- Email: [email protected]
Syncope
S y n c ope Katherine Neal,
MD,
Alicia Clark,
MD*
KEYWORDS Syncope Transient loss of consciousness Presyncope Reflex syncope Cardiovascular syncope Orthostatic hypotension KEY POINTS Syncope is a common problem and accounts for approximately 1% of all emergency room visits. Causes of syncope include reflex (neurally mediated), cardiovascular, and orthostatic hypotension. Collect a thorough history to determine if syncope has truly occurred; obtaining collateral history from a bystander may be necessary. Any abnormal vital sign can indicate a more serious underlying etiology for syncope and should be investigated. All patients presenting with syncope should have postural vital signs checked as this has been proven to be cost-effective and leads to a diagnosis in about 10% of cases. All patients aged 60 years and older presenting to the emergency room with syncope should be evaluated with an electrocardiogram. Carotid ultrasound and brain imaging with computed tomography scan or magnetic resonance imaging are not indicated unless there is a focal neurologic deficit. Consider cardiology consultation for patients with a suspected cardiac cause for syncope.
DEFINITIONS
How are syncope and presyncope defined? The European Society of Cardiology defines syncope as a transient loss of consciousness caused by cerebral hypoperfusion and characterized by quick onset, short duration, and complete recovery. The term presyncope is used to describe the prodromal symptoms of syncope, which are not followed by loss of consciousness; it is not known whether the mechanisms behind syncope and presyncope are the same.1
Disclosures: None. Hospital Medicine Program, Duke University Medical Center, Box 100800, Durham, NC 27710, USA * Corresponding author. E-mail address: [email protected] Hosp Med Clin 4 (2015) 65–73 http://dx.doi.org/10.1016/j.ehmc.2014.09.011 2211-5943/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
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What are the most common presentations confused with syncope? Syncope is distinguished from other causes of loss of consciousness by the mechanism by which an individual loses consciousness: global cerebral hypoperfusion. Conditions that cause partial or complete loss of consciousness not caused by cerebral hypoperfusion include: Epilepsy/seizures Metabolic disorders (eg, hypoglycemia, hypoxia, hyperventilation) Intoxication syndromes Vertebrobasilar transient ischemic attacks In contrast, multiple disorders exist that do not cause loss of consciousness but can be confused with syncope because of the description of the event and difficulty obtaining an accurate history. These disorders include: Falls Cataplexy Drop attacks Pyschogenic pseudosyncope Carotid transient ischemic attack1 What are the different causes of syncope? There are 3 main causes of syncope: reflex (neurally mediated), cardiovascular (eg, encompassing arrhythmias, structural heart disease), and orthostatic hypotension. Reflex (neurally mediated) syncope includes a varied group of conditions in which the usual cardiovascular reflexes that are typically useful in controlling hemodynamics are transiently inappropriate, caused by a specific trigger. This condition results in vasodilatation and/or bradycardia, which lead to a decrease in blood pressure.1 Causes of reflex syncope include: Vasovagal causes Mediated by emotional distress (fear, pain, blood or other phobia, instrumentation) Mediated by orthostatic stress Situational causes Cough/sneeze Gastrointestinal stimulation (eg, swallow, visceral pain, defecation) Micturition and postmicturition Postexercise Postprandial Other (laugh, playing brass instrument, weightlifting) Carotid sinus irritation Atypical forms (no apparent trigger or atypical presentation) Causes of cardiovascular syncope include: Arrhythmia Bradycardia - Sinus node dysfunction (including tachy-brady syndrome) - Atrioventricular conduction system disease - Implanted device malfunction Tachycardia - Supraventricular - Ventricular
Syncope
Drug-induced bradyarrhythmia or tachyarrhythmias Structural disease Cardiac - Cardiac valvular disease (most commonly aortic stenosis) - Acute myocardial infarction/ischemia, caused by arrhythmia or sudden decrease in cardiac output - Hypertrophic cardiomyopathy - Cardiac masses (eg, atrial myxoma and other tumors) - Pericardial disease/tamponade - Congenital anomalies of coronary arteries - Prosthetic valve dysfunction Noncardiac - Pulmonary embolus - Acute aortic dissection - Pulmonary hypertension Orthostatic hypotension is defined as a decrease of at least 20 mm Hg in systolic blood pressure and/or at least 10 mm Hg in diastolic blood pressure within 2 to 5 minutes of standing after a period of 5 minutes of supine rest.2 Causes of orthostatic hypotension and resulting syncope include: Primary autonomic failure Pure autonomic failure Parkinson disease with autonomic symptoms Multiple system atrophy (including Shy-Drager syndrome) Lewy body dementia Secondary autonomic failure Diabetes mellitus Uremia Spinal cord injury (particularly in quadriplegia)3 Amyloidosis Drugs or toxins Alcohol Vasodilators (eg, nitrates, hydralazine) Antihypertensives (eg, a-blockers, some b-blockers) Diuretics (eg, furosemide, hydrochlorothiazide) Antidepressants (eg, selective serotonin reuptake inhibitors, tricyclic antidepressants) Antipsychotics (eg, risperidone, olanzapine) Volume depletion Hemorrhage Nausea with vomiting Diarrhea Adapted from Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30(21):2631–71. EPIDEMIOLOGY
How common is syncope? It is often difficult to determine the incidence of syncope because of variation in definitions and patient under-reporting. The incidence of syncope increases with age and
