You are on page 1of 6

Practice Guidelines

AHA/ACCF Statement on the Evaluation of Syncope

Laura Coughlin

The American Heart Association (AHA) and the American College of Cardiology Foundation (ACCF) recently released a scientific statement on the evaluation of syncope. The statement was published in the January 17, 2006, issue of Circulation and is available at cgi/content/full/113/2/316. Syncope (i.e., transient loss of consciousness) often has a cardiovascular cause and is associated with a high mortality rate in patients with underlying heart disease, transient myocardial ischemia, or other cardiac abnormalities. The evaluation of a patient with syncope should be focused on determining if the patient is at increased risk of death and should seek to identify if the patient has an underlying condition causing the syncope (i.e., heart disease, myocardial ischemia, Wolff-Parkinson-White syndrome, long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia). Once these conditions are excluded, the goal of treatment is to improve the quality of life for the patient and to reduce the risk of injury to the patient and others. The cause of syncope can be determined in most cases by a thorough history and physical examination (see accompanying figure); however, 40 percent of syncopal episodes are unexplained even after a careful evaluation. Overall, the most common causes of syncope are neurocardiogenic, followed by primary arrhythmias. Causes of syncope also are highly associated with age: children and young adults are most likely to have neurocardiogenic syncope, psychiatric causes, or primary arrhythmic causes; middle-aged patients are most likely to have neurocardiogenic syncope; and older patients are more likely than younger patients to have syncope caused by obstructions to cardiac output.

The thorough history of the patient with syncope should begin with the observations of onlookers. Tonic-clonic, seizure-like activity is associated with neurologic and cardiac causes of syncope. Neurocardiogenic syncope (also called vasovagal syncope) often is associated with postepisode fatigue or weakness. Prodromal symptoms are common with neurocardiogenic syncope, whereas the absence of a prodrome is associated with cardiac arrhythmia or a central neurodegenerative disorder (e.g., Parkinsons disease). Auras, premonitions, postepisode confusion, or focal neurologic signs suggest a neurologic cause of syncope; however, syncope with focal neurologic signs also can be associated with basilar artery or severe carotid artery disease. History of myocardial infarction or repaired congenital heart disease raises the possibility of ventricular arrhythmia. Past head trauma in a younger person without underlying heart disease can suggest a neurologic cause, and syncope on head turning raises the possibility of carotid sinus hypersensitivity, especially in older patients. Carotid sinus hypersensitivity can be assessed with carotid massage but should not be performed on patients who have had a recent ischemic attack or stroke, ipsilateral to significant carotid artery stenosis, or carotid artery bruit. All patients should be asked if they have a family history of sudden cardiac death. The history also should include the identification of aggravating and alleviating factors, especially the additions of new medications. Antiarrhythmic and antihypertensive medications raise the possibility of proarrhythmia or orthostasis. Phenothiazines and tricyclic medications predispose older patients to orthostasis. Over-thecounter medications and supplements also can contribute to syncope.

of cial use one individual user of the Contact for copyright questions and/or permission requests. 179 July 1, 2006 Volume 74, Number 1 Web site. All other rights reserved.  American Family Physician

Downloaded from the American Family Physician Web site at Copyright 2006 American Academy of Family Physicians. For the private, noncommer-

Diagnostic Approach to the Patient with Syncope

The rights holder did not grant the American Academy of Family Physicians the right to sublicense this mateSyncope rial to a third party. For the missing item, see the original print version of this publication.
History, physical examination, electrocardiography

Diagnostic for orthostatic hypotension or neurocardiogenic syncope

Unexplained syncope

Echocardiogram, exercise test, and ischemia evaluation

If found, treat for structural heart disease and ischemia. For arrhythmia evaluation, consider electrophysiologic testing if there is a history of a myocardial infarction. Consider implantable defibrillator if the left ventricular ejection fraction is 0.3 or less, with or without a history of myocardial infarction.


Single, benign episode

Frequent episodes

Infrequent episodes

Evaluation complete

Correlate symptoms with rhythm with Holter or event monitor, or an implantable loop recorder, as appropriate.

