Author: Rumm Morag, MD, FACEP, Member of Salem Emergency Physician Services, PC (SEPS), Salem Hospital
Coauthor(s): Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Contributor Information and Disclosures
Updated: Dec 7, 2009
Syncope is defined as a transient, self-limited loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery. The term syncope excludes seizures, coma, shock, or other states of altered consciousness.
Syncope is a prevalent disorder, accounting for 1-3% of emergency department (ED) visits and as many as 6% of hospital admissions each year in the United States. As much as 50% of the population may experience a syncopal event during their lifetime. Although many etiologies for syncope are recognized, studies suggest categorization into cardiac, noncardiac, and unknown groups for the purposes of future risk stratification may be helpful in the initial evaluation. Cardiac syncope is associated with increased mortality, whereas noncardiac syncope is not. In addition, significant morbidity may result from falls or accidents that result from syncope.
Syncope is usually benign; however, in a subset of patients, this symptom presages a life-threatening event. As a result of this risk, hospital admission is frequent because of the difficulties encountered in promptly addressing causes of syncope, the lack of a diagnostic criterion standard, and concern about potentially dangerous arrhythmias.
Once a diagnostic category is identified, limited therapies are available. Little is known regarding the effects of therapies on longevity. Those with initially unknown causes may require further costly testing. Most individual tests have low diagnostic yield and provide limited insight into guiding future clinical management.
Syncope occurs due to global cerebral hypoperfusion. Brain parenchyma depends on adequate blood flow to provide a constant supply of glucose, the primary metabolic substrate. Brain tissue cannot store energy in the form of high-energy phosphates found elsewhere in the body; therefore, a cessation of cerebral perfusion lasting only 3-5 seconds results in syncope. Cerebral perfusion is maintained relatively constant by an intricate and complex feedback system involving cardiac output, systemic vascular resistance, arterial pressure, intravascular volume status, cerebrovascular resistance with intrinsic autoregulation, and metabolic regulation. A clinically significant defect in any one of these or subclinical defects in several of these systems may cause syncope.
Cardiac output can be diminished secondary to mechanical outflow obstruction, pump failure, hemodynamically significant arrhythmias, or conduction defects. Systemic vascular resistance can drop secondary to vasomotor instability, autonomic failure, or vasodepressor/vasovagal response. Arterial pressure decreases with all causes of hypovolemia. A CNS event, such as a hemorrhage or an unwitnessed seizure, can also present as syncope. Syncope can occur without reduction in cerebral blood flow in patients who have severe metabolic derangements (eg, hypoglycemia, hyponatremia, hypoxemia).
Framingham data demonstrate a first occurrence rate of 6.2 cases per 1000 patient-years.1,2 Syncope reoccurs in 3% of affected individuals, and approximately 10% of affected individuals have a cardiac etiology.
Data suggest that patients with cardiac syncope are more likely to experience a poor outcome. Patients who have a significant cardiac history and those who seem to have a cardiac syncope (because of associated chest pain, dyspnea, cardiac murmur, signs of congestive heart failure [CHF], or ECG abnormalities) should be considered to be at increased risk. Most published methods of risk stratification take into account cardiac symptoms and risk factors.
Morbidity from syncope includes recurrent syncope, which occurs in 20% of patients within one year of the initial episode. Lacerations, extremity fractures, head injuries, and motor vehicle accidents can occur secondary to syncope.
- Syncope in a patient with poor baseline cardiac function portends a poor prognosis irrespective of etiology. Middlekauff et al studied 491 patients with New York Heart Association (NYHA) functional class III or IV disease and noted that, regardless of the cause, 45% of those with syncope died within 1 year, whereas 12% of those without syncope died during the same interval.3
- Patients with cardiac syncope appear to do worse than patients with noncardiac syncope. Soteriades et al followed 7814 patients with syncope for 17 years and found a higher mortality rate for patients with cardiac syncope compared with noncardiac syncope.4 Suzuki et al studied 912 patients with syncope for an average of 3 years and found the same result.5
- Decision rules may assist in identifying patients who are at risk. Martin et al describes a risk stratification system that predicts an increased incidence of death at 1 year based on the presence of abnormal ECG findings, a history of ventricular arrhythmia, a history of CHF, and age older than 45 years.6
- Sarasin et al demonstrates a risk of arrhythmia that is proportional to the number of cardiac risk factors, including abnormal ECG findings, history of CHF, and age older than 65 years.7
- The San Francisco Syncope Rule identifies patients who are at immediate risk for serious outcomes within 7 days, with a 96% sensitivity based on the presence of abnormal ECG findings, a history of CHF, dyspnea, a hematocrit level of less than 30, and hypotension.8 The presence of these findings should prompt serious consideration for hospital admission. In an external retrospective review, validation of the San Francisco Syncope Rule in a Canadian emergency department was undertaken. The rule performed with a sensitivity of 90% (44/49 outcomes; 95% confidence interval [CI] 79-96%) and a specificity of 33%, which was much lower than previously reported. Based on results of this study, implementation of this rule would have significantly increased admission rates. These authors concluded further study is needed.9 Another study was also unable to validate the rule, with sensitivity of 74% and specificity of 57% reported.10
- Constantino et al discovered that 6.1% of patients had severe outcomes within 10 days of syncope evaluation.11 The mortality rate was 0.7%, and 5.4% of patients were readmitted or experienced major therapeutic intervention. Risk factors associated with severe short-term outcomes included abnormal ECG, history of CHF, age older than 65 years, male gender, history of chronic obstructive pulmonary disease (COPD), structural heart disease, presence of trauma, and lack of prodromal symptoms.
