Prim Care Clin Office Pract

35 (2008) 475–487

Hypertensive Crises
Christopher J. Hebert, MD*, Donald G. Vidt, MD
Department of Nephrology and Hypertension, Cleveland Clinic, Suite A51,
9500 Euclid Avenue, Cleveland, OH 44195, USA

Hypertension is the most common reason for a physician office visit in

the United States [1]. The primary care physician should therefore expect
to see the occasional patient with very elevated blood pressure, defined as
greater than 180/110 mm Hg. Expedited triage of such patients is necessary
to identify the minority of patients that would benefit from acute reduction
in blood pressure. Hypertensive crises are those situations in which mark-
edly elevated blood pressure is accompanied by progressive or impending
acute target organ damage. The discussion that follows addresses the assess-
ment, treatment, and follow-up care for patients with very elevated blood
pressure, with an emphasis on hypertensive crises.

Definitions
Patients presenting with very high blood pressuredblood pressure
greater than 180/110 mm Hgdshould be triaged into one of three mutually
exclusive groups.
1. Severe hypertension is present when blood pressure exceeds 180/110 mm
Hg in the absence of symptoms beyond mild or moderate headache, and
without evidence of acute target organ damage.
2. Hypertensive urgency is present when blood pressure exceeds 180/
110 mm Hg in the presence of significant symptoms, such as severe
headache or dyspnea, but no or only minimal acute target organ
damage.
3. Hypertensive emergency is present when very high blood pressure
(often O220/140 mm Hg) is accompanied by evidence of life-threaten-
ing organ dysfunction. Box 1 lists the important causes of hypertensive
emergencies.

* Corresponding author.
E-mail address: hebertc@ccf.org (C.J. Hebert).

0095-4543/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved.
doi:10.1016/j.pop.2008.05.001 primarycare.theclinics.com
476 HEBERT & VIDT

Box 1. Examples of hypertensive emergencies

Acute ischemic or hemorrhagic stroke
Subarachnoid hemorrhage
Hypertensive encephalopathy
Acute myocardial ischemia/infarction
Acute heart failure
Acute aortic dissection
Eclampsia
Head trauma
Catecholamine excess states
Beta-blocker or clonidine withdrawal
Cocaine, phencyclidine hydrochloride use
Pheochromocytoma crisis
Hemorrhage
Postsurgical
Severe epistaxis

The term hypertensive crisis is used to indicate either a hypertensive

urgency or emergency.
There are two older terms that are notable. Malignant hypertension repre-
sents markedly elevated blood pressure accompanied by papilledema (grade
4 retinopathy). Accelerated hypertension is considered present if markedly
elevated blood pressure is accompanied by grade 3 retinopathy, but no papil-
ledema. However, the three numbered terms above usually suffice for the
description of all clinical scenarios involving very high blood pressure.

Epidemiology
Among the 65 million Americans with hypertension, the minority have
controlled blood pressure, with estimates falling between 38% and 44%
[1,2]. Hypertensive crises, however, occur in less than 1% of individuals
with hypertension [3].
Although crises are infrequent, very elevated blood pressure is a common
clinical scenario facing the physician. In the United States, more that
250,000 emergency department visits in 2005 were attributed to the diagnosis
of hypertension (International Classification of Diseases, Ninth Revision [ICD9]
diagnoses 401.0, 401.1, 401.9), with 14% resulting in hospital admission [4].
Some have suggested that hospitalization for hypertensive emergency
reflects upon the quality of ambulatory care (ie, an ambulatory care–
sensitive condition) [5]. There are two ways in which an emergency depart-
ment evaluation might indicate poor-quality ambulatory care. First, the
treating physician may have failed to achieve good blood pressure control,
 HYPERTENSIVE CRISES 477

resulting in less effective care [6]. Secondly, a patient with very elevated
blood pressure may have been referred to the emergency department
when office management was possible, making care less efficient. With
high effectiveness and high efficiency being two key aims of high quality
care [6], failure to achieve good blood pressure control and inappropriate
referral undermine efforts to streamline and improve health care. An appro-
priate assessment of patients with very elevated blood pressure will identify
the few patients requiring admission and acute reduction in blood pressure
among the many who require initiation of oral medication on an outpatient
basis and follow-up care.
Bender and colleagues [7] studied 50 patients who presented to an emer-
gency department and found that the most common reason precipitating the
crisis was running out of medication. Furthermore, the average cost was
$1543 per visit, which underscores the importance of effective primary
care. Particularly common is rebound hypertension after abrupt discontin-
uation of clonidine or a beta-blocker [8]. This rebound hypertension is
thought to be due to an acute increase in sympathetic outflow.

