Differential Diagnosis in Primary Care, 4th Edition

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 (see page 104), syncope is due to a diminished supply of oxygen and glucose in the brain cell. Anything that produces hypoglycemia (see page 255) 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 (Table 55).

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 (see page 260), and vasovagal syncope. True vertigo (see page 129) 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. 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)

Syncope

Syncope

Case Presentation #81

A 68-year-old mayor's wife suffered sudden attacks of syncope for several years. The attacks occurred without warning, and she would fall to the floor in a stupor for a minute or two, only to recover with no postictal confusion or other symptomatology. It was rare that she suffered any injuries from the attacks. She had been evaluated by several multispecialty clinics without a definitive diagnosis.

Question #1. Utilizing your knowledge of physiology, what is your differential diagnosis?

Complete physical examination was within normal limits. An electrocardiogram (EKG) showed first degree heart block, but 24-hour Holter monitoring was unremarkable. Echocardiography was normal. Electrophysiologic studies were not available at this time.

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Question #2. What is your diagnosis now?

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