National Hospital Ambulatory Medical Care Survey (NHAMCS) data show that syncope occurs in all age groups but is most common in adult populations. Noncardiac causes tend to be more common in young adults, whereas cardiac syncope becomes increasingly more frequent with advancing age.
- Syncope is relatively uncommon in pediatric populations. One small retrospective study by Pratt and Fleisher reports a prevalence of less than 0.1% in children.12 Pediatric syncope warrants prompt detailed evaluation.
- Advancing age is an independent risk factor for both syncope and death. Various studies suggest categorizing patients older than 45 years, 65 years, and 80 years as "higher risk." Advancing age correlates with increasing frequency of coronary artery and myocardial disease, arrhythmia, vasomotor instability, autonomic failure, polyneuropathy, and use of polypharmacy.
History and physical examination are the most specific and sensitive ways to evaluate syncope. The diagnosis is achieved with a thorough history and physical examination in 50-85% of patients. No single laboratory test has greater diagnostic efficacy.
- A detailed account of the event must be obtained from the patient. The account must include the circumstances surrounding the episode: the precipitant factors, the activity the patient was involved with prior to the event, and the patient's position when it occurred.
- Precipitant factors can include fatigue, sleep or food deprivation, warm ambient environment, alcohol consumption, pain, and strong emotions such as fear or apprehension.
- Activity prior to syncope may give a clue as to the etiology of symptoms. Syncope may occur at rest; with change of posture; on exertion; after exertion; or with specific situations such as shaving, coughing, voiding, or prolonged standing.
- Assessing whether the patient was standing, sitting, or lying supine when the syncope occurred may assist in differentiating cardiac from noncardiac syncope.
- The clinician should attempt to gather all information with respect to symptoms preceding the syncope.
- Prior faintness, dizziness, or light-headedness occurs in 70% of patients experiencing true syncope. Other symptoms, such as vertigo, weakness, diaphoresis, epigastric discomfort, nausea, blurred or faded vision, pallor, or paresthesias, may also occur in the presyncopal period.
- Symptoms of nausea or diaphoresis prior to the event may suggest syncope rather than seizure when the episode was not witnessed, whereas an aura may suggest seizure.
- Patients with true syncope do not remember actually impacting the ground. Presyncope involves the same symptoms and pathophysiology but terminates prior to loss of consciousness and can occasionally include loss of postural tone.
- The duration of symptoms preceding a syncopal episode has been reported to be an average of 2.5 minutes in vasovagal syncope and an average of only 3 seconds in arrhythmia-related cardiac syncope.
- Clinicians should specifically inquire as to red flag symptoms, such as exertional onset, chest pain, dyspnea, low back pain, palpitations, severe headache, focal neurologic deficits, diplopia, ataxia, or dysarthria prior to the syncopal event.
- Patients should be asked to estimate the duration of their loss of consciousness. Syncope is associated with patient estimates ranging from seconds up to 1 minute in most cases. To discriminate from seizures, patients should also be asked if they remember being confused about their surroundings after the event or whether they have oral trauma, incontinence, or myalgias.
- A detailed account of the event must also be obtained from any available witnesses. Witnesses can aid the clinician in differentiating among syncope, altered mental status, and seizure.
- Convulsive activity, automatisms, or attempts to elicit focality can indicate seizure. Witnesses may be able to estimate the duration of unconsciousness and to assist in ascertaining whether the patient experienced postevent confusion.
- Postevent confusion is the most powerful tool for discriminating between syncope and seizure. A postictal phase suggests that a seizure has occurred. Postevent confusion has been described with syncope, but the confusion should not last more than 30 seconds. Seizurelike activity can occur with syncope if the patient is held in an upright posture.
