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Hypertensive Emergencies 

  • Author: Christy Hopkins, MD, MPH; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
Updated: Aug 18, 2015

Uncontrolled Blood Pressure

Hypertensive emergencies encompass a spectrum of clinical presentations in which uncontrolled blood pressures (BPs) lead to progressive or impending end-organ dysfunction. In these conditions, the BP should be lowered aggressively over minutes to hours.

Neurologic end-organ damage due to uncontrolled BP may include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, subarachnoid hemorrhage, and/or intracranial hemorrhage.[1] Cardiovascular end-organ damage may include myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and/or aortic dissection. Other organ systems may also be affected by uncontrolled hypertension, which may lead to acute renal failure/insufficiency, retinopathy, eclampsia, or microangiopathic hemolytic anemia.[1]

With the advent of antihypertensives, the incidence of hypertensive emergencies has declined from 7% to approximately 1% of patients with hypertension.[2] In addition, the 1-year survival rate associated with this condition has increased from only 20% (prior to 1950) to a survival rate of more than 90% with appropriate medical treatment.[3]

History and physical examination

The history and the physical examination determine the nature, severity, and management of the hypertensive event. The history should focus on the presence of end-organ dysfunction, the circumstances surrounding the hypertension, and any identifiable etiology.

The most common clinical presentations of hypertensive emergencies are cerebral infarction (24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart failure (12%). Other clinical presentations associated with hypertensive emergencies include intracranial hemorrhage, aortic dissection, and eclampsia,[4] as well as acute myocardial infarction.

In pregnant patients, acute hypertensive crisis usually results from severe preeclampsia and can lead to maternal stroke, cardiopulmonary decompensation, fetal decompensation caused by reduced uterine perfusion, abruption, and stillbirth.[5]

The duration and severity of the patient’s preexisting hypertension (including the degree of BP control) should be evaluated, as well as the patient's medication history. Details of antihypertensive drug therapy and compliance, intake of over-the-counter (OTC) preparations such as sympathomimetic agents, and use of illicit drugs such as cocaine are important elements of the medication history. In addition, it is important to elicit information about the presence of previous end-organ dysfunction, particularly renal and cerebrovascular disease, and any other medical problems (eg, thyroid disease, Cushing disease, systemic lupus). In female patients, determine the date of their last menstrual period.

Patients may complain of specific symptoms that suggest end-organ dysfunction may be present. Chest pain may indicate myocardial ischemia or infarction, back pain may denote aortic dissection; and dyspnea may suggest pulmonary edema or congestive heart failure. The presence of neurologic symptoms may include seizures, visual disturbances, and altered level of consciousness and may be indicative of hypertensive encephalopathy.

The physical examination should assess whether end-organ dysfunction is present. BP should not only be measured in both the supine position and the standing position (assess volume depletion), but it should also be measured in both arms (a significant difference may suggest aortic dissection).

The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive emergency. Evaluate for the presence of heart failure, which may be indicated jugular venous distention, crackles on auscultation, and peripheral edema. Central nervous system (CNS) findings may include changes in the patient's level of consciousness and visual fields, and/or the presence of focal neurologic signs. Abdominal masses or bruits may be noted.

Evaluation of uncontrolled hypertension

Obtain electrolyte levels, as well as measurements of blood urea nitrogen (BUN) and creatinine levels to evaluate for renal impairment. A dipstick urinalysis to detect hematuria or proteinuria and microscopic urinalysis to detect red blood cells (RBCs) or RBC casts should also be performed

A complete blood cell (CBC) and peripheral blood smear should be obtained to exclude microangiopathic anemia, and a toxicology screen, pregnancy test, and endocrine testing may be obtained, as needed.

Imaging should be directed by clinical presentation. If there is clinical evidence of pulmonary edema or the patient has chest pain, chest radiography and ECG are indicated. Patients with neurological signs should be evaluated with a head CT scan initially, with more advanced imaging determined by clinical presentation.

Malignant hypertension

Malignant hypertension and accelerated hypertension are both hypertensive emergencies, with similar outcomes and therapies. Malignant hypertension may or may not be associated with clinical conditions present in hypertensive urgency. A patient with malignant hypertension always has retinal papilledema (as seen in the image below),[6] as well as flame-shaped hemorrhages and exudates. Other clinical features of malignant hypertension may include encephalopathy, confusion, left ventricular failure, intravascular coagulation, and impaired renal function, with hematuria and weight loss.

The pathologic hallmark of malignant hypertension is fibrinoid necrosis of the arterioles, which occurs systemically, but specifically in the kidneys. These patients develop fatal complications if untreated, and more than 90% will not survive beyond 1-2 years. See Malignant Hypertension.

