Syncope is defined as a transient loss of consciousness. Pathophysiologically, syncope is due to a temporary loss of cerebral blood flow. The evaluation of syncope begins with a careful history and physical examination the first step in evaluating patients. Determining the etiology of syncope is critical to proper diagnosis and treatment, although it should be noted that in about 40% of cases, the precise cause of syncope is never found.2 The patient's age can provide an immediate clue.3 In children and young adults, syncope is usually neurally mediated. However, this is the most frequently encountered form of syncope in patients of all ages. This loss of consciousness is the result of a cardioinhibitory and/or vasodepressor phenomenon in which postural tone and/or heart rate drops abruptly, leading to diminished cerebral perfusion and syncope. Psychiatric causes and primary arrhythmias such as the congenital Long QT (LQTS) and Wolff-Parkinson White (WPW) syndromes are the next most common etiologies of syncope in pediatric patients. In middle-aged adults, neurocardiogenic syncope is by far the most frequent etiology and may be brought out by micturition, defecation, or cough. In the elderly, underlying heart disease is the most frequent basis for syncope, which can result from brady- or tachyarrhythmias, aortic stenosis, or even pulmonary embolus. A careful history and physical examination can also unearth other critical clues. Any history of cardiovascular disease for instance, prior myocardial infarction must be an immediate alert to the risk of life-threatening ventricular arrhythmias. In contrast, a history of syncope with head turning often seen in the elderly suggests carotid sinus hypersensitivity, an important but less grave mechanism of syncope. The potential role of medications in causing syncope can also be brought out by the history. Key features of the physical examination that can be informative include the resting pulse and blood pressure (and associated orthostatic changes, which may suggest dehydration), the presence of carotid bruits, evidence of left ventricular dysfunction (e.g., heart failure), and neurological deficits (which may suggest seizures). The next critical component of the workup of syncope is the electrocardiogram (ECG), which should be obtained in all patients. The ECG can reveal evidence of cardiac conduction system disease, such as sinus node dysfunction or atrioventricular block. A short PR interval and delta wave are ECG hallmarks of pre-excitation due to WPW. The ECG can also diagnose the LQT and Brugada syndromes, which can result in syncope and sudden death. Non-sustained ventricular tachycardia or frequent premature ventricular contractions can also be caught on an ECG and may be a marker for arrhythmic, life-threatening arrhythmias, particularly in the presence of left ventricular dysfunction. Evaluation of structural heart disease and ischemia is also important. Echocardiography to assess the presence of structural heart disease, such as left ventricular dysfunction, hypertrophic cardiomyopathy, and valvular disease, for example, can be useful in appropriate patients. Identifying cardiac ischemia by stress testing or cardiac catheterization, for instance and intervening as needed are appropriate. At this point, patients with syncope who are at risk for life-threatening arrhythmias should have been identified. Patients with important structural heart disease are frequently treated with an implantable cardioverter defibrillator (ICD). Syncope in the remaining category of patients those without underlying cardiovascular disease is not directly associated with increased mortality.1 Management of these patients should be directed toward improving quality of life and minimizing the risk of physical injury from recurrent syncope. Evaluation of this lower risk group of patients can be aided by several diagnostic tools. The ultimate objective here is to document the cardiac rhythm that precisely correlates with the syncopal event. This is often a difficult task. Ambulatory ECG monitoring can be useful. A 24- to 48-hour Holter recording is appropriate for patients with frequent episodes of syncope, but longer monitoring is necessary for infrequent episodes. Implantable loop recorders can be used for arrhythmia surveillance for up to 14 months. Tilt table testing is another diagnostic method that can assist in diagnosing neurally mediated syncope. Controversy exists on the value of tilt table testing because of its variable sensitivity, reproducibility, and diagnostic yield.4 Indeed, it should be remembered that patients with syncope who lack structural heart disease and ECG abnormalities are highly likely to have neurally mediated syncope, irrespective of the results of a tilt table test. Diagnostic electrophysiology study (EPS) is a method of assessing cardiac conduction invasively by placement of intracardiac catheters to measure conduction intervals and perform programmed cardiac stimulation. Again, in patients with normal hearts, the yield of an EPS is low, both in uncovering pathologic bradyarrhythmias or tachyarrhythmias.5,6 EPS can be particularly useful, though, in cases of recurrent unexplained syncope with associated injury for example, syncope that occurs while the patient is driving, resulting in an accident. EPS also can be very helpful in making the diagnosis of ventricular tachyarrhythmia in patients with coronary artery disease who have syncope, left ventricular dysfunction (ejection fractions ? 35%), and who recently underwent an ischemic workup/intervention.1 A schematized flowchart for working up syncope adapted from the ACC/AHA Scientific Statement on the Evaluation of Syncope1 is shown in Figure 1. Management of patients with syncope must be directed at the underlying cause. Hospital admission is generally necessary for potentially life-threatening cases, such as syncope in the setting of structural heart disease. For patients with syncope caused by ventricular tachyarrhythmias in the absence of a reversible cause (e.g., acute myocardial infarction), ICD implantation is indicated as it confers significant survival benefit.7 In patients with ischemic or non-ischemic cardiomyopathy with severe left ventricular dysfunction (i.e., EF ? 35%), ICD therapy is indicated as primary prevention (even in the absence of any documented arrhythmia or syncope) as it has been shown to save lives.8,9 ICD therapy is also indicated in patients with syncope in the setting of hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, LQTS, and Brugada syndrome.10,13 Management of neurally mediated syncope is based on improving patient quality of life and reducing the risk of physical injury. Treatment options include patient training (e.g., avoiding syncopal triggers, tilt training), volume expansion (with salt and fluid supplementation), pharmacologic agents such as vasoconstrictors (e.g., midodrine, paroxetine). In patients with very symptomatic and recurrent syncope in whom evidence of a cardioinhibitory response is found on tilt table testing, permanent pacing may be an effective therapy, but definitive recommendations on use of this therapy await further investigation.2 Syncope is a frequently encountered clinical problem and may indicate potentially lethal pathology. All patients presenting with syncope should undergo a careful evaluation to distinguish those who are at high risk (e.g., with structural heart disease) from those who are not. Subsequent management is based on providing life-saving intervention for high-risk patients and symptom management for those at lower risk.