Syncope overview

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Overview
Historical Perspective
Classification
Pathophysiology
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Differentiating Syncope from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
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CT
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Sahar Memar Montazerin, M.D.[3]

Overview

Syncope is defined as abrupt, transient complete loss of consciousness, inability to keep postural tone, rapid spontaneous recovery with the mechanism of cerebral hypoperfusion. Syncope is usually classified based on the underlying mechanisms leading to hypoperfusion. Syncope is classified to reflex-mediated, orthostatic hypotension, and cardiovascular and syncope of unknown origin subtypes. Neurally mediated syncope (common faint) is the most common type of reflex syncope in younger patients occurs during upright position ( standing , sitting) with prodrome symptoms including diaphoresis, warmth, nausea, and pallor, usually after emotional stress, pain, medical setting. Orthostasis hypotension is defined as reduction in systolic blood pressure of ≥20 mmHg or diastolic blood pressure of ≥10 mm Hg within 3 minutes of standing position and is common in older patients. Carotid sinus syndrome is a type of reflex syncope due to carotid sinus hypersensitivity defined as pause ≥3 seconds and/or a reduction of systolic blood pressure ≥50 mm Hg during stimulation of the carotid sinus, and is more common in older patients. Taking history and [[physical examination] may helpful for the diagnosis. There are some conditions that are incorrectly diagnosed as syncope. These conditions are usually associated with partial or complete loss of consciousness such as epilepsy, metabolic disorders, transient ischemic attack or conditions with loss of posture and without loss of consciousness like cataplexy, drop attacks, falls and pseudo-syncope.There is limited information about the historical perspective of syncope.There are several pathways to explain its pathophysiology, depending on if it is either reflex syncope, orthostatic intolerance, or cardiovascular syncope. Peripheral vascular resistance and cardiac output are the two main determinants for the presentation of syncope. autonomic nervous system impairment due to drugs or an autonomic failure, can lead to a decrease in peripheral vascular resistance. Reflex activity impairment may also cause a decrease of peripheral vascular resistance, as the body normal compensation reflexes fail. Decrease in cardiac output may be due to venous pooling, cardioinhibitory reflexes, arrhythmia, hypertension, pulmonary embolism, and volume depletion leading to diminished venous return, among others. Syncope should be differentiated from other conditions causing partial or complete loss of consciousness. These disorders may include, coma, dizziness, seizure, and vertigo. There are conditions that may mistakenly be diagnosed as syncope. These conditions include epilepsy, hypoglycemia, intoxication, cataplexy, and transient ischemic attacks. The incidence of syncope ranges from 260 to 1950 cases per 100,000 individuals worldwide. It increases with age and especially after age 70 years old. Syncope affects men and women equally. Syncope is a sign of insufficient cerebral blood flow and it should be evaluated for the underlying cause. Possible underlying risk factors of cardiac syncope include Older age (>60 y), male sex, presence of known ischemic heart disease, structural heart disease, previous arrhythmias, or reduced ventricular function, brief prodromes such as palpitations or sudden loss of consciousness without a prodrome, syncope during exertion, syncope in the supine position, low number of syncope episodes (1 or 2), abnormal cardiac examination, family history of inheritable conditions or premature sudden cardiac death (SCD) (<50 y of age), Presence of known congenital heart disease. Common risk factors associated with noncardiac causes of syncope include younger age, no known cardiac disease, syncope only in the standing position, positional change from supine or sitting to standing, presence of prodrome: nausea, vomiting, feeling warm, presence of specific triggers ||||( dehydration, pain, stressful stimulus, medical environment), situational triggers( cough, laugh, micturition, defecation, deglutition), history of syncope with similar characteristics and frequent recurrence.Patients with syncope are at risk of the development of complications, such as trauma from frequent falls and Sudden cardiac death. The prognosis of syncope depends on underlying causes. Syncope caused by cardiovascular diseases may be life-threatening and is an important cause of sudden cardiac death. Prognosis of vasovagal syncope is favorable. Syncope itself is a symptom. Patients with syncope may feel balcking out, dizziness, lightheadedness, and temporary loss of consciousness. Patients may experience