Papilledema. Note the swelling of the optic disc, Papilledema. Note the swelling of the optic disc, with blurred margins

A study by Amraoui et al found a higher all-cause mortality rate in patients with malignant hypertension than in persons who were normotensive or hypertensive, even though the cardiovascular risk profile for the malignant hypertension patients was more favorable than that for the hypertensive controls. The study, which compared 120 patients with a history of malignant hypertension with 120 normotensive and 120 hypertensive persons, found that the malignant hypertension patients had lower total cholesterol, low-density lipoprotein cholesterol, and body mass index values than did the hypertensive controls. However, the median estimated glomerular filtration rate was higher in the normotensive and hypertensive controls than in the malignant hypertension group. Annual all-cause mortality per 100 patient-years was 2.6 for the patients with malignant hypertension, compared with 0.2 and 0.5 for the normotensive and hypertensive controls, respectively.[7]

To see complete information on hypertension, please go to the main article by clicking here.


Management of Hypertensive Emergencies

Approximately 3-45% of adult patients have at least one incident of increased BP during their stay in the emergency department (ED). The fundamental principle in determining the necessary ED care of the hypertensive patient is the presence or absence of end-organ dysfunction. Many patients present to the ED with elevated BPs; however, only a small proportion of patients will require emergency treatment. An important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number."

The primary goal of the emergency physician is to determine which patients with acute hypertension are exhibiting symptoms of end-organ damage and require immediate intravenous (IV) parenteral therapy. In contrast, patients presenting with acutely elevated BP (systolic BP [SBP] >200 mm Hg or diastolic BP [DBP] >120 mm Hg) without symptoms and whose BP stays significantly elevated to this level on discharge should have initiation of medical therapy and close follow-up in the outpatient setting.[8]

Thus, optimal control of hypertensive situations balances the benefits of immediate decreases in BP against the risk of a significant decrease in target organ perfusion. The emergency physician must be capable of appropriately evaluating patients with an elevated BP, correctly classifying the hypertension, determining the aggressiveness and timing of therapeutic interventions, and making disposition decisions.

Acutely lowering BP in the ED for clinical situations other than those listed below is controversial and generally should be avoided.


Optimal pharmacotherapy is dependent upon the specific organ at risk (see individual sections below). In patients presenting with hypertensive emergencies, antihypertensive drug therapy has been shown to be effective in acutely decreasing blood pressure.[9]

Sodium nitroprusside is a commonly used medication. It is a short-acting agent, and the BP response can be titrated from minute to minute. However, patients must have constant monitoring in an intensive care unit. The potential exists for thiocyanate and cyanide toxicity with prolonged use or if the patient has renal or hepatic failure.

Labetalol, an alpha- and beta-blocking agent, has proven to be quite beneficial in the treatment of patients with hypertensive emergencies. Labetalol is particularly preferred in patients with acute dissection and patients with end-stage renal disease. Boluses of 10-20 mg may be administered, or the drug may be infused at 1 mg/min until the desired BP is obtained. Once an adequate BP level is obtained, oral hypertensive therapy should be initiated, and patients are gradually weaned from parenteral agents.

Fenoldopam, a peripheral dopamine-1-receptor agonist is given as initial IV dose of 0.1 µg/kg/min titrated every 15 minutes.

Clevidipine, a dihydropyridine calcium channel blocker, is administered intravenously for rapid and precise BP reduction.[10] It is rapidly metabolized in the blood and tissues and does not accumulate in the body. Initiate IV infusion of clevidipine at 1-2 mg/h; titrate the dose at short intervals (ie, 90 s) initially by doubling the dose.

As the BP approaches its goal, increase the clevidipine dose by less than double, and lengthen the time between dose adjustments to every 5-10 minutes. An approximately 1-2 mg/h increase produces an additional 2-4 mm Hg decrease in SBP. Typically, the therapeutic response is achieved with 4-6 mg/h, although severe hypertension may require higher doses. Most patients have received maximum doses of 16 mg/h or less; experience is limited with short-term dosing as high as 32 mg/h. Because of lipid load restrictions, do not exceed 1000 mL or an average of 21 mg/h within a 24-hour period; experience is limited with use beyond 72 hours.

Neurologic emergencies

Rapid BP reduction is indicated in neurologic emergencies, such as hypertensive encephalopathy, acute ischemic stroke, acute intracerebral hemorrhage, and subarachnoid hemorrhage.

In hypertensive encephalopathy, the treatment guidelines are to reduce the MAP 25% over 8 hours.[11] Labetalol, nicardipine, esmolol are the preferred medications; nitroprusside and hydralazine should be avoided.