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is more common in women than in men. The incidence in women aged 20 to 29 years is approximately 5%, compared with 50% for women more than 80 years of age. In a Dutch study, one-third of medical students (mean age 21 years) reported having a syncopal episode. A more recent data set of adults more than 50 years of age found that 4.4% had a syncopal event in the past year.4 How often is a cause of syncope found? In a review of patients enrolled in the Framingham Heart Study from 1971 to 1988 and reporting a syncopal event, an underlying cause was determined in 63.4% of cases; among those for whom a cause was found, vasovagal events accounted for 21.2%. Cardiovascular causes were implicated in 9.5% of cases, and orthostatic hypotension accounted for 9.4% of cases. For the remaining 36.6% of patients, there was no cause found.5 Other studies indicate that no cause for syncope is found in up to 50% of patients.6 What is the cost of working up syncope? Data from the United States Healthcare Utilization Project indicate that, for hospital admissions with a discharge diagnosis of syncope, annual hospital costs are nearly $3.8 billion with a mean cost of $8700 per admission.7 HISTORY AND EXAMINATION
What historical features help to differentiate the cause of syncope? Obtaining collateral history from a bystander can provide valuable information because an accurate history is often difficult to obtain from the patient and the description of the event can be the most important information for determining potential causes. Key features of the history that the evaluating physician should obtain include:
Circumstances of the event (preceding activities or situation) Hydration status of the patient8 The presence or absence of any prodromal symptoms (eg, palpitations) A description of the event itself, including the duration and what occurred during the event (eg, abnormal rhythmic jerking movements of the limbs, eye or head deviation, trauma during the event) The presence of any symptoms after the event (eg, postictal confusion) Past medical history, particularly any history of cardiac disease Family history, particularly a history of sudden cardiac death or other cardiac disease A full list of medications, including antihypertensives, diuretics, antidepressants, and antipsychotics6
What physical examination findings help determine the cause of syncope? Any abnormal vital sign (eg, bradycardia, tachycardia, or hypotension) Evidence of orthostatic hypotension Clinical evidence of heart failure (eg, increased jugular venous pressure, pulmonary crackles, an S3 or S4 on cardiac examination, hepatomegaly, or lowerextremity edema) Pronounced systolic ejection murmur or diastolic murmur suggesting valvular disease
Syncope
Any focal neurologic deficits Evidence of facial trauma attributable to the syncopal event6 DIAGNOSIS
What diagnostic tests are indicated when evaluating syncope? Given the high yield of postural blood pressure recording, this should be performed in all patients presenting with syncope who do not have a clearly identified alternate cause. The Agency for Healthcare Quality recommends checking orthostatic vital signs in the following manner: Ask the patient to lie in bed with the head flat for at least 3 minutes, but preferably 5 minutes. Measure the blood pressure and pulse while the patient is supine. Instruct the patient to sit for 1 minute. Ask about symptoms brought on by position change. Measure blood pressure and pulse. Instruct the patient to stand. Ask about symptoms brought on by position change. Measure blood pressure and pulse immediately after the patient has stood up and again 3 minutes after the patient stands. If at any time the patient is symptomatic or has a blood pressure less than 90/60 mm Hg, assist the patient back to a supine position. As noted earlier, orthostasis is defined as a decrease of at least 20 mm Hg in systolic blood pressure and/or at least 10 mm Hg in diastolic blood pressure. Additional testing that should be considered includes: Electrocardiogram (ECG) to evaluate for potential cardiovascular causes of syncope and to screen for risk of sudden cardiac death. Findings that put a patient in a higher risk category include evidence of underlying structural heart disease (eg, Q waves) or conduction disease (eg, PR/AV conduction delays, prolonged QT interval, Brugada, or preexcitation). The yield of ECG in determining a cause of syncope is less than 5%.9 Basic laboratory tests, including a complete blood count to rule out an acute anemia, as well as a basic metabolic panel with calcium and blood glucose. If the history, physical examination, or ECG suggests structural heart disease, a transthoracic echocardiogram should be obtained for diagnosis and risk stratification.1,10 Tilt table testing can be considered for cases in which reflex syncope is suspected but is not confirmed by initial evaluation.1 If a cardiac cause of syncope is identified, the patient should be evaluated by a cardiologist. Which tests are least cost-effective in the work-up of syncope? Elderly patients present more commonly than young patients with syncope and are more likely to be admitted to hospital for further evaluation. In a review of 2106 patients more than 65 years of age who presented with syncope and were admitted for evaluation, investigators found that the test with the highest yield (postural blood pressure recording) was performed less than 40% of the time. That review found that the results from cardiac enzymes, computed tomography (CT) scans, transthoracic echocardiogram, carotid ultrasonography, and electroencephalogram affected diagnosis or management in less than 5% of cases and was helpful in determining the cause of syncope less than 2% of the time.11
