Syncope

Eric H. Yang, MD, Hunter C. Champion, MD, Ph.D, Mark Linzer, MD Fast Facts
Syncope is a transient loss of consciousness with loss of postural tone and spontaneous recovery. 6% of hospital admissions and 3% of emergency room visits are due to syncope. Syncope can be classified as: orthostatic hypotension, neurogenic, cardiogenic, neurocardiogenic, and syncope of unknown etiology. $ A thorough history and physical exam provides a diagnosis in 45% of cases. $ Neuroimaging and electroencephalogram have a low diagnostic yield (<2%) and should only be used in patients with a history suggestive of neurogenic syncope and or a focal neurological exam. $ All patients suspected of having cardiogenic syncope should be evaluated with an EKG, holter monitor or telemetry, and echocardiography. $ Electrophysiologic studies should be reserved for those with organic heart disease or conduction abnormalities. $ Event monitors should be used in patients with frequent spells(once per week to once every 2 to 3 months) and a negative cardiac work up. $ Tilt table testing should be used in patients with structurally normal hearts and relatively infrequent syncope (< once every 3 months.) It should also be used in those with nondiagnostic loop /Holter monitoring or symptoms suggesting vasovagal syncope but without an obvious precipitating event. $ $ $

I. Background Syncope is a transient loss of consciousness that is accompanied by loss of postural tone with spontaneous recovery. Approximately 6% of hospital admissions and 3% of emergency room visits are due to syncope. It is therefore important for the house officer to be familiar with the

pathophysiology and diagnosis of the various etiologies of syncope. The common causes of syncope are shown in Table X1 and can be divided into five general categories: orthostatic hypotension, neurogenic, cardiogenic, neurocardiogenic, and syncope of unknown etiology. 1. Orthostatic hypotension accounts for about 8% of syncopal episodes and is due to inadequate intravascular volume. It occurs when a person suddenly rises from a seated or lying position. The sudden rise results in decreased cerebral perfusion and subsequent lost of

consciousness. It is considered benign. 2. Neurogenic syncope is loss of consciousness caused by a neurologic disorder and is responsible for 10% of syncopal episodes. Common neurological diseases associated with

syncope are migraines, transient ischemic attacks, and seizures. Syncope can be accompanied with seizure activity, hemiparesis, visual disturbances, or headache. 3. Cardiogenic syncope is syncope involving cardiovascular pathophysiology. The mechanism of syncope can be either from organic heart disease or from an arrhythmia. Organic heart disease is the cause of 4% of syncopal episodes and includes coronary artery disease, valvular abnormalities, cardiomyopathy, and congenital heart disease. Arrhythmias can be

classified as either bradyarrhythmias, or tachyarrhythmias and accounts for 14% of syncopal episodes . The key feature of cardiogenic syncope is sudden loss of consciousness without prodrome. 4. Neurocardiogenic syncope accounts for 24% of cases and is caused by a neurally mediated reflex mechanism known as the Bezold Jarrish reflex. There is inappropriate vasodilation resulting in an increase in venous pooling and a subsequent decrease in ventricular preload. In order to maintain cardiac output, the left ventricle contracts vigorously against an undefiled ventricle. This Aover exertion@ of the left ventricle is potentially harmful and the body protects itself through a neurally mediated reflex mechanism. The afferent limb of the reflex begins with C fibers in the left ventricle that detect the sudden increase in pressure. This information is processed in the central nervous system and an efferent response is mediated by the vagus nerve. Bradycardia or asystole is induced which protects against vigorous contraction but also leads to a decrease in cardiac output and a potential for syncope. Included in this category are vasovagal syncope, situational syncope (e.g. cough syncope, micturition syncope), and carotid sinus hypersensitivity. 5. Syncope of unknown etiology is unfortunately the most common category for syncope and is responsible for 34% of cases. It is important to note that the original epidemiologic studies were performed several years ago when current diagnostic tools were not widely used. Thus, the actual portion of patients with unexplained syncope is probably lower than 34%. II. Diagnosis
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Diagnosing the cause of syncope can be both costly and frustrating because there is no gold standard test. Table X2 shows the numerous diagnostic tools commonly used in working up syncope. When deciding which test to order it is important to remember that a thorough history and physical exam is the best diagnostic tool. It also helps guide the clinician in deciding which diagnostic test(s) to use. A helpful algorithm for diagnosing syncope is shown in Figure X1. 1. History and Physical Exam: The etiology of a syncopal episode can be diagnosed in 45% of cases by the history and physical exam. Important questions to ask in the history of present illness are what happened before, during and after the syncopal episode. Table X3 shows the key events and symptoms that are characteristic of the various etiologies of syncope. It is also important to ask about possible triggers and if any injury occurred during the event. The past medical history provides insight into the frequency of syncopal episodes, underlying medical conditions predisposing the patient to syncope, and helps guide which diagnostic test(s) to order. A thorough review of medications is important because they frequently cause syncope, especially in the elderly. The physical exam should include checking for orthostatic blood pressures and a thorough cardiovascular and neurological exam. 2. Electrocardiogram: Although the 12 lead EKG provides a diagnosis in only 5% of cases, it should be obtained in all patients with syncope. Structural or conduction abnormalities in a resting EKG help guide further more expensive and invasive evaluation for a cardiac etiology. 3. Neuroimaging and Electroencephalography: These tests are of extreme low yield (02%) when used to find the etiology of a syncopal episode. Neuro-imaging and electroencephalography should therefore not be performed in patients without a history suggesting neurogenic syncope or focal neurological signs on exam. 4. Echocardiography: Transthoracic Echocardiography provides a diagnosis for syncope in 5-10% of cases and its cost-effectiveness in diagnosing syncope has not been studied. As shown

