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EARN CATEGORY I CME CREDIT by reading this article and the article beginning on page 20 and successfully
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LEARNING OBJECTIVES

Understand the distinction between hypertensive emergency and urgency

Describe the pathogenesis of hypertensive crisis and hypertensive encephalopathy
Discuss the clinical manifestations and initial evaluation of a patient in a hypertensive crisis
Identify the conditions associated with hypertensive emergency and urgency

Emergency or urgency? Effective

management of hypertensive crises
PAs need to identify the patients condition in order to select the most appropriate
intervention while avoiding overaggressive treatment of the nonemergent patient.

Kishore Kuppasani, MS, MPA, PA-C;

Alluru S. Reddi, MD, PhD

ypertensive crisis is a significant increase in

BP, usually to levels higher than 180/110
mm Hg. Hypertensive crises are classified
as emergency or urgency. Depending on the
type of crisis, BP should be reduced gradually or must be reduced immediately to prevent target organ
damage. Recognition of the type of manifest hypertensive
crisis is paramount to successful management and treatment
of the at-risk patient.

stress, thus limiting further dissection of the aorta. On the

other hand, a previously nonadherent hypertensive patient
who presents to the ED for a reason other than hypertension
but has a BP of 220/130 mm Hg and is otherwise asymptomatic does not require immediate BP reduction. The distinction between emergency and urgency should always be made
in the ED to prevent overaggressive treatment (Table 1).
PREVALENCE AND INCIDENCE

An estimated 1% of all hypertensive patients will experience

a hypertensive crisis during their lifetimes.1 However, the per-

of BPusually 220/130 mm Hg or higherwith acute and

ongoing target organ damage to the kidneys, heart, vascular system, brain, or eyes. Hypertensive emergency requires
the initiation of BP reduction within minutes to hours to
prevent further progression of target organ damage. BP
should not be lowered to less than 140/90 mm Hg, except
in patients with aortic dissection or eclampsia.
Hypertensive urgency is defined as an elevation of
BPusually 180/110 mm Hg or higherwithout target
organ damage. BP should be lowered gradually over
12 to 24 hours, but not to a normal level (target level,
approximately 160/110 mm Hg).
The clinical status of the patient, not the degree of BP elevation, defines an emergency in certain cases. For example,
in a patient with acute aortic dissection who presents to the
emergency department (ED) with a BP of 160/110 mm Hg,
the systolic BP (SBP) must be lowered to less than 120 mm
Hg within 20 minutes. The rapid reduction reduces shear
44 JAAPA AUGUST 2010 23(8) www.jaapa.com

ISM / Phototake

TYPES OF HYPERTENSIVE CRISES

Hypertensive emergency is defined as a severe elevation

A fundus view of hypertensive retinopathy in the right eye shows

hemorrhages and exudates caused by hypertension.

centage of patients who present to an ED with hypertensive

crisis is not known. A 1-year study reported that hypertensive crises accounted for 27.5% of all ED visits for medical
urgenciesemergencies;2 of those, 20.8% were for hypertensive urgencies and 6.4% were hypertensive emergencies. The
prevalence of hypertensive crisis in this study was 3%.
Little is known about what factors can precipitate a hypertensive crisis. However, a previous diagnosis of hypertension,
nonadherence to antihypertensive medication regimens, and
elevated BP that is not adequately controlled were found to
increase a patients risk for hypertensive crisis.3
PATHOPHYSIOLOGY