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According to the American Academy of Neurology as part of the Choosing Wisely campaign, occlusive carotid artery disease does not cause syncope but it can cause unilateral weakness or focal neurologic deficits. They recommend against performing carotid imaging in the work-up of syncope because it does not yield a diagnosis but does increase cost.12 The Canadian Cardiovascular Society recommends that CT scans of the brain should only be performed in patients with focal neurologic signs/symptoms or seizure activity or to rule out hemorrhage in patients with trauma.13 MANAGEMENT
Which patients with syncope require hospitalization? According to the European Society of Cardiology and the Canadian Cardiovascular Society, the following high-risk features should prompt hospitalization or urgent evaluation: Evidence or history of severe structural disease or coronary artery disease (eg, heart failure with low ejection fraction, previous myocardial infarction) ECG features suggesting arrhythmia-mediated syncope (eg, nonsustained ventricular tachycardia, bifascicular block, inappropriate sinus bradycardia, preexcited QRS complex, ECG suggesting inherited arrhythmogenic disorder) Clinical history suggesting an arrhythmic cause (eg, syncope during exertion or from the supine position, prodromal palpitations, lack of any prodromal symptoms, and family history of sudden cardiac death) Acute laboratory test abnormalities including severe anemia or electrolyte disturbance Vital sign abnormalities at the time of presentation (eg, systolic blood pressure <90 mm Hg)1,13,14 There are multiple emergency room decision rules that seek to stratify risk for patients presenting with syncope. At this time, according to the Canadian Cardiovascular Society, no decision rule increases diagnostic specificity or sensitivity or reduces costs.13 Which patients with syncope should be evaluated by a cardiologist? Any patient who has a clinical history and work-up that suggests cardiac syncope, especially patients with a family history of sudden cardiac death, ECG monitoring with evidence of arrhythmia, or a new diagnosis of structural heart disease, should undergo evaluation by a cardiologist. What are the indications for electrocardiographic monitoring? In general, electrocardiographic monitoring is indicated when there is a high pretest probability of detecting an arrhythmia associated with syncope (discussed earlier). Options for monitoring include in-hospital monitoring (telemetry), Holter monitoring, event monitoring, external or implantable loop recorders, and remote (at home) telemetry.1 In-hospital telemetry should be used when the patient is at high risk for a lifethreatening arrhythmia. This type of monitoring mitigates immediate risk to the patient while other work-up is underway.
Syncope
Holter monitors record continuously for 24 or 48 hours (or up to 7 days). Given that most syncopal events are infrequent, the limited time window of a Holter monitor often does not capture the event. However, for patients experiencing frequent events, this type of monitoring may be helpful in excluding arrhythmia as a cause for symptoms. Event recorders are used in the evaluation of palpitations but not syncope because they are devices activated by the patient after symptoms have started. External loop recorders are worn for about a month at a time and the patient activates the ECG monitoring when symptoms occur (electrodes are worn continuously). These recorders have been shown to have higher yield in the diagnosis of syncope than Holter monitors, but because of patient noncompliance and infrequent episodes of syncope, the yield is still only 25% at best.1 Implantable loop recorders should be considered only with input from a cardiologist because of cost and need for a minor surgical procedure. What are the treatments for the most common causes of syncope? The most common cause of syncope is reflex syncope, and there is limited efficacy in pharmacologic treatment of this condition. Management consists of patient education and awareness of this predisposition with specific avoidance of triggers. Patients are encouraged to maintain adequate hydration and immediately sit or get supine to decrease the risk of injury at the onset of any prodromal symptoms. The concept of physical counterpressure maneuvers is being more widely accepted in treatment of reflex syncope; isometric maneuvers such as leg crossing or hand grip have been shown to increase blood pressure sufficiently to abort the syncopal event.1,15,16 There are no conclusive data that any medications, including b-blockers and alpha-agonists such as midodrine, are effective for reflex syncope. Placement of a pacemaker has been shown to be effective in carotid sinus syndrome.1 Cardiovascular syncope is treated according to the primary underlying condition and should be guided by a cardiology consultant. Patients with symptomatic bradycardia causing syncope should be considered for pacemaker placement. Patients with primary arrhythmia as the cause for syncope may be treated with antiarrhythmic medications and/or ablation. Implantable cardiac defibrillators (ICDs) are considered in patients with high risk of sudden cardiac death. Valvular disease and outflow tract obstructions are managed with a combination of medications, percutaneous valve replacement, cardiac surgery, and consideration of an ICD.8 Orthostatic hypotension is most often managed acutely with volume expansion using crystalloid, repletion of electrolytes, and reversal of the process causing volume depletion. This management may include holding diuretics, supportive care for diarrheal illness, and blood transfusion for hemorrhagic anemia. Patients with orthostatic hypotension that persists after appropriate volume expansion should be worked up for other causes of autonomic failure. Patients may use abdominal binders or compression stockings to combat venous pooling in the lower extremities.1 There are more robust data for the use of the alpha-agonist midodrine in patients with orthostatic hypotension and autonomic failure; doses of 5 to 20 mg 3 times daily have been shown to be effective in 3 separate randomized placebo-controlled trials.1 What are the long-term outcomes for patients with syncope? In population-based studies, approximately one-third of patients with a syncopal event had a recurrence in 3 years. The strongest predictor of recurrence is the number of prior syncopal events; in patients with 1 or 2 lifetime events, recurrence rates were
