Syncope
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Syncope is defined as a transient, self-limited loss of consciousness [1] with an inability to maintain postural tone that is followed by spontaneous recovery. This definition excludes seizures, coma, shock, or other states of altered consciousness. Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients.
History and physical examination are the most specific and sensitive ways of evaluating syncope. These measures, along with 12-lead electrocardiography (ECG), were the only current level A recommendations listed in the 2007 American College of Emergency Physicians (ACEP) Clinical Policy on Syncope. [2]
A detailed account of the event must be obtained from the patient, including the following:
The following questions should be asked:
If the answers are positive, syncope is highly likely; if 1 or more are negative, other forms of loss of consciousness should be considered. [3]
Presyncopal symptoms reported may include the following:
Other information that should be obtained includes the following:
A complete physical examination is required, with particular attention to the following:
See Presentation for more detail.
No specific laboratory testing has sufficient power to be absolutely indicated for evaluation of syncope. Tests may not be necessary and can be tailored to any signs or symptoms that raise concern for a specific underlying illness. Research-based and consensus guideline recommendations are as follows:
Imaging studies that may be helpful include the following:
A standard 12-lead ECG is a level A recommendation in the 2007 ACEP consensus guidelines for syncope. [2] The following considerations are relevant:
Other diagnostic tests and procedures include the following:
See Workup for more detail.
Prehospital management of syncope may require the following:
Advanced triage decisions, such as direct transport to multispecialty tertiary care centers, may be required in select cases.
In patients brought to the emergency department with a presumptive diagnosis of syncope, appropriate initial interventions may include the following:
The treatment choice for syncope depends on the cause or precipitant of the syncope, as follows:
See Treatment and Medication for more detail.
Syncope is defined as a transient, self-limited loss of consciousness [1] 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, categorization into reflex (neurally mediated), orthostatic, and cardiac (cardiovascular) may be helpful during the initial evaluation. Cardiac syncope is associated with increased mortality, whereas noncardiac syncope is not. Syncope may result in significant morbidity and disability due to falls or accidents that occur as a result. [6] In the United States alone, an estimated $2 billion annually is spent on patients hospitalized with syncope.
Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients. It is unclear whether hospital inpatient admission of asymptomatic patients after syncope affects outcomes. No current criterion standard exists for diagnosing undifferentiated syncope.
Many physicians continue to admit patients because of perceived risk. Reviews of the 2001 American College of Emergency Physician (ACEP) clinical policy suggested that evidence-based criteria may decrease admission rates by nearly half by identifying cardiac causes of syncope. Inpatient admission should be reserved for patients in whom identification of specific immediate risk is needed (eg, those with structural heart disease or a history of ventricular arrhythmia). Outpatient management can be used for patients who are at low risk for a cardiac etiology to define a precise cause so that mechanism-specific treatment can be effected.
Syncope occurs as a consequence of global cerebral hypoperfusion. [1] 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 the high-energy phosphates found elsewhere in the body; consequently, a cessation of cerebral perfusion lasting only 3-5 seconds can result in syncope.
Cerebral perfusion is maintained relatively constant by an intricate and complex feedback system involving cardiac output (CO), systemic vascular resistance (SVR), mean arterial pressure (MAP), intravascular volume status, cerebrovascular resistance with intrinsic autoregulation, and metabolic regulation. A clinically significant defect in any one of these systems or subclinical defects in several of them may cause syncope.
CO can be diminished secondary to mechanical outflow obstruction, pump failure, hemodynamically significant arrhythmias, or conduction defects. SVR can drop secondary to vasomotor instability, autonomic failure, or vasodepressor/vasovagal response. MAP decreases with all causes of hypovolemia. Medications can affect CO, SVR, or MAP.
Other conditions can mimic syncope. A central nervous system (CNS) event, such as a hemorrhage or an unwitnessed seizure, can present as syncope. Syncope can occur without reduction in cerebral blood flow in patients who have severe metabolic derangements (eg, hypoglycemia, hyponatremia, hypoxemia, hypercarbia).
Cardiac (cardiopulmonary) 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 electrocardiogram (ECG) is mandatory if any of these causes are possible for the differential diagnosis.
Low flow states, such as those associated with advanced cardiomyopathy, congestive heart failure (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 myocardial infarction (MI), acute aortic dissection, and pulmonary embolus. 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.
Reflex (neurally mediated) syncope may be due to vasovagal syncope, which is mediated by emotional distress such as fear or physical pain. Situational syncope describes syncope that occurs with a fixed event such as micturition, deglutition, exercise induced, and carotid sinus syncope. These causes tend to be more benign and do not predict poor outcomes.
Vasovagal syncope is the most common type in young adults [7] 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. The 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.
Situational syncope is essentially a reproducible vasovagal syncope with a known precipitant. Micturition, defecation, deglutition, 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.
Syncope due to orthostatic hypotension can occur through several mechanisms. Pure autonomic failure can be associated with Parkinson disease or dementia. Secondary autonomic insufficiency can be due to diabetes, uremia, or spinal injury. Drugs such as alcohol cause orthostatic intolerance, and medications such as vasodilators and antidepressants block orthostatic reflexes. Volume depletion due to blood loss, vomiting, diarrhea, poor oral intake, and diuretics also causes orthostatic syncope.
Dehydration and decreased intravascular volume contribute to orthostasis. Orthostatic syncope describes a causative relation 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 it is suspected, patients should be referred to a primary care provider for outpatient tilt-table testing.