The pathophysiology of hypertensive crisis is poorly understood. A sudden increase in BP seems to further accentuate
shear stress in the vessel wall, which leads to additional endothelial damage, further activation of the neurohormonal
(renin-angiotensin II-aldosterone, sympathetic nervous system,
and vasopressin) system, induction of oxidative stress, and
inflammatory cytokines. The coagulation cascade is also activated by the resultant platelet aggregation and fibrin deposition. These changes lead to vasoconstriction, thrombosis, and
fibrinoid necrosis and result in hypoperfusion and ischemia.3-8
Cerebral edema and hypertensive encephalopathy
may result from impaired autoregulation of the brain. A
sudden increase in BP causes forced vasodilation of the
cerebral vessel to accommodate hyperperfusion. This
vasodilation is initially segmental, giving the appearance
of a sausage-string pattern on magnetic resonance angiography or conventional angiography, but soon becomes
diffuse. The endothelium becomes more dysfunctional
than before, allowing plasma components to diffuse into
the surrounding interstitium, leading to cerebral edema
and, finally, hypertensive encephalopathy.
Hypertensive patients in an emergency state present with
target organ damage, and patients in an urgency state do
not have target organ damage. Table 2 lists conditions associated with hypertensive emergency and urgency. The
frequency of target organ damage is not uniform. Target
organ damage reported in one study included cerebral infarction (24.5%), intracerebral or subarachnoid hemorrhage
(4.5%), hypertensive encephalopathy (16.3%), acute pulmonary edema (22.5%), acute heart failure (14.3%), acute
MI or unstable angina (12%), aortic dissection (4.5%), and
eclampsia (2%).2
SYMPTOMS AND EVALUATION

In a hypertensive emergency, the patient presents with

severe headache, nausea, vomiting, chest pain, dyspnea,
neurologic deficit, and vertigo.2 In a hypertensive urgency,
the patient may present with severe headache, dyspnea,
epistaxis, or severe anxiety. These symptoms may overlap
in patients in both types of crisis.
Early triage is an important part of the initial evaluation and establishes the appropriate therapeutic strategies
to improve morbidity and mortality (Figure 1). Patient

TABLE 1. Characteristics of hypertensive emergency

and urgency
Hypertensive
emergency

Hypertensive
urgency

Signs and symptomsa

More
frequent

Less frequent
or minimal

Acute severe increase in BP

Yes

Yes

Acute target organ damage

Yes

No

Acute BP reduction needed

Yes

No

IV medications needed

Yes

No

Hospitalization

Admit to
ICU and
monitor BP

Discharge from
ED with followup in 2-4 d

Characteristic

Key: ED, emergency department.

a
Signs and symptoms seen in a hypertensive emergency include severe headache,
nausea, vomiting, chest pain, dyspnea, neurologic decit, and vertigo. Signs and
symptoms seen in a hypertensive urgency include severe headache, dyspnea,
epistaxis, or severe anxiety. These may overlap in patients in both types of crisis.

TABLE 2. Conditions associated with hypertensive crisis

Hypertensive emergency
(symptomatic and with target organ damage)
Acute aortic dissection
Acute left ventricular failure with pulmonary edema
Acute MI
Acute renal failure
Adrenergic crisis (pheochromocytoma crisis, cocaine ingestion,
clonidine or beta-blocker withdrawal, amphetamine overdose)
Eclampsia
Hypertensive encephalopathy
Ischemic and hemorrhagic stroke
Hypertensive urgency
(asymptomatic and without target organ damage)
Epistaxis
Postoperative hypertension
Renovascular hypertension
Scleroderma crisis
Severe hypertension
Severe hypertension associated with burns or organ transplantation
Severe hypertension with coronary artery disease

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45

CME Hypertensive crisis

HYPERTENSIVE CRISIS

BP >220/130 mm Hg
Symptomatic
Acute target organ
damage

BP ~180/110 mm Hg
Asymptomatic
No target organ
damage

urinalysis. Laboratory studies for serum renin, aldosterone,

catecholamines, or urine metanephrines should be ordered if
secondary hypertension is suspected. Urine toxicology may be
indicated in select cases. An ECG may suggest ischemia and/
or left ventricular hypertrophy. Chest radiography is needed
to evaluate heart size and lungs. A widened mediastinum on
chest radiography is suggestive of aortic dissection and can be
confirmed with CT or MRI. Both CT and MRI are helpful
in the evaluation of cerebral or abdominal pathology. Table:
Hypertensive crisis evaluation and differential diagnosis (in
the online version of this article) lists the possible diagnoses
indicated by the initial findings.
TREATMENT