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15% and 20% after 1 and 2 years, respectively. Patients with 3 or more lifetime events had recurrence rates of 36% and 42% after 1 and 2 years, respectively. Severity of the initial event, presence of structural heart disease, gender, and tilt table response have little or no predictive value in determining risk for recurrent events.1 Major traumatic morbidity, such as motor vehicle accidents and fractures, resulting from syncopal events affects about 6% of patients; minor traumatic morbidity, such as lacerations and bruises, affects about 29% of patients. Elderly patients experience morbidity from syncopal events in the form of depressive symptoms, fear of falling, loss of confidence, and fractures/traumatic injuries.1 CLINICAL GUIDELINES
European Society of Cardiology. Available at: http://eurheartj.oxfordjournals.org/ content/30/21/2631.full.pdf. Moya A, Sutton R, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30(21):2631–71. American Heart Association/American College of Cardiology Foundation. Available at: http://circ.ahajournals.org/content/113/2/316.full.pdf1html. Strickberger SA, Benson DW, et al. 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: endorsed by the American Autonomic Society. Circulation 2006;113(2): 316–27. Canadian Cardiovascular Society position paper. Available at: http://www. onlinecjc.ca/article/S0828-282X%2810%2900003-6/. Sheldon RS, Morillo CA, et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol 2011;27(2): 246–53. PRACTICE IMPROVEMENT
Patients aged 60 years and older presenting to the emergency room with syncope should be evaluated with an ECG. This recommendation is endorsed by the National Quality Forum and is included in Medicare’s Physician Quality Reporting Initiative (http://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/ PQRS/downloads/2008PQRIMeasurespecs.pdf) for patients discharged from the emergency room with a discharge diagnosis of syncope. Patients more than 65 years old presenting with syncope should have postural blood pressure evaluation because it has been shown to be high yield and costeffective in the evaluation and management of syncope.11 Choosing Wisely Campaign
From the American Academy of Neurology: Do not perform imaging of the carotid arteries for simple syncope without other neurologic symptoms. Occlusive carotid artery disease does not cause fainting but causes focal neurologic deficits such as unilateral weakness. Thus, carotid imaging will not identify the cause of the fainting and increases cost. Fainting is a frequent complaint, affecting 40% of people during their lifetime (http://www.choosingwisely.org/doctor-patient-lists/ american-academy-of-neurology/).
Syncope
From the American College of Physicians: In the evaluation of simple syncope and a normal neurologic examination, do not obtain brain imaging studies (CT or MRI). In patients with witnessed syncope but with no suggestion of seizure and no report of other neurologic symptoms or signs, the likelihood of a central nervous system cause of the event is extremely low and patient outcomes are not improved with brain imaging studies (http://www.choosingwisely.org/doctor-patient-lists/americancollege-of-physicians/). REFERENCES
1. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30(21):2631–71. 2. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res 2011;21(2):69–72. 3. Illman A, Stiller K, Williams M. The prevalence of orthostatic hypotension during physiotherapy treatment in patients with an acute spinal cord injury. Spinal Cord 2000;38(12):741–7. 4. Kenny RA, Bhangu J, King-Kallimanis BL. Epidemiology of syncope/collapse in younger and older Western patient populations. Prog Cardiovasc Dis 2013; 55(4):357–63. 5. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002;347(12):878–85. 6. Saklani P, Krahn A, Klein G. Syncope. Circulation 2013;127(12):1330–9. 7. Sun BC. Quality-of-life, health service use, and costs associated with syncope. Prog Cardiovasc Dis 2013;55(4):370–5. 8. Shukla GJ, Zimetbaum PJ. Cardiology patient page. Syncope. Circulation 2006; 113(16):e715–7. 9. Martin GJ, Adams SL, Martin HG, et al. Prospective evaluation of syncope. Ann Emerg Med 1984;13(7):499–504. 10. Krahn AD, Andrade JG, Deyell MW. Selecting appropriate diagnostic tools for evaluating the patient with syncope/collapse. Prog Cardiovasc Dis 2013;55(4): 402–9. 11. Mendu ML, McAvay G, Lampert R, et al. Yield of diagnostic tests in evaluating syncopal episodes in older patients. Arch Intern Med 2009;169(14):1299–305. 12. American Academy of Neurology Choosing Wisely working group. Choosing wisely: five things physicians and patients should question. 2013. Available at: http://www. choosingwisely.org/doctor-patient-lists/american-academy-of-neurology/. Accessed October 14, 2013. 13. Sheldon RS, Morillo CA, Krahn AD, et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol 2011;27(2):246–53. 14. Brignole M, Hamdan MH. New concepts in the assessment of syncope. J Am Coll Cardiol 2012;59(18):1583–91. 15. Brignole M, Croci F, Menozzi C, et al. Isometric arm counter-pressure maneuvers to abort impending vasovagal syncope. J Am Coll Cardiol 2002;40(11):2053–9. 16. Krediet CT, van Dijk N, Linzer M, et al. Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation 2002; 106(13):1684–9.
