Hypertensive Emergencies

in the Emergency
Department
Omoyemi Adebayo, MD*, Robert L. Rogers, MD

KEYWORDS
 Hypertension  Hypertensive emergency  Hypertensive crisis

KEY POINTS
 Hypertensive emergency cannot be diagnosed based only on the combination of severely
increased blood pressure with symptoms such as headache, shortness of breath, and
blurred vision.
 Hypertensive urgency is defined as severe hypertension in a patient with comorbidities
that place the patient at higher risk of end-organ dysfunction. Hypertensive emergency
is defined as objective findings of end-organ damage.
 Asymptomatic and otherwise healthy patients with severe essential hypertension should
be referred to a primary care doctor within a week for nonurgent blood pressure control;
treatment of this group with aggressive intravenous medications can precipitate hypoten-
sion and subsequent end-organ damage.
 Select a therapeutic agent that has rapid and reliable pharmacodynamics that can be
turned on and off easily.
 The goal in treating most hypertensive emergencies is to reduce the blood pressure 25%
within the first 24 hours after diagnosis. An exception is in patients with aortic dissection,
which calls for much more rapid blood pressure reduction.

INTRODUCTION

In 2014, the American Heart Association (AHA) estimated that 77.9 million Americans
older than 20 years of age have hypertension (HTN).1 That is approximately 1 in every 3
adults, which is a staggering figure compared with other common diseases such as
diabetes and hyperlipidemia. In 2009, the AHA reported that almost a third of the pop-
ulation with HTN was unaware of their underlying diagnosis2; this percentage has
decreased to 19% according to recent figures from the National Health and Nutrition

Disclosures: The authors have no relevant financial relationships to disclose.

Department of Emergency Medicine, University of Maryland School of Medicine, 110 South
Paca Street, 6th Floor, Suite 200, Baltimore, MD 21201, USA
* Corresponding author.
E-mail address: yadebayo@umem.org

Emerg Med Clin N Am - (2015) --

http://dx.doi.org/10.1016/j.emc.2015.04.005 emed.theclinics.com
0733-8627/15/$ see front matter 2015 Elsevier Inc. All rights reserved.
2 Adebayo & Rogers

Examination Survey.1 Nearly 70% of all patients with a first-time myocardial infarction,
stroke, or congestive heart failure have poorly controlled blood pressure.1 However,
the 2014 Joint National Committee (JNC) guidelines for blood pressure management
recommend a less aggressive treatment approach for older hypertensive patients than
that proposed in the JNC 7 guidelines,3 which could increase the number of patients
found to be in a hypertensive crisis in the emergency department (ED).4
HTN is associated with significant short-term and long-term morbidity and mortality.
The effects of HTN often build to hypertensive crises that can affect numerous organ
systems either individually or simultaneously. The JNC 7 recommendations laid the
groundwork for the identification and treatment of hypertensive crisis, but they did
not clearly distinguish hypertensive urgency from hypertensive emergency. This
distinction is important because their treatment approaches for blood pressure control
are different. Despite the lack of large randomized controlled trials designed to estab-
lish evidence-based guidelines for the management of hypertensive emergencies,
general consensus exists regarding the need for a timely response to prevent adverse
outcomes.
This article discusses essential concepts in the evaluation and treatment of hyper-
tensive emergencies that are encountered commonly in the ED. These emergencies
include encephalopathy, pulmonary edema, myocardial ischemia, aortic dissection,
nephropathy, and eclampsia (Box 1).

DEFINITION

Hypertension is defined as a systolic blood pressure greater than 140 mm Hg or a dia-

