Sodium nitroprusside is no longer the treatment of choice for acute hypertensive problems; in most situations, appropriate control of blood pressure is best achieved using combinations of nicardipine or clevidipine plus labetalol or esmolol. (Table 11–16 lists drugs, dosages, and adverse effects.)
Table 11–16.Drugs for hypertensive emergencies and urgencies (in descending order of preference). ||Download (.pdf) Table 11–16. Drugs for hypertensive emergencies and urgencies (in descending order of preference).
|Agent ||Action ||Dosage ||Onset ||Duration ||Adverse Effects ||Comments |
|Hypertensive Emergencies |
|Nicardipine (Cardene) ||Calcium channel blocker ||5 mg/h intravenously; may increase by 1–2.5 mg/h every 15 minutes to 15 mg/h ||1–5 minutes ||3–6 hours ||Hypotension, tachycardia, headache. ||May precipitate myocardial ischemia. |
|Clevidipine (Cleviprex) ||Calcium channel blocker ||1–2 mg/h intravenously initially; double rate every 90 seconds until near goal, then by smaller amounts every 5–10 minutes to a maximum of 32 mg/h ||2–4 minutes ||5–15 minutes ||Headache, nausea, vomiting. ||Lipid emulsion: contraindicated in patients with allergy to soy or egg. |
|Labetalol (Trandate) ||Beta- and alpha-blocker ||20–40 mg intravenously every 10 minutes to 300 mg; 2 mg/min infusion ||5–10 minutes ||3–6 hours ||Nausea, hypotension, bronchospasm, bradycardia, heart block. ||Avoid in acute LV systolic dysfunction, asthma. May be continued orally. |
|Esmolol (Brevibloc) ||Beta-blocker ||Loading dose 500 mcg/kg intravenously over 1 minute; maintenance, 25–200 mcg/kg/min ||1–2 minutes ||10–30 minutes ||Bradycardia, nausea. ||Avoid in acute LV systolic dysfunction, asthma. Weak antihypertensive. |
|Fenoldopam (Corlopam) ||Dopamine receptor agonist ||0.1–1.6 mcg/kg/min intravenously ||4–5 minutes ||< 10 minutes ||Reflex tachycardia, hypotension, increased intraocular pressure. ||May protect kidney function. |
|Enalaprilat (Vasotec) ||ACE inhibitor ||1.25 mg intravenously every 6 hours ||15 minutes ||6 hours or more ||Excessive hypotension. ||Additive with diuretics; may be continued orally. |
|Furosemide (Lasix) ||Diuretic ||10–80 mg orally or intravenously ||15 minutes ||4 hours ||Hypokalemia, hypotension. ||Adjunct to vasodilator. |
|Hydralazine (Apresoline) ||Vasodilator ||5–20 mg intravenously; may repeat after 20 minutes ||10–30 minutes ||2–6 hours ||Tachycardia, headache, vomiting, diarrhea ||Avoid in coronary artery disease, dissection. Rarely used except in pregnancy. |
|Nitroglycerin ||Vasodilator ||0.25–5 mcg/kg/min intravenously ||2–5 minutes ||3–5 minutes ||Headache, nausea, hypotension, bradycardia. ||Tolerance may develop. Useful primarily with myocardial ischemia. |
|Nitroprusside (Nitropress) ||Vasodilator ||0.25–10 mcg/kg/min intravenously ||Seconds ||3–5 minutes ||Anxiety, increased intracranial pressure, vomiting, bowel obstruction; thiocyanate and cyanide toxicity, especially with kidney and liver dysfunction; hypotension. Coronary steal, decreased cerebral blood flow, increased intracranial pressure. ||No longer the first-line agent. |
|Hypertensive Urgencies |
|Clonidine (Catapres) ||Central sympatholytic ||0.1–0.2 mg orally initially; then 0.1 mg every hour to 0.8 mg orally ||30–60 minutes ||6–8 hours ||Sedation. ||Rebound may occur. |
|Captopril (Capoten) ||ACE inhibitor ||12.5–25 mg orally ||15–30 minutes ||4–6 hours ||Excessive hypotension. || |
|Nifedipine (Adalat, Procardia) ||Calcium channel blocker ||10 mg orally initially; may be repeated after 30 minutes ||15 minutes ||2–6 hours ||Excessive hypotension, tachycardia, headache, angina, myocardial infarction, stroke. ||Response unpredictable. |
Intravenous nicardipine is the most potent and the longest acting of the parenteral calcium channel blockers. As a primarily arterial vasodilator, it has the potential to precipitate reflex tachycardia, and for that reason it should not be used without a beta-blocker in patients with coronary artery disease.