Framingham data demonstrate a first occurrence rate of 6.2 cases per 1000 patient-years. [8, 9] Syncope reoccurs in 3% of affected individuals, and approximately 10% of affected individuals have a cardiac etiology.
Data from Europe and Japan suggest an occurrence rates similar to that in the United States, accounting for 1-3.5% of ED visits.
No significant differences regarding race are observed with respect to syncope risk. Larger prospective studies fail to show clinically significant differences between men and women.
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 reported a prevalence of less than 0.1% in children. [10] 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 being at higher risk. Advancing age correlates with increasing frequency of coronary artery and myocardial disease, arrhythmia, vasomotor instability, autonomic failure, polyneuropathy, and use of polypharmacy.
Cardiac syncope has a poorer prognosis than other forms of syncope. The 1-year endpoint mortality has been shown to be as high as 18-33%. Studies evaluating mortality 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 New York Heart Association (NYHA) functional class III or IV who have any type of syncope have a mortality as high as 25% within 1 year.
However, some patients do well after definitive surgical treatment or pacemaker placement. Evaluation by a cardiologist for pacemaker placement should be considered in select patients older than 40 years who have recurrent syncope that is confirmed to be neurally mediated syncope (NMS) with a documented period of asystole. Preliminary data suggests that although syncope may recur in this subset of patients, the frequency is reduced by more than 50%. [11]
Noncardiac syncope seems to have no effect on overall mortality 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, 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.
Recurrent falls due to syncope can result in lacerations, orthopedic injuries, and intracranial trauma.
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 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. [12]
Morbidity from syncope includes recurrent syncope, which occurs in 20% of patients within 1 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 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. [13]
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 for patients with cardiac syncope than for those with noncardiac syncope. [14] Suzuki et al studied 912 patients with syncope for an average of 3 years and found the same result. [15]
Risk of serious outcome and death in patients with syncope increases with higher peak troponin concentrations, according to a prospective cohort study of 338 patients who had plasma troponin I levels measured with a sensitive assay 12 hours after syncope. [16] The percentage of patients with a serious outcome increased across patients divided into quintiles on the basis of peak troponin concentration at 1 month (0%, 9%, 13%, 26%, 70%) and at 1 year (10%, 22%, 26%, 52%, 85%). [16]
Decision rules may assist in identifying patients who are at risk. Martin et al described a risk stratification system that predicted an increased incidence of death at 1 year on the basis of abnormal ECG findings, a history of ventricular arrhythmia, a history of CHF, and age older than 45 years. [17]
Sarasin et al demonstrated 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. [18]
The San Francisco Syncope Rule (SFSR) was determined to have a 96% sensitivity for identifying patients at immediate risk for serious outcomes within 7 days, on the basis of the presence of abnormal ECG findings, a history of CHF, dyspnea, a hematocrit level lower than 0.30, and hypotension. [19] The presence of these findings should prompt serious consideration for hospital admission.
In an external retrospective review, validation of the SFSR in a Canadian ED 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. The results of this study suggested that implementation of the rule would have significantly increased admission rates. The authors concluded that further study was needed. [20] Another study was also unable to validate the rule, with a sensitivity of 74% and a specificity of 57% reported. [21]
The ROSE (Risk stratification Of Syncope in the Emergency department) criteria suggested that an elevated B-type natriuretic peptide (BNP), Hemoccult-positive stool, anemia, low oxygen saturation, and presence of Q waves on ECG predict serious outcomes at 30 days. [22] These rules had a 87% sensitivity and a 98.5% negative predictive value to help risk-stratify patients. In this study, the isolated finding of BNP greater than 300 pg/mL was a major predictor of serious outcomes and was present in 89% of patients who died within 30 days.
Constantino et al discovered that 6.1% of patients had severe outcomes within 10 days of syncope evaluation. [23] The mortality 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.
The Evaluation of Guidelines in SYncope Study 2 (EGSYS 2) prospectively followed nearly 400 patients at 1 month and 2 years. The death rate was 2% at 1 month and 9% at 2 years. Patients with advancing age, presence of structural heart disease, and/or abnormal ECG had higher risk. [24]
Clinical judgment, Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) score, [25] and SFSR criteria all have relatively low sensitivities individually for predicting severe short-term outcomes. Some evidence suggests that combining various risk stratification tools may increase sensitivity and reduce unnecessary admissions. [26] A review and meta-analysis by Serrano et al assessed the methodologic quality and prognostic accuracy of the SFSR and the OESIL risk score. [27] The analysis of 18 eligible studies determined that the quality and accuracy of both sets of clinical decision rules are limited.
Patients who present to the ED with syncope should be cautioned to avoid tall ledges and instructed not to drive. Syncope-related injury during driving is rare, but it has been documented.
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.
For patient education resources, see Brain and Nervous System Center, as well as Fainting.
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Rumm Morag, MD, FACEP Member of Salem Emergency Physician Services, PC (SEPS), Salem Hospital
Rumm Morag, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Sanz Laniado Medical Center, Netanya, Israel
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada
Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians
Disclosure: Nothing to disclose.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
David A Peak, MD Associate Residency Director of Harvard Affiliated Emergency Medicine Residency; Attending Physician, Massachusetts General Hospital; Assistant Professor, Harvard Medical School
David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, American Medical Association
Disclosure: Partner received salary from Pfizer for employment.
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