Implantable loop recorder

Sinus rhythm with symptoms

Arrhythmia with symptoms

Cardiac evaluation complete


Figure. Flow chart for the diagnostic approach to the patient with syncope.
Reprinted with permission from AHA/ACCF scientific statement on the evaluation of syncope. From the American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes Research Interdisciplinary Working Group; and the American College of Cardiology Foundation in collaboration with the Heart Rhythm Society. Circulation 2006;113:317.

The physical examination of a patient with syncope should include measurements of blood pressure and pulse rate in the upper and lower extremities while the patient is in the supine and upright positions to identify orthostatic hypotension, autonomic dysfunction, or possible organic heart disease. Checking for carotid bruits can find impaired cerebral blood flow or underlying coronary artery disease. On examination, the physician also may find signs of pulmonary hypertension, left ventricular dysfunction, valvular heart disease, or other forms of organic heart disease. Neurologic disorder is suggested by abnormal cognition, speech, visual field, motor strength, sensation, tremor, or gait disturbance. Electrocardiography, echocardiography, and ischemia 180 American Family Physician

evaluation also can help discover the cause of syncope. Electrocardiograms provide information about heart rhythm and atrioventricular (AV) conduction and can identify sinus bradycardia, prolonged P-R interval, bundle branch block, or a delta wave, all of which can be associated with syncope. Electrocardiograms also can identify genetic disease of the cardiac channels that can cause syncope and life-threatening ventricular arrhythmias (e.g., long QT syndrome, Brugada syndrome). Discovering ventricular ectopy or nonsustained ventricular tachycardia in a patient with underlying heart disease raises the possibility of an arrhythmic origin of syncope. When the history, physical examination, and electrocardiography fail to provide a reason for a patients syncope,
Volume 74, Number 1

July 1, 2006

Practice Guidelines
or if heart disease is suspected, echocardiography can be a useful diagnostic tool. Echocardiograms can help identify underlying heart disease, valvular disease, and pulmonary embolism. Patients who are at risk of or have a history of coronary artery disease also should be evaluated for ischemia. Exercise testing should be performed on these patients, especially if the episode of syncope was exercise related. Syncope in Patients with a Normal Evaluation Syncope is not associated with increased mortality when no underlying heart disease is present. When the initial evaluation is normal, it is often challenging to discern the origin of syncope. Although many of the most serious possible causes of syncope can be excluded by a normal evaluation, the possibilities of neurocardiogenic syncope, carotid sinus hypersensitivity, paroxysmal bradyarrhythmia, supraventricular tachycardia, ventricular tachycardia, and many noncardiac causes still exist.
noninvasive electrocardiographic monitoring electrophysiologic study

After the evaluation for ischemia, the patient should undergo electrophysiologic testing to assess sinus node function, atrioventricular conduction, and ventricular tachyarrhythmias. Electrophysiologic study is appropriate for patients with coronary artery disease, syncope, and mild or moderate left ventricular dysfunction; this is because of the significant implications of inducible ventricular tachycardia. Patients with syncope and severe ischemic cardiomyopathy are appropriate candidates for implantable defibrillators regardless of the result of electrophysiologic testing. Syncope in Patients with Nonischemic Dilated Cardiomyopathy Syncope is associated with an increased risk of mortality in patients with nonischemic dilated cardiomyopathy. The differential diagnosis of syncope in patients with nonischemic dilated cardiomyopathy includes bradycardia, tachycardia, orthostatic hypotension, and pulmonary embolism. There is no evidence to support the use of arrhythmic drugs in patients with nonischemic dilated cardiomyopathy and unexplained syncope; however, implantable defibrillator therapy is an option.
electrophysiologic study

The duration and type of ambulatory electrocardiographic monitoring (e.g., Holter monitor, event monitor, implantable loop monitor) should be dictated by the frequency of symptoms. In patients with unexplained syncope, the use of an implantable loop monitor for one year yielded diagnostic information in more than 90 percent of patients.
tilt-table testing

Tilt-table testing can be used to help establish the diagnosis of neurocardiogenic syncope; however, the sensitivity ranges from 26 to 80 percent, with a specificity of nearly 90 percent.
electrophysiologic study