in figure X1, Echocardiography along with telemetry/holter monitoring should be the initial work up in all patients suspected of having cardiogenic syncope. Those with abnormalities should then proceed with further cardiac evaluation. 5. 24-Hour Holter Monitoring and Inpatient Telemetry: Both of these methods can be used to evaluate for rhythm disturbances in patients suspected to have cardiogenic syncope. Inpatient telemetry can be used in place of out-patient holter monitoring. It is important to remember that the presence of an arrhythmia on monitoring is not diagnostic unless the disturbance reproduces symptoms associated with the patient=s syncope. When used for 24 hours, these tests can provide a diagnosis for syncope in 19% of patients. One study evaluating the effect of duration of monitoring on diagnostic yield showed that although 72 hours of monitoring revealed more arrhythmias, there was no increase in the yield for arrhythmias associated with symptoms (Arch Intern Med. 1990;113:53-68) . Thus Holter monitoring or in-patient telemetry for 24 hours is recommended for all patients suspected of having cardiogenic syncope. Patients with non

diagnostic in-patient telemetry should, in general, not be sent home with further Holter monitoring. 6. Electrophysiolgic Studies: EPS (electrophysiologic studies) are invasive studies thatn use electric stimulation and monitoring to discover abnormalities that predispose patients to arrhythmias (bradycardias and tachycardias). EPS are safe, expensive, and have a diagnostic yield of 32%. Patients without organic heart disease and normal electrocardiograms should rarely undergo EPS. EPS should be reserved for patients who after echocardiography and telemetry have been shown to have organic heart disease and or conduction abnormalities. 7. Loop Recorders and Event Monitors: These devices consist of two chest electrocardiographic leads that are connected to a small monitor. The monitor constantly records and erases the cardiac rhythm. When the patient has and event, a button is pressed and the cardiac rhythm occurring before and after the event is frozen on the monitor. The data is then transmitted to a heart station where it is interpreted. The diagnostic yield varies from 24 to 47%.
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Patients must be able to put the leads on themselves every day and be cognitive enough to activate the memory when an event occurs. Event monitors should be used in patients with frequent spells(once per week to once every 2 to 3 months) and a negative cardiac work up. They should not be used in patients with infrequent syncopal episodes or patients who are incapable of operating the device (e.g. elderly). Implantable event monitors are currently being investigated. These devices can be implanted for long periods of time and do not require daily maintenance. Initial studies of impalantbale event monitors appears promising. (Circ 1999;99:406-10) 8. Tilt Table Testing: This test consists of two phases. The first is known as the passive phase and consists of tilting the patient from a supine position to a 60 degree angle. The patient is left in this position for 10 to 15 minutes. If an end point (syncope or hypotension) is not reached, the patient is brought back to the supine position and isoproterenol is infused at 1g/min. The patient is then retilted and the isoproterenol infusion is continued. If an end point is not reached the patient is returned to the supine position and the infusion rate in increased. The patient is then retilted. This protocol is repeated until either and endpoint is obtained or the maximum infusion rate of 3 to 5 g/min is reached. It is recommended that women of child bearing age have a pregnancy test and that all men older than 45 years of age and women older than 55 years of age have a stress testing prior to tilt-table testing. The overall sensitivity of tilt table testing is between 67 and 83% and specificity is approximately 75%. Tilt table testing should be used in patients with structurally normal hearts and relatively infrequent syncope (< once every 3 months.) It should also be used in those with nondiagnostic loop /Holter monitoring or symptoms suggesting vasovagal syncope but without an obvious precipitating event. III. Treatment The first treatment decision is whether or not to admit the patient. Table X4 provides some general indications for admission, but the clinician=s clinical judgement should always take precedent. The next step is to treat the underlying cause of syncope. Fluid rehydration is the treatment of choice
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for orthostatic hypotension.

