Syncope comes from the Greek word synkoptein, meaning “to cut short.” Hippocrates was the first to use the term and describe the symptom.⁵ Syncope has many causes, but the pathophysiology of the final pathway is the same: hypoperfusion of the cerebral cortex and reticular activating system, which after 8 to 10 seconds of interrupted perfusion causes loss of consciousness; a shorter period results in lightheadedness or dizziness and is referred to as near syncope.

Presenting Signs and Symptoms

The symptoms of syncope can be dramatic. Patients may or may not have a warning, or prodrome, and frequently suffer a fall and have associated trauma. Those with a prodrome frequently experience lightheadedness, diaphoretic warmth, nausea and vomiting, or any combination of these symptoms. Those witnessing the event often fear that the patient has died or was dead for a short period, thus making it an emotionally charged and anxiety-provoking event.

Classification of Syncope

The American College of Physicians lists four major prognostic categories of syncope: neurally mediated, orthostatic, neurogenic, and cardiac; actually, a fifth category (“syncope of unknown cause”) is recognized because in most cases the cause of the syncope remains unknown even after extensive investigation.^6,⁷

Neurally Mediated Syncope

Neurally mediated syncope is syncope associated with inappropriate vasodilation, bradycardia, or both as a result of inappropriate vagal or sympathetic tone.⁸ It is a benign type of cardiovascular syncope that is often associated with a sensation of increased warmth and may be accompanied by preceding lightheadedness (prodrome) along with sweating and nausea. A slow, progressive onset suggests the subcategory vasovagal syncope. Sweating and nausea do not occur with orthostatic hypotension, which is another cause of syncope preceded by lightheadedness.⁵

Neurally mediated or vasovagal syncope may occur after exposure to an unexpected or unpleasant sight, sound, or smell; fear or other emotional distress; severe pain; or surgical procedure. It may also occur in association with prolonged standing or kneeling in a crowded or warm place or after exertion. As a result, the vagus nerve is stimulated, which causes reflex bradycardia and vasodilation.

Situational syncope occurs during or immediately after coughing, micturition, defecation, or swallowing via a similar mechanism. Carotid sinus syncope can be associated with neck pressure (shaving, tight collar) or head turning resulting in stimulation of the carotid sinus in the neck.

Orthostatic Syncope

Orthostatic syncope occurs in individuals with documented postural hypotension associated with syncope or symptoms of presyncope.⁴ In cases of orthostatic syncope, measurement of blood pressure is recommended, first after the patient is supine for 5 minutes and then after the patient is able to stand for 1 to 3 minutes. A decrease of more than 20 mm Hg in systolic pressure is considered abnormal, as is a drop in pressure below 90 mm Hg independent of the development of symptoms.⁹

Because orthostatic hypotension occurs in asymptomatic individuals, vital signs are neither particularly sensitive nor specific. In fact, positive orthostatic changes have been documented in up to 40% of asymptomatic patients older than 70 years and in 25% of those younger than 60 years. Similarly, a notable number of children who are asymptomatic have been documented to have orthostatic hypotension.^5,¹⁰

The most common cause of orthostatic syncope is intravascular volume loss, which may be due to dehydration or bleeding. Orthostatic syncope is not always benign because many patients with serious causes can have this symptom.¹¹

Neurologic Syncope

Neurologic causes of apparent syncope include seizures, transient ischemic attacks, migraine headaches, subarachnoid hemorrhage, and subclavian steal syndrome. Confusion after apparent syncope that lasts more than 5 minutes, tongue biting, incontinence, and epileptic aura suggest a seizure. A significant differential in blood pressure between the two arms suggests subclavian steal or dissection. For neurologic causes to be considered true syncope, they must by definition be transient in nature and result in a return to baseline neurologic function. Thus, loss of consciousness with persistent neurologic deficits or altered mental status is not true syncope. In fact, according to this criterion very few neurologic events (especially strokes or subarachnoid hemorrhage) meet the definition of syncope.