stolic pressure greater than 90 mm Hg.4 Hypertensive crises are separated into 2
broad categories of urgency and emergency. They are both defined by a systolic
blood pressure greater than 180 mm Hg and a diastolic pressure greater than
120 mm Hg but are differentiated by the absence or presence, respectively, of end-
organ damage.4 End-organ damage is typically manifested by dysfunction in the
cerebrovascular, cardiovascular, pulmonary, or renovascular systems. Organ
dysfunction is the sole element that dictates the rapidity and modality of treatment
required in a hypertensive crisis.
Hypertensive urgency is characterized by an acute increase of blood pressure that
is not associated with end-organ damage. Recognition of hypertensive urgency can
generate anxiety in emergency physicians (EPs), leading to the decision to administer
intravenous (IV) medications. This therapeutic approach could inadvertently cause hy-
potension and organ hypoperfusion. In its definition of hypertensive urgency, the JNC
includes symptoms such as headache, shortness of breath, and epistaxis. Many EPs
are opposed to the term hypertensive urgency, citing its lack of meaningful definition.
They prefer to refer to this entity as severe HTN.
Patients with hypertensive urgency are typically either noncompliant with pre-
scribed medications or have been lost to follow-up and therefore lack proper titration
of their medication dosages. Optimal treatment in this population is close outpatient
follow-up with a gradual move toward oral antihypertensive medications.5 No vali-
dated studies have shown that acutely reducing blood pressure in ED patients who
present with severe HTN has any benefits in short-term risk reduction. In its 2013 clin-
ical policy, the American College of Emergency Physicians discouraged initiation of
blood pressure medication in the ED for asymptomatic patients with HTN.6
In contrast, hypertensive emergencies are associated with significant short-term
and long-term morbidity and mortality: 5-year mortality approaches 100%.7 Hyperten-
sive emergencies represent up to one-fourth of all ED visits.4 The JNC recommends
 Hypertensive Emergencies in the ED 3

Box 1
Causes of hypertensive crises

Essential hypertension
Endocrine
Pheochromocytoma
Cushing syndrome
Renin-secreting tumor
Primary hyperaldosteronism
Renovascular disease
Renal artery stenosis
Polyarteritis nodosa
Takayasu arteritis
Drugs
Cocaine
Phencyclidine
Sympathomimetics
Antihypertensive medication withdrawal
Amphetamines
Lead intoxication
Tyramine reaction with use of monoamine oxidase inhibitors
Serotonin syndrome from selective serotonin reuptake inhibitor use
Central nervous system
Cerebral edema
Cerebral hemorrhage
Brain tumor
Spinal cord injury
Coarctation of the aorta
Pain
Burns

the following therapeutic approach after a hypertensive emergency has been diag-
nosed: (1) mean arterial pressure reduction by w25% in the first 1 hour of treatment,
and (2) avoidance of precipitously reducing blood pressure (except in patients with
aortic dissection) to preclude organ hypoperfusion.4

EVALUATION
History
Hypertensive emergencies can be identified based on the patients past and present
history, results of the physical examination, laboratory analysis, and imaging. Any pa-
tient who presents to the ED with severely increased blood pressure should have a
thorough evaluation. The EPs evaluation and treatment algorithms are different for
4 Adebayo & Rogers

an acutely increased blood pressure in a patient with no history of HTN compared with
another patient with known chronic HTN. For example, a previously normotensive
woman who comes to the ED after her twentieth week of gestation with a severely
increased blood pressure and headache raises concern for preeclampsia requiring
emergent management; however, if the same gravid woman presents to the ED
with chronic pregestational HTN and a headache, the level of concern and manage-
ment approach are different than for the patient described earlier.
The EP should obtain the patients current complete medication list: drug names,
doses, any recent changes in their administration, and sudden discontinuations
from previously taken prescriptions. Sympatholytic medications such as clonidine
are notorious for causing severe rebound HTN. Another pertinent piece of information
to obtain from the patient is the use of illicit substances. Cocaine and phencyclidine
are sympathomimetics that cause severe increases in blood pressure, as well as other
symptoms. A family history of sudden death, premature cardiac disease, or endocrine
disorders should prompt the EP to consider pheochromocytoma, multiple endocrine
neoplasm, and hyperthyroidism as possible causes of episodic blood pressure in-
crease and tachycardia in a young healthy patient. The most vital part of the history
is assessment of signs and symptoms associated with the patients chief complaint
(eg, chest pain, shortness of breath, urine output, weakness, or sensory loss) and tar-
geted evaluation of end organs. The presence of symptoms alone does not confirm a
hypertensive emergency, but it suggests that an organ might be affected, requiring
further assessment.

