Hypertension Crisis in the

Emergency Department
Wallace Johnson, MDa,*, My-Le Nguyen, MDb,
Ronak Patel, MDb

KEYWORDS
 Hypertension crisis  Hypertensive urgency  Hypertensive emergency  Malignant hypertension
 Guidelines  Management  Treatment

KEY POINTS
 An elevated blood pressure (BP) reading in the emergency department should be confirmed in more
than one anatomic location based on JNC 7 guidelines and reassessed multiple times before and
during therapy.
 Patients with severely (>180/120 mm Hg) or moderately (140–179/90–119 mm Hg) elevated BP sus-
pected of having end-organ damage should undergo appropriate testing to determine if they have
hypertensive urgency versus emergency. Absolute BP cutoffs are not as important as the presence
or absence of target end-organ damage.
 In general, patients with hypertensive emergency should have their mean arterial pressure (MAP)
reduced by 20% to 25% in the first hour of this diagnosis. Exceptions are patients with ischemic
stroke, in whom MAP should be reduced by 15% to 20%, and patients with aortic dissection that
requires more aggressive BP reduction.
 Hypertensive patients with nausea/vomiting, headache, visual complaints, confusion, stupor, pap-
illedema, or seizures may have hypertensive encephalopathy from cerebral edema. BP reduction
should be gradual, and cerebral perfusion pressure should not be decreased too rapidly.
 Patients with evidence of myocardial ischemia attributable to hypertensive emergency should
receive nitrates to reduce preload and improve coronary perfusion as well as b-blockers, which
can reduce cardiac oxygen demand by lowering heart rate and afterload. b-Blockers should not
be given if there is evidence of acute heart failure or an unstable bradyarrhythmia.
 In pregnant patients with hypertensive emergencies, consider the effects of antihypertensive medi-
cations on the fetus.

INTRODUCTION BP of 120 to 139 mm Hg and/or a diastolic BP of

80 to 89 mm Hg. This definition reflects the fact
Hypertension is a chronic, modifiable risk factor for that patients with prehypertension have a tendency
cardiovascular disease; however, approximately to develop full-blown hypertension over time. As
1% to 2% of patients with hypertension will BP increases there is a continuous, graded rela-
present with a hypertensive emergency at some tionship between BP and cardiovascular risk, but
time in their lives.1 Hypertension is defined as as levels exceed 180/120 mm Hg, a hypertensive
a systolic blood pressure (BP) of 140 mm Hg or crisis may emerge.
higher and/or a diastolic BP of 90 mm Hg or higher The terms malignant hypertension and acceler-
(Box 1).2 Prehypertension is defined as a systolic
cardiology.theclinics.com

ated hypertension were used in the past, but

a
Division of Cardiology, Hypertension Section, University of Maryland School of Medicine, 419 W. Redwood
St, Suite 620, Baltimore, MD 21201, USA; b Division of Cardiology, University of Maryland School of Medicine,
419 W. Redwood St, Suite 620, Baltimore, MD 21201, USA
* Corresponding author.
E-mail address: WJohnson@medicine.umaryland.edu

Cardiol Clin 30 (2012) 533–543

http://dx.doi.org/10.1016/j.ccl.2012.07.011
0733-8651/12/$ – see front matter Ó 2012 Elsevier Inc. All rights reserved.
534 Johnson et al

