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Hypertensive Emergencies


George L. Bakris

, MD, University of Chicago School of Medicine

Last full review/revision Mar 2021| Content last modified Mar 2021

A hypertensive emergency is severe hypertension with signs of damage to target organs (primarily the brain, cardiovascular system, and kidneys). Diagnosis is by blood pressure (BP) measurement, ECG, urinalysis, and serum blood urea nitrogen (BUN) and creatinine measurements. Treatment is immediate BP reduction with IV drugs (eg, clevidipine, fenoldopam, nitroglycerin, nitroprusside, nicardipine, labetalol, esmolol, hydralazine).

(See also Overview of Hypertension.)

Target-organ damage includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection, and renal failure. Damage is rapidly progressive and often fatal.

Hypertensive encephalopathy may involve a failure of cerebral autoregulation of blood flow. Normally, as blood pressure increases, cerebral vessels constrict to maintain constant cerebral perfusion. Above a mean arterial pressure (MAP) of about 160 mm Hg (lower for normotensive people whose BP suddenly increases), the cerebral vessels begin to dilate rather than remain constricted. As a result, the very high BP is transmitted directly to the capillary bed with transudation and exudation of plasma into the brain, causing cerebral edema, including papilledema.

Although many patients with stroke and intracranial hemorrhage present with elevated BP, elevated BP is often a consequence rather than a cause of the condition. Whether rapidly lowering BP is beneficial in these conditions is unclear; it may even be harmful.

Hypertensive urgencies

Very high blood pressure (eg, diastolic pressure > 120 to 130 mm Hg) without target-organ damage (except perhaps grades 1 to 3 retinopathy) may be considered a hypertensive urgency. BP at these very high levels often worries physicians; however, acute complications are unlikely, so immediate BP reduction is not required. Patients should be started on a 2-drug oral antihypertensive combination , and close evaluation (with evaluation of treatment efficacy) should be continued on an outpatient basis. Very high BP without organ damage commonly occurs in highly anxious patients or those who have had very poor sleep quality over a period of weeks.

Symptoms and Signs of Hypertensive Emergencies

Blood pressure is elevated, often markedly (diastolic pressure > 120 mm Hg). Central nervous system symptoms include rapidly changing neurologic abnormalities (eg, confusion, transient cortical blindness, hemiparesis, hemisensory defects, seizures). Cardiovascular symptoms include chest pain and dyspnea. Renal involvement may be asymptomatic, although severe azotemia due to advanced renal failure may cause lethargy or nausea.

Physical examination focuses on target organs, with neurologic examination, funduscopy, and cardiovascular examination. Global cerebral deficits (eg, confusion, obtundation, coma), with or without focal deficits, suggest encephalopathy; normal mental status with focal deficits suggests stroke. Severe retinopathy (sclerosis, cotton-wool spots, arteriolar narrowing, hemorrhage, papilledema) is usually present with hypertensive encephalopathy, and some degree of retinopathy is present in many other hypertensive emergencies. Jugular venous distention, basilar lung crackles, and a 3rd heart sound suggest pulmonary edema. Asymmetry of pulses between arms suggests aortic dissection.

Diagnosis of Hypertensive Emergencies

  • Very high blood pressure
  • Identify target-organ involvement: ECG, urinalysis, blood urea nitrogen (BUN), creatinine; if neurologic findings, head CT

Testing typically includes ECG, urinalysis, and serum BUN and creatinine.

Patients with neurologic findings require head CT to diagnose intracranial bleeding, edema, or infarction.

Patients with chest pain or dyspnea require chest x-ray.

ECG abnormalities suggesting target-organ damage include signs of left ventricular hypertrophy or acute ischemia.

Urinalysis abnormalities typical of renal involvement include red blood cells (RBCs), RBC casts, and proteinuria.

Diagnosis is based on the presence of a very high BP and findings of target-organ involvement.

Treatment of Hypertensive Emergencies

  • Admit to intensive care unit (ICU)
  • Short-acting IV drug: nitrates, fenoldopam, nicardipine, or labetalol
  • Goal: 20 to 25% reduction MAP in 1 to 2 hours

Hypertensive emergencies are treated in an ICU; blood pressure is progressively (although not abruptly) reduced using a short-acting, titratable IV drug. Choice of drug and speed and degree of reduction vary somewhat with the target organ involved, but generally a 20 to 25% reduction in MAP over an hour or so is appropriate, with further titration based on symptoms. Achieving “normal” BP urgently is not necessary. Typical first-line drugs include nitroprusside, fenoldopam, nicardipine, and labetalol (see table Parenteral Drugs for Hypertensive Emergencies). Nitroglycerin alone is less potent.