Hypertensive
emergency

Hypertensive
urgency

IV medications
Monitor patient in
ICU

Oral medications
Follow-up in 2-4 d

FIGURE 1. Triage of patients in hypertensive crisis

history should focus on signs and symptoms, such as

headache, dyspnea, seizures, nausea, vomiting, epistaxis,
mental status, previous history of hypertension, and
medications. Physical examination should include brief
fundoscopic, cardiac, lung, and neurologic examinations.
Establishing the patients volume status is essential because heart failure and acute glomerulonephritis may
manifest with volume overload. Pheochromocytoma and,
at times, renovascular hypertension may manifest with
volume depletion.
Eye examination may reveal papilledema or other grades of
retinopathy. Laboratory studies include a CBC with peripheral smear, serum electrolytes, creatinine, BUN, glucose, and

Management of a specific hypertensive crisis depends on

the signs and symptoms as well as the target organ damage.
Drug therapy should be individualized (Table 3).
Hypertensive emergency The patient should be admitted to the ICU for continuous BP monitoring. Once a
hypertensive emergency is identified, IV administration
of an appropriate drug should be started in the ED. The
initial goal is to lower BP by 25% of the mean arterial
BP within minutes to 1 hour and stabilize BP to approximately 160/100 to 110 mm Hg over the next 2 to 6 hours.9
Rapid BP reduction below this level may precipitate renal,
coronary, or cerebral ischemia. If the patient is stable and
tolerates a BP of 160/100 to 110 mm Hg, further reduction to near normal can be attempted over 24 to 48 hours.
However, normal BP levels should not be achieved in
the patient with ischemic stroke. SBP should be lowered
to less than 120 mm Hg in the patient with aortic dissection.9 Table 4 describes the signs and symptoms, preferred
agent(s), and agents to be avoided when treating a patient
in a hypertensive emergency. Suggested target BP levels
are also listed.
Hypertensive urgency Patients will not have sustained
target organ damage; therefore, their BP can be followed
and treated with short-acting oral agents after eliminating
any triggering factors, such as pain. If the patient does not
have any triggering factors and severe hypertension persists, the patient is considered to have chronic hypertension.
Parenteral drugs are not needed, nor is a rapid reduction
of BP, as there is no evidence to suggest that these patients

KEY POINTS
Depending on the type of crisis (emergency or urgency), BP should be reduced gradually or must be reduced immediately to prevent

target organ damage. Recognition of the type of manifest hypertensive crisis is paramount to successful management and treatment
of the at-risk patient.
Hypertensive emergency is dened as a severe elevation of BPusually 220/130 mm Hg or higherwith acute and ongoing target
organ damage to the kidneys, heart, vascular system, brain, or eyes. Hypertensive urgency is dened as an elevation of BPusually
180/110 mm Hg or higherwithout target organ damage.
The most important task for the ED clinician is to identify whether the patients condition is a hypertensive emergency or urgency.
The goal is to avoid overaggressive treatment of the nonemergent patient while initiating the most appropriate treatment.

46 JAAPA AUGUST 2010 23(8) www.jaapa.com

TABLE 3. Commonly used drugs in hypertensive crises3-9,13

Drug

Dosage

Onset

Duration

Adverse effects

PARENTERAL DRUGS USED IN HYPERTENSIVE EMERGENCIES

ADRENERGIC INHIBITORS
Esmolol (Brevibloc, generics)

250-500 mcg/kg/min,
then 50-100 mcg/kg/min;
may repeat bolus after
5 min or increase to 300
mcg/kg/min

1-2 min

10-30 min

Asthma First-degree heart block

Heart failure Hypotension
Nausea

Labetalol (generics)

20-80 mg bolus q10min

5-10 min

2-6 h

Bronchospasm Heart block

Nausea Scalp tingling Vomiting

Phentolamine (Oraverse, Regitine)

5-10 mg/min

1-2 min

10-30 min

Flushing Headache Tachycardia

20-40 mg in 5 min

5-15 min

2-3 h

Hypokalemia Volume depletion

Enalaprilat (generics)

1.25-5 mg q6h

15-30 min

4-6 h

Angioedema Hypotension
Renal failure

Fenoldopam (Corlopam, generics)