Physical Examination
If high blood pressure is detected during the triage process, the measurement must be
repeated in the examination room after the patient has rested for 5 minutes without
perturbation. The one-size-fits-all approach to blood pressure cuffs can produce
falsely high or low blood pressure readings; a cuff of appropriate size for each patient
is required for accurate measurements.8
When examining a patient with suspected hypertensive emergency, several crucial
parts of the examination indicate whether further testing is needed. Assessment of
mental status is one of the first steps in a thorough neurologic examination. Confusion,
delirium, or seizure without other cause or reason suggests hypertensive encephalop-
athy. Other telltale signs of neurologic impairment are motor or sensory deficits and
papilledema on funduscopic evaluation. A complete ocular examination is vital; if
not performed by the EP, ophthalmologic consultation is warranted to guard against
permanent vision damage. The pulmonary examination should focus on evidence of
rales, hypoxia, or tachypnea, which imply flash pulmonary edema. Murmurs heard
on cardiac examination (specifically, a diastolic decrescendo murmur of aortic regur-
gitation that was not previously known to exist in the patient) could signify a type A
aortic dissection. A careful vascular assessment of proximal and distal pulses and
blood pressures allows stratification of the likelihood of this rare, and potentially
deadly, diagnosis. Auscultation of an abdominal bruit should raise concern for renal
artery stenosis. An often-overlooked part of the examination of a hypertensive patient
is evaluation of volume status. An acute increase in blood pressure results in natri-
uresis, a physiologic response that decreases the blood volume in an effort to reduce
the blood pressure. This response becomes extremely important when IV medications
are administered to treat a hypertensive emergency; the combination of natriuresis
and the effects of a potent antihypertensive agent could induce a dangerously fast
reduction in blood pressure.
 Hypertensive Emergencies in the ED 5

Diagnostic Testing
Laboratory analysis should be based on which organ system the EP thinks could be
damaged. Any patient thought to have had a stroke, seizure, or any neurologic
derangement secondary to hypertensive emergency should undergo computed to-
mography of the head as a priority. Based on a small study, Roque and colleagues9
concluded that measurements of optic nerve sheath diameter by bedside ultrasonog-
raphy can accurately predict which patients have increased intracranial pressure.
Every patient presenting with chest pain should have an electrocardiogram (ECG) to
assess for signs of cardiac ischemia or infarct. If the patients history of present illness
suggests acute coronary syndrome (ACS) (exertional chest pain, dyspnea, diapho-
resis, fatigue, jaw/arm pain, and nausea with epigastric pain), cardiac biomarker mea-
surements should also be obtained. Dyspnea has a myriad of causes (eg, an anginal
equivalent, pulmonary edema, renal failure, and anemia), all of which could stem from
a hypertensive emergency. Obtaining both a screening ECG and chest radiograph
(CXR) in dyspneic patients is recommended. If renal dysfunction is suspected, urinal-
ysis and a basic metabolic panel should be requested. Abnormalities that suggest hy-
pertensive nephropathy include proteinuria, muddy casts, and an increased blood
urea nitrogen or creatinine level. A complete blood count with manual differentiation
showing schistocytes suggests microangiopathic hemolytic anemia, which is another
sign of end-organ damage. Diagnostic testing should be tailored to focus on patient
complaints and the end organ in question to both maximize ED efficiency and mini-
mize costly unnecessary work-ups.10

MANAGEMENT OF HYPERTENSIVE EMERGENCIES

Definitive treatment of any hypertensive emergency is the acute reduction of blood

pressure to prevent ongoing organ damage. The JNC 7 guidelines recommend that
this be done within the first hour.4 Therapy decisions should be considered carefully,
weighing risks and benefits and taking into account which end organ is compromised
as well as the patients comorbidities. A patient in a hypertensive emergency should
be admitted to an intensive or intermediate care unit for meticulous IV titration of anti-
hypertensive medications and close cardiopulmonary monitoring. With the number of
critically ill patients increasing and hospital overcrowding, EPs are likely to be respon-
sible for managing patients with hypertensive emergencies for longer periods of time,
including adjusting the therapeutic approach if the patients condition improves or de-
teriorates in the ED. For patients who improve, it is important for the EP to institute oral
antihypertensive agents for long-acting therapy before discontinuation of IV agents. If
the patient was already on an oral antihypertensive at home, restarting that medication
is appropriate, keeping in mind its side effect profile, onset of action, and half-life,
because iatrogenic hypotension is common in this population.