Electrophysiologic testing is less useful for patients with nonischemic dilated cardiomyopathy than for patients with a history of myocardial infarction, and it has a low negative predictive value for these patients. Syncope in Patients with Other Forms of Heart Disease
hypertrophic cardiomyopathy

The yield of electrophysiologic testing is approximately 3 percent in patients with a normal evaluation, and the sensitivity for detecting bradyarrhythmias is low; therefore, electrophysiologic testing is not routinely recommended for patients with syncope. However, given the low risk involved with electrophysiologic testing, the risk-to-benefit ratio might be favorable in patients with extremely disruptive syncopal episodes. Syncope in Patients with Coronary Artery Disease Identifying a potentially life-threatening diagnosis is the main goal of the evaluation of a patient who has syncope and coronary artery disease. The risk of death in these patients is directly proportional to the severity of left ventricular dysfunction. It is necessary to evaluate these patients for ischemia, underlying heart disease, and arrhythmias. 182 American Family Physician

One out of 500 persons has hypertrophic cardiomyopathy, a genetically determined myocardial disease. The prognosis for these patients is variable, and the annual risk of sudden death is between 0.6 and 1.0 percent. Syncope, especially syncope that repeatedly occurs with exertion, is a major risk factor for sudden death in patients with hypertrophic cardiomyopathy. Studies have shown that implantable defibrillator therapy is effective for high-risk patients with hypertrophic cardiomyopathy.
arrhythmogenic right ventricular dysplasia/cardiomyopathy

Thirty to 50 percent of cases of arrhythmogenic right ventricular dysplasia/cardiomyopathy are thought to be familial, but sporadic cases do occur and may represent a different disease process. Sudden cardiac death may be the first manifestation of arrhythmogenic right ventricular dysplasia/cardiomyopathy, but patients
Volume 74, Number 1

July 1, 2006

Practice Guidelines
usually present with premature ventricular beats, syncope, or sustained ventricular tachycardia with a left bundle branch block. Syncope is viewed as an ominous finding in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy. Implantable defibrillator therapy may be effective for this group. Syncope in Patients with Inherited Cardiac Ion Channel Abnormalities Inherited cardiac ion channel abnormalities such as long QT syndrome and Brugada syndrome can cause syncope and sudden death as a result of ventricular arrhythmias in the absence of structural heart disease.
long qt syndrome

cause syncope in a seemingly healthy child, and the syncope usually is caused by palpitations; other symptoms (e.g., lightheadedness, chest pain, dyspnea, pallor, nausea) may be present.
underlying heart disease

Syncope is considered an ominous sign in patients with long QT syndrome and is assumed to be secondary to an episode of torsades de pointes polymorphic ventricular tachycardia that terminated spontaneously. Treatment options for long QT syndrome include beta blockers and implantable defibrillators. Other interventions include the restriction of strenuous activities, avoidance of medications that prolong the Q-T interval, and a family screening.
brugada syndrome

When underlying heart disease is present, syncope is potentially life threatening. Syncope caused by hypercyanotic spells in children with untreated congenital heart disease is uncommon and should be considered an indication for surgical intervention. Complete AV block or ventricular tachycardia may cause syncope in patients with a history of surgery involving the ventricles. Syncope and young age are risk factors for sudden cardiac death in patients with hypertrophic cardiomyopathy, which is the most common cause of sudden cardiac death in adolescents. Syncope is an ominous sign in children with aortic stenosis and often occurs with exercise. Syncope often occurs in children with primary pulmonary hypertension. Syncope and sudden cardiac death may be the presenting symptom of coronary artery abnormalities in children (present in approximately 1 percent of the population). Special Considerations for Syncope in Older Patients Syncope may cause up to 30 percent of falls in older patients. Clinical presentation of syncope in older patients often is variable, atypical, and multifactorial. Age-related changes such as autonomic dysfunction and reductions in thirst, ability to preserve sodium and water levels, baroreceptor response, and heart rate response to orthostatic stress should be considered when evaluating older patients with syncope. These changes, with the use of multiple medications, are risk factors for orthostatic intolerance and syncope. Classic clinical features of syncope often are absent in older patients. Complete amnesia of the event may be present in up to 40 percent of older patients with syncope. Common clinical presentations of syncope in older patients include postprandial hypotension (often confused with transient ischemic attacks or seizures), carotid sinus hypersensitivity, neurally mediated causes, and cardiovascular medications. Unexplained syncope can be one of the first signs of degenerative disorders such as Parkinsons disease Neurologic Evaluation in Patients with Syncope Syncope is an uncommon manifestation of neurologic processes but should be considered in patients when it is suggested by history or physical examination. If a neurologic cause of syncope is suspected, computed
American Family Physician 183