- A medication history must be obtained in all patients with syncope with special emphasis placed on cardiac and antihypertensive medications. Drugs commonly implicated in syncope include the following:
- Agents that reduce blood pressure (eg, antihypertensive drugs, diuretics, nitrates)
- Agents that affect cardiac output (eg, beta-blockers, digitalis, antiarrhythmics)
- Agents that prolong the cardiac output (QT) interval (eg, tricyclic antidepressants, phenothiazines, quinidine, amiodarone)
- Agents that alter sensorium (including alcohol, cocaine, analgesics with sedative properties)
- Agents that alter serum electrolytes (especially diuretics)
- Inquiry must be made into any personal or familial past medical history of cardiac disease. Patients with a history of myocardial infarction (MI), arrhythmia, structural cardiac defects, cardiomyopathies, or CHF have a uniformly worse prognosis than other patient groups.
- Remember to consider the broad differential diagnosis of syncope. Assess whether the patient has a history of seizure disorder, diabetes, stroke (CVA), deep venous thrombosis (DVT), or abdominal aortic aneurysm or if pregnancy is a possibility.
A complete physical examination is requisite for all patients who present to the ED. Special attention must be paid to certain aspects of the physical examination in patients who present with syncope.
- Always analyze the vital signs. Fever may point to a precipitant of syncope, such as a urinary tract infection (UTI) or pneumonia. Postural changes in blood pressure (BP) and heart rate may point toward an orthostatic cause of syncope but are generally unreliable. Tachycardia may be an indicator of pulmonary embolism, hypovolemia, tachyarrhythmia, or acute coronary syndrome. Bradycardia may point toward a vasodepressor cause of syncope, a cardiac conduction defect, or acute coronary syndrome.
- A glucose level, checked by rapid fingerstick (eg, Accu-Chek), should be evaluated in any patient with syncope. Hypoglycemia can produce a clinical picture identical to syncope, including the prodromal symptoms, absence of memory for the event, and spontaneous resolution.
- A detailed cardiopulmonary examination is essential. Irregular rhythms, ectopy, bradyarrhythmias, and tachyarrhythmias should be detected. Auscultation of heart sounds may reveal murmurs indicating high-grade valvular defects. Search for objective evidence of CHF, including jugular venous distension, lung rales, hepatomegaly, and pitting-dependent edema. Examine the abdomen for the presence of a pulsatile abdominal mass.
- A detailed neurologic examination assists in establishing a baseline as well as defining new or worsening deficits. Patients with syncope should have a normal baseline mental status. Confusion, abnormal behavior, headache, fatigue, and somnolence must not be attributed to syncope; a toxic, metabolic, or CNS cause must be considered. The patient should have a detailed neurologic examination, including evaluation for carotid bruits, cranial nerve deficits, motor deficits, deep tendon reflex lateralization, and sensory deficits. Severe neuropathies may correlate with vasodepressor syncope.
- The patient must be examined for signs of trauma. Trauma may be sustained secondary to syncope with resultant head injury, lacerations, and extremity fractures. Tongue trauma is thought to be more specific for seizures. Remember to consider antecedent head trauma resulting in loss of consciousness as opposed to syncope with resultant trauma if the history or findings are unclear.
- All patients with syncope require a stool guaiac examination. In one study, all patients with anemia contributing to syncope were guaiac-positive.
- A few bedside examinations may help to elucidate the origin of a patient's syncope.
- The Hallpike maneuver may be performed in patients who describe short, intermittent prodromes with primarily vertiginous components to assess for benign paroxysmal positional vertigo.
- Orthostatic changes marked by a decrease in systolic BP by 20 mm Hg, a decrease in diastolic BP by 10 mm Hg, or an increase in heart rate by 20 beats per minute (bpm) with positional changes or systolic BP less than 90 mm Hg with the presence of symptoms may indicate postural hypotension. Bradycardia coinciding with the examination indicates vasodepressor syncope. Be aware that this examination is notoriously insensitive and has limited use.
- Carotid sinus massage has been used with some success to diagnose carotid sinus syncope but can prompt prolonged sinus pauses and hypotension.
Previously, syncope was described based on the specific underlying etiology, which included vasovagal, situational, orthostatic, arrhythmogenic, and other causes. Recently, this practice has shifted to an outcomes-based model, yielding the prognostic categories of cardiac, noncardiac, and unknown.
- Cardiac syncope may be due to vascular disease, cardiomyopathy, arrhythmia, or valvular dysfunction and predicts a worse short-term and long-term prognosis. Obtaining an initial ECG is mandatory if any of these causes are possible for the differential diagnosis.