Most cases involving neurologic causes of syncope are easily predicted. In general, when these patients have symptoms suggesting a specific disease process, the need for intervention based on neurologic symptoms is usually obvious. It is not recommended that a routine neurologic work-up be performed in all patients with syncope unless related neurologic symptoms are present. It has been determined that routine neurologic testing and investigation, such as computed tomography (CT), is not cost-effective in patients without neurologic symptoms.¹²

Cardiac-Related Syncope

Syncope in this class can be caused by many types of arrhythmias (benign and malignant), valvular and ischemic heart disease, and cardiomyopathies. Although it is clear that patients with known cardiac disease and syncope have a significantly increased incidence of cardiac-related death, cardiac disease may not be recognized in many patients with cardiac syncope, and persons with a history of cardiac disease may appear to be very stable. Therefore, depending on the history and age of the patient, a relatively aggressive search for cardiac problems may be necessary. However, the urgency of these investigations and whether they should be done in the ambulatory or inpatient setting (e.g., monitoring) are unclear.

Syncope of Unknown Cause

Syncope of unknown cause is the largest category of syncope, with estimates as high as 40%, even with extensive work-up.¹ Some studies have found that after evaluation in the ED, physicians are uncertain of the cause of the syncope more than 50% of the time.¹⁴ As a result, many serious cases are initially classified in this category, which causes a dilemma for emergency physicians who must decide whether to admit or discharge these patients. It is this largest group of patients who present the greatest challenge for physicians.

Recommended Diagnostic Tests

Ongoing or related symptoms associated with syncope should direct the ED investigation. CT is not indicated for all patients, but one should not ignore associated symptoms, for which a complete work-up should be performed ⁷ (e.g., CT in patients with associated headache or abdominal pain, urine pregnancy tests in females, ultrasonography in pregnant women, troponin assay and CT angiography in patients with chest pain and dyspnea).

A routine electrocardiogram (ECG) is almost always indicated, as are rhythm strips and monitoring while the patient is in the ED. Any nonsinus rhythms or new changes on the ECG should be a concern. Routine basic laboratory tests in asymptomatic patients are not recommended, and their use should be guided by the history and physical examination. Recent work has focused on the value of brain natriuretic peptide (BNP) as a predictor of risk in patients with syncope.¹⁵ BNP may have some utility but requires further consideration before becoming a recommended test. In particular, the value of a single reading and the timing of drawing blood in relation to the event require further work. In addition, although it makes sense that BNP may be helpful because it is a predictor of congestive heart failure (CHF) and structural heart disease, it remains unclear whether it provides any greater value over taking a good history, especially given the added cost of the test.¹⁶

Prognosis

Perhaps the best investigation of the prognosis of patients with syncope was done by Soteriades et al., who used data from the Framingham study.¹³ This study assessed the risk for death in a prospective cohort of 7814 patients over a 17-year period. The results were dramatic. Those with documented heart disease and syncope had twice the mortality rate of patients without syncope, and patients with syncope with a neurologic cause were 50% more likely to die. People with syncope of unknown cause also had a significantly increased risk for death of 30%, whereas those with neurally mediated (vasovagal) syncope had a lower risk. The study clearly shows that the increased risk for death in this group requires further scrutiny, as does ED disposition and management.

Other studies suggest that cardiac-related syncope represents 5% to 40% of the causes of syncope and is associated with a significant increase in mortality. ED management of patients with cardiac symptoms such as chest pain in addition to syncope is obvious; however, of most concern are asymptomatic patients with syncope.

The absence of cardiac symptoms is not reassuring because patients can have serious “silent symptoms” (silent myocardial infarction and silent arrhythmia, such as Brugada syndrome ¹⁷) that may not be obviously associated with syncope on initial evaluation. Such patients may not have a history of cardiac disease, and syncope may be the first symptom. Patients with cardiac symptoms and syncope clearly need thorough and timely evaluation and thus in most cases require emergency hospitalization.¹⁸

Physicians evaluating patients with syncope who are asymptomatic and without a clear cause are faced with the following questions:

1. Is the syncope a symptom indicating that known underlying heart disease is active, unstable, and related to the episode?

2. Is the syncope a symptom of occult underlying heart disease?

3. Is the syncope a symptom of an occult noncardiac life-threatening process (e.g., pulmonary embolism, occult bleeding, transient ischemic attack, subarachnoid hemorrhage)?

To maximize the sensitivity of detecting underlying disease, physicians frequently admit low-risk patients for further evaluation, although the cost-effectiveness and value of such decisions are often questioned.¹⁹ It is this group of asymptomatic patients with syncope who are most likely to benefit from risk stratification strategies to guide disposition decisions.