Brugada syndrome is a heritable cardiac disorder. Patients with Brugada syndrome who present with syncope have a two-year risk of sudden cardiac death of 30 percent. Implantable defibrillator therapy often is recommended. Evaluation of Children with Syncope Syncope in children generally is benign because underlying heart disease is less common in young persons; however, the differential diagnosis and evaluation of syncope is similar in children and adults. The main goal of the evaluation of a child with syncope is the identification of underlying heart disease, which may include genetic abnormalities. Hypertrophic cardiomyopathy and catecholaminergic polymorphic ventricular tachycardia in children often present as syncope associated with high-intensity physical activity and can be evaluated with echocardiography and an exercise stress test. In children, syncope with a normal electrocardiogram and echocardiogram may be caused by breath-holding spells resulting from emotional upset (found in 2 to 5 percent of patients).
bradycardia and tachycardia

In children, transient but profound sinus pauses or sustained bradycardia may cause syncope as a result of a neurocardiogenic reflex; however, syncope caused by isolated bradycardia is uncommon. Tachycardia may
July 1, 2006

Volume 74, Number 1

Practice Guidelines
tomography or magnetic resonance imaging of the brain is indicated. When cerebrovascular disease is suspected, imaging of the extracranial and intracranial carotid arteries is appropriate. Syncope that occurs in the supine position and is preceded by an aura or followed by confusion or amnesia is possibly caused by a neurologic disorder. Neurologic disorders that cause syncope often result in orthostatic hypotension from dysautonomia. These disorders can be suspected by history, neurologic examination, and bedside testing of orthostatic vital signs. Tilt-table testing, cardiac responses to deep breathing, the Valsalva maneuver, and sweat testing can confirm the presence of a dysautonomia, distinguish central from peripheral causes of syncope, and guide patient management. Disorders that increase intracranial pressure also can result in syncope. Cardiac involvement is common in patients with neuromuscular diseases. Evaluation of patients with neuromuscular disease should include electrocardiography, echocardiography, and assessment for cardiac ischemia; these patients can be treated with a pacemaker or implantable defibrillator. before 10 weeks gestation; one or more unexplained fetal deaths at 10 weeks gestation or later; severe preeclampsia or placental insufficiency requiring birth before 34 weeks gestation; unexplained venous or arterial thrombosis; or small-vessel thrombosis in any tissue or organ with no significant evidence of vessel-wall inflammation. Treatment of antiphospholipid syndrome during pregnancy reduces the risks of pregnancy loss, preeclampsia, placental insufficiency, preterm birth, and thrombosis. ACOG states that women with antiphospholipid syndrome and no history of thrombosis should receive prophylactic doses of heparin and low-dose aspirin during pregnancy and for six to eight weeks postpartum. For women with recurrent miscarriage, the combination of prophylactic heparin and low-dose aspirin may reduce pregnancy loss and is more effective than low-dose aspirin alone or prednisone. Although ACOG found few data on the effectiveness of treatments for women with severe preeclampsia or uteroplacental insufficiency, prophylactic heparin and aspirin generally are recommended. Initiation of heparin before conception is not supported by evidence. Women with antiphospholipid syndrome and a history of thrombosis should receive full heparin anticoagulation throughout pregnancy and for six to eight weeks postpartum to minimize the risk of maternal thromboembolism. This can be achieved safely with warfarin (Coumadin) after delivery. The benefit of adding aspirin is unknown. After the postpartum period, patients should be referred to a physician with expertise in treating the syndrome for further anticoagulation therapy. The effectiveness of corticosteroids and intravenous immune globulin for the treatment of antiphospholipid syndrome is uncertain. Women with antiphospholipid syndrome who are pregnant should be instructed about the signs and symptoms of preeclampsia and thrombosis and should be examined frequently. Serial ultrasonic assessment should be considered because of the risk for growth restriction. Antepartum testing should be considered after 32 weeks gestation (or earlier if growth restriction is evident). Long-term risks of antiphospholipid syndrome include thrombosis and stroke. Patients with antiphospholipid syndrome should be referred to a physician with expertise in treating the syndrome for long-term follow-up. The use of estrogen-containing oral contraceptives has been shown to increase the risk for thrombosis in women with antiphospholipid syndrome and therefore should be avoided in these women.