Parenteral Drugs for Hypertensive Emergencies



Selected Adverse Effects*

Special Indications


1–21 mg/hour IV

Atrial fibrillation, fever, insomnia, nausea, headache

Most hypertensive emergencies

Should be used cautiously in patients with acute heart failure


0.625–5 mg IV every 6 hours

Precipitous fall in blood pressure in high-renin states, variable response

Acute left ventricular failure

Should be avoided in acute myocardial infarction


250–500 mcg/kg/minute IV for 1 minute, then 50–100 mcg/kg/minute for 4 minutes; may repeat sequence

Hypotension, nausea

Aortic dissection perioperatively


0.1–0.3 mcg/kg/minute IV infusion; maximum dose 1.6 mcg/kg/minute

Tachycardia, headache, nausea, flushing, hypokalemia, elevation of intraocular pressure in patients with glaucoma

Most hypertensive emergencies

Should be used cautiously in patients with myocardial ischemia


10–40 mg IV every 4–6 hours

10–20 mg IM every 4–6 hours

Tachycardia, flushing, headache, vomiting, aggravation of angina



20 mg IV bolus over 2 minutes, followed every 10 minutes by 40 mg, then up to 3 doses of 80 mg; or 0.5–2 mg/minute IV infusion

Vomiting, scalp tingling, burning in throat, dizziness, nausea, heart block, orthostatic hypotension

Most hypertensive emergencies, except acute left ventricular failure

Should be avoided in patients with asthma


5–15 mg/hour IV

Tachycardia, headache, flushing, local phlebitis

Most hypertensive emergencies, except acute heart failure

Should be used cautiously in patients with myocardial ischemia


5–100 mcg/minute IV infusion†

Headache, tachycardia, nausea, vomiting, apprehension, restlessness, muscular twitching, palpitations, methemoglobinemia, tolerance with prolonged use

Myocardial ischemia, heart failure


0.25–10 mcg/kg/minute IV infusion† (maximum dose for 10 minutes only)

Nausea, vomiting, agitation, muscle twitching, sweating, cutis anserina (if blood pressure is reduced too rapidly), thiocyanate and cyanide toxicity

Most hypertensive emergencies

Should be used cautiously in patients with high intracranial pressure or azotemia


1–15 mg IV bolus followed by 1–40 mg/hour IV infusion

Tachycardia, flushing, headache

Rarely used unless patient has a confirmed diagnosis of pheochromocytoma

* Hypotension may occur with all drugs.

† A special delivery system (eg, infusion pump for nitroprusside, nonpolyvinyl chloride tubing for nitroglycerin) is required.

Oral drugs are not indicated because onset is variable and the drugs are difficult to titrate. Although short-acting oral nifedipine reduces blood pressure rapidly, it may lead to acute cardiovascular and cerebrovascular events (sometimes fatal) and is therefore not recommended.

Clevidipine is an ultra-short-acting (within 1 to 2 minutes), 3rd-generation calcium channel blocker that reduces peripheral resistance without affecting venous vascular tone and cardiac filling pressures. Clevidipine is rapidly hydrolyzed by blood esterases and, thus, its metabolism is not affected by renal or hepatic function. It has been shown to be effective and safe in the control of perioperative hypertension and hypertensive emergencies and was associated with lower mortality than nitroprusside.

Starting dose of clevidipine is 1 to 2 mg/hour, doubling the dose every 90 seconds until approaching target BP, at which time dose is increased by less than double every 5 to 10 minutes. Clevidipine may thus be preferred over nitroprusside for most hypertensive emergencies, although it should be used with caution in acute heart failure with reduced ejection fraction as it may have negative inotropic effects. If clevidipine is not available, then fenoldopam, nitroglycerin, or nicardipine are reasonable alternatives.

Nitroprusside is a venous and arterial dilator, reducing preload and afterload; thus, it is the most useful for hypertensive patients with heart failure. It is also used for hypertensive encephalopathy and, with beta-blockers, for aortic dissection. Starting dose is 0.25 to 1.0 mcg/kg/minute titrated in increments of 0.5 mcg/kg to a maximum of 8 to 10 mcg/kg/minute; maximum dose is given for ≤ 10 minutes to minimize risk of cyanide toxicity. The drug is rapidly broken down into cyanide and nitric oxide (the active moiety). Cyanide is detoxified to thiocyanate. However, administration of > 2 mcg/kg/minute can lead to cyanide accumulation with toxicity to the central nervous system and heart; manifestations include agitation, seizures, cardiac instability, and an anion gap metabolic acidosis.