0.1-0.3 mcg/kg/min

5-10 min

30 min

Headache Nausea Tachycardia

Hydralazine (generics)

10-20 mg bolus

10-20 min

1-4 h

Flushing Headache Tachycardia

Vomiting

Nicardipine (Cardene, generics)

5-15 mg/h

5-10 min

2-4 h

Headache Flushing
Reex tachycardia

Nitroglycerin (generics)

5-100 mcg/min

1-3 min

5-10 min

Headache Hypotension Vomiting

Sodium nitroprusside (Nitropress)

0.25-10 mcg/kg/min

Immediate

1-2 min

Cyanate toxicity Hypotension

Nausea Vomiting

DIURETICS
Furosemide (generics), used with
other agents
VASODILATORS

ORAL DRUGS FOR HYPERTENSIVE URGENCIES

Amlodipine (Norvasc, generics)

5-10 mg

30-50 min

18-24 h

Headache Flushing
Peripheral edema Tachycardia

Captopril (Capoten, generics)

12.5-25 mg

15-60 min

4-6 h

Cough
Renal failure with bilateral renal
artery stenosis

Clonidine (Catapres, Jenloga,

generics)

0.2 mg

30-120 min

8-12 h

Dry mouth Hypotension

Sedation

Furosemide (Lasix, generics)

20-40 mg

30-60 min

4-5 h

Hypokalemia Volume depletion

Labetalol (Trandate, generics)

200-400 mg

20-120 min

8-12 h

Bronchospasm
Decreased myocardial contractility
Heart block

Nicardipine (Cardene, generics)

20-30 mg

30-120 min

6-8 h

Headache Tachycardia

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CME Hypertensive crisis

TABLE 4. Preferred IV therapy in hypertensive emergency
Emergency

Signs and symptoms

Drug(s) of choice

Drug(s) to be avoided

Target BP

Acute MI

Chest pain Dyspnea

Esmolol Labetalol
Nitroglycerine

Hydralazine (may
increase heart rate and
O2 consumption)

Gradual reduction
to 5%-10% of MAP

Acute renal failure

and hematuria

No specic signs or
symptoms unless
uremia or HF is present

Fenoldopam
Nicardipine

Nitroprusside (rapid
BP reduction causes
further alteration in
autoregulation)

Gradual reduction to 10%

of MAP over several hours

Aortic dissection

Chest pain
(intrascapular region)
Headache Syncope

Esmolol
Labetalol plus
nitroprusside

Hydralazine (may
increase mechanical
stress)

SBP <120 mm Hg within

20 min

Cocaine withdrawal

Agitation AMS

Phentolamine

Propranolol (complete
beta blockade and
increases BP)

10%-15% reduction
of MAP

Eclampsia

Headache Seizures

Hydralazine Labetalol
MgSO4 Nicardipine
Nifedipinea

ACE inhibitors (fetal

abnormalities)
Nitroprusside (cyanate
toxicity)

DBP <90 mm Hg gradually

(<1 h)

Hypertensive
encephalopathy

Headache AMS
Papilledema
(common but not
always present)

Fenoldopam Labetalol
Nicardipine

Clonidine (sedation)
Nitroglycerine
Nitroprusside
(increases ICP)

25% reduction of MAP

over 2-3 h

Intracerebral
hemorrhage

AMS
Headache
Neurologic (focal)
decit

SBP >200 mm Hg or
MAP >150 mm Hg:
Esmolol
Labetalol
Nicardipine

Hydralazine
(increases ICP)
Nitroglycerine
Nitroprusside

High ICP: Maintain MAP

<130 mm Hg or SBP <180
mm Hg for the rst 24 h
Normal ICP: Maintain MAP
<110 mm Hg or SBP <160
mm Hg for rst 24 h

Ischemic stroke

AMS
Headache
Neurologic (focal)
decit

BP >180/120 mm Hg or
MAP >140 mm Hg:
Labetalol
Nicardipine

Clonidine (sedation)

15% reduction of MAP

BP <140/90 mm Hg
should be avoided
Maintain a BP of
<180/105 mm Hg for
24 h after thrombolysis