For acute ischemic stroke, the preferred medications are labetalol and nicardipine. Withhold antihypertensive medications unless the SBP is >220 mm Hg or the DBP is >120 mm Hg, UNLESS the patient is receiving IV or intra-arterial (IA) fibrinolysis; then, the goal BP is an SBP of < 185 mm Hg and DBP < 110 mm Hg. After treatment with fibrinolysis, the SBP should be maintained < 180 mm Hg and the DBP at < 105 mm Hg for 24 hours.[11]

For acute intracerebral hemorrhage, the preferred medications are labetalol, nicardipine, and esmolol; avoid nitroprusside and hydralazine. The treatment is based on clinical/radiographic evidence of increased intracranial pressure (ICP). If there are signs of increased ICP, maintain the MAP just below 130 mm Hg (or SBP < 180 mm Hg) for the first 24 hours after onset. In patients without increased ICP, maintain the MAP < 110 mm Hg (or SBP < 160 mm Hg) for the first 24 hours after symptom onset.[11]

Recent evidence shows that in cases of acute intracerebral hemorrhage, early intensive BP control is well tolerated and can reduce hematoma growth in patients treated within 6 hours after the onset of intracerebral hemorrhage.[12, 13] The target systolic pressure for these studies was 140 mm Hg and routine IV medications were used. The target SBP was maintained over 7 days.[12, 13]

In subarachnoid hemorrhage, nicardipine, labetalol, and esmolol are also the preferred agents; again, nitroprusside and hydralazine should be avoided. Maintain the SBP < 160 mm Hg until the aneurysm is treated or cerebral vasospasm occurs. Although oral nimodipine is used to prevent delayed ischemic neurologic deficits, it is NOT indicated for treating acute hypertension.[11]

Cardiovascular emergencies

Rapid BP reduction is also indicated in cardiovascular emergencies, such as aortic dissection, acute coronary syndrome, and acute heart failure.

In aortic dissection, the preferred medications are labetalol, nicardipine, nitroprusside (with beta-blocker), esmolol, and morphine sulfate. However, avoid beta-blockers if there is aortic valvular regurgitation or suspected cardiac tamponade. Maintain the SBP at < 110 mm Hg, unless signs of end-organ hypoperfusion are present. The preferred treatment includes a combination of narcotic analgesics (morphine sulfate), beta blockers (labetalol, esmolol), and vasodilators (nicardipine, nitroprusside). Calcium channel blockers (verapamil, diltiazem) are an alternative to beta blockers.[14]

For acute coronary syndrome, beta blockers and nitroglycerin are the preferred drugs. Treatment is indicated if the SBP is >160 mm Hg and/or the DBP is >100 mm Hg. Reduce the BP by 20-30% of baseline. Note that thrombolytics are contraindicated if the BP is >185/100 mm Hg.[15]

In acute heart failure, the preferred medications are IV nitroglycerin or sublingual nitroglycerin and IV enalaprilat. Treat with vasodilators (in addition to diuretics) for a SBP =140 mm Hg.[15]

Cocaine toxicity/pheochromocytoma

Diazepam, phentolamine, and nitroglycerin/nitroprusside are the preferred drugs. However, avoid beta-adrenergic antagonists before administering phentolamine.

Hypertension and tachycardia from cocaine toxicity rarely require specific treatment. Alpha-adrenergic antagonists (phentolamine) are the preferred agents for cocaine-associated acute coronary syndromes.[16] Pheochromocytoma treatment guidelines are similar to that of cocaine toxicity. Only after alpha blockade can beta blockers be added for BP control.


The preferred medications are hydralazine, labetalol, and nifedipine. Avoid - Nitroprusside, angiotensin-converting enzyme inhibitors, esmolol. In women with eclampsia or preeclampsia, the SBP should be < 160 mm Hg and the DBP should be < 110 mm Hg in the antepartum and intrapartum periods. If the platelet count is less than 100,000 cells mm3, the BP should be maintained below 150/100 mm Hg. Patients with eclampsia or preeclampsia should also be treated with IV magnesium sulfate to avoid seizures.[17]

Perioperative hypertension

Nitroprusside, nitroglycerin, and esmolol are preferred. Target the perioperative BP to within 20% of the patient's baseline pressure, except if there is the potential for life-threatening arterial bleeding. Perioperative beta blockers are the first choice in patients undergoing vascular procedures or in patients with an intermediate or high risk of cardiac complications.[14]

Contributor Information and Disclosures

Christy Hopkins, MD, MPH Associate Professor, Department of Surgery, University of Utah School of Medicine; Medical Director, Division of Emergency Medicine, University Health Care

Christy Hopkins, MD, MPH is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Department of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, National Association of EMS Physicians

Disclosure: Medical Director for: SironaHealth.

Chief Editor

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians

Disclosure: Nothing to disclose.

Additional Contributors

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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Papilledema. Note the swelling of the optic disc, with blurred margins
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