Glenn N. Levine, MD, FACC, FAHA

1. What is the word syncope derived from?

    According to text in the European Society of Cardiology (ESC) Guidelines on the Management of Syncope, the word syncope is derived from the Greek words syn, meaning “with,” and the verb kopto, meaning “I cut” or “I interrupt.”

2. What is the underlying mechanism causing syncope?

    Transient global cerebral hypoperfusion. Note that other conditions that do not cause transient global cerebral hypoperfusion can cause a transient loss of consciousness, and some experts believe these conditions should be referred to as transient loss of consciousness instead of syncope.

3. Cessation of cerebral blood flow of what duration causes syncope?

    Cessation of cerebral blood flow for as short a period as 6 to 8 seconds can precipitate syncope.

4. What is the most common cause of syncope in the general population?

    Neurocardiogenic syncope is the most common cause of syncope in the general population. This is also variably referred to in the literature as vasovagal syncope, neurally mediated syncope, and vasodepressor syncope.

5. What are the most common causes of syncope in pediatric and young patients?

    According to the scientific statement on syncope from the 2006 American Heart Association/American College of Cardiology Foundation (AHA/ACCF), the most common causes of syncope in pediatric and young patients are neurocardiogenic syncope, conversion reactions (psychiatric causes), and primary arrhythmic causes (e.g., long QT syndrome, Wolff-Parkinson-White syndrome). In contrast, elderly patients have a higher frequency of syncope caused by obstructions to cardiac output (e.g., aortic stenosis, pulmonary embolism) and by arrhythmias resulting from underlying heart disease.

6. What is the most common cause of sudden cardiac death in young athletes?

    Hypertrophic cardiomyopathy, followed by anomalous origin of a coronary artery. Other causes of sudden cardiac death in younger persons, in general, include long QT syndrome, Brugada syndrome, and arrhythmogenic right ventricular dysplasia (ARVD), as well as pulmonary embolism.

7. What are the common causes of syncope?

Box 60-1 lists the causes of syncope and loss of consciousness.

8. What are the important causes of ventricular tachyarrhythmias (VTs)?

9. What is the approach to the patient with syncope?

    The goals of the evaluation of patients with syncope are not only to identify the cause of syncope but also to determine if the cause is cardiac or noncardiac. Noncardiac causes of syncope generally have a relatively benign course (overall 1-year mortality rates of 0% to 12% and an approximately 0% mortality rate with neurally mediated syncope). Unexplained and undiagnosed causes have an intermediate 1-year mortality rate of 5% to 6%. Cardiac causes, in contrast, are associated with 1-year mortality risk of 18.5% to 33%. Thus, there is a premium on excluding a cardiac cause of syncope, even if the exact cause of syncope cannot be determined.

    A detailed history and physical examination, along with electrocardiogram (ECG) examination, can identify the presumptive cause of syncope in 40% to 50% of cases. Premonitory symptoms such as nausea or diaphoresis, especially in a younger person, or symptoms caused by anxiety, pain, or emotional distress, suggest neurocardiogenic syncope. Syncope during or immediately after urination, defecation, or certain other activities suggests situational syncope. Recent initiation of certain blood pressure–lowering medications, particularly α-adrenoceptor blockers (such as those used to treat benign prostatic hypertrophy), raise suspicion for orthostatic hypotension, which can be confirmed on examination. A history of prior MI or depressed EF raises the concern for VT. Cardiac systolic murmurs suggest aortic stenosis or HCM. Table 60-1 gives the factors on history, physical examination, and ECG that may suggest a specific cause for the patient’s syncope.

10. How does one properly test for orthostatic hypotension?

    Recommendations vary, but according to the ESC Guidelines on the Management of Syncope, one first has the patient lie supine for 5 minutes. Blood pressure is then measured 3 minutes after the patient stands, with subsequent blood pressure measurements each minute thereafter if the blood pressure falls and continues to fall compared with supine values. Orthostatic hypotension is defined as a 20 mm Hg or greater drop in systolic blood pressure or systolic blood pressure falling to less than 90 mm Hg. Some other experts also consider falls of diastolic blood pressure of 10 mm Hg or more or increases in heart rate of 20 beats/min or more as criteria to diagnose orthostatic hypotension.

