “fainting.” Examples include unpleasant smell, sudden pain, acute blood loss, and sustained upright posture. Vasovagal reactions are often preceded by an increase in heart rate and blood pressure.
a. Neurocardiogenic syncope is thought to be the result of autonomic overactivity followed by a fall in peripheral vascular resistance, without a significant rise in cardiac output. In susceptible individuals, the stimulation of mechanoreceptors located in the inferior and posterior wall of the left ventricle by stretch, cardiac distention, or rapid systolic contraction leads to increased neural discharges through unmyelinated C fibers to the vasomotor center in the medulla, resulting in enhanced parasympathetic and decreased sympathetic activities. The withdrawal of the sympathetic nervous system results in sudden bradycardia or hypotension. Animal studies suggest that cardiac afferents may not be required to initiate a vasodepressor response and that other potential mechanisms, such as release of endogenous opioids or nitric oxide inhibition of sympathetic nerve firing and primary central nervous system activation, may play a role in vasodepressor syncope.
b. Situational syncope. Patients often recall situational syncopal episodes. Micturition, defecation, cough, and trumpet playing are examples. The action causes a reflex vasodilation (vagally mediated) that is exacerbated if the patient performs a Valsalva maneuver, which decreases the blood return to the right heart.
c. Orthostatic syncope. Postural hypotension is reported in up to 24% of elderly people. Normally when a person stands, the systolic blood pressure drops only 5 to 15 mm Hg, and the diastolic pressure rises slightly. In orthostasis, the decrease in systolic blood pressure exceeds 20 mm Hg; frequently, the diastolic pressure drops by > 10 mm Hg. This finding demands a search for a potential cause.
(1) Common causes include volume depletion, medications, diabetes, alcohol, infection, and varicose veins.
(2) Dysautonomic syndromes causing orthostatic hypotension are divided into two categories: primary and secondary. Primary autonomic failure is idiopathic and includes pure autonomic failure (i.e., Bradbury-Eggleston syndrome) and multisystem atrophy (i.e., Shy-Drager syndrome). Secondary causes include amyloidosis, tabes dorsalis, multiple sclerosis, spinal tumors, and familial dysautonomia.
a. Carotid sinus syncope. Less than 1% of patients presenting with syncope have been given a diagnosis of carotid sinus syncope. This entity should be considered in patients with spontaneous symptoms while shaving, swimming, turning the head, or wearing a tight collar, as well as in older patients with recurrent syncope. A cardioinhibitory response (i.e., bradycardia) occurs in about 70%, and a vasodepressor response (i.e., hypotension) occurs in 10%. The remaining patients have a mixed response (i.e., bradycardia with hypotension). Carotid sinus syncope is elicited by manual pressure on the carotid sinus and can be blocked by atropine. Clinical presentation along with findings of carotid sinus hypersensitivity in the absence of other potential causes is enough to make the diagnosis. Symptom reproduction during carotid massage is not necessary for a diagnosis. A positive carotid test result is defined by cardiac asystole of 3 seconds or longer, a drop in systolic blood pressure of > 50 mm Hg, or a drop of > 30 mm Hg in blood pressure and symptoms. Carotid massage should be avoided in patients with a history of stroke or transient ischemic attack (TIA) within 3 months (unless they have had normal carotid Doppler results) or those patients in whom carotid bruits are heard on clinical examination.
2. Cardiac syncope
a. Mechanical causes
(1) Syncope or related symptoms frequently occur with exertion and arise from left ventricular outflow obstruction, as seen in aortic stenosis or hypertrophic obstructive cardiomyopathy (HOCM). With exertion, peripheral vascular resistance falls, but the cardiac output is fixed, leading to hypotension. Arrhythmias and altered baroreceptor response also play a role in syncope in patients with an obvious mechanical cause, such as aortic stenosis.
(2) Right ventricular outflow obstruction can also result in syncope. This condition can also trigger a vasodepressor component by mechanisms similar to neurocardiogenic syncope.
(3) Myocardial ischemia and infarction, pulmonary embolus, and cardiac tamponade should be kept in mind. Syncope may be the initial complaint in 7% of patients older than 65 years presenting with myocardial infarction.
(4) Patients with hypertrophic obstructive cardiomyopathy have an annual risk of sudden death in nonselective populations of approximately 1% per year. Syncope increases the relative risk of sudden cardiac death by approximately fivefold. The presence or absence of other sudden death risk factors (family history of sudden cardiac death, nonsustained ventricular tachycardia, marked left ventricular hypertrophy, and significant left ventricular outflow tract gradient) influences the risk of sudden cardiac death. Electrophysiologic (EP) testing plays a minimal role in risk stratification, as does genotyping for specific mutations currently. Treatment in high-risk patients usually includes the use of β-blockers, calcium channel blockers, disopyramide and other antiarrhythmics, and frequently implantable cardioverter—defibrillator (ICD) placement.
(5) Arrhythmogenic right ventricular dysplasia is a disorder in which syncope is caused by ventricular tachycardia originating in the right ventricle secondary to replacement of myocardium by adipose tissue
and/or fibrosis. The imaging modality of choice is cardiac magnetic resonance imaging (usually with fat suppression), which usually shows thinning, aneurysms, and replacement of right ventricular myocardium with adipose and fibrotic tissues. It is thought to be a common cause of sudden cardiac death in patients younger than 35 years and may be familial in 30% to 50% of patients. It is usually diagnosed based upon the presenting electrocardiogram (ECG), suggested by the presence of premature ventricular contractions or sustained ventricular tachycardia with a left bundle branch morphology. Treatment of syncope in this setting usually includes ICD implantation, and yearly ICD appropriate therapy rates are usually 15% to 20%.
and/or fibrosis. The imaging modality of choice is cardiac magnetic resonance imaging (usually with fat suppression), which usually shows thinning, aneurysms, and replacement of right ventricular myocardium with adipose and fibrotic tissues. It is thought to be a common cause of sudden cardiac death in patients younger than 35 years and may be familial in 30% to 50% of patients. It is usually diagnosed based upon the presenting electrocardiogram (ECG), suggested by the presence of premature ventricular contractions or sustained ventricular tachycardia with a left bundle branch morphology. Treatment of syncope in this setting usually includes ICD implantation, and yearly ICD appropriate therapy rates are usually 15% to 20%.
(6) Ion Channel disorders
(i) Long QT syndrome.
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