Acute Hypertension: Hypertensive Urgency and Hypertensive Emergency

Gregary D. Marhefka, MD

ABSTRACT: Acute hypertension—blood pressure greater than 180/120 mm Hg—can be classified as either hypertensive urgency or hypertensive emergency. Hypertensive urgency has no associated target organ damage, whereas hypertensive emergency can feature neurologic, aortic, cardiac, renal, hematologic, and/or pregnancy-related damage. Little evidence-based research exists about treatment. Intravenous antihypertensive pharmacotherapy is indicated only for hypertensive emergency, with the use of specific agents tailored to the type of organ damage. Several US and European guidelines provide recommendations for the diagnosis and management of hypertensive urgency and hypertensive emergency. This review summarizes what is known about managing hypertensive urgency and emergency, with an emphasis on guideline-directed therapy.

KEYWORDS: Acute hypertension, hypertensive urgency, hypertensive emergency, hypertensive crisis, malignant hypertension

"There is some truth in the saying that the greatest danger to a man with a high blood pressure lies in its discovery, because ‘then some fool is certain to try and reduce it,’” said British physician John Hay, MD, in 1931.1 We have learned a great deal about acute hypertension in the 85 years since Dr Hay was quoted. Nevertheless, despite dramatic advances in modern medicine, a significant void still exists in its evidence-based management.

Acute hypertension is common and can be divided into hypertensive urgency or hypertensive emergency, which is blood pressure greater than 180/120 mm Hg without or with target organ damage, respectively. In a recent retrospective study of more than 1.2 million patient hospital admissions from 114 US hospitals, Shorr and colleagues2 reported that 13.8% were found to have acute hypertension in the emergency department (ED). From 2006 to 2011, visits to EDs for essential hypertension have increased by 25%.
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The paucity of data about hypertensive urgency and emergency is reflected in the fact that the latest 2014 guideline for the management of high blood pressure in adults from the Eighth Joint National Committee (JNC 8) does not even mention acute hypertension or hypertensive urgency or emergency.4


Definition of hypertensive urgency. Because the JNC 8 does not comment on hypertensive urgency in its 2014 guideline, one must refer to expert opinion from the 2003 JNC 7 guideline.5 Hypertensive urgency is defined as a blood pressure greater than 180/120 mm Hg in the absence of progressive target organ dysfunction. These patients are often therapy-nonadherent or inadequately treated. They may present with headache, shortness of breath, epistaxis, or anxiety but often are asymptomatic.

The JNC 7 notes, “Unfortunately, the term ‘urgency’ has led to overly aggressive management of many patients with severe, uncomplicated hypertension.”5 The American College of Emergency Physicians (ACEP) 2013 policy statement6 chooses the phrase asymptomatic elevated blood pressure rather than hypertensive urgency. The college’s policy statement notes that most clinical trials use a blood pressure above 180/100 mm Hg, but they chose to define asymptomatic elevated blood pressure as that consistent with JNC 7’s stage 2 hypertension, 160/100 mm Hg or greater. The 2013 hypertension management guidelines from the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC) define hypertensive urgency as blood pressure greater than 180/120 mm Hg without acute organ damage7 (Table 1).

hypertensive urgency

aUses phrase asymptomatic elevated blood pressure instead of hypertensive urgency.

Abbreviations: ACCF/AHA, American College of Cardiology Foundation/American Heart Association; ACEP, American College of Emergency Physicians;
ACOG, American College of Obstetrics and Gynecology; AHA/ASA, American Heart Association/American Stroke Association; BP, blood
pressure; ESC/ESH, European Society of Cardiology/European Society of Hypertension; HR, heart rate; HTN, hypertension; JNC 7, Seventh Joint
National Committee; JNC 8, Eighth Joint National Committee; MAP, mean arterial pressure; SBP, systolic blood pressure; STEMI, ST-segment
elevation myocardial infarction; tPA, tissue plasminogen activator.


Treatment of hypertensive urgency. Dr Hay’s 1931 statement is apropos today as it applies to hypertensive urgency. According to expert opinion from the 2003 JNC 7, no evidence exists that specific treatment for hypertensive urgency is warranted.5 Patients likely will need to have their medications adjusted or reinitiated in the presence of nonadherence, but most importantly, patients being discharged from the ED should have a confirmed follow-up appointment in the next few days.

