Emergency Medicine

How to Evaluate the Patient with Syncope

Which patient characteristics should raise your level of concern about syncope? Was the episode really syncopal, or might it have been a seizure? Which forms of structural heart disease should you suspect and when? Should the patient undergo computed tomography scanning of the head? The authors address these and other issues associated with an often innocent but always worrisome symptom.

By Colleen N. Hickey, MD, and Peter S. Pang, MD

Syncope is defined as a transient loss of consciousness and postural tone followed by spontaneous recovery without medical intervention. Its many possible causes share a common pathophysiology: a sudden decrease or brief cessation of blood flow to both cerebral hemispheres or the reticular activating system of the brain.

The overall incidence of syncope is approximately 6.2 cases per 1,000 patient years (or 12% to 48% of the U.S. population), and the frequency increases with age. Although syncope rates in pediatric populations are much lower than in adults, 15% to 50% of the pediatric population will experience an episode of syncope at some point during childhood. There is no question, however, that old age is a significant risk factor for syncope, with the annual incidence in patients aged 75 or older reported at 6%.

Syncope accounts for 1% to 3% of all visits to the emergency department and 1% to 6% of all hospital admissions. Despite extensive research and development of diagnostic pathways and clinical guidelines, the health care costs of a syncope evaluation are significant. Every year in the United States, more than one million people are evaluated for syncope, with an admission rate ranging from 30% to 70%, costing the health care industry billions of dollars. No firm criteria have been established to accurately assess the need for admission or extensive outpatient workup with these patients.

Ultimately, a substantial proportion of patients who present with syncope will have a benign or unknown etiology. Nonetheless, rapid diagnosis of significant etiologies, with careful but efficient consideration of those that may be life-threatening, remains the focus of the initial evaluation.

WHO IS AT RISK

As noted, the majority of patients presenting with syncope will have a benign etiology, but overall morbidity and mortality in this population is still a significant concern. Patients with a cardiac history or underlying structural heart disease have a worse outcome compared to noncardiac patients, with an increased risk of death after their syncopal event. Patients with severe heart failure (NYHA Class III/IV) have been shown to have substantial increases in mortality after their syncopal events compared with patients with the same degree of heart failure but no syncope.

Even patients presenting with a benign cause of syncope may have increased morbidity due to recurrent episodes, which occur in 20% to 30% of patients within one year. Motor vehicle crashes, head injuries, fractures, lacerations, and other injuries can occur secondary to syncopal episodes.

Not all patients who present with fainting have ex-seizures share some clinical features, the underlying perienced syncope. Seizure, for example, should always pathophysiologies are distinct and must be differentibe considered in the differential. Although syncope and ated. Key historical features that may help distinguish seizures are: a history of seizures; a preceding aura; rhythmic movements, such as classic tonic-clonic movements or myoclonic jerks; confusion after the event lasting more than several seconds or a prolonged return to consciousness; loss of bowel or bladder function during the event; injuries such as tongue biting; and unconsciousness lasting more than five minutes. Symptoms more suggestive of syncope include prodromal symptoms such as nausea and vomiting, diaphoresis, or lightheadedness; a rapid return to a clear sensorium; or loss of consciousness preceded by stress, pain, cough, micturition, or defecation.

Nevertheless, confounding factors often make this distinction difficult. Either of these entities may occur suddenly without any prodrome or warning and cause injuries. Convulsive jerking may occur in syncope, and both conditions may coexist in a single patient. Furthermore, seizures may lead to a cardiac arrhythmia resulting in pronounced hypotension, and syncope or seizures may be the presenting feature in a small number of patients with underlying cardiac disease, such as prolonged QT syndrome.

CARDIAC CAUSES OF SYNCOPE

As a result of recent research, current practice is shifting toward dividing etiologies of syncope into cardiac and noncardiac causes due to the prognostic significance of this classification scheme. Although there are several well-established etiologies of syncope, the only one strongly associated with increased mortality and sudden death is syncope due to a cardiac cause. The rates of sudden death and overall mortality are markedly higher in patients with cardiac causes versus neurocardiogenic or unknown causes of syncope, with a one-year mortality ranging from 18% to 33%. A history of congestive heart failure (CHF), ventricular arrhythmias, or abnormal ECG findings must be elucidated during the initial evaluation.

Because of the significant increase in mortality, cardiac causes must be considered in every patient who presents with syncope. The primary concern in this population is an increased risk of arrhythmia leading to sudden death, especially if the patient reports the complete absence of prodromal symptoms.