Practice Guideline Briefs

Diagnosis and Treatment of Antiphospholipid Syndrome
Antiphospholipid syndrome is associated with various conditions, including arterial and venous thromboses, autoimmune thrombocytopenia, fetal loss, preeclampsia, intrauterine growth restriction, placental insufficiency, and preterm delivery. The American College of Obstetricians and Gynecologists (ACOG) has developed guidelines for the diagnosis and treatment of this condition. The guidelines were published in the November 2005 issue of Obstetrics & Gynecology. Diagnosis of antiphospholipid syndrome is based on a combination of clinical history and laboratory testing. Initial diagnosis requires testing for lupus anticoagulant and anticardiolipin antibodies; patients should be diagnosed if lupus anticoagulant is present or if medium to high levels (i.e., greater than 20 binding units) of immunoglobulin G (IgG) or IgM anticardiolipid antibodies are present. Positive test results must be confirmed by a second test after several weeks. Testing for antiphospholipid antibodies should be limited to women with appropriate medical or obstetric histories. The primary manifestations of antiphospholipid syndrome are pregnancy loss and venous or arterial thromboses. Thus, clinical criteria for laboratory testing are three or more consecutive spontaneous abortions 184 American Family Physician

Volume 74, Number 1

July 1, 2006

Management of Dyspepsia

Practice Guidelines

The rights holder did not grant the American Academy of Family Physicians the right to sublicense this mateDyspeptic symptoms rial to a third party. For the missing item, see the original print version of this publication.

Heartburn with or without regurgitation is present (predominant or frequent)

NSAID or COX-2 inhibitor use

Dyspepsia without obvious GERD or NSAID use

Manage as GERD (i.e., acid suppression)

Consider discontinuing NSAID, switching to another agent, or adding PPI.

Age 55 years or younger and no alarm symptoms present

Age older than 55 years or alarm symptoms present

Test for Helicobacter pylori.




Treat for H. pylori infection.

PPI therapy for four to six weeks

Treatment fails

Treatment fails

Reassure patient and reassess diagnosis.

Consider EGD.

Figure. Algorithm for management of dyspepsia. (NSAID = nonsteroidal anti-inflammatory drug; COX = cyclooxygenase; GERD = gastroesophageal reflux disease; PPI = proton pump inhibitor; EGD = esophagogastroduodenoscopy.)
Adapted with permission from American Gastroenterological Association. American Gastroenterological Association medical position statement: evaluation of dyspepsia. Gastroenterology 2005;129:1754.

AGA Releases Updated Recommendations on Dyspepsia

The American Gastroenterological Association (AGA) has released a position statement to reflect new evidence on the evaluation of dyspepsia. The report was published in the November 2005 issue of Gastroenterology. The AGA defines dyspepsia as chronic or recurrent pain or discomfort in the upper abdomen. Because there is considerable overlap in the definitions of dyspepsia and gastroesophageal reflux disease (GERD) (i.e., frequent heartburn or acid regurgitation), the AGA recommends further research to better define dyspepsia. GERD and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) may cause dyspeptic symptoms. If no obvious GERD or NSAID use is present, the AGA

recommends that patients 55 years or younger without alarm symptoms be tested for Helicobacter pylori infection. Esophagogastroduodenoscopy is recommended for patients who are older than 55 years and those who have alarm symptoms. The accompanying figure presents an algorithm for the management of dyspepsia.

Answers to This Issues Clinical Quiz Q1. E Q5. B Q9. A, B, D Q2. D Q6. D Q10. A, B, D Q3. B Q7. A Q11. A, B, C, D Q4. B Q8. C

July 1, 2006

Volume 74, Number 1

American Family Physician 185