Hypertensive Encephalopathy
The brain, like other organs, possesses an autoregulatory system to maintain a certain
cerebral perfusion pressure. The autoregulatory system of a normotensive patient
maintains a steady state, adequate for perfusion, by maintaining a mean arterial pres-
sure (MAP) of 60 to 120 mm Hg. In normotensive patients who suddenly become hy-
pertensive, the regulator system quickly becomes overwhelmed and can no longer
maintain autoregulation through vasoconstriction and dilation. In contrast, in patients
with long-standing hypertension, the autoregulatory system gradually adapts to
severely increased blood pressures and accommodates a higher set-point and thus
decreases the likelihood of a hypertensive emergency at moderately increased
6 Adebayo & Rogers

pressures. When the cerebral regulatory system becomes overwhelmed, the patient is
at risk for cerebral edema. The subsequent syndrome is known as hypertensive en-
cephalopathy. It can manifest in many ways, including acute delirium, lethargy, confu-
sion, severe headache, or seizure. In addition, it is important to consider other equally
dangerous causes of altered mental status (eg, infection and cerebrovascular acci-
dents), because they have entirely different management strategies. In patients expe-
riencing ischemic stroke, the blood pressure should not be reduced by more than 10%
to 15% over the first 24 hours, because it is thought that HTN protects the ischemic
penumbra of the brain.1114
The treatment of hypertensive encephalopathy begins with symptom control. Expert
opinion suggests that medications such as benzodiazepines, fosphenytoin, phenytoin,
or barbiturates should be given for delirium and seizure control; they provide the added
benefit of further blood pressure reduction.15 For blood pressure management of
hypertensive encephalopathy not complicated by cerebral vascular accident, the
MAP should be reduced by about 20% to 25% in the first 1 hour of treatment. Tradi-
tionally used medications include IV nitroprusside, labetalol, nicardipine, and enalapril
(Table 1). Centrally acting medications such as clonidine should be avoided for the
acute management of hypertensive emergencies because their sedative side effects
can make it difficult to appreciate the resolution of encephalopathic symptoms.15

Pulmonary Edema
One of the most harrowing hypertensive emergencies is hypoxic respiratory failure
with acute flash pulmonary edema. Certain patient populations (ie, those with conges-
tive heart failure and end-stage renal disease) are unable to tolerate fluctuations in
their blood pressure easily, resulting in volume overload and pulmonary edema. In
recent years, attention has centered on the use of noninvasive ventilation therapy,
such as bilevel positive airway pressure ventilation, to circumvent the likelihood of
these patients progressing to intubation. Treatment of the underlying cause, along
with blood pressure reduction, is key to clinical improvement.
For patients with flash pulmonary edema, preload and afterload reduction remains
the goal of treatment. One or more medications that work either alone or in conjunction
with each other have been the traditional treatment. Nitrates such as nitroglycerin are
effective in reducing preload because of their venodilatory effects. Afterload reducers,
such as angiotensin-converting enzyme inhibitors, are also used as key treatment of
flash pulmonary edema. Loop diuretics such as furosemide are often used to treat
symptomatic dyspnea secondary to pulmonary edema. In a recent randomized,
double-blind prospective study, Holzer-Richling and colleagues16 found that adminis-
tration of furosemide versus placebo to a cohort of patients did not improve outcomes.
Study participants who received furosemide required lower doses of antihypertensive
agents, suggesting a role for loop diuretics in reducing blood pressure.16 Caution is
needed when giving a diuretic during a hypertensive crisis, because more than half
of patients with pulmonary edema are euvolemic or hypovolemic, not overloaded in
terms of total body volume; in contrast, patients with renal or hepatic failure tend to
be overloaded, so diuretics have benefit in the acute phase to excrete the excess fluid
and off-load the lungs.
Nitroprusside, one of the fastest acting agents in the treatment armamentarium, is
considered ideal for patients with flash pulmonary edema.17 It has the profile benefit
of being rapid in onset as well as a venous and arterial dilator. Its use carries a small
risk of thiocyanate and cyanide toxicity, but that side effect is seen more commonly
with excessive dosing and refractory blood pressure response. Clevedipine, one of
the newest IV antihypertensive medications (approved by the US Food and Drug
 Hypertensive Emergencies in the ED 7

