Syncope is a common clinical entity with a lifetime prevalence between 20% and 40%, and is slightly more common in women than in men.

Key Concepts

• •

  Syncope is defined as a sudden, spontaneous loss of consciousness and postural tone with rapid, complete, and spontaneous recovery. This loss of consciousness typically lasts seconds to minutes and is not followed by a persistent alteration in mental status.

• •

  Syncope is caused by a transient global cerebral hypoperfusion. It is the final common pathway for a wide variety of underlying causes, and requires a systematic approach to diagnosis.

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  Pre-syncope, or near-syncope, is defined as the sudden onset of a sense of impending or incomplete loss of consciousness.

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  Most syncopal episodes have benign causes, but serious underlying conditions are possible. The causes of syncope can be organized into the following three categories: (i) cardiac, (ii) reflex (includes vasovagal syncope), (iii) orthostatic.

• •

  National guidelines recommend a 12-lead electrocardiogram for all patients with syncope but most patients without serious underlying disease will have a normal or nondiagnostic electrocardiogram (ECG).

• •

  National guidelines do not recommend routine laboratory testing or imaging (e.g., chest x-ray, neuroimaging, echocardiogram) and these tests should be obtained only when history or physical examination suggests such evaluation.

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  Hospitalization or placement in an observation unit after emergency department (ED) evaluation for syncope is based on the specific, identified cause (e.g., gastrointestinal hemorrhage, malignant arrhythmia, pulmonary embolism).

• •

  Patients with a clear description of reflex syncope (e.g., vasovagal syncope) without serious underlying disease are generally appropriately discharged directly from the ED.

• •

  Several syncope clinical risk scores have been developed for ED use, but none have been definitively shown to outperform unaided clinical gestalt with respect to risk stratification and resource utilization.

The age distribution for syncope is bimodal, with a peak in early adulthood, around age 20 years, and a second peak in later adulthood, around and after age 60 years. Pre-syncope is a less common complaint than syncope for emergency department (ED) visits, perhaps because many patients with pre-syncope do not seek evaluation. Pre-syncope and syncope are associated with similar clinical outcomes at 30 days.

Syncope is defined as a transient, spontaneous loss of consciousness and postural tone with rapid, complete, and spontaneous recovery, caused by global cerebral hypoperfusion, generally from a drop in cardiac output or systemic blood pressure. Loss of consciousness typically lasts seconds to minutes and is not followed by a persistent alteration in mental status. (For a discussion of the approach to altered mental status, see Chapter 12 .) Approximately 8 to 10 seconds of hypoperfusion to both cerebral cortices and the brainstem reticular activating system will result in transient loss of consciousness and the inevitable loss of postural tone. Syncope is the final common pathway for a wide variety of underlying causes, (e.g., dehydration, hemorrhage, cardiac arrhythmia, structural heart disease) making for a broad differential diagnosis.

The causes of syncope can be organized into three broad categories:

• (i)

  Reflex

• (ii)

  Orthostatic

• (iii)

  Cardiac (see Box 11.1 ).

  BOX 11.1

  Cardiac Diagnoses Associated With Syncope

  • •

    Dysrhythmias: (See Box 11.2 for further detail)

    • •

      Tachydysrhythmias

    • •

      Bradydysrhythmias

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    Structural causes:

    • •

      Hypertrophic cardiomyopathy

    • •

      Aortic stenosis

    • •

      Severe pulmonic stenosis

    • •

      Acute myocardial infarction/ischemia

    • •

      Cardiac masses (e.g., atrial myxoma)

    • •

      Pericardial tamponade

    • •

      Prosthetic valve dysfunction

    • •

      Ventricular assist device (VAD) dysfunction

  • •

    Cardiopulmonary causes:

    • •

      Acute aortic dissection

    • •

      Pulmonary embolism

    • •

      Pulmonary hypertension

Reflex syncope , also known as neurally mediated syncope, is the most common cause of syncope, particularly among younger patients. It is caused by inappropriate vasodilation, bradycardia, or both, and includes vasovagal syncope, carotid sinus syndrome, and situational syncope. Vasovagal syncope is commonly encountered in the ED and is typically characterized by a prodrome of some combination of the following associated symptoms: nausea, pallor, diaphoresis, lightheadedness, warmth, chills, and blurred or darkening vision. Common triggers include intense fear, emotion, anxiety, or pain; being in a warm, crowded place; prolonged standing; or other noxious stimuli, such as when a layperson encounters a traumatized traffic accident victim. Vasovagal syncope is a clinical diagnosis based on history, physical examination, and eyewitness accounts, if available. Carotid sinus syndrome is caused by carotid sinus hypersensitivity, which is defined as a pause of ≥3 seconds and/or a ≥50 mm Hg decrease in systolic blood pressure upon stimulation of the carotid sinus. This entity is more common in older patients and in men. Situational syncope is defined by its close association with a specific action such as urination, defecation, recent or overeating, coughing, sneezing, swallowing, laughing, breath holding, or post-exercise. It can be preceded by the same prodromal symptoms as vasovagal syncope.

Orthostatic syncope , also known as postural hypotension, is defined by a decrease in blood pressure of at least 20 mm Hg systolic, and at least 10 mm Hg diastolic within 3 minutes of standing. This condition is associated with dehydration, blood loss, adverse medication effects, autonomic dysfunction, alcohol consumption, and older age. Syncope or pre-syncope will occur when the autonomic response is insufficient to counteract the drop in blood pressure associated with postural change. Measuring orthostatic vital signs in the ED setting is not generally useful since they do not appear to independently predict 30-day serious outcomes, nor do they reliably diagnose or exclude orthostatic syncope, unless the vital sign changes upon standing reproduce the symptoms with which the patient presented.

Cardiac syncope is divided into three general categories: Dysrhythmic, structural, and cardiopulmonary (see Box 11.1 ). This is the most serious form of syncope and must be distinguished from reflex or orthostatic syncope, when feasible. Cardiac dysrhythmias most often occur in patients with underlying structural heart disease, a prior diagnosis of a dysrhythmia syndrome, or a recent or acute myocardial infarction. Several dysrhythmias can lead to syncope or pre-syncope, including both brady- and tachydysrhythmias (see Box 11.2A ). The symptoms caused by a given dysrhythmia will vary depending on the severity of the disruption of cardiac output and the patient’s cardiovascular reserve. Patients with underlying heart disease, such as coronary artery disease (CAD), valvular disease, congenital heart disease, cardiomyopathy, or cardiac channelopathy (e.g., Brugada syndrome, long QT syndrome), are at higher risk for dysrhythmias. Various ECG findings are suggestive of such underlying heart disease (see Box 11.2B ). Dysrhythmic syncope classically presents without a prodrome, although patients with tachydysrhythmias may report palpitations or chest discomfort prior to losing consciousness.

Structural heart disease has a significant morbidity and mortality without intervention, and also predisposes patients to serious dysrhythmia, making early diagnosis key to maximizing good outcomes. Structural causes of syncope include valvular disease (e.g., aortic stenosis), hypertrophic cardiomyopathy, pericardial tamponade, and atrial myxoma, among others (see Box 11.1 ).

Cardiopulmonary causes of syncope include conditions such as pulmonary embolism (PE), pulmonary hypertension, acute myocardial infarction (MI), and acute aortic dissection. Syncope is only a part of their presentation, and patients will have associated signs and symptoms of these conditions. Generally healthy patients with typical syncope and no findings suggestive of cardiopulmonary causes should not undergo specific testing, such as d-dimer assay or CT angiography. Routine testing of all ED syncope patients for PE, for example, with a d-dimer assay or CT pulmonary angiogram, is not indicated, and would lead to significant over-testing due to the low prevalence of this disease in this cohort.