The ACEP 2013 policy statement on asymptomatic elevated blood pressure recommends against routine screening for acute target organ injury unless the patient is less likely to follow up, or if there is question of admission to the hospital, in which case screening for an elevated creatinine level is suggested.6 In primary care, JNC 7 guidelines suggest a thorough physical examination including assessment of bilateral blood pressures, body mass index, and optic fundi; palpation and auscultation of carotid arteries, femoral arteries, abdominal aorta, thyroid, heart, lungs, abdomen (for enlarged kidneys or distended bladder), and extremities (for edema and pulses); and a neurologic examination. Screening tests should include electrocardiography for left ventricular hypertrophy, urinalysis, and serum glucose, hematocrit, potassium, creatinine, and lipid levels.5

The 2013 ESH/ESC guideline states, “Isolated large BP elevations without acute [organ dysfunction] … should not be considered an emergency.”7 They recommend reinstitution or intensification of oral drug therapy without any mention of specific agents (Table 1).

In 1989, Zeller and colleagues8 prospectively followed 64 asymptomatic ED patients with severe hypertension (diastolic blood pressure of 116-139 mm Hg) not recently on antihypertensives. Each patient initially had received oral clonidine and hydrochlorothiazide, then each was randomized to 1 of 3 treatment arms: (1) up to 4 hourly doses of oral clonidine until a 20 mm Hg drop in diastolic pressure or to a diastolic pressure of 105 mm Hg, followed by maintenance therapy; (2) an initial dose of oral clonidine followed by hourly oral placebo and subsequent maintenance therapy; or (3) no serial doses and only oral maintenance therapy. They found no difference in the time required to achieve blood pressure control between groups 1 and 2, and no difference at 24 hours in pressure reduction between groups 1, 2, and 3. Of the 44 patients who followed up at 1 week, blood pressure had been adequately controlled across all groups, with no difference between groups.

Levy and colleagues9 retrospectively reported on 1016 patients discharged from an urban teaching hospital ED in 2008 with a primary diagnosis of hypertensive urgency (> 180/100 mm Hg) without target organ damage. A total of 435 patients (42.8%) (average age, 49.2 years; 94.5% African American) were treated, mostly with oral clonidine (in 88.5% of those treated). The authors observed that most of the treated patients had a history of hypertension (93.1% vs 84.3%) and a higher initial mean blood pressure (202/115 vs 185/106 mm Hg). They found no significant difference between treated patients and untreated patients in ED revisits at 24 hours (4.4% vs 2.4%) and at 30 days (18.9% vs 15.2%), or mortality at 30 days (0.2% vs 0.2%) and 1 year (2.1% vs 1.6%).

Grassi and colleagues10 studied 549 ED patients (average age 59 years; 51% men) with asymptomatic blood pressure greater than 180/100 mm Hg, without preexisting cardiovascular, cerebrovascular, or renovascular disease. All patients were placed in a quiet room for 30 minutes of rest; 175 patients (31.9%) had a significant reduction in blood pressure of at least 20/10 mm Hg to below 180/100 mm Hg with rest alone. The remaining patients then were given oral amlodipine, perindopril, or labetalol (decided by the attending physician of record), of which 296 of 394 (75%) had a significant reduction in blood pressure of at least 20/10 mm Hg to below 180/100 mm Hg. There were no complications noted in any of the groups at follow-up within 48 to 72 hours.

These studies demonstrate the safety and importance of rest and oral antihypertensive therapy with close outpatient follow-up for the treatment of hypertensive urgency.


Definition of hypertensive emergency. Because JNC 8 guidelines do not make reference to hypertensive emergencies, one must refer to the 2003 JNC 7 guidelines, which define hypertensive emergency as a blood pressure greater than 180/120 mm Hg in the presence of target organ damage.5 The 2013 ACEP guidelines6 do not have a specific policy regarding hypertensive emergency. The ESH/ESC guideline7 defines hypertensive emergency as a blood pressure greater than 180/120 mm Hg in the presence of impending or progressive organ damage. The 2015 American College of Obstetrics and Gynecology (ACOG) guidelines define hypertensive emergency in pregnancy as acute-onset, severe hypertension of 160/110 mm Hg or above persisting more than 15 minutes.11 The type of target organ damage includes encephalopathy (including posterior reversible encephalopathy syndrome [PRES]), stroke, seizure, retinopathy, acute aortic dissection, acute myocardial infarction (MI), acute heart failure/acute pulmonary edema, acute renal failure, microangiopathic hemolytic anemia, severe preeclampsia, HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome, and eclampsia (Table 2).

organ damage

aThere is no specific ICD-10 code for hypertensive urgency or hypertensive
emergency. These are considered synonymous under ICD-10 code I10, primary
(essential) hypertension.

