Cardiovascular Syncope
A. Definition
Syncope is a sudden loss of consciousness of brief duration.
B. Pathophysiology
Cardiovascular syncope occurs when the brain's metabolic needs cannot be met by the available blood supply. Adequate perfusion is dependent on an adequate systemic blood pressure: BP = CO أ— SVR (where BP = blood pressure, CO = cardiac output, and SVR = systemic vascular resistance). Therefore, a fall in cardiac output or a fall in systemic vascular resistance can precipitate a fall in blood pressure, leading to syncope. Because CO = SV أ— HR (where SV = stroke volume and HR = heart rate), either inadequate stroke volume or inadequate heart rate reduces cardiac output, potentially leading to hypotension and syncope.
C. Etiology
1. Reduced cardiac output
a. Bradycardia
(1) Heart block. A block in the cardiac conduction pathway may prevent the SA nodal electrical signal for ventricular contraction from being transmitted, in turn causing bradycardia. Whether syncope occurs depends on whether an alternative, lower pacemaker (e.g., the AV junction) produces an escape rate that is sufficiently fast to maintain blood pressure.
(2) Sick sinus syndrome occurs when there is a deficit in impulse generation from the SA node, which may lead to bradycardia and syncope.
(a) Profound sinus bradycardia, sinus arrest, and the tachycardia–bradycardia syndrome are the arrhythmias that constitute the sick sinus syndrome. The tachycardia–bradycardia syndrome is one of atrial instability where supraventricular tachycardia halts abruptly and is followed by severe bradycardia.
(b) Sick sinus syndrome may result from ischemic heart disease and idiopathic or inflammatory degeneration of the SA node.
b. Impaired stroke volume. The rhythmic filling and emptying of the left ventricle generates its stroke volume; therefore, conditions that either inhibit left ventricular filling or inhibit left ventricular emptying can severely reduce stroke volume, leading to hypotension and syncope.
(1) Conditions that limit left ventricular filling
(a) Obstruction to inflow. Any mechanical block in the cardiovascular system that inhibits filling of the left ventricle impairs its output. Such obstructions include mitral stenosis, left atrial myxoma, right atrial myxoma, pulmonary embolism, and pulmonic stenosis.
(b) Tachycardia. Both ventricular tachycardia and very rapid supraventricular tachycardia reduce the diastolic filling period of the left ventricle, limiting its filling and reducing its stroke volume. In ventricular tachycardia, the shortened diastolic filling period is compounded by incomplete ventricular relaxation, which further limits filling.
(c) Impaired systemic venous return. Failure of adequate systemic venous return to the right heart subsequently impairs its output to the left heart, impairing left ventricular stroke volume.
(i) Typically, impaired venous return occurs when the supine patient assumes the upright posture.
(ii) Normally, the tendency for gravity-induced venous pooling of blood in the legs is offset by venous vasoconstriction, which helps maintain venous return. However, in the face of dehydration, antihypertensive drugs, or autonomic dysfunction, impaired venous return may produce orthostatic syncope. Autonomic dysfunction may be idiopathic; familial; surgically induced; or result from diabetes, alcoholism, or pyridoxine deficiency.
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(2) Conditions that impair left ventricular emptying. The left ventricle may be impaired from emptying either as a result of a severe, sudden depression in myocardial contractile function or as a result of outflow obstruction.
(a) Decreased myocardial contractility. The sudden and severe degree of contractile depression required to cause syncope is almost invariably caused by global ischemia produced by left main or triple-vessel coronary disease, acute MI, ventricular tachycardia, or ventricular fibrillation.
(b) Obstruction to outflow. Obstruction of left ventricular outflow that produces syncope is caused by valvular aortic stenosis and hypertrophic cardiomyopathy.
2. Reduced total peripheral resistance. If cardiac output is maintained but total peripheral resistance falls, blood pressure also falls, potentially causing syncope.
a. An inappropriate fall in total peripheral resistance is usually operative in the common fainting spell. Increased blood flow to the skeletal muscles due to a fall in total peripheral resistance may divert flow from the brain and result in fainting. Venodilation and relative bradycardia may further compound the “vasovagal faint†by reducing venous return and cardiac output.
b. Reduced total peripheral resistance leading to syncope may also occur in drug-induced, familial, or idiopathic autonomic dysfunction.
D. Diagnosis
A single fainting episode or episode of light-headedness occurs in more than 50% of the population at some point in a lifetime. It would be impossible to explore the cause of the event extensively in every affected patient. A good history and physical examination should be adequate to exclude potentially serious causes of a single episode of syncope. However, recurrent syncope requires a more extensive workup.