Box 1 The management of hypertensive emergencies in

Hypertension definitions the ED is challenging because of the lack of
evidence-based guidelines from large clinical trials.
Term Definition Hypertensive urgencies, in contrast to emergen-
Hypertensive crisis cies, can be treated with an oral regimen in an
A. Hypertensive Abrupt rise in BP with outpatient setting. Initiating treatment for hyperten-
urgency no signs of end-organ sive urgencies in the ED remains controversial
damage; diastolic BP because there is no consensus on whether it is
usually >120 mm Hg cost-effective and improves long-term patient care.
B. Hypertensive Abrupt rise in BP with Causes of hypertensive emergency and urgency
emergency acute end-organ
are shown in Box 2.
damage; diastolic BP
usually >120 mm Hg
Prehypertension Systolic BP 120–139 mm NORMAL BLOOD PRESSURE REGULATION
Hg and/or diastolic BP
80–89 mm Hg In persons with normal BP regulation there is an
Hypertension Systolic BP >140 mm Hg appropriate balance between normal vital organ
and/or diastolic perfusion, hypoperfusion, and hyperperfusion. BP
BP >90 mm Hg is dependent on cardiac output and peripheral
vascular resistance. The balance between cardiac
now the term hypertensive crisis can refer to ei- output and peripheral vascular resistance depends
ther a hypertensive emergency or hypertensive on a complex set of integrated actions between the
urgency. In the years since the term malignant cardiovascular, neural, renal, and endocrine
hypertension was initially coined in 1914, a large systems, which is not totally understood. A multi-
number of both oral and intravenous medications system approach to BP regulation allows the
have been developed for the treatment of hyper- body to respond to internal and external demands
tensive emergencies as well as chronic essential such as dehydration, thirst, infection, trauma, and
hypertension.3–5 Malignant hypertension was ini- rapid changes in position or volume. The renin-
tially named as such because the 1-year mortality angiotensin-aldosterone system is one of the key
rate after a hypertensive emergency in 1928 was systems involved in the regulation of BP.3,4
80% (similar to a malignant cancer prognosis); The sympathetic nervous system also plays
later, advances in medical therapy reduced the a major role, particularly during times of physical
1-year mortality to 10% by 1998.6 stress, psychological stress, and heavy exertion.
The significant reduction in the mortality related The sympathetic nervous system can increase
to hypertensive emergencies is undeniably associ- cardiac output and arterial vasoconstriction. Lastly,
ated with the development of both parental and endothelial function is also involved in BP regula-
oral antihypertensive agents, but increased aware- tion. The endothelium found on the vascular wall
ness and published clinical guidelines have also acts a regulator of BP by secreting vasodilators
contributed to better management of hypertensive and/or vasoconstrictors in response to various
emergencies. A recent publication found that stimuli.3
although hospitalizations for hypertensive emer-
gencies increased in 2007 when compared with ALTERED BLOOD PRESSURE REGULATION
the year 2000, the all-cause in-hospital mortality IN HYPERTENSIVE CRISES
rate decreased.1 Deshmukh and colleagues1
believe the reduction in mortality is at least partly The mechanisms underlying both primary (essen-
due to the release of the Seventh Joint National tial) hypertension and hypertensive crises are not
Committee2 report on the prevention, detection, totally understood. There seem to be several
evaluation, and treatment of hypertension in 2003. mechanisms that are found in both chronic
One of the first tasks in the emergency depart- primary hypertension and hypertensive crises.
ment (ED) evaluation is to determine whether The initial event appears to be an abrupt rise in
the patient’s condition represents a hypertensive BP from a known or unknown stimulus followed
emergency or urgency. A hypertensive emergency by compensatory mechanisms arising from the
is defined as acute target end-organ damage vascular endothelium. Initially the endothelium
typically associated with a severely elevated releases the vasodilator nitric oxide in an attempt
BP (systolic BP >180 mm Hg and/or diastolic to compensate for the change in vasoreactivity.
BP >120 mm Hg) versus a hypertensive urgency, The arterioles sense a rise in BP and, in turn, arte-
which is characterized by a similarly elevated BP rial smooth muscle contracts in an effort to reduce
and no target end-organ damage (see Box 1).7 the rise in BP and to limit the effect of the BP at the
 Hypertension Crisis in the ED 535

