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■ History of congestive heart failure

■ Abnormal ECG

■ Syncope in supine position

■ Exertional syncope

■ Syncope associated with chest pain

■ Patient at low risk for cardiac etiology

■ Young patient, normal physical examination, normal ECG

■ Clinical presentation suggestive of vasovagal syncope

Goals of Care (ED core measures) for syncope:ECG for every patient > 60

years old with a discharge diagnosis of syncope from ED

TREATMENT

■ Resuscitation, as needed

■ Identifying and treating the underlying etiology is the mainstay of treatment.

■ Admit for monitoring and echocardiogram: If no identifiable cause in

high-risk patient (one-third of patients).

VENOUS CIRCULATORY DISORDERS

Deep Venous Thrombosis

Deep venous thrombosis (DVT) can occur anywhere in the deep venous sys-

tem, but is most common in the deep veins of the legs.

In the legs, the deep venous system constitutes a network of veins that extend from

the calf veins to the femoral (which is, in fact, a deep vein, although it is often

called the “superficial femoral vein”) and iliac veins. The superficial veins in the

legs include the greater and short saphenous veins and the perforator veins.

There are many clinical factors that increase the susceptibility to DVT forma-

tion (see Table 2.27).

PATHOPHYSIOLOGY

■ Damage to the vessel wall, venostasis, or hypercoagulable state (Virchow’s

triad)→thrombus formation.

■ Once formed, thrombus can propagate or embolize proximally.

■ Massive thrombus can cause vasospasm of adjacent artery.

CARDIOVASCULAR EMERGENCIES

TABLE 2.27. Clinical Risk Factors for Deep Venous Thrombosis

T Trauma, travel

H Hypercoagulable, hormone replacement

R Recreational drugs (intravenous drugs)

O Old (age > 60 y)

M Malignancy

B Birth control pill, blood group A

O Obesity, obstetrics

S Surgery, smoking

I Immobilization

S Sickness

(Reproduced, with permission, from Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine:

A Comprehensive Study Guide, 6th ed. New York: McGraw-Hill, 2004:409.)

Virchow’s triad: Damage to

vessel wall, venostasis,

hypercoagulable state.