Assessment
A timely and focused history, physical examination, and select testing is
important in the initial assessment of the patient with very elevated blood
pressure.

History
The history should be completed in a timely manner and capture several
key pieces of information. The physician should assess the duration and
severity of hypertension. The relevant symptoms to address include head-
ache, chest pain, dyspnea, edema, acute fatigue, weakness, epistaxis, seizure,
or change in level of consciousness. Such symptoms as tachycardia, diapho-
resis, and tremor may suggest pheochromocytoma, and thinning of skin and
weight gain may suggest Cushing syndrome. Any history of comorbid
conditions or end organ damage is important, such as left ventricular hyper-
trophy, chronic kidney disease, or prior stroke or myocardial infarction.
Direct questioning regarding adherence to any prescribed antihypertensive
medications is necessary, as well as recent use of such medications as oral
contraceptives, monoamine oxidase inhibitors, nonsteroidal anti-inflamma-
tory drugs, cyclosporine, stimulant/anorectic agents, and prednisone. The
patient should be questioned for use of alcohol as well as recreational drugs,
particularly cocaine, amphetamines, and phencyclidine hydrochloride.

Physical examination
The measurement of blood pressure should be performed with proper
technique and, in the setting of diminished pedal pulses, should include
478 HEBERT & VIDT

both arms and at least one leg measurement. A fundus examination

should be performed to assess for papilledema, hemorrhages, and exudates.
A careful cardiovascular examination should include assessment of the
jugular venous pulse, auscultation for abdomenal bruits, and assessment
of peripheral pulses. A lung examination and assessment for dependent
edema should be performed to estimate volume status. Finally, a neurologic
examination, including assessment of mental status, is important.

Testing
In the emergency department setting, a limited but expeditious battery of
tests should include a chemistry panel, urinalysis with microscopic examina-
tion of the sediment, and ECG. A chest radiograph is important if there is
a suspicion of heart failure or pulmonary disease. A CT scan of the head is
indicated if history or examination suggests a central nervous system disor-
der. In the office setting or with less severe elevations of blood pressure,
clinical judgment should guide testing, but in all cases a careful history
and examination are critical.
In practice, emergency department evaluations often are lacking. For
example, Karras and colleagues [9] observed care for patients with severely
elevated blood pressure at four academic emergency departments. Serum
chemistry was performed in only 73% of cases, ECG in 53%, and urinalysis
in 43%. The goal should be a timely evaluation that includes the essential
clinical tests.

Goals of treatment
Proper triage prepares the physician to establish short- and long-term
goals for the patient with very elevated blood pressure (Table 1).
There is a distinct lack of trial evidence that patients with severe hyper-
tension (without crisis) benefit from acute lowering of blood pressure, and
it may be associated with risk. For example, short-acting nifedipine has
been associated with severe hypotension, stroke, acute myocardial infarc-
tion, and death, and is no longer a part of the management of severe hyper-
tension [10]. Although other oral medications for acute blood pressure
reduction may not have such clear documentation of harm, the evidence
of benefit is lacking, and the edict ‘‘first, do no harm’’ is advisable.
Therefore, management of severe hypertension should include brief office
observation (hours), initiation or resumption of oral antihypertensive med-
ication, and arrangement for timely follow-up care, usually within 72 hours.
For patients with hypertensive urgency, again clear evidence of benefit of
acute lowering of blood pressure is lacking, but expert opinion [11–13] favors
judicious acute treatment with an oral agent with rapid onset of action. The
short-term goal is to reduce the blood pressure within 24 to 72 hours, and
appropriate follow-up should be mandatory. For noncompliant patients,
Table 1
Triage of patients with very elevated blood pressure
Severe hypertension Hypertensive urgency Hypertensive emergency
Blood Pressure O180/110 mm Hg O180/110 mm Hg Often O220/140 mm Hg
Clinical features: symptoms May be asymptomatic; headache Severe headache, dyspnea, edema Chest pain, severe dyspnea,
altered mental status, focal
neurologic deficit
Clinical features: findings No acute target organ damage Acute target organ damage usually Life-threatening target organ