Box 2
Causes of hypertensive emergency and urgency

Essential hypertension
Renovascular disease
Renal artery stenosis: atheroma or fibromuscular dysplasia
Polyarteritis nodosa
Takayasu arteritis
Renal parenchymal disease
Glomerulonephritis
Tubulointerstitial nephritis
Systemic sclerosis
Hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
Diabetes mellitus
Systemic lupus erythematosus
Renal aplasia
Renal cell carcinoma
Endocrine
Pheochromocytoma
Cushing syndrome
Primary hyperaldosteronism
Renin-secreting tumor
Drugs
Cocaine, phencyclidine, sympathomimetics, erythropoietin, cyclosporine
Antihypertensive medication withdrawal
Amphetamines
Lead intoxication
Interactions with monoamine oxidase inhibitors
Autonomic hyperreactivity
Guillain-Barré syndrome
Acute intermittent porphyria
Pregnancy related
Preeclampsia
Eclampsia
Central nervous system disorders
Head injury
Cerebral infarction
Cerebral hemorrhage
Brain tumor
Spinal cord injury
Coarctation of the aorta
Burns
Postoperative pain and/or anesthesia complications
536 Johnson et al

cellular level. A vicious cycle occurs, with pro- but the difference seems to be that the abrupt
longed arterial smooth muscle contraction leading rise in BP promotes acute target end-organ
to more endothelial dysfunction and an inability to damage. The target end-organ damage may actu-
release more nitric oxide, only resulting in a further ally accelerate the rise in the BP, leading to organ
increase in BP. tissue hyperperfusion and endothelial damage
Inflammation is also a part of the pathophysi- owing to blunted or inadequate compensatory
ology of endothelial dysfunction. The mechanical mechanisms. This hypertensive emergency BP
shear forces on the vascular wall result in endothe- threshold can occur at markedly different levels
lial damage and dysfunction. Endothelial dysfunc- in individual patients. Patients with chronic hyper-
tion results in the expression of inflammatory tension have more smooth muscle hypertrophy
markers such as endothelin-1, endothelial adhe- because of a sustained elevation in BP, allowing
sion molecules, and cytokines.3,8,9 The inflamma- temporary and incomplete end-organ protection
tory component of hypertension is believed to at the capillary level. By contrast, normotensive
promote coagulation, platelet aggregation, endo- patients who undergo an abrupt increase in BP
thelial layer permeability, and vasoconstriction. do not have the same degree of smooth muscle
Thus, “hypertension begets hypertension,” and hypertrophy. Thus, even small abrupt rises in BP
there appears to be a complex interaction of the can induce a hypertensive crisis in normotensives,
renin-angiotensin-aldosterone system, sympa- partly due to the capillary damage that occurs.3 At
thetic nervous system, and endothelial dysfunction present, there is not enough evidence to support
regardless of the initial stimulus. There is also a treatment approach based on the potential
evidence that angiotensin II activates the expres- underlying pathophysiology of hypertensive crisis,
sion of genes for proinflammatory cytokines and so clinicians should achieve disease-specific BP
activation of transcription factor NF-kB, causing targets in these patients using whatever agents
a direct toxic effect to the vessel wall.10 An necessary, as long as there are no contraindica-
increased level of von Willebrand factor, von tions (Tables 1 and 2).
Willebrand factor prepeptide, plasmin-antiplasmin
complexes, and reduced levels of ADAMTS13 are CLINICAL MANIFESTATIONS OF
seen in patients with hypertensive crisis, suggest- HYPERTENSIVE CRISIS
ing that thrombotic microangiopathy may play
a role.11 The central nervous system is particularly sus-
Hypertensive crisis appears to have a similar ceptible to high BP and its associated hyperperfu-
pathophysiology to primary chronic hypertension, sion and shear mechanical forces. In one

Table 1
Parenteral medications used for treatment of hypertensive crisis

Cardiac
Dosing Onset of Action Preload Afterload Output
Sodium 0.25–10 mg/kg/min IV infusion Within seconds to Y YY No effect
nitroprusside minutes
Nitroglycerin 5–100 mg/min IV infusion 1–5 min YY Y No effect
Labetalol 20–80 mg bolus every 10 min, 5–10 min No effect Y Y
or 0.5–2 mg/min IV infusion
Esmolol 80 mg bolus over 30 secs then 1–2 min No effect No effect Y
150 mg/kg/min IV infusion
Hydralazine 10–20 mg IV bolus 10–20 min No effect Y [
Phentolamine 5–15 mg IV bolus 1–2 min No effect Y [
Nicardipine 2–15 mg/h IV infusion 5–10 min No effect Y [
Clevidipine 1–2 mg/h then titrate to 1–4 min No effect Y [
maximum 16 mg/h IV
infusion
Fenoldopam 0.1–0.6 mg/kg/min IV infusion 5–10 min No effect Y [
Enalaprilat 1.25–5 mg every 6 h IV bolus 15–30 min No effect Y [

Abbreviation: IV, intravenous.

