What is syncope and what causes it?
Syncope is a transient loss of consciousness, followed by spontaneous recovery without specific resuscitative measures. This is caused by a sudden and global drop in blood flow to the brain stem. It is a common clinical problem, often disabling, costly and sometimes the only warning before sudden death. The prognosis often depends on the diagnosis. Syncope can account for 1 percent of hospital admissions and 3 percent of emergency room visits with an annual cost estimated to be $800 million.
Causes of syncope can be divided into six categories:

• Vascular – hypovolemia or neurocardiogenic
• Cardiac – anatomic or arrhythmic
• Neurologic – seizure
• Metabolic – drugs
• Psychogenic – panic disorder
• Unknown origin.

Etiologies vary among different age groups with neurocardiogenic (vasovagal) being the most common among the general population. Young patients are likely to have neurocardiogenic syncope, followed by primary arrhythmias like Long QT Syndrome. In the middle age or elderly, neurocardiogenic syncope may also occur, but triggered by deglutition, micturition, defecation or cough. Orthostatic hypotension due to autonomic dysfunction or medications should be evaluated. Cardiovascular causes include outlet obstructions, such as aortic stenosis or pulmonary embolism. Arrhythmias are related to underlying structural heart disease, such as previous myocardial infarction or cardiomyopathy, but may also include supraventricular tachycardias and bradyarrhythmias.

Where do we begin? Or Risk stratification
The main reason to evaluate patients with syncope is to determine whether the patient is at increased risk of sudden death, especially those with underlying heart disease. In most patients, the reasons for the syncope can be determined from a meticulous history and physical exam including assessment of medications, especially anti-arrhythmic agents and anti-hypertensives (diuretics). Non – specific seizure-like activity can be seen both with neurologic and cardiac etiologies. Neurocardiogenic syncope is often followed by fatigue, weakness and nausea. The absence of prodromal symptoms is suggestive of a cardiac arrhythmia. The physical exam is used to evaluate for orthostasis, carotid bruits, or structural heart disease. An echocardiogram and stress test help to rapidly subdivide the high risk from the low risk individual. The EKG can be a useful adjunct in evaluating bradyarrhythmias, structural heart disease, or sources of supraventricular or ventricular tachycardias. Mortality in those with structural heart disease and syncope is extraordinarily high, approaching 50 percent at five years if untreated. I call this “Cardiac Cancer”, a high risk, and a high profile scenario where appropriate intervention can save lives. Those who have known heart disease, risk factors, or symptoms of angina or congestive heart failure would merit at least an expedited, if not an inpatient workup. Many studies have documented a low cardiovascular mortality in those without intrinsic cardiac abnormalities, such as neurocardiogenic syncope.

Which patients require EP studies?
This study is a direct assessment of the patient’s conduction system and screens for inducible arrhythmias. It can pinpoint numerous treatable abnormalities which cause loss of consciousness. These range from abnormalities of impulse formation or conduction, which cause bradycardia, to inducible arrhythmias. EP testing, though invasive, is done via venous access, uses no dye, and is very low risk even in very high risk patients. After assessing for ischemia and LV function, it is an early tool in the evaluation of syncope for those with cardiac disease. The mortality from outpatient cardiac arrest is in the 95% range, therefore identification of these individuals before this happens is critical.

What is the role of Tilt Table testing in the evaluation of syncope?
A tilt table test is a helpful aid in the evaluation of recurrent neurocardiogenic syncope. The head up tilt promotes accumulation of the majority of the blood volume in the leg veins, mimicking hypovolemia. The decrease in venous return activates the sympathetic nervous system in an effort to maintain an adequate cardiac output. Drug stimulation consists of sympathetic stimulation with isoproterenol or further increase in venous pooling with nitroglycerin. The objective is to trigger a parasympathetic reflex which results in bradycardia and/or hypotension, in turn resulting in syncope from decreased cerebral perfusion. Once the patient’s clinical scenario is replicated, the table is immediately lowered, resulting in restoration of cerebral blood flow by gravity. The test is exceedingly safe and is usually performed in an outpatient or office setting. The test’s usefulness depends on the replication of the patient’s symptoms surrounding recurrent syncopal events. It is less important to achieve actual syncope than to recreate the typical symptoms that accompany syncope. Very often patients will report diaphoresis, nausea, dyspnea, flushing, clamminess and other typical symptoms. Syncope can be induced in many patients that have never before had it; therefore a test is only “positive” if it also replicates the patient’s symptoms. A “negative” test is of little value as it does not exclude the presence of syncope, it just tells you that on that given instance you were unable to produce the clinical syndrome. This is why the test cannot be used to “clear” a patient following a syncopal event. Only clinical observation on therapy, showing a prolonged absence of syncopal events, is of significance.

January 2008

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