Use of implantable pacemakers and or defibrillators could be

considered in cardiogenic syncope. A recently published consensus on the treatment of vasovagal syncope suggest use of beta-blockers in those who have an increase in heart rate prior to syncope in tilt table testing. Those with no significant increase in heart rate should be treated with fludrocortisone (AJC. 1999;84:33Q-39Q).

Table X1: Causes of Syncope

Etiology of syncope Orthostatic hypotension Neurogenic syncope Migraines Transient ischemic attacks Seizures Cardiogenic syncope Organic heart disease Aortic stenosis Hypertrophic cardiomyopathy Congenital heart disease Myocardial infarction Arrhythmias Bradyarrhythmias Tachyarrhythmias Neurocardiogenic syncope Vasovagal Situational Cough Micturition/Defecation Swallow Carotid sinus hypersensitivity Syncope of unknown etiology Characteristics Occurs with standing Seizure activity, hemiparesis, visual disturbances, headache Prevalence, % 8 10

Chest pain, exertional syncope, dyspnea

Sudden syncope without prodrome, subsequent injury

14

Warmth and nausea

18 5

1 Negative work up 34%

Based on 5 population-based studies in unselected patients with syncope Adapted from Ann Intern Med. 1997;126:989-96

Table X2: Diagnostic Tests for Evaluating Syncope

Test History and Physical Electrocardiogram Neuroimaging and Electroencephalography Echocardiography Holter monitoring/telemetry Electrophysiolgic Studies Loop Recorders Cost $ 160 90 888 493 580 468 4678 284 Indications for use All patients with syncope All patients with syncope Patients with history suggesting neurogenic syncope and or focal neurological findings on exam. Patients suspected to have cardiogenic syncope. Patients suspected to have cardiogenic syncope. Patients with organic heart disease and or conduction abnormalities Patients with frequent spells and no known structural heart disease. Recurrent syncope in those with negative electrophysiolgic studies. Patients with normal hearts and infrequent syncope or those with symptoms suggesting vasovagal syncope but without obvious precipitating event. Diagnostic Yield% 45 5 0-2 5-10 19 32 24-47

Tilt Table Testing

683

Average of cost from University of Wisconsin Hospital, University of Pittsburgh Medical Center, New England Medical Center, and Duke University Medical Center.

Table X3: Characteristic Syncopal Symptoms

Etiology Before syncope Orthostatic Hypotension Patients was sitting or lying. Headache, visual disturbances no prodromal symptoms prodrome with feelings of warmth, nausea. Situational trigger present Symptoms During syncope Rising from sitting or lying position. Begins feeling lightheaded. Convulsions, seizure like activity, urinary/fecal incontinence patient has sudden lost of consciousness none After syncope No residual effects.

Neurogenic Syncope

residual effects, patient is disoriented after event no residual effects, injury residual feelings of nausea and warmth

Cardiogenic Syncope Neurocardiogenic Syncope

Table X4: Criteria for Admission

Strong Indication Cardiogenic Syncope Syncope in patients with heart disease Coronary artery disease, heart failure, electrocardiograhic findings (serious bradycardia or tachycardia, increased QT interval, or bundle branch block) Syncope with accompanying chest pain. Stroke or focal neurological disorder Moderate Indication Sudden loss of consciousness resulting in injury. Exertional syncope Age > 70 Moderate-to-severe orthostatic hypotension Frequent spells
Based on 6 population-based studies of patients with syncope presenting to the emergency department. Adapted from Ann Intern Med. 1997;127:76-86

Figure X1: Algorithm for diagnosing syncope.

Adapted from Linzer, Yang, et al Ann Int Med. 1997;126:989-96

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References Linzer M, Yang EH, Estes N, Wang P, Vorperian V, Kapoor W. Diagnosing Syncope Part 1: Value of History, Physical Examination, and Electrocardiography Ann Int Med. 1997;126:989996 Linzer M, Yang EH, Estes N, Wang P, Vorperian V, Kapoor W. Diagnosing Syncope Part 2: Unexplained Syncope Ann Int Med. 1997;127:76-86 Calkins H. Pharmacologic Approaches to Therapy for Vasovagal Syncope Am J Cardiol 1999;84:20Q-25Q Zimetbaum PJ. Josephson ME. The evolving role of ambulatory arrhythmia monitoring in general clinical practice Ann Int Med. 1999;130(10):848-56 Bloomfield D, Sheldon R, Grubb B, Calkins H, Sutton R. Putting it Together: A New Treatment Algorithm for Vasovagal Syncope and Related Disorders Am J Cardiol. 1999;84:33Q-39Q

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