11. What other testing can be performed when the cause of syncope remains unclear?

    When the diagnosis is still not clear, echocardiography can be obtained, looking for unsuspected depressed LV ejection fraction or right ventricular dysfunction, HCM (which may predispose to VT), or obstructive heart disease (aortic stenosis, HCM, rare left atrial myxoma). Note that although echocardiography has become part of the shotgun evaluation of syncope for many practitioners, and is recommended as a diagnostic test to consider by both the AHA/ACCF and the ESC, its yield in patients with unremarkable cardiac histories, physical examination, and ECGs is low. In cases in which neurocardiogenic syncope is suspected and further testing is desired, a tilt table test can be obtained. Exercise stress testing has been suggested by some to assess for cardiac ischemia or exercise-induced arrhythmias in appropriately selected patients. In patients in whom a bradyarrhythmia or tachyarrhythmia is suspected, a Holter monitor, event monitor, or implantable loop recorder can be considered or, under certain circumstances, electrophysiologic testing can be performed.

12. During carotid sinus massage, what is considered a diagnostic response?

    According to the ESC Guidelines on Management of Syncope, a ventricular pause lasting 3 seconds or longer, or a fall in systolic blood pressure of 50 mm Hg or more, is considered abnormal and defines carotid sinus hypersensitivity. Note that carotid sinus massage should not be performed in patients with a recent transient ischemic attack (TIA) or stroke, or those with carotid bruits.

13. What is a tilt table test?

    Tilt table testing is most commonly performed on patients with neurally mediated syncope (e.g., neurocardiogenic syncope). The patient first lies supine on a board with a foot support. The table is then rotated to a tilt angle of 60 to 80 degrees, so that the patient is almost in the standing position. This maneuver leads to venous pooling and later loss of plasma volume as a result of movement into interstitial spaces. Overall, there is an approximate 15% to 20% (700 mL) decrease of plasma volume. The normal neuroregulatory mechanisms of the body will usually compensate for this, maintaining blood pressure. Vasovagal reactions can occur during monitoring, leading to decrease in heart rate and blood pressure. In a typical protocol, the patient is tilted for 30 minutes, and if no loss of consciousness has occurred, isoproterenol infusion is started and the patient retilted. Other protocols may administer different provocative agents, such as nitroglycerin or adenosine. Criteria have been established to classify the patient responses as cardioinhibitory, vasodepressor, or mixed, based on falls in heart rate, blood pressure, and the occurrence of syncope.

14. How should one decide between ordering a Holter monitor, an event or ambulatory monitor, or an implantable loop monitor?

    A Holter monitor, which is usually worn for 24 to 48 hours, is useful if the patient experiences syncope or presyncope at least once a day. An event or ambulatory monitor, which most commonly is ordered for approximately 4 weeks, is useful if the patient experiences symptoms at least once or several times a month. An implantable loop monitor is reasonable to consider in a patient with occasional symptoms that occur less than once per month.

15. Should a shotgun neurologic evaluation, including computed tomography (CT) scan, carotid ultrasound, and electroencephalogram, be ordered in all patients with syncope?

    No. True syncope (or loss of consciousness) is an unusual manifestation of neurologic syncope (excluding causes such as reflex, situational, or neurocardiogenic syncope and dysautonomia). In one report, electroencephalogram provided diagnostic information in less than 2% of cases of syncope, and almost all those patients had a history of seizures or symptoms suggesting seizure. Neurologic workup should only be undertaken if a neurologic cause is suggested by the history or physical examination. TIAs usually do not cause syncope. Carotid disease and stroke more likely lead to focal neurologic deficits than to global neurologic ischemia and syncope (the rare exception being severe bilateral carotid artery disease). Severe bilateral vertebrobasilar disease can cause syncope, but is not easily diagnosed by screening studies. Importantly, cerebral hypoperfusion caused by ventricular tachycardia can result in seizure-like activity, and the report by family members or other witnesses of the event of “seizure-like” activity in the patient should not cause one to be misled toward a search for neurologic causes based on this alone.

16. What is long QT syndrome?

    Long QT syndrome is characterized by a corrected QT interval (QTc) of greater than 450 ms (Fig. 60-1). The QT interval is prolonged because of delayed repolarization as a result of a genetic defect in either potassium or sodium channels. Syncope in patients in long QT syndrome likely is due to torsade des pointes. The onset of symptoms most commonly occurs during the first two decades of life. The risk of developing syncope or sudden cardiac death increases with QTc, with lifetime risks of approximately 5% in those with QTc less than 440 ms, but 50% in those with QTc more than 500 ms. Patients with long QT syndrome should be referred to electrophysiologists for further evaluation and treatment, which may include medicines or placement of an implantable cardioverter defibrillator (ICD).

17. What is Brugada syndrome?

    Brugada syndrome is a disorder of sodium channels, resulting in sometimes intermittent unusual ST segment elevation in leads V1 through V3, as well as a right bundle branch block–like pattern (Fig. 60-2). Such patients are susceptible to developing polymorphic VT. Patients with suspected Brugada syndrome should be referred for specialized cardiac evaluation and a probable placement of an ICD.

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