HYPERTENSIVE CRISES
absent, but may include elevated damage (eg, acute myocardial
serum creatinine infarction, stroke,
encephalopathy, acute renal
failure, heart failure)
Immediate goal Lower blood pressure within days Lower blood pressure within Immediate blood pressure
24–72 hours reduction; decrease by
15%–25% within 2 hours
Treatment setting Outpatient Usually outpatient Inpatient, intensive care unit
Medications Long-acting, oral Oral medications with rapid onset Intravenous medication
of action; occasionally
intravenously
Follow-up Within 3–7 days Within 24–72 hours As appropriate after hospital
management

479
480 HEBERT & VIDT

resumption of prior medications may be sufficient. For untreated patients,

initiation of long-acting agents is appropriate.
Hypertensive emergency warrants admission to an intensive care unit and
treatment with a parenteral agent. The short-term goal is to reduce the
blood pressure by 15% to 25% within 4 hours. A reduction beyond 25%
may exceed the autoregulatory capacity of the cerebrovascular circulation
[14] and therefore elicit hypoperfusion, ischemia, and stroke.

Pharmacotherapy
For severe hypertension, initiation or resumption of long-acting antihy-
pertensive medication is warranted.
If immediate reduction of blood pressure is indicated (urgency), medica-
tions with rapid onset of action are preferred. Oral medications that may be
appropriate include clonidine, (0.1–0.2 mg), labetalol (200–400 mg), or cap-
topril (12.5–25 mg). Use of drugs with rapid onset carries two caveats. First,
a large dose should be followed by a longer period of observation in the
office or emergency department to assess for hypotension. Secondly, the
effect of a drug with short onset of action (eg, clonidine) may decrease
shortly after discharge to home, resulting in return of very elevated blood
pressure. To avoid this occurrence, one can either continue dosing of the
same drug as an outpatient, or begin a long-acting drug (eg, amlodipine,
extended-release metoprolol, diuretic) in the office. Table 2 lists some com-
monly used oral agents in the treatment of hypertensive crises.
Parenteral agents are indicated for some cases of hypertensive urgency
and all cases of hypertensive emergency. Table 3 lists some commonly
used intravenous medications.

Table 2
Preferred medications for hypertensive urgencies
Agent Dose Onset of action Comment
Labetalol 200–400 mg po 20–120 min Bronchoconstriction, heart block,
aggravate heart failure
Clonidine 0.1–0.2 mg po 30–60 min Rebound hypertension with
abrupt withdrawal
Captopril 12.5–25 mg po 15–60 min Can precipitate acute renal
failure in setting of bilateral
renal artery stenosis
Nifedipine, 30 mg po 20 min Avoid short-acting oral or
extended sublingual nifedipine due to risk
release of stroke, acute myocardial
infarction, severe hypotension
Amlodipine 5–10 mg po 30–50 min Headache, tachycardia, flushing,
peripheral edema
Prazosin 1–2 mg po 2–4 hours Syncope (first dose), tachycardia,
postural hypotension
Table 3
Preferred medications for hypertensive emergencies
Onset/duration of action
Agent Dose (after discontinuation) Precautions
Parenteral vasodilators
Sodium nitroprusside 0.25–10.00 mg/kg/min as intravenous Immediate/2–3 min Nausea, vomiting, muscle twitching; with
infusion; maximal dose for 10 min only after infusion prolonged use, may cause thiocyanate
intoxication, methemoglobinemia acidosis,
cyanide poisoning; bags, bottles, and
delivery sets must be light-resistant
Glyceral trinitrate 5–100 mg as intravenous infusion 2–5 min/5–10 min Headache, tachycardia, vomiting, flushing,
methemoglobinemia; requires special
delivery systems due to the drug’s binding
to polyvinyl chloride tubing