Prolonged administration of nitroprusside (> 1 week or, in patients with renal insufficiency, 3 to 6 days) leads to accumulation of thiocyanate, with lethargy, tremor, abdominal pain, and vomiting. Other adverse effects include transitory elevation of hair follicles (cutis anserina) if BP is reduced too rapidly. Thiocyanate levels should be monitored daily after 3 consecutive days of therapy, and the drug should be stopped if the serum thiocyanate level is > 12 mg/dL (> 2 mmol/L). Because nitroprusside is broken down by ultraviolet light, the IV bag and tubing are wrapped in an opaque covering. Given data showing increased mortality with nitroprusside compared to clevidipine, nitroglycerin, and nicardipine, nitroprusside should probably not be used when other alternatives are available.

Fenoldopam is a peripheral dopamine-1 agonist that causes systemic and renal vasodilation and natriuresis. Onset is rapid and half-life is brief, making it an effective alternative to nitroprusside, with the added benefit that it does not cross the blood-brain barrier. Initial dosage is 0.1 mcg/kg/minute IV infusion, titrated upward by 0.1 mcg/kg every 15 minutes to a maximum of 1.6 mcg/kg/minute.

Nitroglycerin is a vasodilator that affects veins more than arterioles. It can be used to manage hypertension during and after coronary artery bypass graft surgery, acute myocardial infarction, unstable angina pectoris, and acute pulmonary edema. IV nitroglycerin is preferable to nitroprusside for patients with severe coronary artery disease because nitroglycerin increases coronary flow, whereas nitroprusside tends to decrease coronary flow to ischemic areas, possibly because of a “steal” mechanism. Starting dose is 10 to 20 mcg/minute titrated upward by 10 mcg/minute every 5 minutes to maximum antihypertensive effect.

For long-term BP control, nitroglycerin must be used with other drugs. The most common adverse effect is headache (in about 2%); others include tachycardia, nausea, vomiting, apprehension, restlessness, muscular twitching, and palpitations.

Nicardipine, a dihydropyridine calcium channel blocker with less negative inotropic effects than nifedipine, acts primarily as a vasodilator. It is most often used for postoperative hypertension and during pregnancy. Dosage is 5 mg/hour IV, increased every 15 minutes to a maximum of 15 mg/hour. It may cause flushing, headache, and tachycardia; it can decrease glomerular filtration rate (GFR) in patients with renal insufficiency.

Labetalol is a beta-blocker with some alpha-1-blocking effects, thus causing vasodilation without the typical accompanying reflex tachycardia. It can be given as a constant infusion or as frequent boluses; use of boluses has not been shown to cause significant hypotension. Labetalol is used during pregnancy, for intracranial disorders requiring BP control, and after myocardial infarction. Infusion is 0.5 to 2 mg/minute, titrated upward to a maximum of 4 to 5 mg/minute. Boluses begin with 20 mg IV followed every 10 minutes by 40 mg, then 80 mg (up to 3 doses) to a maximum total of 300 mg. Adverse effects are minimal, but because of its beta -blocking activity, labetalol should not be used for hypertensive emergencies in patients with asthma. Low doses may be used for left ventricular failure if nitroglycerin is given simultaneously.

Key Points

  • A hypertensive emergency is hypertension that causes target-organ damage; it requires intravenous therapy and hospitalization.
  • Target-organ damage includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection, and renal failure.
  • Do ECG, urinalysis, serum blood urea nitrogen and creatinine measurement, and head CT for patients with neurologic symptoms or signs.
  • Reduce mean arterial pressure by about 20 to 25% over the first hour using a short-acting, titratable IV drug such as clevidipine, nitroglycerin, fenoldopam, nicardipine, or labetalol.
  • It is not necessary to achieve “normal” blood pressure urgently (especially true in acute stroke).

More Information

The following is an English-language resource that may be useful. Please note that THE MANUAL is not responsible for the content of this resource.

  • 2017 ACC/AHA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults.

Drugs Mentioned In This Article

Drug Name Select Trade
nitroprusside NITROPRESS
nitroglycerin NITRO-DUR
Phentolamine No US brand name
nicardipine CARDENE
clevidipine CLEVIPREX
fenoldopam CORLOPAM

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