- Low flow states, such as those associated with advanced cardiomyopathy, CHF, and valvular insufficiency, may result in hypotension and cause transient global cerebral hypoperfusion. Often these patients are on medications that reduce afterload, which may contribute to the cause of syncope.
- Ventricular arrhythmias, such as ventricular tachycardia and torsade de pointes, tend to occur in older patients with known cardiac disease. These patients tend to have fewer recurrences and have a more sudden onset with few, if any, presyncopal symptoms. Associated chest pain or dyspnea may be present. This type of syncope is generally unrelated to posture and can occur during lying, sitting, or standing. Often, these arrhythmias are not revealed on the initial ECG but may be captured with prolonged monitoring.
- Supraventricular tachyarrhythmias include supraventricular tachycardia and atrial fibrillation with rapid response. These may be associated with palpitations, chest pain, or dyspnea. Patients typically have prodromal symptoms and may have syncope while attempting to stand or walk because of resultant hypotension. These symptoms may spontaneously resolve prior to evaluation but are often noted during initial triage and assessment. Be sure to scrutinize ECG findings for evidence of Wolff-Parkinson-White syndrome, Brugada syndrome, and long QT syndrome.
- Bradyarrhythmias include sick sinus syndrome, sinus bradycardia, high-grade atrioventricular blocks, pacemaker malfunction, and adverse medication reactions. Generally, these patients have a history of cardiac problems and are symptomatic. Chest pain, dyspnea, decreased exercise tolerance, and fatigue may all be present. Consider cardiac ischemia and medication side effects as additional causes.
- Cardiac outflow obstruction may also result in sudden-onset syncope with little or no prodrome. One critical clue is the exertional nature, and the other is the presence of a cardiac murmur. Young athletes may present with this etiology for syncope. Specific pathology includes aortic stenosis, hypertrophic obstructive cardiomyopathy, mitral stenosis, pulmonary stenosis, pulmonary embolus, left atrial myxoma, and pericardial tamponade.
- Syncope can also result from an acute MI or an aortic dissection. These conditions can have associated chest pain, neck pain, shoulder pain, dyspnea, epigastric pain, hypotension, alteration of mental status and can result in sudden death.
- Noncardiac syncope may be due to a vasovagal response to pain, dehydration with orthostasis, situational syncope, autonomic dysfunction, psychiatric disease, and, rarely, neurovascular causes. With the exception of the latter, these causes tend to be more benign and do not predict poor outcomes.
- Vasovagal syncope is the most common type in young adults but can occur at any age. It usually occurs in a standing position and is precipitated by fear, emotional stress, or pain (eg, after a needlestick). Autonomic symptoms are predominant. Classically, nausea, diaphoresis, fading or "graying out" of vision, epigastric discomfort, and light-headedness precede syncope by a few minutes. Syncope is thought to occur secondary to efferent vasodepressor reflexes by a number of mechanisms, resulting in decreased peripheral vascular resistance. It is not life threatening and occurs sporadically.
- Dehydration and decreased intravascular volume contribute to orthostasis. Orthostatic syncope describes a causative relationship between orthostatic hypotension and syncope. Orthostatic hypotension increases in prevalence with age as a blunted baroreceptor response results in failure of compensatory cardioacceleration. In elderly patients, 45% of these cases are related to medications. Limited evidence suggests that polydipsia may reduce recurrences. Orthostasis is a common cause of syncope and tends to be recurrent. Bedside orthostatics cannot exclude this as an etiology; if suspected, patients should be referred to a primary care provider for outpatient tilt-table testing.
- Situational syncope is essentially a reproducible vasovagal syncope with a known precipitant. Micturition, defecation, tussive, and carotid sinus syncope are types of situational syncope. These stimuli result in autonomic reflexes with a vasodepressor response, ultimately leading to transient cerebral hypotension. These are not life-threatening but can cause morbidity. The treatment involves avoidance of the precipitant when possible and the initiation of counter maneuvers when anticipated.
- Neurologic syncope may have prodromal symptoms such as vertigo, dysarthria, dysphagia, diplopia, and ataxia. Syncope results from preexisting bilateral vertebrobasilar insufficiency with some superimposed acute process. Circulation is briefly obstructed from the reticular activation system in the brain stem, resulting in loss of consciousness. Neurologic syncope may uncommonly result from transient large cerebral vessel obstruction or a transient ischemic attack.