other symptoms based on the underlying causes of the syncope.Patients with syncope usually appear normal. Physical examination of patients with syncope is usually remarkable for cardiac murmur, orthostatic hypotension, and altered level of consciousness during the episode of syncope.There are no diagnostic laboratory findings associated with syncope. Some patients with syncope may have acidosis, which is usually suggestive of insufficient blood flow. Other possible laboratory findings may include hypoglycemia, increased lactate level, hypoxia, and hypercapnia. Generally, the ECG of individuals with syncope is normal. However, ECG may be remarkable for an arrhythmia. The arrhythmia may be seen on the EKG include sinus bradycardia <40 beats/min or repetitive sinoatrial blocks or sinus pauses > 3s, Mobitz II 2nd or 3rd-degree atrioventricular block, alternating left and right bundle branch block, rapid paroxysmal supraventricular tachycardia, ventricular tachycardia, and pacemaker malfunction with cardiac pauses.CXR is necessary for evaluation of patients presented with syncope and abnormal findings may be suggestive of adverse event. Transthoracic echocardiography can be useful in the diagnostic workup of patients presenting with syncope. This evaluation is especially warranted in patients who are suspected to have structural heart disease. CT scan is useful when other modalities are inconclusive for evaluation of structural heart disease in the presence of syncope.If syncope is suspected due to pulmonary thromboembolism CT scan is recommended. Cardiac MRI can be useful in the presence of syncope and suspected structural or infiltrative heart disease such as arrhythmogenic right ventricular dysplasia or cardiac sarcoidosis. Other diagnostic studies for syncope include tilt table test and Exercise Stress Test. Tilt table test is especially useful in differentiating syncope from other possible causes of transient loss of consciousness, such as epilepsy and conversion disorder. A tilt table test can help to reveal Vasovagal syncope or hypotensive syncope. The patient is on the table is tilted at 70 degrees for 45 minutes. A positive test is defined induced hypotension with or without bradycardia or asystole suggestive of vasovagal syncope. If hypotension occurs within the first 3 minutes of test orthostasis hypotension is concerned. In delay orthostasis hypotension fall in blood pressure occurs after 3 minutes. Exercise stress test (EST) is recommended in the presence of syncope during exercise or syncope during the occurrence of angina pectori suspected myocardial ischemia. Contraindications for EST in patients with syncope include: hypertrophic obstructive cardiomyopathy, severe aortic stenosis,Catecholaminegic polymorphic ventricular tachycardia(CPVT), pulmonary artery hepertension,Interarterial anomalous coronary artery ,Long QT syndrome type 1. Medical therapy is the mainstay of the treatment based on the cause and mechanism of syncope for preventing syncope recurrences and traumatic injuries and prolong survival. All patients with cardiac syncope should be hospitalized. If the machanism of syncope is bifascicular block, permanent pacemaker is recommended. In the setting of inferior myocardial infarction and complete heart block, implantation of permanent pacemaker is not the first decision and the best approach is treatment of myocardial infarction. In syncope secondary to documented VT, VF due to structural heart disease such as ischemic and non-ischemic cardiomyopathy and decreased left ventricular ejection fraction treatment of arrhythmia and ICD implantation is warranted. In VT secondary to sarcoidosis and frequent syncope due to reentry arrhythmia loop around the granulom formation in myocardium, ICD implantation is necessary. In inherent causes of ventricular tachyarrhythmia such as Long QT syndrome, Short QT syndrome, Brugada, Cathecolaminegic polymorphic ventricular tachycardia (CPVT), Arrhythmogenic right ventricular dysplasia(ARVC) making decision for ICD implantation is associated with documented ventricular tachyarrhythmia. For other type of syncope increasing salt and discontinuation of causing medications and education of the patient is recommended. Patients with neurally mediated syncope should be educated about participate factors such as dehydration,prolong standing, alcohol,diuretic, vasodilators and sitting down or lie-down at the onset of symptoms and doing counterpressure maneuvers( hand gripping, leg crossing, arm tensing). Medications may be helpful in neurally mediated syncope include betablocker,midoderine, SSRI. Ingestion of 500 cc water acutely prevents hypotensive syncope. Some of the measures that can be taken to prevent vasovagal syncopal episodes include avoidance of prolonged standing, hot environment, humid atmosphere. Secondary prevention strategies following syncope include ICD implantation in ventricular arrhythmia and avoidance of driving for a specific time based on the guideline.