Data from Refs.2–4
 Hypertension Crisis in the ED 537

Table 2
Special indications and warnings for parenteral medications

Special Indications Warnings

Sodium Most hypertensive Caution with renal insufficiency; can develop cyanide toxicity,
nitroprusside emergencies acidosis, methemoglobinemia, increased intracranial
pressure, nausea, vomiting, muscle twitching, theoretical
“coronary steal” (shunting of blood from diseased vessels
to well-perfused vessels may produce coronary ischemia)
Nitroglycerin Most hypertensive Headache; can develop tolerance, tachycardia, vomiting,
emergencies, methemoglobinemia, flushing
coronary ischemia
Labetalol Most hypertensive Avoid in acute heart failure, bradycardia, and
emergencies, bronchoconstrictive disease
aortic dissection
Esmolol Aortic dissection Avoid in acute heart failure, bronchoconstrictive disease, and
heart block
Hydralazine Eclampsiaa Can cause reflex tachycardia, headache
Phentolamine Catecholamine excess Flushing, headache, tachycardia
Nicardipine Most hypertensive Avoid in acute heart failure and coronary ischemia; causes
emergencies reflex tachycardia, nausea, vomiting, headache, increased
intracranial pressure
Clevidipine Most hypertensive Atrial fibrillation; avoid in soy allergy
emergencies
Fenoldopam Most hypertensive Caution with glaucoma; can cause headache, flushing,
emergencies, acute tachycardia, local phlebitis
renal impairment,
and/or hematuria
Enalaprilat Acute left ventricular Avoid in acute myocardial ischemia
failure

a
Labetalol is safer during pregnancy.
Data from Aggarwal M, Khan I. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiol Clin 2006;24:135–46;
and Acelajado MC, Calhoun DA. Resistant hypertension, secondary hypertension, and hypertensive crises: diagnostic evalu-
ation and treatment. Cardiol Clin 2010;28:639–54.

representative study of the prevalence of end- the authors believe that patients presenting to
organ complications, cerebral infarctions were the ED with hypertensive crisis should undergo
noted in 24%, intracerebral or subarachnoid electrocardiography (ECG), chest radiography,
hemorrhage in 4%, and hypertensive encephalop- computed tomography (CT) of the brain if neu-
athy in 16% of patients. Cardiovascular complica- rologic symptoms are present, urinalysis, elec-
tions in the same study included acute heart failure trolytes/creatinine, complete blood count, and
in 36% of patients and acute myocardial infarction cardiac enzymes if acute coronary syndrome is
and/or unstable angina in 12%. Aortic dissection suspected. This guideline is based on expert
was noted in 2% of patients and eclampsia of opinion and not on data from large randomized
pregnancy in 4.5%.12 In the ED, clinicians need clinical trials. As always, sound clinical judgment
to be aware that substance abuse, medical non- should be used in the ED setting for each individual
compliance, and secondary hypertension are patient.
major causes of hypertensive crisis. Initial evalua-
tion of hypertensive crisis should be focused on Neurologic Syndromes
assessment of potential cardiovascular, cerebro-
vascular, and renal damage. The brain relies on a fairly constant cerebral BP to
function properly. The cerebral vasculature must
CLINICAL EVALUATION OF HYPERTENSIVE help maintain this steady perfusion pressure
CRISIS IN THE ED despite changes in mean arterial pressure (MAP)
through autoregulation. When this autoregulation
The usefulness of routine testing for patients with fails in the setting of sudden and severely elevated
severely elevated BP is controversial. However, MAP, cerebral edema and microhemorrhages can
538 Johnson et al