Acute Risk Stratification in the Emergency Department

Martin et al. developed the first risk stratification scheme for patients evaluated in the ED for syncope.²⁰ The stratification was premised on 1-year prognosis for death or cardiac morbidity. Four predictors of death at 1 year were found: age older than 45 years, history of ventricular dysrhythmias, history of CHF, and abnormal findings on an ECG. A similar study found that an abnormal ECG and history of structural heart disease (primarily CHF) predicted mortality but that a much higher age cutoff (older than 65 years) could predict death at 1 year.³

Sarasin et al. developed a risk score for ED patients with syncope.²¹ The score was based on three factors associated with increased risk for an arrhythmia: abnormal findings on an ECG, age older than 65 years, and a history of any cardiac disease (primarily CHF).

Finally, Quinn et al. derived and validated a decision rule that addresses short-term risk (7 days) to better determine immediate risk in patients in the ED.^2,²² Again, a history of CHF and abnormal findings on an ECG were the most important predictors. The decision rule considered all patients with syncope and also determined that shortness of breath, hematocrit higher than 30, and systolic blood pressure greater than 90 mm Hg were important risk factors. Age older than 75 years was found to be sensitive but nonspecific in this cohort and not useful as a predictor.

Others have tried to validate this work with variable success.²³^–²⁵ The key to studies being able to most closely validate the work is using the proper ECG definition, which includes not only new changes on the ECG but also any nonsinus rhythms that are found not only on the ECG but also during monitoring throughout the patient’s ED stay.²⁶

Other important prospective risk stratification studies are from Italy. The OESIL study found that age older than 65 years, history of cardiovascular disease, syncope without a prodrome, and ECG abnormalities were risk factors.³ The EGSYS study found an abnormal ECG, history of heart disease, absence of a prodrome, supine status, palpitations, and effort-related syncope to be risk factors.²⁷ Finally, the STePS study found ECG abnormalities, concomitant trauma, absence of a prodrome, and male gender to be short-term risks.²⁸

Age as a risk factor deserves specific mention because physicians often admit patients with syncope just because of age. For almost all diseases, older people die sooner than younger people, and health problems in general increase with age. Recommending that all people older than 45 years (or even those older than 65 or 75 years) be admitted because this factor predicts 1-year death is impractical. Although it may be sensitive as a predictor, age by itself is a poor discriminator; many younger people have significant illness that puts them at even greater risk. This was demonstrated in a study of the short-term outcomes of asymptomatic patients who had syncope of unknown cause and were older than 50 years; all had benign outcomes.¹⁴ Furthermore, comparison of age solely as a risk versus other risk factors has shown that risk factors perform better than age alone.²⁹

In summary, advanced age is a risk, but no practical age cutoff for risk has been established, and it should be considered with other risk factors. In particular, almost every study on risk factors has found that an abnormal ECG, including abnormalities detected on cardiac monitoring, is important, as is a history of cardiac disease, specifically CHF. The lack of a prodrome or vagal symptoms is also important in every study, but one study that looked at its subjective nature found that physicians had poor agreement on the presence of vagal symptoms.

Improved Diagnostic Strategies in the Emergency Department

Some investigators have reported that diagnostic and prognostic ability improve with more invasive testing such as echocardiography. This makes sense in that this procedure may identify patients with structural heart disease and a limited ejection fraction; however, another study found that patients who would benefit from echocardiography could be identified by their history and physical examination and that this procedure may not be cost-effective.³⁰ Another group in the United Kingdom found that risk stratification could be improved by implementing a protocol of more aggressive strategies such as tilt-table testing and echocardiography but noted that such strategies may not be cost-effective or practical in the ED.³¹ An Italian group thought that diagnosis could be improved just with more aggressive history taking and physical examination.³²

Because echocardiography and other invasive tests are not routinely available in the ED 24 hours per day, investigators have started to use observation units to avoid inpatient admission for a select group of intermediate-risk patients evaluated in the ED.³³ There appears to be some promise for syncope observation units, with the goal being to move more low- and intermediate-risk syncope patients from the traditional inpatient work-up to a more structured and efficient observation or outpatient work-up.

Guidelines for Admission and Disposition

Many specialty societies have devised consensus guidelines for admission to the hospital that have focused on the best available data.^34,³⁵ The American College of Emergency Physicians recommends that patients with evidence of cardiac and neurologic causes of syncope, as well as other serious outcomes diagnosed in the ED, be admitted to the hospital. Admission is also recommended for patients with undifferentiated syncope who have risk factors for adverse outcomes (Fig. 64.1).