Historical Perspective

There is limited information about the historical perspective of syncope.

Classification

Syncope is defined as abrupt, transient complete loss of consciousness, inability to keep postural tone, rapid spontaneous recovery with the mechanism of cerebral hypoperfusion. Syncope is usually classified based on the underlying mechanisms leading to hypoperfusion. Syncope is classified to reflex-mediated, orthostatic hypotension, and cardiovascular subtypes. Neurally mediated syncope (common faint) is the most common type of reflex syncope in younger patients occurs during upright position ( standing , sitting) with prodrome symptoms including diaphoresis, warmth, nausea, and pallor, usually after emotional stress, pain, medical setting. Orthostasis hypotension is defined as reduction in systolic blood pressure of ≥20 mmHg or diastolic blood pressure of ≥10 mm Hg within 3 minutes of standing position and is common in older patients. Carotid sinus syndrome is a type of reflex syncope due to carotid sinus hypersensitivity defined as pause ≥3 seconds and/or a reduction of systolic blood pressure ≥50 mm Hg during stimulation of the carotid sinus is more common in older patients. Taking history and physical examination may helpful for the diagnosis. There are some conditions that are incorrectly diagnosed as syncope. These conditions are usually associated with partial or complete loss of consciousness such as epilepsy, metabolic disorders, transient ischemic attack or conditions with loss of posture and without loss of consciousness like cataplexy, drop attacks, falls and pseudo-syncope.

Pathophysiology

Syncope is an entity in which loss of conscience due to cerebral hypoperfusion presents. There are several pathways to explain its pathophysiology, depending on if it is either reflex syncope, orthostatic intolerance, or cardiovascular syncope.

Causes

Peripheral vascular resistance and cardiac output are the two main determinants for the presentation of syncope. autonomic nervous system impairment due to drugs or an autonomic failure, can lead to a decrease in peripheral vascular resistance. Reflex activity impairment may also cause a decrease of peripheral vascular resistance, as the body normal compensation reflexes fail. Decrease in cardiac output may be due to venous pooling, cardioinhibitory reflexes, arrhythmia, hypertension, pulmonary embolism, and volume depletion leading to diminished venous return, among others.

Differentiating Syncope from other Diseases

Syncope should be differentiated from other conditions causing partial or complete loss of consciousness. These disorders may include, coma, dizziness, seizure, and vertigo. There are conditions that may mistakenly be diagnosed as syncope. These conditions include epilepsy, hypoglycemia, intoxication, cataplexy, and transient ischemic attacks.

Epidemiology and Demographics

The incidence of syncope ranges from 260 to 1950 cases per 100,000 individuals worldwide. It increases with age and especially after age 70 years old. Syncope affects men and women equally.

Risk Factors

Syncope is a sign of insufficient cerebral blood flow and it should be evaluated for the underlying cause. Possible underlying risk factors of cardiac syncope include Older age (>60 y), male sex, presence of known ischemic heart disease, structural heart disease, previous arrhythmias, or reduced ventricular function, brief prodromes such as palpitations or sudden loss of consciousness without a prodrome, syncope during exertion, syncope in the supine position, low number of syncope episodes (1 or 2), abnormal cardiac examination, family history of inheritable conditions or premature sudden cardiac death (SCD) (<50 y of age), Presence of known congenital heart disease. Common risk factors associated with noncardiac causes of syncope include younger age, no known cardiac disease, syncope only in the standing position, positional change from supine or sitting to standing, presence of prodrome: nausea, vomiting, feeling warm, presence of specific triggers ||||( dehydration, pain, stressful stimulus, medical environment), situational triggers( cough, laugh, micturition, defecation, deglutition), history of syncope with similar characteristics and frequent recurrence.

Natural History, Complications, and Prognosis

Patients with syncope are at risk of the development of complications, such as trauma from frequent falls and Sudden cardiac death. The prognosis of syncope depends on underlying causes. Syncope caused by cardiovascular diseases may be life-threatening and is an important cause of sudden cardiac death. Prognosis of vasovagal syncope is favorable.

Diagnosis

History and Symptoms

Syncope itself is a symptom. Patients with syncope may feel balcking out, dizziness, lightheadedness, and temporary loss of consciousness. Patients may experience other symptoms based on the underlying causes of the syncope.

Physical Examination

Patients with syncope usually appear normal. Physical examination of patients with syncope is usually remarkable for cardiac murmur, orthostatic hypotension, and altered level of consciousness.

Laboratory Findings

There are no diagnostic laboratory findings associated with syncope. Some patients with syncope may have acidosis, which is usually suggestive of insufficient blood flow. Other possible laboratory findings may include hypoglycemia, increased lactate level, hypoxia, and hypercapnia.