HYPERTENSIVE CRISES
Nicardipine 5–15 mg/h intravenous infusion 1–5 min/15–30 min, but may Tachycardia, nausea, vomiting, headache,
exceed 12 h increased intracranial pressure, possible
after prolonged infusion protracted hypotension after prolonged infusions
Verapamil 5–10 mg intravenous; can follow with 1–5 min/30–60 min Heart block (first-, second-, and third-degree),
infusion of 3–25 mg/h especially with concomitant digitalis or
b-blockers; bradycardia
Fenoldopam 0.1–0.3 mg/kg/min intravenous infusion !5 min/30 min Headache, tachycardia, flushing, local phlebitis
Hydralazine 10–20 mg as intravenous bolus or 10–40 mg 10 min intravenous/O1 h Tachycardia, headache, vomiting, aggravation
intramuscularly; repeat every 4–6 h (intravenous); of angina pectoris
20–30 min intramuscularly/
4–6 h intramuscularly
Enalaprilat 0.625–1.250 mg intravenous every 6 h 15–60 min/12–24 h Renal failure in patients with bilateral renal
artery stenosis; hypotension
Parenteral adrenergic inhibitors
Labetalol 10–80 mg as intravenous bolus every 10 min; 2–5 min/2–4 h Bronchoconstriction, heart block, orthostatic
up to 2 mg/min as intravenous infusion hypotension
Esmolol 500 mg/kg bolus injection intravenously 1–5 min/15–30 min First-degree heart block, congestive
or 25–100 mg/kg/min by infusion; may heart failure, asthma
repeat bolus after 5 min or increase infusion
rate to 300 mg/kg/min

481
Phentolamine 5–15 mg as intravenous bolus 1–2 min/10–30 min Tachycardia, orthostatic hypotension
482 HEBERT & VIDT

Sodium nitroprusside is very appropriate in the treatment of hypertensive

emergencies because it is easily titratable, having an onset of action that is
immediate and a duration of action only 2 to 3 minutes after discontinua-
tion. It is a nonspecific vasodilator that has the same mechanism of action
as endogenous nitric oxide. Adverse effects include nausea and vomiting,
and thiocyanate intoxication with prolonged use is an important precaution.
Despite these drawbacks, the drug is easily titrated and has become a main-
stay of the management of hypertensive emergencies. When used in the set-
ting of aortic dissection, concomitant use of a beta-blocker is important.
Nitroglycerin improves coronary blood flow and is the drug of choice for
hypertensive emergency associated with acute myocardial infarction when
blood pressure is moderately elevated. It is a vasodilator of capacitance
vessels more so than arteries, and is less potent than nitroprusside. Disad-
vantages include side effects, such as headache and vomiting, and tolerance
with prolonged use is a limitation.
Labetalol is commonly used for hypertensive emergencies, particularly
aortic dissection. Its mechanism of action includes both alpha and beta
blockade, and has a rapid onset of action. It can be continued orally on
an outpatient basis, although it requires multiple doses per day. The disad-
vantages are those common to the beta-blocker class, including the potential
for bradycardia, heart block, and bronchoconstriction. Esmolol is an intra-
venous beta-blocker that has very rapid onset of action along with short
duration of action after discontinuation, making it particularly useful in
the perioperative setting. It does not come in an oral form.
Enalaprilat is an intravenous angiotensin-converting enzyme (ACE)
inhibitor that has a fairly rapid onset of action. Like all ACE inhibitors,
it carries the risk of acute renal failure in the setting of bilateral renal artery
stenosis.
Fenoldopam is particularly useful in the setting of renal insufficiency in
that it has been shown to improve renal blood flow [15,16]. The drug acts
as a dopamine receptor agonist and therefore causes renal as well as
systemic vasodilatation. Like nitroprusside, it is easily titrated, but it is
a much more costly drug.
For hypertensive urgency, oral amlodipine or extended-release nifedipine
may be useful if the goal is to lower the blood pressure within 72 hours. As
mentioned previously, immediate-release nifedipine should be avoided
because of risk of hypotension.
Verapamil has a rapid onset of action and is available in both intravenous
and oral forms, but carries a risk of heart block. Nicardipine is a calcium
blocker without substantial risk of heart block, but tachycardia and the
tendency toward prolonged action after discontinuation are limitations.
Hydralazine is a direct vasodilator of arterioles and for years has been
a useful drug in the management of hypertensive crises, particularly eclamp-
sia of pregnancy. Its advantages include a rapid onset of action, intravenous
and oral dosing, and a track record of safety in the setting of pregnancy.
 HYPERTENSIVE CRISES 483