Abbreviations: HELLP, hemolysis, elevated liver enzymes, low platelet count;
ICD-10, 10th revision of the International Statistical Classification of Diseases and
Related Health Problems; NSTEMI, non-ST segment elevation myocardial infarction;
PRES, posterior reversible encephalopathy syndrome.


Treatment of hypertensive emergency. The goal of treatment of hypertensive emergency is to reduce the blood pressure safely enough to reverse the target organ damage without resulting in detrimental sequelae from iatrogenically caused organ malperfusion. Organs such as the brain, heart, and kidneys contain a microcirculation that is sensitive to broad fluctuations in systemic blood pressure.5 In chronic hypertension, a rightward shift in the pressure-flow autoregulation curve helps protect the brain, for example, from the deleterious effects of chronic hypertension (Figure). In the setting of chronic hypertension, a sudden and severe reduction in blood pressure to what would otherwise be considered normal could result in malperfusion. Therefore, the vast majority of patients with hypertensive emergency should be managed in an intensive care unit (ICU), where they can be closely monitored for signs of iatrogenic target organ damage from overly aggressive blood pressure lowering and/or progression of the original target organ damage secondary to inadequate blood pressure control.

cerebral microvasculature autoregulation

Figure. Cerebral microvasculature autoregulation. In a chronic severely hypertensive
patient, acute reduction in blood pressure to the “normal” level could result in
cerebral malperfusion (black arrows). Abbreviations: HTN, hypertension; MAP, mean
arterial pressure.


In these situations, intra-arterial blood pressure monitoring often is required, especially if the patient is on potent intravenous (IV) antihypertensive therapy. Referring to the JNC 7 expert opinion,5 mean arterial blood pressure (MAP) should be reduced by 25% or less within the first hour. Between hours 2 to 6, the target blood pressure is 160/100 to 160/110 mm Hg, followed by gradual normalization over 24 to 48 hours.5 The 2013 ESH/ESC guideline7 recommends reducing blood pressure by less than 25% within the first hour and then subsequent cautious reduction thereafter.

The one diagnosis that mandates an immediate rather than gradual reduction to normal blood pressure levels is acute aortic syndrome (Table 1).12,13

Neurologic Damage

Examples of neurologic damage in acute hypertensive emergencies are hypertensive encephalopathy, including PRES, acute stroke, seizure, and retinopathy. The medications of choice for treating neurologic emergencies are those that do not increase intracranial pressure (Table 3). The IV dihydropyridine calcium-channel blockers nicardipine and clevidipine, or the IV dual α1- and β12-adrenergic receptor blocker labetalol, are generally well tolerated and are the medications of choice.

hypertensive emergency medications

Abbreviation: dP/dtmax, change in ventricular pressure over change in time.


Nitroprusside, nitroglycerin, and hydralazine all have the potential to increase intracranial pressure and therefore are generally contraindicated in this setting. Hydralazine in particular as an as-needed, bolus IV medication has little role in any acute hypertension treatment, except perhaps for pregnancy-related acute hypertension, owing to the unpredictability of response and prolonged duration of action.14

PRES is a neuroradiologic and clinical diagnosis that typically is associated with hypertensive encephalopathy but also can be seen in pregnancy-associated, acute-onset, severe hypertension syndromes (preeclampsia, eclampsia, HELLP syndrome) and with certain organ transplant immunosuppressive medications such as tacrolimus and cyclosporine.15

The 2013 American Heart Association/American Stroke Association (AHA/ASA) guidelines for the early management of patients with acute ischemic stroke16 recommend treatment of blood pressures greater than 220/120 mm Hg in the setting of acute ischemic stroke. If the use of tissue plasminogen activator (tPA) is indicated, the goal is to reduce blood pressure in these patients to less than 185/110 mm Hg before tPa administration in order to reduce the risk of hemorrhagic conversion. For systolic blood pressure greater than 140 mm Hg but less than 220 mm Hg, there is no proof that any treatment is beneficial. If systolic blood pressure is less than 120 mm Hg in the setting of acute ischemic stroke, the guidelines recommend placing the patient flat and providing isotonic saline to minimize the potential for cerebral malperfusion. As the AHA/ASA guidelines note, “Unfortunately, … an ideal blood pressure range has not yet been scientifically determined.”16

Seizures are a possible symptom of hypertensive encephalopathy and/or acute stroke and are treated with benzodiazepines or antiepileptic agents. Retinopathy is a relatively common complication of hypertension. Historically, retinopathy, along with acute nephropathy, was the first organ pathology identified in malignant hypertension described in the 1920s.17 These chronic hypertensive conditions had been considered malignant because of the associated high mortality rates—of the 81 patients observed by Keith and colleagues,17 91% died within 4 years, and the average lifespan of these patients was 8 months.