Cerebrovascular conditions associated with loss of consciousness should be considered, however, these will typically present with other cardinal signs and symptoms, and would generally not meet the strict definition of syncope. For example, a spontaneous subarachnoid hemorrhage (SAH) or basilar artery migraine could present with syncope but would generally be preceded and accompanied by an acute headache, vertigo, or alteration in mental status. Acute stroke or transient ischemia attack does not cause syncope because it does not produce global hypoperfusion.

Syncope mimics are any of several conditions encountered in the ED that can mimic syncope, such as mechanical fall, intoxication, hypoglycemia, head trauma, and seizures (see Box 11.3 ). Differentiating these conditions from true syncope can be challenging, particularly without collateral history from witnesses. Seizures can be confused with syncope partly due to the fact that convulsions and incontinence, although classically associated with seizure, can also be seen with syncope as well. Rhythmic motor activity in the setting of syncope is often referred to as “convulsive syncope” and is usually brief (under 20 seconds). Unlike epileptic seizure, the motor activity and loss of consciousness of syncope are not associated with any post-ictal state.

Taking a careful history is key to determining the etiology of the syncopal episode. In particular, the setting (e.g., bathroom after voiding, restaurant after a large meal, blood draw, crowded place), body position (e.g., seated, prone, standing, changing position), and context (e.g., exertion, emotional event, painful stimulus, fasting state) should be established. Age, current medications, personal history of prior syncope, family history, and past medical history are important, as with any cardiopulmonary compliant. The risk of adverse events increases gradually with age, and is low under age 45 years. A careful medication history can also lead to a diagnosis of drug-related orthostatic hypotension (see Box 11.4 ). Any family history of sudden cardiac death, recurrent syncope, significant dysrhythmia, or early CAD should raise concern for cardiac syncope. Many comorbidities can place a patient at higher risk for adverse events, particularly a history of heart failure, CAD, dysrhythmia, or structural heart disease. Risk factors for PE should also be explored.

These clinical variables, along with associated signs or symptoms (see the following sections) can inform the pretest probability of cardiac, orthostatic, situational, or vasovagal syncope. For example, syncope occurring after quickly rising from supine to a standing position may indicate orthostatic hypotension. Syncope occurring during a blood draw likely represents a vasovagal episode. Syncope during or immediately after urination (micturition syncope), defecation (defecation syncope), eating a large meal (post-prandial syncope), coughing or swallowing may indicate a situational syncope. Syncope during exercise may prompt concern for cardiac outflow obstruction such as hypertrophic cardiomyopathy or aortic stenosis or inability to increase cardiac rate in response to exercise (e.g., heart block).

Any prior episodes and relevant previous testing (e.g., recent echocardiography, stress test) should be explored in an attempt to reduce low-value repeat testing. The clinical approach to pre-syncope is the same as for syncope—pre-syncope exists on a continuum with syncope, with similar rates of adverse events. Thorough ED evaluation fails to identify the etiology of syncope/pre-syncope roughly 50% of the time.

Symptoms

Several symptoms should be explored during the history-taking process including chest pain, dyspnea, palpitations, abdominal or back pain, vaginal bleeding, headache, and any associated neurologic symptoms. Chest pain could suggest a diagnosis of acute coronary syndrome with dysrhythmia, PE, or aortic dissection, while dyspnea could suggest PE or underlying heart failure. Palpitations may suggest a dysrhythmia. Abdominal or back pain could suggest a rupturing aortic aneurysm. Vaginal bleeding suggests possible ectopic pregnancy; severe headache may indicate SAH. Prodromal symptoms such as lightheadedness, warmth, nausea or vomiting, and pallor help make the diagnosis of vasovagal syncope.

Other symptoms may suggest the presence of a syncope mimic. A preceding aura or prolonged confusion/somnolence could indicate a seizure with a post-ictal state. Convulsions can occur with either syncope or seizure, but epileptic convulsions generally last longer (>20 myoclonic jerks). A mechanical fall leading to blunt head trauma and loss of consciousness could represent a mild traumatic brain injury, and not syncope, although differentiating between the two can be difficult in practice, especially in older patients with cognitive deficits or in those whose head trauma induces retrograde amnesia.