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MD,
Alicia Clark,
MD*
KEYWORDS Syncope Transient loss of consciousness Presyncope Reflex syncope Cardiovascular syncope Orthostatic hypotension KEY POINTS Syncope is a common problem and accounts for approximately 1% of all emergency room visits. Causes of syncope include reflex (neurally mediated), cardiovascular, and orthostatic hypotension. Collect a thorough history to determine if syncope has truly occurred; obtaining collateral history from a bystander may be necessary. Any abnormal vital sign can indicate a more serious underlying etiology for syncope and should be investigated. All patients presenting with syncope should have postural vital signs checked as this has been proven to be cost-effective and leads to a diagnosis in about 10% of cases. All patients aged 60 years and older presenting to the emergency room with syncope should be evaluated with an electrocardiogram. Carotid ultrasound and brain imaging with computed tomography scan or magnetic resonance imaging are not indicated unless there is a focal neurologic deficit. Consider cardiology consultation for patients with a suspected cardiac cause for syncope.
DEFINITIONS
How are syncope and presyncope defined? The European Society of Cardiology defines syncope as a transient loss of consciousness caused by cerebral hypoperfusion and characterized by quick onset, short duration, and complete recovery. The term presyncope is used to describe the prodromal symptoms of syncope, which are not followed by loss of consciousness; it is not known whether the mechanisms behind syncope and presyncope are the same.1
Disclosures: None. Hospital Medicine Program, Duke University Medical Center, Box 100800, Durham, NC 27710, USA * Corresponding author. E-mail address: [email protected] Hosp Med Clin 4 (2015) 65–73 http://dx.doi.org/10.1016/j.ehmc.2014.09.011 2211-5943/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
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What are the most common presentations confused with syncope? Syncope is distinguished from other causes of loss of consciousness by the mechanism by which an individual loses consciousness: global cerebral hypoperfusion. Conditions that cause partial or complete loss of consciousness not caused by cerebral hypoperfusion include: Epilepsy/seizures Metabolic disorders (eg, hypoglycemia, hypoxia, hyperventilation) Intoxication syndromes Vertebrobasilar transient ischemic attacks In contrast, multiple disorders exist that do not cause loss of consciousness but can be confused with syncope because of the description of the event and difficulty obtaining an accurate history. These disorders include: Falls Cataplexy Drop attacks Pyschogenic pseudosyncope Carotid transient ischemic attack1 What are the different causes of syncope? There are 3 main causes of syncope: reflex (neurally mediated), cardiovascular (eg, encompassing arrhythmias, structural heart disease), and orthostatic hypotension. Reflex (neurally mediated) syncope includes a varied group of conditions in which the usual cardiovascular reflexes that are typically useful in controlling hemodynamics are transiently inappropriate, caused by a specific trigger. This condition results in vasodilatation and/or bradycardia, which lead to a decrease in blood pressure.1 Causes of reflex syncope include: Vasovagal causes Mediated by emotional distress (fear, pain, blood or other phobia, instrumentation) Mediated by orthostatic stress Situational causes Cough/sneeze Gastrointestinal stimulation (eg, swallow, visceral pain, defecation) Micturition and postmicturition Postexercise Postprandial Other (laugh, playing brass instrument, weightlifting) Carotid sinus irritation Atypical forms (no apparent trigger or atypical presentation) Causes of cardiovascular syncope include: Arrhythmia Bradycardia - Sinus node dysfunction (including tachy-brady syndrome) - Atrioventricular conduction system disease - Implanted device malfunction Tachycardia - Supraventricular - Ventricular
Syncope
Drug-induced bradyarrhythmia or tachyarrhythmias Structural disease Cardiac - Cardiac valvular disease (most commonly aortic stenosis) - Acute myocardial infarction/ischemia, caused by arrhythmia or sudden decrease in cardiac output - Hypertrophic cardiomyopathy - Cardiac masses (eg, atrial myxoma and other tumors) - Pericardial disease/tamponade - Congenital anomalies of coronary arteries - Prosthetic valve dysfunction Noncardiac - Pulmonary embolus - Acute aortic dissection - Pulmonary hypertension Orthostatic hypotension is defined as a decrease of at least 20 mm Hg in systolic blood pressure and/or at least 10 mm Hg in diastolic blood pressure within 2 to 5 minutes of standing after a period of 5 minutes of supine rest.2 Causes of orthostatic hypotension and resulting syncope include: Primary autonomic failure Pure autonomic failure Parkinson disease with autonomic symptoms Multiple system atrophy (including Shy-Drager syndrome) Lewy body dementia Secondary autonomic failure Diabetes mellitus Uremia Spinal cord injury (particularly in quadriplegia)3 Amyloidosis Drugs or toxins Alcohol Vasodilators (eg, nitrates, hydralazine) Antihypertensives (eg, a-blockers, some b-blockers) Diuretics (eg, furosemide, hydrochlorothiazide) Antidepressants (eg, selective serotonin reuptake inhibitors, tricyclic antidepressants) Antipsychotics (eg, risperidone, olanzapine) Volume depletion Hemorrhage Nausea with vomiting Diarrhea Adapted from Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30(21):2631–71. EPIDEMIOLOGY
How common is syncope? It is often difficult to determine the incidence of syncope because of variation in definitions and patient under-reporting. The incidence of syncope increases with age and