Administration in 2008) has shown great promise in clinical trials for treatment of se-
vere hypertension, particularly for pulmonary edema and postoperative hyperten-
sion.18 Clevedipine is a dihydropyridine calcium channel blocker that has the added
benefit of not being metabolized by the kidney or liver.1921

Myocardial Ischemia
Classically, ACS develops as the result of an acute coronary thrombus. Cardiac
ischemia can also be the result of other uncommon causes, such as hypertensive
emergency. Patients with cardiac ischemia typically present with chest pain, dyspnea,
diaphoresis, vomiting, and, especially in the elderly, generalized fatigue. Severe hyper-
tension is usually associated with increased myocardial work and oxygen demand.
Patients with previously diseased hearts are at increased risk of further myocardial
ischemia. Electrocardiographic abnormalities and increased cardiac biomarkers indi-
cate hypertension-induced cardiac ischemia or infarction. Treatment of ischemic
chest pain is 3-fold: (1) reduction in myocardial work, (2) reduction in myocardial ox-
ygen consumption, and (3) improvement in coronary artery perfusion.
The first intervention that should be performed in a patient with suspected ACS is
administration of aspirin.22 Severely hypertensive patients with suspected ACS should
be given an IV b-blocker (class IIa recommendation by the AHA).23 Other commonly
recommended agents are nitroglycerin and labetalol. Nitroglycerin is often titrated
to resolution of chest pain or hypotension, whichever occurs first. Nitroglycerin has
the added effect of coronary vasodilation, which improves cardiac tissue perfusion.
No specific recommendations exist on which b-blocker is preferred, but it is best to
use a medication with a quick pharmacokinetic profile so that it can be titrated easily.
Care should be used with medications such as hydralazine and nitroprusside. Hydral-
azine causes reflex tachycardia, which increases myocardial work and oxygen con-
sumption. It also has an extremely variable dose response curve from patient to
patient, which can cause a precarious situation for EPs when the blood pressure
decreases precipitously. Nitroprusside has the potential to cause coronary steal syn-
drome, which worsens ischemia and could increase risk of death if it is given after
acute myocardial infarction (AMI).24,25 Similarly, b-blockers should not be adminis-
tered after AMI because of the risk that they could worsen underlying congestive heart
failure and cause cardiogenic shock.

Aortic Dissection
When a patient describes the sudden-onset chest pain that radiates to the back, the
EP should put aortic dissection (AD) at the top of the differential diagnosis. However,
more subtle presentations should not be overlooked: chest pain accompanied by pain
in any extremity, neurologic symptoms, abdominal or back pain, or gastrointestinal
bleeding should raise concern for AD. The mortality for AD increases 1% to 2% every
hour during the first 24 hours after the onset of symptoms. The Stanford classification
distinguishes dissections as either type A or type B. Type A involves the aortic arch
only; type B involves the descending aorta. Most type B dissections and some type
A dissections can be managed with medical therapy but that determination should
be made by the vascular surgeon. All type A dissections should be referred to a
vascular surgeon for likely surgical repair.
Whenever AD is suspected, it is important to measure the blood pressure in both arms
and to assess the pulses in all 4 extremities. It is critical not to rely on classic findings:
w19% of patients with type A dissections and w9% of those with type B dissections
have no identifiable pulse deficits.26 More reliable is identification of a new diastolic
murmur suggestive of aortic regurgitation, which is seen in up to 44% of type A
 8
Adebayo & Rogers
Table 1
Pharmacologic agents for hypertensive emergencies

