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March 10, 2016

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Gregary D. Marhefka, MD

Consultant. 2016;56(3):222-232.
ABSTRACT: Acute hypertensionblood 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%.3
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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.5Hypertensive 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 colleges 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 7s 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).
Uses phrase asymptomatic elevated blood pressure instead of hypertensive


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 Hays 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).
There 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
Related Health Problems; NSTEMI, non-ST segment elevation myocardial
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.
Figure. Cerebral microvasculature autoregulation. In a chronic severely
patient, acute reduction in blood pressure to the normal level could result in
cerebral malperfusion (black arrows). Abbreviations: HTN, hypertension; MAP,
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 1- and 1/2-adrenergic receptor blocker labetalol, are generally well
tolerated and are the medications of choice.
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 ratesof 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/dt max), the rate
of ventricular contraction, and the blood pressure with -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 -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 -
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 -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 1- and 1/2-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.26Treatment 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

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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