Syncope consists of a sudden loss of consciousness leading to an inability to preserve postural tonus. The episode is self-limited. Cardiogenic syncope may arise in a wide variety of heart conditions and may predict an ulterior catastrophic event in some cases.
An individual that has experienced a cardiogenic syncope may describe the presence of an aura prior to the event, consisting of dizziness, amaurosis, diaphoresis, nausea or blurred vision. The duration of the aura is different in various cases, depending on the mechanism of the disease. If the substrate is arrhythmic, the aura lasts for about 3 seconds, whereas in vasovagal episodes its duration may be as long as 2.5 minutes. This period is followed by a complete, short duration loss of consciousness. Convulsions, myoclonic jerks or tonic spasms caused by brain hypoperfusion  may occur during the episode. Urine and fecal matter loss, confusion and oral trauma suggest epilepsy, whereas dysarthria and focal neurologic signs imply cerebrovascular disease. The recovery after a cardiogenic syncope is usually complete and spontaneous.
A careful history inquiry is a key tool in evaluating a syncope patient . It should always be combined with clinical examination and a 12 lead electrocardiogram (class A recommendations ). The victim should be asked about the position of the body before symptoms set in  , the activity he or she was involved in and other precipitating factors. Anamnesis should determine if the person has a history of myocardial infarction, structural heart disease, arrhythmia, channelopathy or cardiomyopathy. Prior medication (diuretics, beta blockers, vasodilators, nitrates, antiarrhythmic, tricyclic antidepressants) is always important to know.
The physical evaluation must highlight the vital signs and heart auscultation. Tachycardia is suggestive for an acute cardiovascular event, such as a myocardial infarction, pulmonary embolism or signifies an ongoing tachyarrhythmia. An acute coronary syndrome may also be accompanied by bradycardia, especially if a cardiac conduction defect is present. Murmurs also point to a cardiac cause of the syncope but do not warrant it. Cardiovascular evaluation should be completed by assessment of the jugular veins, auscultation of lung rales, palpation of the liver and possible abdominal masses signifying abdominal aneurysms and evaluation of peripheral edema.
A Schellong test is a useful maneuver, indicating orthostatic hypotension if positive. A carotid sinus massage should only be performed by an experienced physician since it can induce prolonged cardiac pauses or severe bradycardia. The maneuver is to be avoided if carotid bruits are present.
Multiple recurrences during a short period of time require immediate cause diagnosis and therapeutic intervention.
Blood workup is nonspecific in this disease, but certain tests may show predisposing factors for a cardiogenic syncope: abnormal electrolytes levels, heart enzymes or B-type natriuretic peptide . An echocardiography is indicated when mechanical cardiac causes are suspected, whereas an electrocardiogram is useful in all cardiogenic syncope patients. A normal aspect implies good prognosis, but clinical judgment may still dictate the need for Holter monitoring or loop event recording . The standard electrocardiogram may show atrioventricular blocks of various degrees , Brugada syndrome, Wolff-Parkinson-White syndrome or acute ischemia. Sinus pauses, sustained and nonsustained ventricular tachycardia episodes may also be substrates for a cardiogenic syncope. A positive tilt table test indicates a vasodepressor mechanism.