Cardiac causes of syncope can be divided into structural cardiovascular abnormalities and primary cardiac rhythm disturbances. Structural heart disease has emerged as the most important risk factor for predicting death in patients presenting with syncope. Broadly defined, structural heart disease includes coronary heart disease, valvular disease (especially aortic or mitral stenosis), aortic dissection, cardiac tamponade, hypertrophic obstructive cardiomyopathy, and cardiac tumors (myxomas). Severe heart conditions, such as advanced cardiomyopathy, CHF, and valvular insufficiency, may result in low-flow states that can lead to transient global hypoperfusion.

Structural heart disease may lead to cardiac outflow obstruction, resulting in the sudden onset of syncope with little or no prodrome. Syncope may be the presenting sign in patients with moderate to severe aortic stenosis. Young athletes presenting with syncope, especially during exercise, should be evaluated for hypertrophic obstructive cardiomyopathy. Mitral stenosis, pulmonary stenosis, atrial myxomas, pulmonary hypertension, and pericardial tamponade can also manifest with syncope secondary to outflow obstruction or poor right heart filling.

While acute coronary syndromes (ACS) may not be classically considered structural heart disease, they are categorized in this category as the most significant subset of coronary heart disease. The potential for an ACS leading to an arrhythmogenic event should never be overlooked. However, in the majority of cases, significant historical symptoms and signs will accompany syncope due to ACS or aortic dissection.

Primary rhythm disturbances can be divided into bradyarrhythmias and tachyarrhythmias. Bradyarrhythmias include sinus bradycardia, sick sinus syndrome, high-grade atrioventricular blocks, and pacemaker malfunction. Most patients presenting with these abnormalities have a history of cardiac disease or are symptomatic from their underlying disease. Historical clues to a bradyarrhythmia include chest pain, dyspnea, decreased exercise tolerance, dizziness, and fatigue. Medication side effects are an important potential cause of symptomatic bradycardia and are often overlooked during the initial evaluation.

Both ventricular and supraventricular tachyarrhythmias may induce syncope. Ventricular tachycardia and torsade de pointes primarily present in older patients with underlying cardiac disease, with the rare exceptions of commotio cordis or structural heart disease in young persons combined with vigorous exercise. Also in this category is prolonged QT syndrome, which can be hereditary and present at any age or as a side effect of medications, including amiodarone, procainamide, and tricyclic antidepressants. The Brugada syndrome, with its characteristic ECG findings of a pseudo-right bundle branch block and ST-segment elevation in leads V1 through V3, is another etiology to consider.

Syncope due to ventricular arrhythmias tends to occur suddenly without prodromal symptoms. Furthermore, aside from prolonged QT syndrome, these arrhythmias are often not seen on the initial ECG; instead, they are found only after a period of prolonged rhythm monitoring.

Syncope patients with known structural heart disease or ECG abnormalities on presentation should be admitted for further cardiac workup, including continuous telemetry monitoring, echocardiography, and consideration of risk stratification with stress testing. Due to the likelihood of an arrhythmia going undetected during routine cardiac monitoring, 24-hour rhythm monitoring or additional long-term monitoring should be considered. Additional follow-up with a cardiologist or electrophysiologist should also be considered for patients with known heart disease and syncope.

NONCARDIAC CAUSES OF SYNCOPE

Noncardiac syncope has multiple etiologies. The most common is neurocardiogenic (or vasovagal) syncope, which accounts for approximately 50% to 65% of previously unexplained syncope. This is the most common cause of syncope in young adults, but it may occur at any age. Examples of this benign cause of syncope include situational syncope, emotionally induced syncope, and carotid sinus hypersensitivity. Neurocardiogenic syncope tends to occur while the person is standing and is usually precipitated by prolonged standing, fear, pain, or emotional stress. Most patients experience some type of prodromal symptoms such as lightheadedness, diaphoresis, blurry vision, nausea, weakness, or the sensation of feeling flushed or warm. These symptoms may last from several seconds to several minutes prior to the syncopal episode. Many of these patients will have a history of prior presyncopal symptoms without prior syncope or even a history of syncope in a similar situation in the past. However, as patients age, prodromal symptoms may decrease or be altogether absent, making this diagnosis more difficult.

Situational or reflex syncope is a subset of neurocardiogenic syncope that occurs with a known precipitant such as micturition, defecation, or coughing. These specific stimuli result in an autonomic reflex leading to vagal stimulation and sympathetic withdrawal, ultimately causing decreased cerebral perfusion. Carotid sinus syncope occurs in patients who are thought to have increased sensitivity of the baroreceptors in the carotid sinus. Syncope may occur with rotation of the neck, turning the head, or pressure on the carotid sinus such as from carotid massage, shaving, or a tight collar.