1. History. A thorough patient interview can reveal clues that may point to a specific etiology for the recurrent syncope.
a. A history of palpitations might indicate an arrhythmia.
b. The observation that syncope occurred upon assumption of an upright position suggests orthostatic hypotension.
c. A history of chest pain might indicate an ischemic event or pulmonary embolism.
d. A change in antihypertensive medication or a recent episode of dehydration are additional clues.
e. A history of a prior MI and reduced left ventricular function suggests the possibility of a ventricular arrhythmia.
2. Physical examination. Those maneuvers that might reveal a reason for hypotension and possible syncope should be emphasized.
a. Blood pressure
(1) The blood pressure should be recorded in both arms in both the supine and the sitting or standing positions.
(2) On assuming an upright posture, it is normal for systolic blood pressure to fall slightly while diastolic pressure increases. There is also usually a slight increase in heart rate.
(a) A frank decline in systolic and diastolic pressure on assuming an upright posture may indicate volume depletion or sympathetic compensation that is inadequate to counteract the change in posture.
(b) A fall in diastolic pressure of more than 10 mm Hg is significant and may suggest an orthostatic etiology of the syncope.
b. Heart rate and rhythm. The pulse should be examined for an extended period of time in an effort to detect arrhythmia or bradycardia.
c. Valvular obstruction. The murmurs and physical findings associated with mitral stenosis, aortic stenosis, pulmonic stenosis, or idiopathic hypertrophic subaortic stenosis should be recognized as indications of potentially correctable mechanisms for syncope.
d. Thromboembolism. Thrombophlebitis in the lower limbs indicates a source of pulmonary emboli, which can cause syncope. Physical evidence that a pulmonary embolus is present includes wheezing, increased intensity of the pulmonary component of the S2, and jugular venous distention.
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3. Electrocardiography. If second- or third-degree AV block is detected, it demonstrates the likely cause of the syncope. Bundle branch block and arrhythmias, or both, on the standard ECG should raise suspicion that heart block or arrhythmia are syncopal etiologies.
4. Holter monitoring. If the history, physical examination, and ECG point to an arrhythmia as the potential cause of the syncope, Holter monitoring may be performed. It records each heart beat over a 24-hour period, which is then reviewed for arrhythmia. Unfortunately, because most arrhythmias occur sporadically, most Holter monitor examinations are negative even when an arrhythmia is the source of the syncope.
5. Event monitors. These devices are worn or carried for several weeks. They are activated by the patient at the time of symptoms and document the rhythm before and after activation. The recording is then reviewed for arrhythmia.
6. Electrophysiologic testing. If the initial work-up demonstrates that heart disease is present but fails to demonstrate a specific cause of syncope, electrophysiologic stimulation may provoke the arrhythmia responsible for the syncope. Having established an arrhythmic cause, the proper therapy may then be instituted.
E. Therapy
1. Therapy for bradyarrhythmias. When a bradyarrhythmia has been established as the cause of the syncope, drug-induced bradycardia should be ruled out as a cause by discontinuing potentially offending drugs. If symptomatic bradycardia persists, a permanent pacemaker is indicated.
2. Therapy for tachyarrhythmias
a. Drug therapy for both ventricular and supraventricular tachyarrhythmias that have caused an episode of syncope is clearly indicated [see II D 1 b (3)]. In general, such therapy should be guided by electrophysiologic testing.
b. Antitachycardia pacemakers or implantable defibrillators may be used to electrically correct arrhythmias if drug therapy fails.
3. Therapy for autonomic dysfunction. If autonomic dysfunction is the cause of orthostatic hypotension and syncope, little can be done directly to treat the underlying cause. Instead, therapies to protect the patient from possible hypotension should be instituted. These include high salt intake or fludrocortisone to ensure volume expansion, support stockings to prevent venous pooling, or midodrine to increase peripheral vascular resistance. There may be a role for permanent cardiac pacing in a select group of patients for whom other forms of therapy have failed.
4. Correction of mechanical obstructions to cardiac inflow or outflow. Any fixed valvular lesion that has caused an episode of syncope should be corrected. If idiopathic hypertrophic subaortic stenosis is determined to be the cause of the syncope, standard therapy with propranolol or verapamil is indicated to reduce the amount of outflow obstruction. If medical therapy fails, myomectomy or alcohol septal ablation may be necessary.