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is more common in women than in men. The incidence in women aged 20 to 29 years is approximately 5%, compared with 50% for women more than 80 years of age. In a Dutch study, one-third of medical students (mean age 21 years) reported having a syncopal episode. A more recent data set of adults more than 50 years of age found that 4.4% had a syncopal event in the past year.4 How often is a cause of syncope found? In a review of patients enrolled in the Framingham Heart Study from 1971 to 1988 and reporting a syncopal event, an underlying cause was determined in 63.4% of cases; among those for whom a cause was found, vasovagal events accounted for 21.2%. Cardiovascular causes were implicated in 9.5% of cases, and orthostatic hypotension accounted for 9.4% of cases. For the remaining 36.6% of patients, there was no cause found.5 Other studies indicate that no cause for syncope is found in up to 50% of patients.6 What is the cost of working up syncope? Data from the United States Healthcare Utilization Project indicate that, for hospital admissions with a discharge diagnosis of syncope, annual hospital costs are nearly $3.8 billion with a mean cost of $8700 per admission.7 HISTORY AND EXAMINATION
What historical features help to differentiate the cause of syncope? Obtaining collateral history from a bystander can provide valuable information because an accurate history is often difficult to obtain from the patient and the description of the event can be the most important information for determining potential causes. Key features of the history that the evaluating physician should obtain include:
Circumstances of the event (preceding activities or situation) Hydration status of the patient8 The presence or absence of any prodromal symptoms (eg, palpitations) A description of the event itself, including the duration and what occurred during the event (eg, abnormal rhythmic jerking movements of the limbs, eye or head deviation, trauma during the event) The presence of any symptoms after the event (eg, postictal confusion) Past medical history, particularly any history of cardiac disease Family history, particularly a history of sudden cardiac death or other cardiac disease A full list of medications, including antihypertensives, diuretics, antidepressants, and antipsychotics6
What physical examination findings help determine the cause of syncope? Any abnormal vital sign (eg, bradycardia, tachycardia, or hypotension) Evidence of orthostatic hypotension Clinical evidence of heart failure (eg, increased jugular venous pressure, pulmonary crackles, an S3 or S4 on cardiac examination, hepatomegaly, or lowerextremity edema) Pronounced systolic ejection murmur or diastolic murmur suggesting valvular disease
Syncope
Any focal neurologic deficits Evidence of facial trauma attributable to the syncopal event6 DIAGNOSIS
What diagnostic tests are indicated when evaluating syncope? Given the high yield of postural blood pressure recording, this should be performed in all patients presenting with syncope who do not have a clearly identified alternate cause. The Agency for Healthcare Quality recommends checking orthostatic vital signs in the following manner: Ask the patient to lie in bed with the head flat for at least 3 minutes, but preferably 5 minutes. Measure the blood pressure and pulse while the patient is supine. Instruct the patient to sit for 1 minute. Ask about symptoms brought on by position change. Measure blood pressure and pulse. Instruct the patient to stand. Ask about symptoms brought on by position change. Measure blood pressure and pulse immediately after the patient has stood up and again 3 minutes after the patient stands. If at any time the patient is symptomatic or has a blood pressure less than 90/60 mm Hg, assist the patient back to a supine position. As noted earlier, orthostasis is defined as a decrease of at least 20 mm Hg in systolic blood pressure and/or at least 10 mm Hg in diastolic blood pressure. Additional testing that should be considered includes: Electrocardiogram (ECG) to evaluate for potential cardiovascular causes of syncope and to screen for risk of sudden cardiac death. Findings that put a patient in a higher risk category include evidence of underlying structural heart disease (eg, Q waves) or conduction disease (eg, PR/AV conduction delays, prolonged QT interval, Brugada, or preexcitation). The yield of ECG in determining a cause of syncope is less than 5%.9 Basic laboratory tests, including a complete blood count to rule out an acute anemia, as well as a basic metabolic panel with calcium and blood glucose. If the history, physical examination, or ECG suggests structural heart disease, a transthoracic echocardiogram should be obtained for diagnosis and risk stratification.1,10 Tilt table testing can be considered for cases in which reflex syncope is suspected but is not confirmed by initial evaluation.1 If a cardiac cause of syncope is identified, the patient should be evaluated by a cardiologist. Which tests are least cost-effective in the work-up of syncope? Elderly patients present more commonly than young patients with syncope and are more likely to be admitted to hospital for further evaluation. In a review of 2106 patients more than 65 years of age who presented with syncope and were admitted for evaluation, investigators found that the test with the highest yield (postural blood pressure recording) was performed less than 40% of the time. That review found that the results from cardiac enzymes, computed tomography (CT) scans, transthoracic echocardiogram, carotid ultrasonography, and electroencephalogram affected diagnosis or management in less than 5% of cases and was helpful in determining the cause of syncope less than 2% of the time.11