Left ventricular
failure and
pulmonary edema

Chest pain
Dyspnea

ACE inhibitors
Furosemide
Nitroglycerine
Nitroprusside

Hydralazine
Labetalol (may
worsen HF)

10%-15% reduction of MAP

Pheochromocytoma

Headache
Sweating

Labetalol
Phentolamine

Diuretics (volume
depletion)
Nitroprusside
(hypotension)

Gradual reduction until

symptoms improve

Subarachnoid
hemorrhage

AMS
Headache
Neurologic
(focal decit)

MAP >130 mm Hg:

Esmolol
Labetalol
Nicardipine
Oral nimodipineb

Hydralazine
(increases ICP)
Nitroglycerine
Nitroprusside

Maintain SBP <160 mm Hg

(MAP >130 or <70 mm Hg
carries poor prognosis)

Key: AMS, altered mental status; DBP, diastolic BP; ICP, intracranial pressure; HF, heart failure; MAP, mean arterial pressure; MgSO4, magnesium sulfate; SBP, systolic BP.
a
Only long-acting nifedipine is used.
b
Oral nimodipine has a hypotensive effect but is not used to treat hypertension. It is used to prevent delayed ischemic neurologic decit.

48 JAAPA AUGUST 2010 23(8) www.jaapa.com

experience immediate (from hours to a few days) target

organ damage if left untreated. BP will fall by 6% within 1
hour even before antihypertensive drugs are started.8 Thus,
parenteral use of antihypertensive agents should be avoided
in the uncomplicated patient with severe hypertension.
Some clinicians hesitate to treat hypertensive urgency
in the ED. Oral agents should be considered if the patients BP is higher than 180/110 mm Hg and are indicated when the patients BP is higher than 220/120 mm
Hg.10,11 BP should be reduced to approximately 160/110
mm Hg over a period of 12 to 24 hours after triggering
factors are corrected to avoid myocardial, cerebral, and
renal ischemia.
Follow-up within 2 to 4 days after the ED visit is extremely
important. Patients should be instructed to schedule a followup appointment with a primary care physician or an outpatient clinic as soon as possible.
Prognosis Patient prognosis after a hypertensive crisis is
poor. A 30-year follow-up of 315 patients with hypertensive
emergency showed a 5-year survival of 74%.12 The most
common causes of death were renal failure (40%), stroke
(24%), MI (11%), and heart failure (10%).
CONCLUSION

The most important task for the ED clinician is to identify whether the patients condition is a hypertensive
emergency or urgency. The goal is to avoid overaggressive treatment of the nonemergent patient while initiating
the most appropriate treatment. Effective management
of hypertensive crises improves both morbidity and
mortality. JAAPA

ONLINE EXTRAS AT
www.jaapa.com
Table: Hypertensive crisis evaluation and
differential diagnosis

Kishore Kuppasani is a hospitalist PA at the University Hospital, UMDNJ,

Newark, New Jersey. Alluru Reddi is professor of medicine, Department of
Medicine, Division of Nephrology and Hypertension, UMDNJ-New Jersey
Medical School, Newark. The authors have indicated no relationships to
disclose relating to the content of this article.
REFERENCES
1. Kinkaid-Smith P, McMichael J, Murphy EA. The clinical course and pathology of hypertension
with papilloedema (malignant hypertension). Quart J Med. 1958;27(105):117-153.
2. Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies: prevalence and clinical presentation. Hypertension. 1996;27(1):144-147.
3. Patel HP, Mitsnefes M. Advances in the pathogenesis and management of hypertensive crisis.
Curr Opin Pediatr. 2005;17(2):210-214.
4. Kitiyakara C, Guzman NJ. Malignant hypertension and hypertensive emergencies. J Am Soc
Nephrol. 1998;9(1):133-142.
5. Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet. 2000;356(9227):411-417.
6. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiol
Clin. 2006;24(1):135-146.
7. Marik PE, Varon J. Hypertensive crises: challenges and management. Chest. 2007;131(6):1949-1962.
8. Nolan CR, Linas SL. Malignant hypertension and other hypertensive crises. In: Schrier RW, ed.
Diseases of the Kidney & Urinary Tract. 8th ed. Philadelphia, PA: Wolters Kluwer/Lippincott,
Williams & Wilkins; 2007:1370-1436.
9. Chobanian AV, Bakris GL, Black HR, Cushman WC, et al. Seventh report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206-1252.
10. Shayne P. Against routine initiation of antihypertensive therapy in the emergency department.
Ann Emerg Med. 2009;54(6):792-793.
11. Slovis CM, Reddi AS. Increased blood pressure without evidence of acute end organ damage.
Ann Emerg Med. 2008;51(3S):S7-S9.
12. Lip GY, Beevers M, Beevers DG. Complications and survival of 315 patients with malignant-phase
hypertension. J Hypertens. 1995;13(8):915-924.
13. Rosei EA, Salvetti M, Farsang C. European Society of Hypertension Scientic Newsletter: treatment of hypertensive urgencies and emergencies. J Hypertens. 2006;24(12):2482-2485.