Hypertensive emergencies can be associated with acute retinopathy or acute choroidopathy and associated vision loss. Involvement of the choroid typically is a sign of acute, dramatic rise in blood pressure, often in a young person, in the setting of hypertensive emergency.18

Aortic Damage

Type A aortic dissection involves the ascending aorta and is a surgical emergency requiring immediate operative repair, given that the mortality rate of nonsurgically treated cases is 50% within the first 48 hours. Type B aortic dissection involves only the descending thoracic aorta and generally is treated medically unless there are signs of organ malperfusion on presentation, such as spinal cord or abdominal viscera ischemia.

The 2010 American College of Cardiology Foundation (ACCF) and AHA task force guidelines for the diagnosis and management of thoracic aortic disease recommend reducing the velocity of ventricular contraction (dP/dtmax), the rate of ventricular contraction, and the blood pressure with β-blockers, targeting a heart rate of less than 60 beats/min and a systolic blood pressure between 100 and 120 mm Hg while maintaining adequate organ perfusion.12

The 2014 ESC guidelines on the diagnosis and treatment of aortic diseases recommend treatment with IV β-blockers to reduce heart rate and lower systolic blood pressure to 100 to 120 mm Hg (Table 1).13 It is essential to start with a negative inotrope such as esmolol, because starting with vasodilator therapy actually may increase dP/dt and therefore the sheer stresses on the acutely injured aorta, leading to dissection progression and rupture. After β-blockers have been maximized, pure vasodilator medications such as nicardipine, clevidipine, nitroprusside, or nitroglycerin may be needed to achieve the target blood pressure (Table 3).

Acute aortic syndromes also are unique because, unlike with other hypertensive emergencies, the goal is to reduce systolic blood pressure to 100 to 120 mm Hg as quickly as possible, not only by 25% in the first hour or so. This requires strict ICU-level monitoring for sequelae of overly rapid reduction of blood pressure that can occur due to potential loss of microvasculature autoregulation at suddenly lower blood pressures. If this occurs, finding a median blood pressure that reduces dP/dt on the injured aorta but allows other organ perfusion is individualized by patient.

Cardiac Damage

Acute hypertension sometimes can be associated with acute MI, acute heart failure, or acute pulmonary edema. In the differential diagnosis of ST segment elevation MI (STEMI), one must always remember the possibility of acute type A aortic dissection with the dissection flap occluding right coronary artery flow or, more rarely, left coronary artery flow.19

For hypertensive emergency with acute MI not associated with type A aortic dissection, treatment with nitroglycerin is indicated, along with goal-directed therapies for non-ST segment elevation MI or STEMI (Table 3). Nitroglycerin should not be used in cases of suspected right ventricular infarction or if the patient recently has taken a phosphodiesterase type 5 inhibitor for erectile dysfunction within the preceding 24 to 48 hours.

Per the 2013 ACCF/AHA guideline for the STEMI management,20 fibrinolytic therapy is absolutely contraindicated in severe uncontrolled hypertension greater than 180/110 mm Hg that is unresponsive to emergency medical therapy (Table 3). If there is severe hypertension greater than 180/110 mm Hg at the time of admission, fibrinolytic therapy is relatively contraindicated (Table 1). In addition to IV nitroglycerin, an IV β-blocker (eg, metoprolol) also is reasonable for ongoing hypertension or ischemia in the absence of acute heart failure, low cardiac output, or bradyarrhythmias. Nitroprusside should be used carefully if at all in the setting of acute coronary syndrome due to its potential for inducing coronary steal. The true clinical significance of this potential complication is unknown.21

In acute heart failure, IV diuretics and IV nitroglycerin or nitroprusside are indicated. The IV negative inotropes such as esmolol, labetalol, and diltiazem are generally contraindicated in acute heart failure, because they could induce a low cardiac output state. Furthermore, the dihydropyridine calcium-channel blockers nicardipine and clevidipine also have some degree of negative inotrope properties and should be used sparingly in the setting of acute heart failure. High-dose nicardipine continuous drips also contain a significant volume of fluid, which also can potentiate heart failure.