Cardiac outflow obstruction
Hypertrophic subaortic stenosis
Paroxysmal supraventricular tachycardia
Paroxysmal ventricular tachycardia
Primary pulmonary hypertension
Prolonged QT syndrome
Sick sinus syndrome
Sinus pause (>3 s)
Carotid sinus syncope
Cough (posttussive) syncope
- Serum glucose level
- In one study, 2 of 170 patients with syncope tested for serum glucose were found to be hypoglycemic.
- Despite this low yield, rapid blood glucose assessment is easy, fast, and may be diagnostic, leading to efficient intervention.
- CBC count
- If performed empirically, a CBC count has an exceedingly low yield in syncope. Some risk stratification protocols use a low hematocrit level as a poor prognostic indicator.
- A prospective evaluation of syncope found that 4 of 170 patients had signs and symptoms of GI hemorrhage with a confirmatory CBC count. No occult bleeding was diagnosed on the basis of an empiric CBC count in this study.
- Serum electrolyte levels with renal function
- These tests if performed empirically have an exceedingly low yield in syncope. Some risk stratification protocols use electrolyte level abnormalities and renal insufficiency as poor prognostic indicators.
- In the study by Martin et al, 134 patients with syncope had electrolytes drawn as part of the routine workup.13 One patient was unexpectedly found to be hyponatremic secondary to diuretic use.
- Serum electrolyte tests are indicated in patients with altered mental status or in patients in whom seizure is being considered.
- Cardiac enzymes: These tests are indicated in patients who give a history of chest pain with syncope, dyspnea with syncope, or exertional syncope; those with multiple cardiac risk factors; and those in whom a cardiac origin is highly suspected.
- Total creatine kinase (CK): A rise in CK levels may be associated with prolonged seizure activity or muscle damage secondary to a prolonged period of loss of consciousness.
- Urinalysis/dipstick: In elderly and debilitated patients, UTI is common, easily diagnosed, and treatable and may precipitate syncope. UTIs may occur in the absence of fever, leukocytosis, and symptoms in this population.
- Chest radiography
- In elderly patients and in patients who are debilitated, pneumonia is common, easily diagnosed, and treatable and may precipitate syncope. Pneumonia may occur in the absence of fever, leukocytosis, and symptoms in this population.
- Evaluation of a select number of etiologies of syncope may be aided by chest radiography. Pneumonia, CHF, lung mass, effusion, and widened mediastinum can all be seen if present and may guide therapy.
- Head CT scanning (noncontrast)
- Head CT scanning is not indicated in a nonfocal patient after a syncopal event. This test has a low diagnostic yield in syncope.
- Of 134 patients prospectively evaluated for syncope using CT scanning, 39 patients had abnormal findings on scans.13 Only 1 head CT scan was diagnostic in a patient not expected to have intracranial pathology. Of the remaining scans, 5 showed subdural hematomas thought to be secondary to syncope.
- Head CT scanning may be clinically indicated in patients with new neurologic deficits or in patients with head trauma secondary to syncope.
- Chest/abdominal CT scanning: This imaging study is indicated only in select cases, such as cases in which aortic dissection, ruptured abdominal aortic aneurysm, or pulmonary embolus is suspected.
- Brain MRI/magnetic resonance arteriography (MRA): These tests may be required in select cases to evaluate vertebrobasilar vasculature and are more appropriately performed on an inpatient basis in consultation with a neurologist or a neurosurgeon.
- Ventilation-perfusion (V/Q) scanning: This test is appropriate for patients in whom pulmonary embolus is suspected.
- In patients with known heart disease, left ventricular function and ejection fraction have been shown to have an accurate predictive correlation with death.
- Echocardiography is the test of choice for evaluating suspected mechanical cardiac causes of syncope.
- ECG is indicated in syncope because of the high morbidity and mortality rates associated with cardiac syncope.
- Normal ECG findings are a good prognostic sign.
- ECG can be diagnostic for acute MI or myocardial ischemia and can provide objective evidence of preexisting cardiac disease or dysrhythmia such as Wolff-Parkinson-White syndrome or atrial flutter (3:1 or 4:1 block).
- Bradycardia, sinus pauses, nonsustained ventricular tachycardia and sustained ventricular tachycardia, and atrioventricular conduction defects occur with increasing frequency with age and are truly diagnostic only when they coincide with symptoms.
- Clinicians may choose to forego ECG in young, healthy patients with a clear noncardiac precipitant, vasovagal symptoms, and normal physical examinations.
- Holter monitor/loop event recorder
- This is an outpatient test. In the past, all patients with syncope were monitored for 24 hours in a hospital. Later, loop recorders and signal-averaged event recorders allowed for monitoring over longer time periods, which increased the yield of detecting an arrhythmia.