Drug Dose Onset of Action (min) Duration of Action Adverse Effects Indications
Vasodilators
Nitroglycerin 5100 mg/min as IV infusion 25 530 min Headache, vomiting, Cardiac ischemia; flash
methemoglobinemia; pulmonary edema; caution
caution in right ventricular with recent use of
infarct phosphodiesterase
inhibitors
Sodium 0.2510 mg/kg/min as IV Immediate 12 min Nausea, vomiting, muscle Most hypertensive
nitroprusside infusion twitching, sweats, emergencies; caution with
thiocyanate and cyanide high intracranial pressure
toxicity or azotemia
Nicardipine 515 mg/h IV 510 1530 min, may last Tachycardia, headache, Most hypertensive
hydrochloride several hours flushing, local phlebitis emergencies; caution of
coronary steal with cardiac
ischemia
Fenoldopam 0.10.3 mg/kg per min <5 30 min Tachycardia, headache, Best for hypertensive
mesylate IV fusion nausea, flushing nephropathy emergencies
Enalaprilat 1.255 mg every 6 h IV 1530 612 h Significant reductions in Acute left ventricular failure
blood pressure in high- and flash pulmonary
renin states edema; avoid in AMI
Hydralazine 1020 mg IV 1020 IV 14 h IV Tachycardia, flushing, Eclampsia; caution given
hydrochloride 1040 mg IM 2030 IM 46 h IM headache, vomiting, erratic response
worsening angina
 Clevidipine Initial infusion of
12 mg/h, titrate
every 510 min
Adrenergic Antagonists
Esmolol 250500 mg/kg/min IV bolus, 12
hydrochloride then 50100 mg/kg/min by
infusion; repeat bolus after
5 min if needed or increase
infusion to 300 mg/min
Labetalol 2080 mg IV bolus every
hydrochloride 10 min; alternatively, 0.5
2 mg/min IV infusion
Phentolamine 5-mg to 15-mg IV bolus
Abbreviations: AMI, acute myocardial infarction; IM, intramuscular.
Adapted from Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure. Hypertension 2003;42:120652.
24 515 min Headache, nausea, vomiting, Postoperative hypertension,
hypotension, rebound hypertensive emergency in
hypertension, reflex renal dysfunction or acute
tachycardia heart failure
1030 min Hypotension, nausea, asthma Aortic dissection,
exacerbation, first-degree perioperative
heart block, heart failure
510 36 h Vomiting, scalp tingling, Most hypertensive
bronchoconstriction, emergencies except acute
dizziness, nausea, heart heart failure; ideal for
block, orthostatic preeclampsia
hypotension
12 1030 min Tachycardia, flushing, Pheochromocytoma and
headache other catecholamine excess
states
Hypertensive Emergencies in the ED
9
10 Adebayo & Rogers

dissections.26 A CXR obtained as part of the work-up might show a widened medias-
tinum, but as many as 15% of patients with AD have normal chest radiographs.27
The goal of medical therapy for AD is rapid and large reduction of vascular sheer
stress and blood pressure. The initial medication should be able to reduce the sheer-
ing force; a b-blocker is typically used for this purpose, because this drug group both
decreases the heart rate (HR) and prevents reflex tachycardia when arteriodilators are
introduced. Esmolol is an ideal agent for this purpose because of its rapid on/off qual-
ities and its ability to reduce the HR to less than 60 beats per minute. A medication is
also needed to reduce the systolic blood pressure to less than 120 mm Hg. Nitroprus-
side has long been used for this purpose and is a reasonable option for fast and reli-
able blood pressure control.27

Acute Renal Failure

Acute renal failure (ARF) can be either the direct cause or an observed effect of a hy-
pertensive emergency. A patients history, specifically renal transplant and renal func-
tion, can help differentiate cause from effect. Assessment of the patients volume
status is also important to determine the need for adjunctive therapies, such as
positive-pressure ventilation or diuretics for patients who present with dyspnea from
fluid overload. Calcium channel blockers (eg, nicardipine) are typically preferred in
ARF because they do not affect renal perfusion or clearance. Nitroprusside and fenol-
dopam are also commonly used. Nitroprusside is effective in reducing blood pressure,
but it places the patient at risk of cyanide toxicity because it decreases renal clearance
and thus causes a buildup of metabolites. Fenoldopam is a more desirable second-
line medication. An arterial vasodilator, it not only decreases blood pressure but
also promotes renal excretion via its specific effects on the dopamine receptors in
the nephron. It produces no toxic metabolites and has been shown to be as effective
in blood pressure reduction as nitroprusside.28,29 In the special case of scleroderma
renal crisis, angiotensin-converting enzyme inhibitors (eg, captopril and enalapril)
are first-line agents for effect management.30