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49

TABLE. Hypertensive crisis evaluation and differential diagnosis

Assessment and/or ndings

Differential diagnosis

HISTORY
Chest pain radiates to left arm and back

Acute MI Aortic dissection

Dyspnea, pulmonary edema

Left ventricular failure

Headache, nausea, vomiting, altered mental status, seizures,

focal neurologic decit

Stroke

Hematuria, red blood cell casts

Acute glomerulonephritis Vasculitis

Illicit drug use

Cocaine ingestion

Nonadherence to previous antihypertensive therapy

Clonidine or beta-blocker withdrawal

IMAGING STUDIES
Chest CT (false or double lumen of aorta)

Aortic dissection

Chest MRI (intramural hematoma appearing as crescentic

thickening around aortic wall)

Aortic dissection

Chest radiography
Rib notching caused by dilated intercostal arteries
Widening of mediastinum

Aortic dissection
Coarctation of aorta

ECG
Deep T-wave inversions in the absence of MI
Q waves, ST-T abnormalities

Subarachnoid hemorrhage
Acute MI

Head CT or MRI (ischemia or hemorrhage)

Stroke

Transesophageal echocardiography (intimal ap, double lumen)

Aortic dissection

LABORATORY STUDIES
CBC (anemia) and schistocytes on peripheral blood smear

Microangiopathic hemolytic anemia

Serum potassium (low) and serum bicarbonate (high)

Metabolic alkalosis associated with renovascular hypertension

Primary aldosteronism

Serum creatinine and BUN (elevated)

Renal failure

Serum glucose
Elevated
Low

Diabetes mellitus Pheochromocytoma

Precipitates hypertensive encephalopathy

Serum renin (low) and serum aldosterone (high)

Primary aldosteronism

Plasma catecholamines and urine metanephrine (elevated)

Pheochromocytoma

Urinalysis (red blood cells, red blood casts)

Acute glomerulonephritis Vasculitis

Urine toxicology

Cocaine ingestion

Pregnancy test (positive)

<20 weeks
>20 weeks with seizures
>20 weeks without seizures

Acute or chronic hypertension

Preeclampsia
Eclampsia

PHYSICAL EXAMINATION
Systolic BP
High in arms and low in legs
Difference >20 mm Hg in arms, pulse decit, weak pulses

Coarctation of aorta
Aortic dissection

Orthostatic BP and pulse changes

Pheochromocytoma Volume depletion

Eyes
Grade 2 retinopathy (arteriovenous nicking, narrowing)
Grades 3 (hemorrhages, exudates) and 4 (papilledema) retinopathy

Chronic hypertension
Target organ damage (previously called malignant hypertension)

Neck (jugular vein distension)

Left ventricular failure

Heart (S3 sound)

Left ventricular failure

Lungs (crackles, congestion)

Left ventricular failure

Abdomen
Bruits
Gravid uterus

Aneurysms Renal artery stenosis

Preeclampsia-eclampsia

Peripheral edema

Left ventricular failure

Neurologic decit with seizures

Eclampsia Hypertensive encephalopathy Stroke