Although the exact mechanism of neurocardiogenic syncope is not well understood, it is thought to result from an abnormal autonomic response that results in peripheral vasodilation and increased vagal tone, leading to reduced cardiac filling and bradycardia. Neurocardiogenic syncope tends to occur sporadically and has never been shown to be associated with increased mortality.

There are several other less common causes of syncope. Some examples are hypovolemia resulting from benign causes such as dehydration and orthostasis or more serious causes such as hemorrhage; anemia; hyperventilation; hypoxia; hypoglycemia; alcohol or other substance abuse; psychiatric conditions such as generalized anxiety disorder, panic disorder, and somatization disorder; breath holding (especially in children); and subclavian steal syndrome.

There are also several life-threatening etiologies that rarely present as syncope but should be considered in every patient who presents with the condition. These include pulmonary embolism, transient ischemic attack or stroke (usually from pre-existing vertebral-basilar insufficiency), cerebral aneurysm, abdominal aortic aneurysm, epidural or subdural hematoma, and ruptured ectopic pregnancy.

Medication-related syncope, which accounts for approximately 3% of all cases, should be considered in the differential, especially in patients with multiple medical problems who are taking several drugs. Many different medications, even when taken at prescribed doses, may precipitate syncopal episodes. Most common among these are diuretics, beta blockers, calcium channel blockers, vasodilators, antiarrhythmics, and nitrates. Other medications that may be implicated include digitalis, alpha blockers, angiotensin-converting enzyme inhibitors, sildenafil, tricyclic antidepressants, quinidine, phenothiazines, sedatives, and analgesics. A thorough medication history, including over-the-counter medications and herbal remedies, is essential.

HISTORY AND PHYSICAL EXAM ARE KEY

The history and physical examination will reveal the diagnosis in up to 45% of patients presenting with syncope. The initial goal should be to differentiate true syncope from other alterations in consciousness, including seizure or psychiatric disorders. Important historical questions include: Is there any history of syncope or seizures? Was the patient standing or sitting when the syncopal episode occurred? Were there any prodromal symptoms, especially chest pain or dyspnea? Were there any surrounding events or stressors, such as cough, strong emotion, or micturition? Did anyone witness the event? Did the patient have prolonged confusion or altered mental status after the event?

These questions can help risk-stratify the patient and guide the initial workup. The presence or absence of any personal or family history of cardiac disease is a key finding. As mentioned above, medication lists should be carefully reviewed to assess for the possibility of medication-induced syncope.

A complete physical exam should be performed on every patient. Abnormal vital signs may point toward key etiologies. The importance of a thorough cardiovascular and neurologic exam cannot be overemphasized. Additionally, a rectal exam to assess for gastrointestinal bleeding should be considered in all patients presenting with syncope.

Careful carotid sinus massage may be helpful in a small number of patients in whom carotid sinus hypersensitivity appears to be a key feature of their presentation. Cardiac and continuous blood pressure monitoring with atropine should be initiated at the bedside. The carotid sinus is massaged for at least five seconds to assess for hypersensitivity, which manifests as decreased heart rate and blood pressure. This procedure must be done with care, however, as one review revealed an embolic stroke incidence of 0.28%. Assessment for carotid artery disease with documentation of the absence of bruits or thrills must be performed prior to massage.

DIAGNOSTIC TESTING

Several conditions that may result in syncope can be detected on routine lab work and urinalysis. Although uncommon as a cause of syncope, anemia can be diagnosed by a simple complete blood cell count. Hypoglycemia and electrolyte abnormalities can be detected on a basic chemistry panel. Urinalysis can demonstrate a urine infection, which may be the cause of a syncopal episode in an older individual; it can also be used to determine if a woman is pregnant. Cardiac enzymes should be evaluated in patients presenting with syncope and symptoms of chest pain or dyspnea or a history of cardiovascular disease. However, it should be noted that these studies have a very low diagnostic yield and should only be obtained if clinically indicated, not routinely.

The most significant adjunctive study for evaluating patients with syncope is a 12-lead ECG. An abnormal ECG on presentation strongly suggests underlying cardiac disease, with the resultant increased risk of sudden death and overall mortality. While significant ECG abnormalities are helpful when present, it is not uncommon for an arrhythmia to be missed on a single ECG reading. Holter monitoring or longer-term event monitoring has been suggested for patients in whom the suspicion of an arrhythmia is moderate to high, patients who have been admitted for telemetry monitoring without an additional event, and patients with recurrent syncopal events. Understandably, event monitors have shortcomings for those patients without prodromal symptoms and continuous recorders are recommended.