A. Definition
Syncope is a sudden loss of consciousness of brief duration.
B. Pathophysiology
Cardiovascular syncope occurs when the brain's metabolic needs cannot be met by the available blood supply. Adequate perfusion is dependent on an adequate systemic blood pressure: BP = CO أ— SVR (where BP = blood pressure, CO = cardiac output, and SVR = systemic vascular resistance). Therefore, a fall in cardiac output or a fall in systemic vascular resistance can precipitate a fall in blood pressure, leading to syncope. Because CO = SV أ— HR (where SV = stroke volume and HR = heart rate), either inadequate stroke volume or inadequate heart rate reduces cardiac output, potentially leading to hypotension and syncope.
C. Etiology
1. Reduced cardiac output
a. Bradycardia
(1) Heart block. A block in the cardiac conduction pathway may prevent the SA nodal electrical signal for ventricular contraction from being transmitted, in turn causing bradycardia. Whether syncope occurs depends on whether an alternative, lower pacemaker (e.g., the AV junction) produces an escape rate that is sufficiently fast to maintain blood pressure.
(2) Sick sinus syndrome occurs when there is a deficit in impulse generation from the SA node, which may lead to bradycardia and syncope.
(a) Profound sinus bradycardia, sinus arrest, and the tachycardia–bradycardia syndrome are the arrhythmias that constitute the sick sinus syndrome. The tachycardia–bradycardia syndrome is one of atrial instability where supraventricular tachycardia halts abruptly and is followed by severe bradycardia.
(b) Sick sinus syndrome may result from ischemic heart disease and idiopathic or inflammatory degeneration of the SA node.
b. Impaired stroke volume. The rhythmic filling and emptying of the left ventricle generates its stroke volume; therefore, conditions that either inhibit left ventricular filling or inhibit left ventricular emptying can severely reduce stroke volume, leading to hypotension and syncope.
(1) Conditions that limit left ventricular filling
(a) Obstruction to inflow. Any mechanical block in the cardiovascular system that inhibits filling of the left ventricle impairs its output. Such obstructions include mitral stenosis, left atrial myxoma, right atrial myxoma, pulmonary embolism, and pulmonic stenosis.
(b) Tachycardia. Both ventricular tachycardia and very rapid supraventricular tachycardia reduce the diastolic filling period of the left ventricle, limiting its filling and reducing its stroke volume. In ventricular tachycardia, the shortened diastolic filling period is compounded by incomplete ventricular relaxation, which further limits filling.
(c) Impaired systemic venous return. Failure of adequate systemic venous return to the right heart subsequently impairs its output to the left heart, impairing left ventricular stroke volume.
(i) Typically, impaired venous return occurs when the supine patient assumes the upright posture.
(ii) Normally, the tendency for gravity-induced venous pooling of blood in the legs is offset by venous vasoconstriction, which helps maintain venous return. However, in the face of dehydration, antihypertensive drugs, or autonomic dysfunction, impaired venous return may produce orthostatic syncope. Autonomic dysfunction may be idiopathic; familial; surgically induced; or result from diabetes, alcoholism, or pyridoxine deficiency.
P.40
(2) Conditions that impair left ventricular emptying. The left ventricle may be impaired from emptying either as a result of a severe, sudden depression in myocardial contractile function or as a result of outflow obstruction.
(a) Decreased myocardial contractility. The sudden and severe degree of contractile depression required to cause syncope is almost invariably caused by global ischemia produced by left main or triple-vessel coronary disease, acute MI, ventricular tachycardia, or ventricular fibrillation.
(b) Obstruction to outflow. Obstruction of left ventricular outflow that produces syncope is caused by valvular aortic stenosis and hypertrophic cardiomyopathy.
2. Reduced total peripheral resistance. If cardiac output is maintained but total peripheral resistance falls, blood pressure also falls, potentially causing syncope.
a. An inappropriate fall in total peripheral resistance is usually operative in the common fainting spell. Increased blood flow to the skeletal muscles due to a fall in total peripheral resistance may divert flow from the brain and result in fainting. Venodilation and relative bradycardia may further compound the “vasovagal faint†by reducing venous return and cardiac output.
b. Reduced total peripheral resistance leading to syncope may also occur in drug-induced, familial, or idiopathic autonomic dysfunction.
D. Diagnosis
A single fainting episode or episode of light-headedness occurs in more than 50% of the population at some point in a lifetime. It would be impossible to explore the cause of the event extensively in every affected patient. A good history and physical examination should be adequate to exclude potentially serious causes of a single episode of syncope. However, recurrent syncope requires a more extensive workup.