- Recent studies show that age-matched asymptomatic populations have an equivalent number of arrhythmic events recorded by ambulatory monitoring. Loop recorders have a higher diagnostic yield than Holter monitor evaluation with a marginal cost savings.15
- A study completed through an ECG outpatient registry in Vermont by Gibson and Heitzman involving 1512 patients referred for syncope, showed that symptomatic arrhythmias were found in just 0.5% of patients.16 In fact, patients had symptoms without arrhythmias more often than symptoms with arrhythmias, advancing the notion that ambulatory monitoring has a higher negative than positive diagnostic yield.
- Head-up tilt-table test
- This test is useful for confirming autonomic dysfunction and can generally be safely arranged on an outpatient basis.
- The test involves using a tilt table to stand a patient at 70 degrees for 45 minutes. Various modified protocols with concomitant medications, fasting, and maneuvers exist. Normally norepinephrine (NE) levels rise initially and are maintained to hold BP constant.
- A positive result occurs when NE levels fatigue with time and a falling BP and pulse rate produce symptoms.
- The head-up tilt-table test is less sensitive than electrophysiologic stress testing, and a negative result does not exclude the diagnosis of neurogenic syncope.
- Electroencephalography (EEG) can be performed at the discretion of a neurologist if seizure is considered a likely alternative diagnosis.
- Stress test/electrophysiologic studies (EPS) have a higher diagnostic yield than the Holter monitor and should be obtained for any patient with a suspected arrhythmia as a cause of syncope.
- A cardiac stress test is appropriate for patients in whom cardiac syncope is suspected and in whom have risk factors for coronary atherosclerosis. This test can assist with cardiac risk stratification and can guide future therapy.
- Patients are placed on a cardiac monitor and beat-to-beat BP monitoring device. Atropine is kept at the bedside.
- Longitudinal massage lasting 5 seconds is initiated at the point of greatest carotid pulse intensity at the level of the thyroid cartilage on one side at a time.
- The maximal response occurs after approximately 18 seconds, and a positive result is one that produces 3 seconds of asystole or syncope. If the result is negative, the process is repeated on the other carotid sinus.
- Carotid sinus massage may theoretically precipitate an embolic stroke in persons with preexisting carotid artery disease.
- Treatment may require the following:
- Intravenous access
- Oxygen administration
- Advanced airway techniques
- Glucose administration
- Pharmacologic circulatory support
- Pharmacologic or mechanical restraints
- Defibrillation or temporary pacing
- Advanced triage decisions, such as direct transport to multispecialty tertiary care centers, may be required in select cases.
In patients brought to the ED with a presumptive diagnosis of syncope, appropriate initial interventions include intravenous access, oxygen administration, and cardiac monitoring. ECG and rapid blood glucose evaluation should be promptly performed. Syncope may be the manifestation of an acute life-threatening process but is generally not emergent. Clinically ruling out certain processes is important. The treatment choice for syncope depends on the cause or precipitant of the syncope. Patients in whom a cause cannot be ascertained in the ED, especially if they have experienced significant trauma, warrant supportive care and monitoring.
- Situational syncope treatment focuses on educating patients about the condition. For example, in carotid sinus syncope, patients should be instructed not to wear tight collars, to use a razor rather than electric shaver, and to maintain good hydration status; they should also be informed of the possibility of pacemaker placement in the future.
- Orthostatic syncope treatment also focuses on educating the patient. Inform patients about avoiding postprandial dips in BP, teach them to elevate the head of their bed to prevent rapid BP fluctuations on arising from bed, and emphasize the importance of assuming an upright posture slowly. Additional therapy may include thromboembolic disease (TED) stockings, mineralocorticoids (eg, fludrocortisone for volume expansion), and other drugs such as midodrine (an alpha1-agonist with vasopressor activity). Patients' medications must be reviewed carefully to eliminate drugs associated with hypotension. Intentional oral fluid consumption is useful in decreasing frequency and severity of symptoms in these patients.
- Cardiac arrhythmic syncope is treated with antiarrhythmic drugs or pacemaker placement. Consider cardiologist evaluation or inpatient management since this is more commonly associated with poor outcomes.14 Trials assessing beta blockade to prevent syncope have conflicting results, but no clear effect has been demonstrated.
- Cardiac mechanical syncope may be treated with beta-blockade to decrease outflow obstruction and myocardial workload. Valvular disease may require surgical correction. This, too, is associated with increased future morbidity and mortality.
- Neurologic syncope may be treated in the same fashion as orthostatic syncope, or it may be treated with antiplatelet medications. Patients are recommended to have neurologic follow-up care to determine whether they need further neurovascular imaging.