Imaging studies, performed routinely, are also of limited value. Unless a specific pathology is suspected, imaging is not recommended. However, because older individuals can have unusual presentations of common diseases, the use of more liberal laboratory testing and imaging studies in this population should be considered. The use of head computed tomography (CT) after syncope is not routinely indicated. Specifically, head CT is rarely indicated in patients with nonfocal neurologic exams. Exceptions include patients with new neurologic deficits or with head trauma, especially patients on blood-thinning medications.

While not an emergent diagnostic study, tilt-table testing can be helpful in confirming autonomic dysfunction. Caution should be used in interpreting the results since both false positives and false negatives can occur, which can be influenced by the method of tilt-table testing used as well as the patient population being evaluated. In a positive tilt-table test, patients will become symptomatic because they do not have an appropriate autonomic response to maintain their blood pressure in that position. However, a negative result does not exclude a neurocardiogenic cause for syncope.

PATIENT DISPOSITION

Even with an extensive and expensive evaluation, 20% to 50% of patients will ultimately have an unknown reason for their syncopal episode. Recent research has targeted accurate risk stratification of patients as well as clinical guidelines and pathways. Despite several studies outlining strategies to decrease the admission rate of this population, however, up to 70% of patients are admitted despite a negative workup in the emergency department.

A derivation study in 2003 established the San Francisco Syncope Rule to predict patients with short term serious outcomes. This study suggested that patients with any of the following should be admitted for further evaluation: an abnormal ECG, shortness of breath, a hematocrit level below 30%, systolic blood pressure less than 90 mm Hg, or a history of CHF. A prospective cohort study published in 2005 suggested that following this rule would decrease admissions by 10% and still predict short-term serious outcomes.

The American College of Emergency Physicians’ Clinical Policies Subcommittee on Syncope outlined a policy for the evaluation and treatment of patients presenting with syncope based on the medical literature from 1985 to 1998. Although no level A recommendations were made, level B recommendations for admission were: a history of CHF or ventricular arrhythmias, associated chest pain or other symptoms compatible with acute coronary syndrome, evidence of significant CHF or valvular heart disease on physical examination, or ECG findings indicating ischemia, arrhythmia, prolonged QT interval, or bundle branch block. The significant increase in one-year mortality in patients with underlying heart disease is evident in these recommendations. Level C recommendations for admission include: age over 60, history of coronary artery disease or congenital heart disease, family history of unexpected sudden death, or exertional syncope in younger patients without an obvious benign cause for the syncope.

Although these recommendations were outlined in 2001, little change has occurred in admission rates since then; they continue to range between 30% to 70% at institutions throughout the country. Patients more likely to be admitted are male, white, and older than 65; those with a prodrome of dyspnea or vomiting; those with a history of coronary artery disease, CHF, hypertension, cerebrovascular disease, or diabetes; and those with abnormal ECGs on presentation.

The difficulty of accurate risk stratification is considerable. The wide range of etiologies, from completely benign to imminently fatal, highlights the difficulty. Furthermore, the fact that syncope occurs in every age group as well as in healthy people and those with multiple comorbidities compounds the problem of safe disposition. Recognizing the significant limitations of broad generalities, it can be said that young, healthy patients with a plausibly benign cause for vasovagal syncope and a negative workup are likely candidates for safe discharge home. Older patients, especially those with underlying cardiac disease, should be strongly considered for admission.

MANAGEMENT STRATEGIES

The management of syncope is aimed at treating the underlying cause, and much of it is beyond the scope of the initial presentation. Patients with arrhythmia, for example, will likely need an electrophysiology evaluation with possible further intervention such as a pacemaker, automated implantable cardioverter defibrillator, or ablation. All patients with syncope due to a cardiac cause and those with syncope who have known underlying cardiac disease should be strongly considered for admission and telemetry monitoring at a minimum, with appropriate specialist follow-up as indicated. Medications that may be the cause of the syncopal episode should be stopped and alternate medications investigated or dosages adjusted.

With some of the more common benign causes of syncope, it may be feasible to initiate outpatient treatment at the time of the patient’s initial presentation.

For instance, patients with situational syncope should receive education about the condition and techniques to recognize early symptoms to avoid syncopal episodes. Patients with neurocardiogenic syncope should also be educated on the importance of adequate salt and fluid intake. Physical maneuvers, such as tensing of the arms and legs and gripping of the hands, may also help prevent syncope if prodromal symptoms are recognized in time.

SIGNIFICANT CHALLENGE

The diagnostic evaluation of syncope remains a significant challenge. Careful consideration of potentially life-threatening causes combined with a realistic understanding of the limitations of the diagnostic workup will lead to a thorough and safe evaluation and appropriate disposition of the patient.