1. History. A thorough patient interview can reveal clues that may point to a specific etiology for the recurrent syncope.
a. A history of palpitations might indicate an arrhythmia.
b. The observation that syncope occurred upon assumption of an upright position suggests orthostatic hypotension.
c. A history of chest pain might indicate an ischemic event or pulmonary embolism.
d. A change in antihypertensive medication or a recent episode of dehydration are additional clues.
e. A history of a prior MI and reduced left ventricular function suggests the possibility of a ventricular arrhythmia.
2. Physical examination. Those maneuvers that might reveal a reason for hypotension and possible syncope should be emphasized.
a. Blood pressure
(1) The blood pressure should be recorded in both arms in both the supine and the sitting or standing positions.
(2) On assuming an upright posture, it is normal for systolic blood pressure to fall slightly while diastolic pressure increases. There is also usually a slight increase in heart rate.
(a) A frank decline in systolic and diastolic pressure on assuming an upright posture may indicate volume depletion or sympathetic compensation that is inadequate to counteract the change in posture.
(b) A fall in diastolic pressure of more than 10 mm Hg is significant and may suggest an orthostatic etiology of the syncope.
b. Heart rate and rhythm. The pulse should be examined for an extended period of time in an effort to detect arrhythmia or bradycardia.
c. Valvular obstruction. The murmurs and physical findings associated with mitral stenosis, aortic stenosis, pulmonic stenosis, or idiopathic hypertrophic subaortic stenosis should be recognized as indications of potentially correctable mechanisms for syncope.
d. Thromboembolism. Thrombophlebitis in the lower limbs indicates a source of pulmonary emboli, which can cause syncope. Physical evidence that a pulmonary embolus is present includes wheezing, increased intensity of the pulmonary component of the S2, and jugular venous distention.
P.41
3. Electrocardiography. If second- or third-degree AV block is detected, it demonstrates the likely cause of the syncope. Bundle branch block and arrhythmias, or both, on the standard ECG should raise suspicion that heart block or arrhythmia are syncopal etiologies.
4. Holter monitoring. If the history, physical examination, and ECG point to an arrhythmia as the potential cause of the syncope, Holter monitoring may be performed. It records each heart beat over a 24-hour period, which is then reviewed for arrhythmia. Unfortunately, because most arrhythmias occur sporadically, most Holter monitor examinations are negative even when an arrhythmia is the source of the syncope.
5. Event monitors. These devices are worn or carried for several weeks. They are activated by the patient at the time of symptoms and document the rhythm before and after activation. The recording is then reviewed for arrhythmia.
6. Electrophysiologic testing. If the initial work-up demonstrates that heart disease is present but fails to demonstrate a specific cause of syncope, electrophysiologic stimulation may provoke the arrhythmia responsible for the syncope. Having established an arrhythmic cause, the proper therapy may then be instituted.
E. Therapy
1. Therapy for bradyarrhythmias. When a bradyarrhythmia has been established as the cause of the syncope, drug-induced bradycardia should be ruled out as a cause by discontinuing potentially offending drugs. If symptomatic bradycardia persists, a permanent pacemaker is indicated.
2. Therapy for tachyarrhythmias
a. Drug therapy for both ventricular and supraventricular tachyarrhythmias that have caused an episode of syncope is clearly indicated [see II D 1 b (3)]. In general, such therapy should be guided by electrophysiologic testing.
b. Antitachycardia pacemakers or implantable defibrillators may be used to electrically correct arrhythmias if drug therapy fails.
3. Therapy for autonomic dysfunction. If autonomic dysfunction is the cause of orthostatic hypotension and syncope, little can be done directly to treat the underlying cause. Instead, therapies to protect the patient from possible hypotension should be instituted. These include high salt intake or fludrocortisone to ensure volume expansion, support stockings to prevent venous pooling, or midodrine to increase peripheral vascular resistance. There may be a role for permanent cardiac pacing in a select group of patients for whom other forms of therapy have failed.
4. Correction of mechanical obstructions to cardiac inflow or outflow. Any fixed valvular lesion that has caused an episode of syncope should be corrected. If idiopathic hypertrophic subaortic stenosis is determined to be the cause of the syncope, standard therapy with propranolol or verapamil is indicated to reduce the amount of outflow obstruction. If medical therapy fails, myomectomy or alcohol septal ablation may be necessary.
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