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According to the American Academy of Neurology as part of the Choosing Wisely campaign, occlusive carotid artery disease does not cause syncope but it can cause unilateral weakness or focal neurologic deficits. They recommend against performing carotid imaging in the work-up of syncope because it does not yield a diagnosis but does increase cost.12 The Canadian Cardiovascular Society recommends that CT scans of the brain should only be performed in patients with focal neurologic signs/symptoms or seizure activity or to rule out hemorrhage in patients with trauma.13 MANAGEMENT
Which patients with syncope require hospitalization? According to the European Society of Cardiology and the Canadian Cardiovascular Society, the following high-risk features should prompt hospitalization or urgent evaluation: Evidence or history of severe structural disease or coronary artery disease (eg, heart failure with low ejection fraction, previous myocardial infarction) ECG features suggesting arrhythmia-mediated syncope (eg, nonsustained ventricular tachycardia, bifascicular block, inappropriate sinus bradycardia, preexcited QRS complex, ECG suggesting inherited arrhythmogenic disorder) Clinical history suggesting an arrhythmic cause (eg, syncope during exertion or from the supine position, prodromal palpitations, lack of any prodromal symptoms, and family history of sudden cardiac death) Acute laboratory test abnormalities including severe anemia or electrolyte disturbance Vital sign abnormalities at the time of presentation (eg, systolic blood pressure <90 mm Hg)1,13,14 There are multiple emergency room decision rules that seek to stratify risk for patients presenting with syncope. At this time, according to the Canadian Cardiovascular Society, no decision rule increases diagnostic specificity or sensitivity or reduces costs.13 Which patients with syncope should be evaluated by a cardiologist? Any patient who has a clinical history and work-up that suggests cardiac syncope, especially patients with a family history of sudden cardiac death, ECG monitoring with evidence of arrhythmia, or a new diagnosis of structural heart disease, should undergo evaluation by a cardiologist. What are the indications for electrocardiographic monitoring? In general, electrocardiographic monitoring is indicated when there is a high pretest probability of detecting an arrhythmia associated with syncope (discussed earlier). Options for monitoring include in-hospital monitoring (telemetry), Holter monitoring, event monitoring, external or implantable loop recorders, and remote (at home) telemetry.1 In-hospital telemetry should be used when the patient is at high risk for a lifethreatening arrhythmia. This type of monitoring mitigates immediate risk to the patient while other work-up is underway.
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Holter monitors record continuously for 24 or 48 hours (or up to 7 days). Given that most syncopal events are infrequent, the limited time window of a Holter monitor often does not capture the event. However, for patients experiencing frequent events, this type of monitoring may be helpful in excluding arrhythmia as a cause for symptoms. Event recorders are used in the evaluation of palpitations but not syncope because they are devices activated by the patient after symptoms have started. External loop recorders are worn for about a month at a time and the patient activates the ECG monitoring when symptoms occur (electrodes are worn continuously). These recorders have been shown to have higher yield in the diagnosis of syncope than Holter monitors, but because of patient noncompliance and infrequent episodes of syncope, the yield is still only 25% at best.1 Implantable loop recorders should be considered only with input from a cardiologist because of cost and need for a minor surgical procedure. What are the treatments for the most common causes of syncope? The most common cause of syncope is reflex syncope, and there is limited efficacy in pharmacologic treatment of this condition. Management consists of patient education and awareness of this predisposition with specific avoidance of triggers. Patients are encouraged to maintain adequate hydration and immediately sit or get supine to decrease the risk of injury at the onset of any prodromal symptoms. The concept of physical counterpressure maneuvers is being more widely accepted in treatment of reflex syncope; isometric maneuvers such as leg crossing or hand grip have been shown to increase blood pressure sufficiently to abort the syncopal event.1,15,16 There are no conclusive data that any medications, including b-blockers and alpha-agonists such as midodrine, are effective for reflex syncope. Placement of a pacemaker has been shown to be effective in carotid sinus syndrome.1 Cardiovascular syncope is treated according to the primary underlying condition and should be guided by a cardiology consultant. Patients with symptomatic bradycardia causing syncope should be considered for pacemaker placement. Patients with primary arrhythmia as the cause for syncope may be treated with antiarrhythmic medications and/or ablation. Implantable cardiac defibrillators (ICDs) are considered in patients with high risk of sudden cardiac death. Valvular disease and outflow tract obstructions are managed with a combination of medications, percutaneous valve replacement, cardiac surgery, and consideration of an ICD.8 Orthostatic hypotension is most often managed acutely with volume expansion using crystalloid, repletion of electrolytes, and reversal of the process causing volume depletion. This management may include holding diuretics, supportive care for diarrheal illness, and blood transfusion for hemorrhagic anemia. Patients with orthostatic hypotension that persists after appropriate volume expansion should be worked up for other causes of autonomic failure. Patients may use abdominal binders or compression stockings to combat venous pooling in the lower extremities.1 There are more robust data for the use of the alpha-agonist midodrine in patients with orthostatic hypotension and autonomic failure; doses of 5 to 20 mg 3 times daily have been shown to be effective in 3 separate randomized placebo-controlled trials.1 What are the long-term outcomes for patients with syncope? In population-based studies, approximately one-third of patients with a syncopal event had a recurrence in 3 years. The strongest predictor of recurrence is the number of prior syncopal events; in patients with 1 or 2 lifetime events, recurrence rates were