The etiology of syncope dictates the need, if any, for specialty consultation. Select cases may require consultation with a neurosurgeon, a neurologist, a cardiologist, a vascular surgeon, a cardiothoracic surgeon, an endocrinologist, or a toxicologist.
These agents improve conduction through the atrioventricular node by reducing vagal tone via muscarinic receptor blockade. For patients with infranodal block, this therapy is ineffective.
Anticholinergic (or parasympatholytic) drug that exerts its action by competitively inhibiting acetylcholine at muscarinic receptors on postganglionic smooth muscle. Can counteract rapidly heightened vagal tone in response to pathologic carotid sinus syndrome. Additionally, can reverse bradycardia and lessen degree of heart block when vagal activity is etiologic factor. Usual doses are used to reduce severe bradycardia and syncope associated with hyperactive carotid sinus reflex.
0.5 mg (5 mL of 0.1 mg/mL solution) IV/IM/SC
Bradyarrhythmias or heart block: 0.5 mg IV; can be repeated; not to exceed 2 mg for full parasympathetic block; minimal effective dose may need to be repeated q1-2h or prn prior to definitive treatment
Newborns: 0.1 mg (2 mL of a 0.05 mg/mL solution)
<12 years: 0.6 mg (6 mL of a 0.1 mg/mL solution)
In stable patients, administer only after consulting a pediatric cardiologist because children are more susceptible than adults to toxic effects of anticholinergic agents
Other anticholinergics have additive effects; may increase pharmacologic effects of atenolol and digoxin; may decrease antipsychotic effects of phenothiazines; tricyclic antidepressants with anticholinergic activity may increase effects
Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid in Down syndrome and/or in children with brain damage to prevent hyperreactive response; avoid also in coronary heart disease, tachycardia, CHF, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; patients with prostatic hypertrophy or prostatism can have dysuria and may require catheterization; adverse effects include xerostomia, anhydrosis, blurred vision, photophobia, palpitations, tachycardia; constipation and difficulty in micturating may occur in elderly persons; toxic doses lead to restlessness, hallucinations, or delirium, or may progress to coma and death
Parenterally injected dextrose is used in patients unable to sustain adequate oral intake. Its direct oral absorption results in a rapid increase in blood glucose concentrations.
Nutrient replenisher, serves to restore blood glucose levels. Each 100 mL of 5% dextrose contains 5 g of dextrose, whereas each 100 mL of 10% dextrose contains 10 g of dextrose.
Should be given only after demonstrated hypoglycemia.
1-2 ampules of 5% dextrose IV
Administer as in adults
Caution when administering parenteral fluids to patients receiving corticosteroids or corticotropin, especially if solution contains sodium ions
Intracranial or intraspinal hemorrhage; delirium tremens if patient already dehydrated; if administering at the same time as blood products, do not administer without electrolytes through the same infusion set because of the possibility of pseudoagglutination of red cells
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause nausea, which may also occur with hypoglycemia; may result in dilution of serum electrolyte concentrations or overhydration in fluid overload; caution in patients with congested states or pulmonary edema; hypertonic dextrose given peripherally may cause thrombosis (administer instead through central venous catheter); caution in subclinical diabetes mellitus or carbohydrate intolerance; risk of inducing significant hyperglycemia or hyperosmolar syndrome increased if solution administered rapidly, especially in patients with chronic uremia or carbohydrate intolerance; concentrated solutions should not be administered SC or IM; rates of infusion higher than 0.5 g/kg/h may produce glycosuria—at infusion rates of 0.8 g/kg/h, incidence of glycosuria is 5%; monitor fluid balance, electrolyte concentrations, and acid-base balance closely; may produce vitamin B-complex deficiency
CNS agents of the 1,4-benzodiazepine class exert their effects by binding at stereo-specific receptors in the CNS. Their exact mechanism of action has not been clearly elucidated. Benzodiazepines cause a dose-related CNS depression, which varies from mild sedation to hypnosis.
Indicated for treatment of anxiety and management of panic attacks. Following PO administration, absorbed readily. Peak concentrations in plasma occur 1-2 h following administration.