occur. Edema occurs when the vascular endothe- ventricular ejection fraction was unchanged during
lium is disrupted owing to elevated pressure the episodes as well as after treatment. However,
causing leakage of plasma elements.13 Symptoms they did observe segmental wall motion abnormal-
can include headache, stupor, seizures, delirium, ities after treatment. The investigators concluded
agitation, nausea/vomiting, and visual distur- that the cause of acute heart failure in patients
bances. Focal neurologic findings can occur, but with hypertensive crisis may be due to diastolic
are rare, and should raise the suspicion for dysfunction secondary to ischemia.
ischemic stroke or cerebral hemorrhage.14 Patients Sodium nitroprusside is thought to be the best
with long-standing hypertension have a better agent for acute pulmonary edema precipitated by
ability to tolerate increases in MAP without a hypertensive crisis.3 Sodium nitroprusside
increasing cerebral perfusion. This ability is thought decreases both preload and afterload. It has a rapid
to be due to cerebral arteriolar hypertrophy, which onset of action and a short half-life. Cyanide toxicity
reduces the transmission of the elevated pressure is extremely rare. Thiocyanate toxicity is also
to the capillary bed. It is essential not to lower uncommon and occurs only with high doses of ni-
systemic BP too rapidly, as this can lead to a drop troprusside in patients with renal insufficiency.19
in cerebral perfusion pressure and cause ischemia. Angiotensin-converting enzyme (ACE) inhibitors
BP should be lowered within 2 to 6 hours of presen- such as enalapril can be used to reduce afterload
tation to no more than 25% of the initial value.15 and hence improve cardiac output.20 A new
third-generation dihydropyridine calcium-channel
Myocardial Ischemia blocker, clevidipine, was shown in a small study
to be effective in reducing BP without adverse
Elevated systemic vascular resistance increases
events.7 In this study, 89% of patients achieved
left ventricular (LV) myocardial wall tension and
target BP within 30 minutes of starting clevidipine.
oxygen demand. In markedly elevated BP such
Clevidipine selectively inhibits extracellular calcium
as in hypertensive emergencies, myocardial perfu-
influx through L-type channels resulting in smooth
sion may not be able to adequately maintain the
muscle relaxation; thus it decreases peripheral
increased myocardial oxygen demand, which
vascular resistance. An advantage of clevidipine
can lead to myocardial ischemia and even infarc-
is that it undergoes metabolism by plasma ester-
tion. Patients with long-standing hypertension
ases, thus it is independent of renal or hepatic func-
may also have LV hypertrophy, which in itself
tion.11 Loop diuretics such as furosemide are often
increases myocardial oxygen demand. This
used in combination with antihypertensive therapy
increased LV mass can also cause some degree
to induce diuresis in hypertensive pulmonary
of coronary artery compression, leading to de-
edema. This common practice was recently chal-
creased luminal blood flow.3 Preferred agents in
lenged by a prospective, randomized, double-
treating patients with hypertensive emergencies
blinded placebo-controlled study in which the
with evidence of ischemia include nitrates that
effectiveness of furosemide in lowering subjective
can lower LV preload and improve coronary blood
perception of dyspnea was compared with
flow as well as b-blockers that can reduce heart
placebo. The results showed no difference in the
rate, decrease afterload, and improve diastolic
subjective perception of dyspnea between the 2
coronary perfusion.16 Hydralazine should be
groups. Patients in the furosemide group required
avoided, as it can induce a reflex tachycardia
fewer antihypertensive medications, which led to
and increase cardiac work.
a conclusion that furosemide may have some anti-
hypertensive effect via direct venodilation. The
Acute Heart Failure
results of the study challenge the practice of using
Acute heart failure presenting as acute pulmonary loop diuretics to reduce the perception of
edema in a hypertensive crisis occurs with an inci- dyspnea.21
dence of 36%, making it the second most common
sign of end-organ damage.3 Heart failure can occur
Aortic Dissection
in a hypertensive crisis but it can also be a risk
factor for the development of hypertensive crisis.17 Aortic dissection is a rare but potentially deadly
It was initially thought that transient systolic complication of a hypertensive crisis. Aortic dissec-
dysfunction causes pulmonary edema in patients tion can be misdiagnosed as coronary ischemia,
with hypertensive crisis, but this theory has been pleurisy, heart failure, stroke, musculoskeletal
challenged. Gandhi and colleagues18 used pain, or an acute abdomen. One must maintain
transthoracic echocardiography to evaluate LV a high index of suspicion, and cardiologists must
ejection fraction during acute episodes of hyper- be particularly aware that an aortic dissection can
tensive pulmonary edema and found that the left extend into the coronary arteries and present with
 Hypertension Crisis in the ED 539

