Symptom Finder - Syncope
SYNCOPE
The differential of syncope or a brief loss of consciousness is best developed with the use of physiology and, to a lesser extent, anatomy.
Like convulsions , syncope is due to a diminished supply of oxygen and glucose in the brain cell. Anything that produces hypoglycemia may lead to episodes of syncope, but the most common cause is overdose of insulin. It is also important to include
insulinomas and overdose of oral hypoglycemic agents.
Reduced delivery of oxygen to the brain cell accounts for most cases of syncope.
Oxygen must get into the body through the lungs with adequate ventilation. It must then be absorbed through the alveolar–capillary membrane, picked up by an adequate number of red cells, and delivered to the brain by a good functioning heart and unobstructed carotid and vertebral–basilar system. Retracing the above physiology and anatomy will develop the disease entities that must be considered in the differential diagnosis of syncope.
Thus, mechanical obstructions of the larynx (foreign body), the bronchi, bronchioles (asthma and emphysema), or alveolar–capillary membrane (pulmonary fibrosis, sarcoidosis, or pulmonary embolism) may cause anoxia and syncope. Severe anemia prevents the adequate transport of oxygen. Oxygen transport from the heart to the brain may be obstructed mechanically or functionally. It is functionally obstructed by CHF of Stokes–Adams syndrome (heart block) and other arrhythmias, particularly ventricular tachycardia and sick sinus syndrome. Functional obstruction may result from a drop in blood pressure from carotid sinus syncope, postural hypotension and vasovagal syncope.
True vertigo may lead to syncope by way of the latter mechanism. Mechanical obstruction may occur at the aortic valve (aortic stenosis or insufficiency), at the carotid arteries (thrombi or plaques), or focally in the smaller arteries from ischemia due to arterial thrombi or emboli. Less commonly, mechanical obstruction may occur from ball–valve thrombi in the mitral or tricuspid valve, large pulmonary emboli, or cough syncope in which poor venous return to the heart is the cause.
Approach to the Diagnosis
Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Syncope induced by exercise suggests long QT syndrome. There is often a family history of sudden death. Focal neurologic signs during the attack suggest transient ischemia attack (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia).
Transesophageal echocardiography is the procedure of choice to find a cardiac source. A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.
Other Useful Tests
1. CBC (anemia)
2. Chemistry panel (hypoglycemia, hypocalcemia)
3. Serum and urine osmolality (dehydration)
4. Upright-tilt table test (postural hypotension)
5. ECG (cardiac arrhythmia)
6. Carotid sinus massage (carotid sinus syndrome)
7. ECG (CHF, valvular heart disease)
8. Carotid scans (TIA)
9. Four-vessel cerebral angiogram (TIA)
10. Exercise tolerance test (coronary insufficiency)
11. Signal-averaging ECG (ventricular arrhythmia)
12. 72-hour fast with glucose monitoring (insulinoma)
13. Drug screen (drug abuse)
14. 24-hour ambulatory blood pressure monitoring (postural
hypotension)
15. Neurology consult
16. Continuous-loop ECG recording (cardiac arrhythmia)
17. Psychiatric consult
18. Electrophysiologic study (cardiac arrhythmia)
19. MRI or MRA of the brain (cerebrovascular insufficiency)
20. Therapeutic trial of anticonvulsants (seizure disorder)
21. Therapeutic trial of hydrocortisone 20 mg/day (orthostatic,
postural hypotension)
22. Therapeutic trial of an anti-arrhythmia agent (paroxysmal cardiac
arrhythmia)
The differential of syncope or a brief loss of consciousness is best developed with the use of physiology and, to a lesser extent, anatomy.
Like convulsions , syncope is due to a diminished supply of oxygen and glucose in the brain cell. Anything that produces hypoglycemia may lead to episodes of syncope, but the most common cause is overdose of insulin. It is also important to include
insulinomas and overdose of oral hypoglycemic agents.
Reduced delivery of oxygen to the brain cell accounts for most cases of syncope.
Oxygen must get into the body through the lungs with adequate ventilation. It must then be absorbed through the alveolar–capillary membrane, picked up by an adequate number of red cells, and delivered to the brain by a good functioning heart and unobstructed carotid and vertebral–basilar system. Retracing the above physiology and anatomy will develop the disease entities that must be considered in the differential diagnosis of syncope.
Thus, mechanical obstructions of the larynx (foreign body), the bronchi, bronchioles (asthma and emphysema), or alveolar–capillary membrane (pulmonary fibrosis, sarcoidosis, or pulmonary embolism) may cause anoxia and syncope. Severe anemia prevents the adequate transport of oxygen. Oxygen transport from the heart to the brain may be obstructed mechanically or functionally. It is functionally obstructed by CHF of Stokes–Adams syndrome (heart block) and other arrhythmias, particularly ventricular tachycardia and sick sinus syndrome. Functional obstruction may result from a drop in blood pressure from carotid sinus syncope, postural hypotension and vasovagal syncope.
True vertigo may lead to syncope by way of the latter mechanism. Mechanical obstruction may occur at the aortic valve (aortic stenosis or insufficiency), at the carotid arteries (thrombi or plaques), or focally in the smaller arteries from ischemia due to arterial thrombi or emboli. Less commonly, mechanical obstruction may occur from ball–valve thrombi in the mitral or tricuspid valve, large pulmonary emboli, or cough syncope in which poor venous return to the heart is the cause.
Approach to the Diagnosis
Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Syncope induced by exercise suggests long QT syndrome. There is often a family history of sudden death. Focal neurologic signs during the attack suggest transient ischemia attack (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia).
Transesophageal echocardiography is the procedure of choice to find a cardiac source. A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.
Other Useful Tests
1. CBC (anemia)
2. Chemistry panel (hypoglycemia, hypocalcemia)
3. Serum and urine osmolality (dehydration)
4. Upright-tilt table test (postural hypotension)
5. ECG (cardiac arrhythmia)
6. Carotid sinus massage (carotid sinus syndrome)
7. ECG (CHF, valvular heart disease)
8. Carotid scans (TIA)
9. Four-vessel cerebral angiogram (TIA)
10. Exercise tolerance test (coronary insufficiency)
11. Signal-averaging ECG (ventricular arrhythmia)
12. 72-hour fast with glucose monitoring (insulinoma)
13. Drug screen (drug abuse)
14. 24-hour ambulatory blood pressure monitoring (postural
hypotension)
15. Neurology consult
16. Continuous-loop ECG recording (cardiac arrhythmia)
17. Psychiatric consult
18. Electrophysiologic study (cardiac arrhythmia)
19. MRI or MRA of the brain (cerebrovascular insufficiency)
20. Therapeutic trial of anticonvulsants (seizure disorder)
21. Therapeutic trial of hydrocortisone 20 mg/day (orthostatic,
postural hypotension)
22. Therapeutic trial of an anti-arrhythmia agent (paroxysmal cardiac
arrhythmia)