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15% and 20% after 1 and 2 years, respectively. Patients with 3 or more lifetime events had recurrence rates of 36% and 42% after 1 and 2 years, respectively. Severity of the initial event, presence of structural heart disease, gender, and tilt table response have little or no predictive value in determining risk for recurrent events.1 Major traumatic morbidity, such as motor vehicle accidents and fractures, resulting from syncopal events affects about 6% of patients; minor traumatic morbidity, such as lacerations and bruises, affects about 29% of patients. Elderly patients experience morbidity from syncopal events in the form of depressive symptoms, fear of falling, loss of confidence, and fractures/traumatic injuries.1 CLINICAL GUIDELINES
European Society of Cardiology. Available at: http://eurheartj.oxfordjournals.org/ content/30/21/2631.full.pdf. Moya A, Sutton R, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30(21):2631–71. American Heart Association/American College of Cardiology Foundation. Available at: http://circ.ahajournals.org/content/113/2/316.full.pdf1html. Strickberger SA, Benson DW, et al. 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: endorsed by the American Autonomic Society. Circulation 2006;113(2): 316–27. Canadian Cardiovascular Society position paper. Available at: http://www. onlinecjc.ca/article/S0828-282X%2810%2900003-6/. Sheldon RS, Morillo CA, et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol 2011;27(2): 246–53. PRACTICE IMPROVEMENT
Patients aged 60 years and older presenting to the emergency room with syncope should be evaluated with an ECG. This recommendation is endorsed by the National Quality Forum and is included in Medicare’s Physician Quality Reporting Initiative (http://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/ PQRS/downloads/2008PQRIMeasurespecs.pdf) for patients discharged from the emergency room with a discharge diagnosis of syncope. Patients more than 65 years old presenting with syncope should have postural blood pressure evaluation because it has been shown to be high yield and costeffective in the evaluation and management of syncope.11 Choosing Wisely Campaign
From the American Academy of Neurology: Do not perform imaging of the carotid arteries for simple syncope without other neurologic symptoms. Occlusive carotid artery disease does not cause fainting but causes focal neurologic deficits such as unilateral weakness. Thus, carotid imaging will not identify the cause of the fainting and increases cost. Fainting is a frequent complaint, affecting 40% of people during their lifetime (http://www.choosingwisely.org/doctor-patient-lists/ american-academy-of-neurology/).
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From the American College of Physicians: In the evaluation of simple syncope and a normal neurologic examination, do not obtain brain imaging studies (CT or MRI). In patients with witnessed syncope but with no suggestion of seizure and no report of other neurologic symptoms or signs, the likelihood of a central nervous system cause of the event is extremely low and patient outcomes are not improved with brain imaging studies (http://www.choosingwisely.org/doctor-patient-lists/americancollege-of-physicians/). REFERENCES
1. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30(21):2631–71. 2. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res 2011;21(2):69–72. 3. Illman A, Stiller K, Williams M. The prevalence of orthostatic hypotension during physiotherapy treatment in patients with an acute spinal cord injury. Spinal Cord 2000;38(12):741–7. 4. Kenny RA, Bhangu J, King-Kallimanis BL. Epidemiology of syncope/collapse in younger and older Western patient populations. Prog Cardiovasc Dis 2013; 55(4):357–63. 5. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002;347(12):878–85. 6. Saklani P, Krahn A, Klein G. Syncope. Circulation 2013;127(12):1330–9. 7. Sun BC. Quality-of-life, health service use, and costs associated with syncope. Prog Cardiovasc Dis 2013;55(4):370–5. 8. Shukla GJ, Zimetbaum PJ. Cardiology patient page. Syncope. Circulation 2006; 113(16):e715–7. 9. Martin GJ, Adams SL, Martin HG, et al. Prospective evaluation of syncope. Ann Emerg Med 1984;13(7):499–504. 10. Krahn AD, Andrade JG, Deyell MW. Selecting appropriate diagnostic tools for evaluating the patient with syncope/collapse. Prog Cardiovasc Dis 2013;55(4): 402–9. 11. Mendu ML, McAvay G, Lampert R, et al. Yield of diagnostic tests in evaluating syncopal episodes in older patients. Arch Intern Med 2009;169(14):1299–305. 12. American Academy of Neurology Choosing Wisely working group. Choosing wisely: five things physicians and patients should question. 2013. Available at: http://www. choosingwisely.org/doctor-patient-lists/american-academy-of-neurology/. Accessed October 14, 2013. 13. Sheldon RS, Morillo CA, Krahn AD, et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol 2011;27(2):246–53. 14. Brignole M, Hamdan MH. New concepts in the assessment of syncope. J Am Coll Cardiol 2012;59(18):1583–91. 15. Brignole M, Croci F, Menozzi C, et al. Isometric arm counter-pressure maneuvers to abort impending vasovagal syncope. J Am Coll Cardiol 2002;40(11):2053–9. 16. Krediet CT, van Dijk N, Linzer M, et al. Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation 2002; 106(13):1684–9.
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