Syncope and Related Paroxysmal Spells

Etiology

The etiology of syncope varies greatly. Benign causes include dehydration and vasovagal, known as neurocardiogenic syncope. Vasovagal syncope is the predominant cause of syncope worldwide, particularly in young patients. More worrisome etiologies of syncope include dysrhythmias, cardiac conduction disease, valvular heart disease, congenital heart disease (such as Brugada, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, and long QT syndrome), acute anemia or gastrointestinal bleed, and pulmonary embolism. All of these etiologies result in the hypoperfusion of the brain and require evaluation in the emergency department.[6][7]

Epidemiology

The prevalence of syncope is approximately 20% in the general population. The risk of recurrence is approximately 13.5%. Females have a greater prevalence than men. In retrospective studies, the etiology of syncope is undetermined in 37% of cases. Most cases of syncope, especially in young patients, are reflex-mediated neurocardiogenic and benign.[8]

Pathophysiology

The pathophysiology of syncope varies by its etiology. In benign syncope, as vasovagal syncope, the vagus nerve is often over-stimulated, thus causing a transient loss of consciousness. The most common causes are classically due to fear, excitement, or temperature intolerances.

The other etiologies, listed above, require a careful history, physical, and evaluation, as the etiology is most-often cardiac and may be a predictor of a dangerous, life-threatening pathology.

History and Physical

A history and a physical exam are the most important aspects of the workup for syncope. In fact, health care costs and time can be substantially reduced with a proper history. Multiple decision support guidelines have been developed and compared. The Boston Syncope Pathway has a negative predictive value approaching 100%. Specifically, a history should include evaluation of prodrome, including chest pain, obtaining a tailored personal and family history of cardiac disease and cardiac death, and a thorough physical exam, including auscultation for a murmur.

Evaluation

Evaluation of syncope should focus on risk stratifying between low-risk and high-risk syncope. As noted, a complete history and physical exam will help assist with risk stratification. New medications, such as beta-blockers, nitrates, diuretics, and antiarrhythmics, should be carefully considered as possible contributors. A family history of sudden cardiac death is a dangerous predictor of adverse outcome.[9][10][11]

Benign or low-risk characteristics include age younger than 40, syncope after standing from a sitting position, warmth, nausea, cough, or micturition before syncope, and an individualized trigger for syncope (such as pain or emotional distress). In children, these triggers are known as psychogenic. A history of recurring syncope in a young patient in the setting of these benign events indicates a low-risk factor. Dehydration is a common cause of syncope in young patients, and orthostatic evaluation can be considered as part of the workup. Rarely, a cerebrovascular accident, such as an intracranial bleed, can cause a reflex-mediated syncope. Features that indicate high-risk include exertional syncope, chest pain, history of congestive heart failure, aortic stenosis, left ventricular outflow tract disease, dilated cardiomyopathy, coronary artery disease, congenital heart disease, past myocardial infarction, and implantable cardioverter-defibrillator placement. Of note, recurrence of syncope multiple times in 6 months should warrant further evaluation, regardless of age.

Vital sign abnormalities, such as hypotension, may indicate an acute bleed. In older patients and menstruating females, an exam looking for pallor or gastrointestinal bleed should be considered as this can lead to cerebral hypoperfusion, causing syncope. Hemoglobin or hematocrit is indicated in such patients. Other vital sign abnormalities, such as bradycardia, may indicate arteriovenous (AV) dissociation. Hypoxia can indicate a pulmonary embolism. Physical exam findings of a new murmur can indicate dangerous valvular pathologies, such as aortic stenosis or mitral regurgitation.

All patients should receive a screening electrocardiogram (ECG). ECG features, such as a new left bundle branch block, Brugada pattern, arrhythmogenic RV dysplasia, prolonged QTc, and hypertrophic cardiomyopathy patterns, suggest high risk and indicate a need for further workup. Similarly, sinus bradycardia, dysrhythmias, and second or third-degree AV blocks should all warrant further workup.

Treatment / Management

Patients with low-risk syncope, as evaluated by history, physical, and screening ECG, can be discharged home. Without any high-risk features, the likely cause of the syncope is benign; vasovagal and dehydration are the most common. Orthostatic in young patients often delineate between vasovagal and dehydration. Patients can be rehydrated and discharged if symptoms resolve. If the young patient has recurrent syncope without high-risk features, a non-emergent echocardiogram can be scheduled for the patient as an outpatient. Management may include beta-blocker, compression stockings, or fludrocortisone.[12][13][14][15](B2)

Patients with high-risk syncope require further observation or workup. Specifically, studies have been conducted to investigate the utility of observation units in the emergency department for patients with syncope as a means to decrease health care expenditures. These studies have shown similar outcomes, adverse events, and a reduction in costs when compared to inpatient hospitalizations.

Testing done in observation units or as inpatient should be tailored to the patient’s syncopal evaluation and etiology. If there are signs and symptoms of acute coronary syndrome, such as chest pain or ECG ischemic changes, serial troponins should be done. Exercise stress testing may also be useful.

Patients with a worrisome cardiac history, such as significant coronary artery disease, congestive heart failure, or hypertrophic cardiomyopathy, are at high-risk for structural abnormalities and arrhythmia. These patients should have an echocardiogram to evaluate for worsening structural abnormalities that would decrease left ventricular outflow.  The treatment may include an implantable cardioverter defibrillator (IDC). Patients with a history of ventricular dysrhythmias are at high risk for recurrence. Recurrence of syncope in six months may also indicate a dysrhythmia. Patients with an ICD or pacemaker already in place should have their device interrogated to determine further if a dysrhythmia occurred.

All patients with worrisome cardiac history should have 24-hour telemetry observation and evaluation for ICD placement. Patients with conduction disease on ECG, a new murmur on physical exam, or a concerning family history of sudden cardiac death should be evaluated for structural and valvular disorders with an echocardiogram, telemetry, and home telemetry. Often, these patients may require a pacemaker or ICD.

All patients with anemia as the cause of hypovolemia should have a complete blood count (CBC), type and screen, and evaluation for the etiology of the bleed.

Patients with concern for acute intracranial bleed as the cause of syncope should have a CT of their head and likely neurosurgical consultation.

Finally, patients with hypoxia should undergo a workup for pulmonary embolism.

Differential Diagnosis

• Acute aortic dissection

• Acute hypoglycemia

• Adrenal crisis in emergency medicine

• Antidepressant toxicity

• Aortic stenosis imaging

• Asystole

• Atrial fibrillation

• Beta-blocker toxicity

• Brugada syndrome

• Cocaine toxicity