Electrocardiogram

Generally, the ECG of individuals with syncope is normal. However, ECG may be remarkable for an arrhythmia. The arrhythmia may be seen on the EKG include sinus bradycardia <40 beats/min or repetitive sinoatrial blocks or sinus pauses > 3s, Mobitz II 2nd or 3rd-degree atrioventricular block, alternating left and right bundle branch block, rapid paroxysmal supraventricular tachycardia, ventricular tachycardia, and pacemaker malfunction with cardiac pauses.

X-ray

CXR is necessary for evaluation of patients presented with syncope and abnormal findings may be suggestive of adverse event.

CT

CT scan is useful when other modalities are inconclusive for evaluation of structural heart disease in the presence of syncope.(Class2b, 2017AHA/ACC/HRS guideline). If syncope is suspected due to pulmonary thromboembolism CT scan is recommended.

MRI

Cardiac MRI can be useful in the presence of syncope and suspected structural or infiltrative heart disease such as arrhythmogenic right ventricular dysplasia or cardiac sarcoidosis.

Echocardiography

Transthoracic echocardiography can be useful in the diagnostic workup of patients presenting with syncope. This evaluation is especially warranted in patients who are suspected to have structural heart disease.

Other Diagnostic Studies

There are no other imaging findings associated with syncope.

Other Diagnostic Studies

Other diagnostic studies for syncope include tilt table test and Exercise Stress Test. Tilt table test is especially useful in differentiating syncope from other possible causes of transient loss of consciousness, such as epilepsy and conversion disorder. A tilt table test can help to reveal Vasovagal syncope or hypotensive syncope. The patient is on the table is tilted at 70 degrees for 45 minutes. A positive test is defined induced hypotension with or without bradycardia or asystoe suggestive of vasovagal syncope. If hypotension occurs within the first 3 minutes of test orthostasis hypotension is concerned. In delay orthostasis hypotension fall in blood pressure occurs after 3 minutes. Exercise stress test (EST) is recommended in the presence of syncope during exercise or syncope during the occurrence of angina pectori suspected myocardial ischemia. Contraindications for EST in patients with syncope include: hypertrophic obstructive cardiomyopathy, severe aortic stenosis,Catecholaminegic polymorphic ventricular tachycardia(CPVT), pulmonary artery hepertension,Interarterial anomalous coronary artery ,Long QT syndrome type 1.

Treatment

Medical Therapy

Medical therapy is the mainstay of the treatment based on the cause and mechanism of syncope for preventing syncope recurrences and traumatic injuries and prolong survival. All patients with cardiac syncope should be hospitalized. If the machanism of syncope is bifascicular block, permanent pacemaker is recommended. In the setting of inferior myocardial infarction and complete heart block, implantation of permanent pacemaker is not the first decision and the best approach is treatment of myocardial infarction. In syncope secondary to documented VT, VF due to structural heart disease such as ischemic and non-ischemic cardiomyopathy and decreased left ventricular ejection fraction treatment of arrhythmia and ICD implantation is warranted. In VT secondary to sarcoidosis and frequent syncope due to reentry arrhythmia loop around the granulom formation in myocardium, ICD implantation is necessary. In inherent causes of ventricular tachyarrhythmia such as Long QT syndrome, Short QT syndrome, Brugada, Cathecolaminegic polymorphic ventricular tachycardia (CPVT), Arrhythmogenic right ventricular dysplasia(ARVC) making decision for ICD implantation is associated with documented ventricular tachyarrhythmia. For other type of syncope increasing salt and discontinuation of causing medications and education of the patient is recommended. Patients with neurally mediated syncope should be educated about participate factors such as dehydration,prolong standing, alcohol,diuretic, vasodilators and sitting down or lie-down at the onset of symptoms and doing counterpressure maneuvers( hand gripping, leg crossing, arm tensing). Medications may be helpful in neurally mediated syncope include betablocker,midoderine, SSRI.

Surgery

Surgical intervention is not recommended for the management of syncope.

Primary Prevention

Some of the measures that can be taken to prevent vasovagal syncopal episodes include avoidance of prolonged standing, hot environment, humid atmosphere.

Secondary Prevention

Secondary prevention strategies following syncope include ICD implantation in ventricular arrhythmia and avoidance of driving for a specific time based on the guideline.