Limiting its use are several potential side effects, including reflex tachy-
cardia, headache, and vomiting. The reflex tachycardia makes this drug gen-
erally undesirable for treatment of crises associated with acute coronary
syndrome or acute aortic dissection.
Phentolamine is a potent alpha-1 antagonist with a rapid onset of action
that has traditionally been used in cases of catecholamine excess, such as
pheochromocytoma crisis. Side effects can be problematic with this drug, par-
ticularly orthostatic hypotension, flushing, headache, and reflex tachycardia.
Oral clonidine is a useful drug for hypertensive urgency due to its rapid
onset of action. However, multiple doses of clonidine can be a setup for
hypotension if the patient is not observed for a sufficient amount of time.
The practice of clonidine loading has largely fallen out of favor. One small
trial of clonidine loading among patients with severe asymptomatic hyper-
tension found no benefit [17].

Assessment and management of selected hypertensive emergencies

In addition to the general principles outlined above, the clinical features
and management of several specific hypertensive emergencies deserve special
attention.

Neurologic hypertensive emergencies

A neurologic hypertensive emergency is present if severe hypertension is
associated with encephalopathy, stroke, subarachnoid hemorrhage, or acute
head trauma.
When neurologic findings, such as a focal deficit or altered mental status,
are present, the physician should attempt to accurately place the case into
one of the preceding four categories. A careful physical examination is im-
portant both for diagnosis and to establish the level of neurologic function-
ing at the time of presentation. The optic fundus and mental status must be
examined, and the patient must be assessed for motor deficits and cerebellar
dysfunction.
Hypertensive encephalopathy is a manifestation of cerebral edema and is
suggested by such symptoms as severe headache, nausea, vomiting, confu-
sion, seizure, or coma. Papilledema is found on optic fundus examination,
and rapid reduction of blood pressure is indicated. Sodium nitroprusside
is the drug of choice, and a reduction in blood pressure by 20% to 25%
over the first few hours is advisable.
Stroke is typically diagnosed by history and examination indicating
a focal neurologic insult along with corresponding abnormalities on brain
CT or MRI. In such situations, watershed areas of brain parenchyma sur-
rounding the stroke are dependent on perfusion pressure to remain viable.
For that reason, acute and aggressive lowering of blood pressure may confer
a risk.
484 HEBERT & VIDT

Severe hypertension resulting from head trauma (Cushing’s reflex) should

be evident from the clinical presentation. The ideal target blood pressure in
this setting is unknown. Blood pressure reduction should be accomplished
cautiously and with close neurologic surveillance.

Acute aortic dissection

Aortic dissection is a life-threatening condition in which timely diagnosis
and aggressive treatment of blood pressure are key. Severe hypertension and
tachycardia are typically present, and efforts to reduce blood pressure and
heart rate to reduce shear stress will decrease the likelihood of propagation
of the dissection. Upon diagnosis, systolic blood pressure should be reduced
to less than 120 mm Hg within 20 minutes. The drugs of choice are beta-
blockers, such as labetalol or esmolol, as well as sodium nitroprusside.

Acute coronary syndrome

Acute coronary syndrome includes unstable angina and acute myocardial
infarction. In these settings, an elevated adrenergic response is typical, lead-
ing to increased blood pressure and increased myocardial oxygen demand.
The drugs of choice in these situations are intravenous nitroglycerin, which
improves coronary perfusion, and beta-blockers.

Acute pulmonary edema

Treatment of acute heart failure with pulmonary edema requires drugs
that decrease preload and left ventricular volume. Sodium nitroprusside
and fenoldopam are good choices, along with a loop diuretic.

Renal emergencies
Measurement of serum creatinine and a urinalysis with examination of the
sediment is important for all patients with hypertensive emergency. A renal
emergency is present if new or acutely worsening renal dysfunction is pres-
ent or if the urine sediment contains red cell casts or dysmorphic red cells.
Fenoldopam is a strong choice of agent in this case due to its efficacy in
reducing blood pressure along with its action to increase renal blood flow
and urine output. Sodium nitroprusside and labetalol are also useful.
A temporary reduction in glomerular filtration rate may occur with acute re-
duction of severely elevated blood pressure, even in crises of nonrenal causes.
Short-term dialysis is sometimes necessary. Careful monitoring of renal func-
tion, electrolytes, and volume status is necessary throughout the clinical course.