0.25-0.5 mg PO initial for anxiety and hyperventilation
0.25 mg PO initial for elderly patients or those with advanced hepatic disease
<18 years: Not established
>18 years: Administer as in adults
Carbamazepine and disulfiram decrease effects; cimetidine, lithium, contraceptives, ketoconazole, itraconazole, and CNS depressants (including alcohol) increase toxicity
Documented hypersensitivity; severe respiratory depression; narrow-angle glaucoma; preexisting hypotension
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Withdrawal symptoms may occur upon abrupt discontinuation of drug; withdrawal symptoms include heightened sensory perception, impaired concentration, dysosmia, clouded sensorium, paresthesias, muscle cramps, muscle twitch, diarrhea, blurred vision, appetite decrease, weight loss, and seizures
Midodrine forms an active metabolite, desglymidodrine, which is an alpha1-agonist that acts on receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of BP. This drug has minimal beta effects and diffuses poorly across the blood-brain barrier.
Increases standing, sitting, and supine systolic and diastolic BP in patients with orthostatic hypotension of various etiologies. Standing systolic BP elevated by approximately 15-30 mm Hg at 1 h after 10-mg dose, with some effect persisting for 2-3 h. Has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.
10 mg PO tid; take during daytime hours when patient needs to be upright, pursuing activities of daily life
Drugs that stimulate alpha-adrenergic agonists may enhance or potentiate pressor effects; cardiac glycosides may enhance or precipitate bradycardia; psychopharmacologic agents or beta-blockers may precipitate AV block or arrhythmia
Documented hypersensitivity; acute renal disease; severe organic heart disease; pheochromocytoma; urinary retention; persistent and excessive supine hypertension
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in diabetes or visual complications; discontinue and reevaluate if any signs or symptoms suggesting bradycardia occur; do not administer after evening meal or <4 h before bedtime; adverse effects include hypertension (especially supine hypertension), paresthesias, pruritus, piloerection, chills, urinary frequency and urgency, or urinary retention
- The Syncope Evaluation in the Emergency Department Study (SEEDS) data suggest that specialized syncope units with protocoled approaches to ruling out cardiac causes of syncope reduce hospital costs and length of stay without compromising quality of care.17
- Patients with select etiologies of syncope may require transfer for specialty evaluation or procedures.
- Education may have a substantial impact on the prevention of recurrence, especially in situational and orthostatic syncope.
- Patients may be trained to avoid situations that prompt syncope in situational cases.
- In orthostatic syncope, patients should drink 500 mL of fluid each morning in addition to their usual routine and should avoid standing up too quickly.
- Patients with recurrent syncope should be cautioned to avoid tall ledges and to refrain from driving.
- Recurrent falls due to syncope can result in lacerations, orthopedic injuries, and intracranial trauma.
- Cardiac syncope has a poorer prognosis than other forms of syncope. The 1-year end point mortality rate has been shown to be as high as 18-33%. Studies evaluating mortality rates within 4 weeks of presentation and 1 year after presentation both report statistically significant increases in this patient group. Patients with cardiac syncope may be significantly restricted in their daily activities, and the occurrence of syncope may be a symptom of their underlying disease progression.
- Syncope of any etiology in a patient with cardiac conditions (to be differentiated from cardiac syncope) has also been shown to imply a poor prognosis. Patients with NYHA functional class III or IV who have any type of syncope have a mortality rate as high as 25% within 1 year.
- However, some patients do well after definitive surgical treatment or pacemaker placement.
- Noncardiac syncope seems to have no effect on overall mortality rates and includes syncope due to vasovagal response, autonomic insufficiency, situations, and orthostatic positions.
- Vasovagal syncope has a uniformly excellent prognosis. This condition does not increase the mortality rate, and recurrences are infrequent.
- Situational syncope and orthostatic syncope also have an excellent prognosis. They do not increase the risk of death; however, recurrences do occur and are sometimes a source of significant morbidity in terms of quality of life and secondary injury.
- Syncope of unknown etiology generally has a favorable prognosis, with 1-year follow-up data showing a low incidence of sudden death (2%), a 20% chance of recurrent syncope, and a 78% remission rate.
- Patients who present to the ED with syncope should be instructed not to drive. Syncope-related injury during driving is rare but has been documented.
- For excellent patient education resources, visit eMedicine's Brain and Nervous System. Also, see eMedicine's patient education article Fainting.
The medicolegal implications of patients with syncope returning to activities such as sports, driving, and operating machinery have been well publicized. Consultation with a subspecialist and/or a hospital attorney may be prudent prior to making definitive recommendations.
- Failure to consider and diagnose life-threatening etiologies of syncope
- Failure to scrutinize the initial ECG and seek comparison to a prior ECG
- Failure to provide adequate subspecialty and/or primary care follow-up
- Failure to educate patients adequately about the etiology of the syncope and preventive measures to avoid recurrence
- Failure to adequately address short-term recurrence probability and ensure low risk of subsequent morbidity
- Failure to consider and diagnose life-threatening conditions that occur as a result of the syncopal episode