Sympathomimetic Crisis
This category encompasses severe increases in blood pressure secondary to many
causes: cocaine, phencyclidine, or amphetamine abuse; pheochromocytoma; interac-
tion of monoamine oxidase inhibitor drugs with selective serotonin reuptake inhibitors
or with wine and cheese (tyramine reaction); abrupt cessation of sympatholytic medi-
cations such as clonidine; and alcohol withdrawal. The treatment of all these crises is
similar. The sole use of b-blockers is not recommended because of the reflex tachy-
cardia that it induces, which could precipitate a rapid increase in blood pressure and
cardiovascular collapse.31,32 Phenoxybenzamine, phentolamine, nitroprusside, and
labetalol are good first-line medications.33,34 In cocaine-induced crisis, benzodiaze-
pines should be used in conjunction with antihypertensive drugs. In a study involving
378 patients with cocaine-induced chest pain, Ibrahim and colleagues35 found no dif-
ference in the troponin levels of patients who received b-blockers and those who did
not. This observation challenges convention, which has created a culture of fear around
using such drugs in these patients. More studies are needed to validate or challenge
these controversial findings. In the treatment of a hypertensive emergency in patients
with clonidine withdrawal, the first step is to administer clonidine.

Hypertensive Emergency in Pregnancy

Pregnancy causes many deviations from womens pregravid physiology. Blood pres-
sure decreases in the second trimester of pregnancy before increasing back to
 Hypertensive Emergencies in the ED 11

baseline values in the third trimester. Preeclampsia is a poorly understood disorder of

hypertension that occurs for unknown reasons in 2% to 6% of pregnancies after the
20th week of gestation. It can be a serious disorder, with consequences for both
mother and fetus. The dramatic increase in maternal blood pressure affects the
placenta, which is the end organ that is vital to fetal development. Preeclampsia
has mild and severe forms. Mild preeclampsia and severe preeclampsia are essen-
tially distinguished by the degree of hypertension that persists and not the degree
of proteinuria because both forms can exist without proteinuria. The treatment of se-
vere preeclampsia is 2-fold: (1) delivering the fetus as soon as possible (ideally after
the administration of steroids for fetal lung maturity in viable fetuses), and (2) reducing
the blood pressure and reversing end-organ damage. Preeclampsia can also lead to
other end-organ dysfunction such as the HELLP (hemolysis, elevated liver enzymes,
and low platelet count) syndrome. Failure to achieve rapid control of the blood
pressure can lead to the potentially fatal progression to eclampsia, characterized by
seizures, strokes, and death.
The approach to blood pressure management in a preeclamptic patient is a
balancing act. When the fetus is viable and delivery is not imminent, antihypertensive
therapy must be chosen so that precipitous decreases in blood pressure do not cause
placental hypoperfusion and compromise fetal blood flow. Labetalol, nifedipine, nicar-
dipine, and hydralazine have been common choices for this condition for years. How-
ever, the safety of hydralazine and nifedipine in gravid patients has been questioned.
Those medications, particularly hydralazine, should be considered second-line or
third-line choices because of their unpredictability in duration of action and degree
of hypotension. Labetalol and nicardipine are more predictable.36 Another hallmark
in the treatment of severe preeclampsia and eclampsia is the use of magnesium sul-
fate, which is given as a bolus followed by an infusion. Patients should be monitored
closely for the development of magnesium toxicity. Magnesium is thought to be neuro-
protective to the mother, preventing the onset of eclampsia (or terminating seizures
once eclampsia has set in), and possibly to the fetus.37

SUMMARY

Hypertension is a multifaceted disease process that affects the US and global popu-
lations in massive proportions. The most accurate indicator of hypertensive emer-
gency is the presence of end-organ damage. The EPs role is pivotal in rapidly
identifying and differentiating hypertensive emergency from hypertensive urgency
and providing the appropriate intervention. Actions that are fundamental to identifying
individuals at risk include obtaining a targeted history, performing a careful physical
examination, and requesting the appropriate laboratory and diagnostic screening.
Many medications are available to treat hypertensive emergencies but none is univer-
sally recognized as being superior to the others. Important considerations in drug se-
lection include an understanding of the underlying physiology of the crisis, the
patients comorbid conditions, and associated risk factors. Once a drug is chosen,
it should be given quickly because time is tissue in hypertensive emergency. Pa-
tients should be managed in an intensive care unit because critical care monitoring
is required. With appropriate identification and management, hypertensive crises
can be halted and reversed.

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