Intravenous clevidipine is an L-type calcium channel blocker with a 1-minute half-life, which facilitates swift and tight control of severe hypertension. It acts on arterial resistance vessels and is devoid of venodilatory or cardiodepressant effects.
This combined beta- and alpha-blocking agent is the most potent adrenergic blocker for rapid blood pressure reduction. Other beta-blockers are far less potent. Excessive blood pressure drops are unusual. Experience with this agent in hypertensive syndromes associated with pregnancy has been favorable.
This rapidly acting beta-blocker is approved only for treatment of supraventricular tachycardia, but is often used for lowering blood pressure. It is less potent than labetalol and should be reserved for patients in whom there is particular concern about serious adverse events related to beta-blockers.
Fenoldopam is a peripheral dopamine-1 (DA1) receptor agonist that causes a dose-dependent reduction in arterial pressure without evidence of tolerance, rebound, withdrawal, or deterioration of kidney function. In higher dosage ranges, tachycardia may occur. This drug is natriuretic, which may simplify volume management in acute kidney injury.
This is the active form of the oral ACE inhibitor enalapril. The onset of action is usually within 15 minutes, but the peak effect may be delayed for up to 6 hours. Thus, enalaprilat is used primarily as an adjunctive agent.
Intravenous loop diuretics can be very helpful when the patient has signs of heart failure or fluid retention, but the onset of their hypotensive response is slow, making them an adjunct rather than a primary agent for hypertensive emergencies. Low dosages should be used initially (furosemide, 20 mg, or bumetanide, 0.5 mg). They facilitate the response to vasodilators, which often stimulate fluid retention.
Hydralazine can be given intravenously or intramuscularly, but its effect is less predictable than that of other drugs in this group. It produces reflex tachycardia and should not be given without beta-blockers in patients with possible coronary disease or aortic dissection. Hydralazine is used primarily in pregnancy and in children, but even in these situations, it is not a first-line drug.
This agent should be reserved for patients with accompanying acute coronary ischemic syndromes.
This agent is given by controlled intravenous infusion gradually titrated to the desired effect. It lowers the blood pressure within seconds by direct arteriolar and venous dilation. Monitoring with an intra-arterial line avoids hypotension. Nitroprusside—in combination with a beta-blocker—is useful in patients with aortic dissection.
Patients with less severe acute hypertensive syndromes can often be treated with oral therapy. Suitable drugs will reduce the blood pressure over a period of hours. In those presenting as a consequence of noncompliance, it is usually sufficient to restore the patient’s previously established oral regimen.
Clonidine, 0.2 mg orally initially, followed by 0.1 mg every hour to a total of 0.8 mg, will usually lower blood pressure over a period of several hours. Sedation is frequent, and rebound hypertension may occur if the drug is stopped.
Captopril, 12.5–25 mg orally, will also lower blood pressure in 15–30 minutes. The response is variable and may be excessive. Captopril is the drug of choice in the management of scleroderma hypertensive crisis.
The effect of fast-acting nifedipine capsules is unpredictable and may be excessive, resulting in hypotension and reflex tachycardia. Because myocardial infarction and stroke have been reported in this setting, the use of sublingual nifedipine is not advised. Nifedipine retard, 20 mg orally, appears to be safe and effective.
When the blood pressure has been brought under control, combinations of oral antihypertensive agents can be added as parenteral drugs are tapered off over a period of 2–3 days.
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