Signs

The physical examination, which usually is normal, is generally not helpful in the evaluation of syncope. Hypotension may indicate volume loss from dehydration or hemorrhage. Otherwise, unexplained tachypnea, tachycardia, or hypoxia should prompt consideration of PE. Orthostatic blood pressure measurement is not helpful unless the patient’s symptoms are reproduced in synchrony with the fall in blood pressure. Orthostatic hypotension has a sensitivity for hypovolemia of only approximately 70%.

The cardiovascular examination may reveal cardiac murmurs indicative of structural heart disease (e.g., aortic stenosis) or reveal signs of new-onset heart failure (e.g., elevated jugular pressure, bilateral lower extremity edema, third heart sound, rales or wheezes on lung auscultation). A pulse deficit, in the correct context, may raise suspicion for aortic dissection. We do not recommend performing diagnostic carotid sinus massage in the ED due to the lack of high-quality evidence supporting its diagnostic utility in this setting. Carotid sinus massage (CSM) may be considered as part of an inpatient or observation unit evaluation of older patients (>40 years) with syncope associated with abrupt neck movement or neck pressure, and no identified underlying cause on detailed evaluation.

A neurologic examination, including a cognitive assessment, should be performed, and based on the definition of syncope, the patient should be neurologically at their baseline. Any sign of a new neurologic deficit should prompt consideration of an acute neurologic condition.

Examination of the head, neck, and extremities should be done to assess for signs of trauma, since syncope is often associated with fall. Rectal examination for gross blood or melena is recommended if gastrointestinal hemorrhage is suspected and the patient is not able to report recent stool characteristics.

Electrocardiogram

The 12-lead ECG is the most commonly ordered test in the ED evaluation of syncope. Although it is rarely diagnostic, this test is safe, noninvasive, and relatively inexpensive. We recommend a 12-lead ECG in all cases of syncope except in otherwise healthy patients under age 40 with no significant conditions identified by careful history or physical examination, and with a history clearly consistent with vasovagal syncope. If there is uncertainty, we recommend obtaining a 12-lead ECG to evaluate for underlying conduction disturbance or occult myocardial injury. Dysrhythmias, preexcitation, and a shortened PR or prolonged corrected QT interval may be identified on the 12-lead ECG. Certain ECG abnormalities are considered highly likely to be casually related to the syncope, such as sinus bradycardia less than 40 beats/min or sinus pauses greater than 3 seconds, third-degree (complete) heart block, Mobitz II second-degree AV block, and others (see Box 11.2A ). Other ECG abnormalities may raise concern for other serious underlying conditions (see Box 11.2B ). For example, a pseudo-right bundle branch block in association with ST elevation in leads V ₁ through V ₃ suggests Brugada syndrome. Acute myocardial ischemia or cardiac hypertrophy may be revealed. An ECG showing a right ventricular strain pattern may suggest PE, whereas diffuse ST-elevation can help diagnose pericarditis, which may be accompanied by myocarditis. In patients over 40 years of age without a clear causative finding for syncope , continuous cardiac monitoring in the ED for 4 to 6 hours, both at rest and during light exertion, may be helpful in identifying dysrhythmias not evident on the initial ECG .

BOX 11.2A

Dysrhythmias Potentially Associated With Syncope

• •

  Atrioventricular (AV) Block

  • •

    Mobitz type II second degree

  • •

    Third degree (complete heart block)

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  Sinus pause >3 s

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  Sick sinus syndrome

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  Persistent sinus bradycardia (<40 beats/min)

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  Ventricular tachyarrhythmias

  • •

    Monomorphic ventricular tachycardia

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    Polymorphic ventricular tachycardia (i.e., Torsades de pointes)

  • •

    Ventricular fibrillation

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  Supraventricular tachyarrhythmias

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    Atrial flutter/fibrillation

  • •

    AV nodal reentry tachycardia

  • •

    AV reentry tachycardia

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  Alternating left and right bundle branch block

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  Pacemaker or automatic implantable cardioverter-defibrillator malfunction with cardiac pauses

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