Adrenergic crises
Examples of adrenergic crises include pheochromocytoma crisis, cocaine
or amphetamine intoxication, and clonidine withdrawal. Drugs to consider
 HYPERTENSIVE CRISES 485

in these cases include the pure alpha-blocker phentolamine (adding

a beta-blocker if needed), the combined alpha-/beta-blocker labetalol, or
clonidine in the case of clonidine withdrawal.

Pregnancy
Pregnancy-associated crises pose a challenge because many of the com-
monly used drugs for acute lowering of blood pressure are contraindicated
in pregnancy. The drugs of choice include hydralazine, methyldopa, and mag-
nesium sulfate. Beta-blockers or nifedipine are sometimes used in addition.

Follow-up
Studies suggest that patients treated for hypertensive crises often do not
get adequate discharge instructions. Karras and colleagues [9] found that
only 29% of such patients seen in four urban academic emergency depart-
ments received written instructions to follow up with a primary care
provider. For many such patients, the risk attributable to ongoing poor
control of blood pressure clearly outweighs the short-term risk of a transient
rise in blood pressure.

Prevention
Hypertensive crises are largely preventable. Inadequate management of
hypertension by the physician, poor adherence to therapy by the patient,
and insufficient access to care are important factors leading to crises.
Patients presenting with hypertensive crisis often have a history of poorly
controlled blood pressure. Failure to intensify the treatment regimen in
response to an elevated blood pressure in the office has been repeatedly
correlated with poor control. More aggressive and effective execution of
a treatment plan for hypertension is important in the effort to prevent crises.
Another common scenario preceding a crisis is a patient discontinuing
medications. Discontinuation of any antihypertensive medication can pre-
cipitate a crisis as the antihypertensive effect wears off. In addition, rebound
hypertension can follow abrupt discontinuation of high-dose beta-blockers
or clonidine.
Poor access to care may be considered a system-level factor that contrib-
utes to the occurrence of hypertensive crises. Often a timely office visit or
telephone call is all it takes to prevent a crisis.

Pitfalls in office management of very elevated blood pressure

A physician encountering a patient with very high blood pressure in the
office or emergency department should be wary of several common pitfalls
in assessment and treatment.
486 HEBERT & VIDT

The first pitfall is error in measurement of blood pressure. This can be

due to any of several deviations from recommended technique, such as
use of an ill-fitting cuff or omission of a brief rest period before measure-
ment. A thorough discourse on the topic is provided elsewhere [18]. Partic-
ular attention should be given to the white coat effect, in which the patient’s
blood pressure rises when in a medical setting, often due to anxiety about
the blood pressure reading itself or about the examination in general. The
physician then finds the blood pressure elevated and may assume it is nor-
mally this high, when the typical blood pressure is actually lower. This
can lead to treatment based on overestimates of blood pressure. Measure-
ment by a nonphysician provider or with an automated device with physi-
cian absent [19] can help avoid the confusion brought on by the readings
that are possibly misleading because of the white coat effect.
The next pitfall lies in treating the number. As discussed previously, the
symptoms, physical examination, and findings on initial testing (laboratory
tests, EKG, chest radiography) are more appropriate guides to decision-
making than the blood pressure itself. Keep in mind that the clinical status
of the patient rather than the level of blood pressure determines a hyperten-
sive urgency or emergency.
Another common mistake is to overestimate the benefit and underesti-
mate the risk of acute lowering of blood pressure. Blood pressure should
be acutely lowered if there is reason to believe there will be a benefit,
such as in the case of an acute aortic dissection. Where the benefit is less
clear, the physician should proceed with the approach of ‘‘first, do no
harm.’’
Finally, after the urgency of the acutely elevated blood pressure passes,
the physician should not underestimate the risk of chronic elevation of
blood pressure. Consider the faulty logic of the following scenario: A patient
presents to the office with a blood pressure of 190/112 mm Hg, without
symptoms. The patient is medicated in the office to achieve a blood pressure
of 170/100 mm Hg 3 hours later, and is discharged to home. The patient is
then re-evaluated for this chronic condition 2 months later, at which time
the blood pressure is still poorly controlled. In the majority of cases of
patients with very elevated blood pressure, the patient has chronic hyperten-
sion, and the physician and patient should proceed accordingly to achieve
good ongoing blood pressure control.

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