0071643192.pdf

DIAGNOSIS

■ Clinical exam or studies showing evidence of end-organ damage

TREATMENT

Hypertensive emergency mandates immediate treatment, with a goal to reduce
MAP by 25% in 30–60 minutes or reduction of diastolic pressure to about
110 mmHg. Reduction beyond this goal puts the patient at risk for end-organ
ischemia due to relative hypotension. This is especially true for the patient
with chronic HTN in whom the cerebral autoregulation curve has shifted to
the right. An exception to this is in the treatment of aortic dissection, where a
lower MAP is necessary to eliminate shear forces. A short-acting, titratable IV
agent is preferred (see Table 2.24). Oral agents should notbe used.

■ Sodium nitroprusside
■ Drug of choice for most emergencies
■ Arteriolar and venodilator
■ Cerebral vasodilator (careful in stroke syndromes)
■ Dilates normal coronary arteries >diseased →coronary steal
■ Cyanide is a metabolite, so long-term use is limited.
■ Contraindicated in pregnancy
■ Fenoldopam
■ Peripheral dopamine-1 receptor agonist
■ Improves renal function acutely

CARDIOVASCULAR EMERGENCIES

In hypertensive emergencies,

reduction of MAP > 25% puts

the patient at risk for end-

organ ischemia due to relative

hypotension.

Sodium nitroprusside is a

cerebral vasodilator and

should be used carefully in

stroke syndromes.

Nicardipene ↓cerebral

vasospasm, and therefore is a

good agent for stroke

syndromes.

TABLE 2.24. Antihypertensive Agents for Hypertensive Emergencies

CONDITION AGENT OFCHOICE

Accelerated hypertension, hypertensive encephalopathy, Sodium nitroprusside

or acute renal failure Labetalol

Nicardipene

Myocardial ischemia Nitroglycerin

Labetalol

Pulmonary edema Nitroglycerin

Sodium nitroprusside

Fenoldopam

Aortic dissection Esmolol or labetalol (first)

Sodium nitroprusside

Catecholamine crisis Benzodiazepine sedation

Labetalol

Phentolamine

Eclampsia Magnesium

Labetalol

Nicardipine

Hydralazine