Renal Damage

Acute kidney injury in hypertensive emergency is relatively common. In a prospective, cross-sectional study, Derhaschnig and colleagues22 found that levels of creatinine, blood urea nitrogen, cystatin C, and neutrophil gelatinase-associated lipocalin were significantly higher and the estimated glomerular filtration rate was significantly lower in hypertensive emergency patients compared with urgencies or control patients (59 patients in all; patients with chronic kidney disease were excluded).

Acute or preexisting renal impairment may predispose to the development of hypertensive emergency, and hypertensive emergency likewise may lead to direct kidney injury. The IV calcium-channel blockers nicardipine or clevidipine, or the dual α1- and β12-adrenergic receptor blocker labetalol, are acceptable medications for blood pressure control in acute kidney injury in the setting of hypertensive emergency (Table 3). IV nitroprusside also is very effective, but its limitation is in its renal clearance and the potential for thiocyanate poisoning or life-threatening cyanide toxicity.

A less common renal hypertensive emergency is scleroderma renal crisis, which is acute hypertension seen in approximately 5% of patients with systemic sclerosis.23 Scleroderma renal crisis is the new onset of accelerated hypertension in association with oliguric or anuric acute renal failure.24 It also can be associated with acute heart failure, encephalopathy, and thrombotic microangiopathy. Pathologically, it is associated with autoimmunity, vasculopathy, and fibrosis. Regardless of renal failure and function, treatment is with angiotensin-converting enzyme inhibitors (ACEIs) (Table 3). Acutely, oral captopril is the medication of choice, regardless of the serum creatinine level. If needed, hemodialysis may be instituted. Prognosis after an episode of scleroderma renal crisis is significantly worse, with a 5-year survival rate of 65%.24 Lifelong ACEI therapy is indicated following an episode, but interestingly, ACEI therapy before an episode of scleroderma renal crisis has never proven to be preventive.

Hematologic Damage

A rare but often forgotten pathophysiologic process in hypertensive emergency is microangiopathic hemolytic anemia (MAHA).25 Described in malignant hypertension, MAHA is characterized by coinciding thrombocytopenia and elevated serum lactate dehydrogenase that frequently is associated with renal or cerebral dysfunction. Microscopically, there is fibrinoid necrosis with fibrin and platelet thrombi in the lumina of small vessels, resulting in luminal narrowing and intravascular fragmentation of red blood cells with consumption of platelets.26 Treatment is supportive, with blood pressure control typically resulting in resolution. Acutely, any of the IV agents me be used, tailoring therapy to any coexisting conditions (Table 3).


The 2015 ACOG guidelines11 define pregnancy and postpartum acute-onset, severe hypertension as blood pressure of 160/110 mm Hg or greater persisting more than 15 minutes (Table 1). It is associated with severe preeclampsia, eclampsia, and HELLP syndrome.11 It can occur in the second half of pregnancy in previously nonhypertensive women, or in women with preexisting hypertension who develop a superimposed preeclampsia with acutely worsening hypertension. If a pregnant woman is found in the office to have acute-onset, severe hypertension of 160/110 mm Hg or higher for more than 15 minutes, she should be referred immediately to the hospital.

While monitoring the fetus, the recommended first-line agents are IV labetalol, IV hydralazine, or oral nifedipine (Table 3). Magnesium sulfate is not an antihypertensive medication but is used to prophylactically reduce seizure risk in preeclampsia or to treat seizures in eclampsia. Hydralazine can induce maternal hypotension. Labetalol can result in neonatal bradycardia and should be avoided in patients with heart failure or asthma. Nifedipine can lead to maternal tachycardia and hypotension.11


There are no coding diagnoses specific to hypertensive urgency or hypertensive emergency in the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10). These diagnoses are considered synonyms under Essential (Primary) Hypertension, ICD-10 code I10. Table 2 lists some of the ICD-10 billing codes related to target organ damage and illnesses seen in hypertensive emergency.


Acute hypertension is categorized as hypertensive urgency or hypertensive emergency depending on the absence or presence of target organ damage, respectively. Few data exist regarding its evidence-based management. Current US and European guidelines recommend initiation, reinitiation, or intensification of oral antihypertensive therapy for hypertensive urgency, whereas controlled IV antihypertensive therapy is reserved for hypertensive emergencies. 

The optimal IV medication and the rapidity with which optimal blood pressure is achieved depend on the type of end-organ damage.

Gregary D. Marhefka, MD, is the associate director of the Cardiovascular Intensive Care Unit and an associate professor of medicine in the Department of Medicine, Division of Cardiology, at the Sidney Kimmel Medical College at Thomas Jefferson University in Philadelphia, Pennsylvania.


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