both a history and ECG findings identical to those of ophthalmoscopic examination. This variability
an acute myocardial infarction. As far as a patient’s decreases with grade III and IV retinopathy.27
initial presentation is concerned, one should Some studies have shown an association between
remember the 3 Rs, namely rapid onset, ripping, the degree of retinopathy and signs of end-organ
and radiating pain in the chest, back, or both. damage such as LV hypertrophy, microalbuminu-
Many diseases and conditions are associated ria, and coronary artery disease in women.28,29
with aortic dissection, but 75% of patients with Ophthalmoscopy can be useful in recognizing
acute aortic dissection have underlying hyperten- acute end-organ damage in the form of papillede-
sion22,23 In the ED the diagnosis of aortic dissection ma in hypertensive encephalopathy, but the lack
is made using contrast-enhanced CT, magnetic of arteriolar narrowing, retinal hemorrhages, exu-
resonance imaging, or transesophageal echocardi- dates, or papilledema cannot be used to exclude
ography (TEE), although in most settings CT is a diagnosis.
chosen because of the need for rapid diagnosis. A
disadvantage of TEE is that it may not give sufficient Acute Renal Insufficiency
visualization of the distal ascending aorta or the
Renal insufficiency can be the cause or result of
aortic arch.22
hypertensive crisis. There are changes in renal
Once the diagnosis of aortic dissection is made,
arteries in chronic hypertension, including endo-
prompt treatment is essential because the death
thelial dysfunction and impaired vasodilation.
rate in acute aortic dissection may be as high as
Thus renal autoregulation is altered, resulting in
1% per hour during the first 24 hours. A type-A
an increase of intraglomerular pressure with
dissection is a surgical emergency whereas
increasing systemic arterial pressure. This rise in
a type-B dissection can often be managed medi-
pressure can cause ischemic injury and fibrosis.3
cally. If the vascular surgery consultant determines
Hypertensive emergency can occur in acute
that emergency surgery is not needed, prompt BP
glomerulonephritis, hemolytic uremic syndrome,
reduction to a target systolic BP of less than 120
renal artery stenosis, patients on hemodialysis
mm Hg and reduction in heart rate to below 65
receiving erythropoietin with an accelerated rate
beats/min should be instituted. Intravenous b-
of increase in hematocrit,30 and in renal transplant
blockade with esmolol or labetalol is usually
patients, especially those on cyclosporin and
started to reduce shear stress on the aorta. Other
corticosteroids.10
agents such as sodium nitroprusside are often
Clinical presentations that suggest renal in-
added, and if the BP is refractory to multiple anti-
volvement include proteinuria, elevated serum
hypertensive agents, reversible secondary causes
creatinine, hypokalemic metabolic alkalosis, and
of hypertension should be ruled out. Renal artery
microangiopathic hemolytic anemia.31 Uremia
hypertension or acute pain from the dissection
was historically the major cause of death until of
has to be considered as a possible cause of
hemodialysis and improved antihypertensive medi-
refractory hypertension. If the aortic dissection is
cations became available. The level of renal
complicated by organ ischemia, limb ischemia,
recovery relates to the degree of renal impairment
or refractory pain, surgical or endovascular
at presentation and the underlying renal disorder.
therapy may be necessary.22,24
Minoxidil, a direct arteriolar vasodilator, is a potent,
oral agent useful in malignant hypertension associ-
Hypertensive Retinopathy ated with renal failure. Minoxidil may cause reflex
tachycardia and fluid retention.31 ACE inhibitors
Arteriolar narrowing in patients with mild to
such as captopril and enalapril are the drugs of
moderate hypertension has been described since
choice for malignant hypertension in patients who
the late 1800s. Vessel narrowing and arteriolar
present with scleroderma renal crises.32 Fenoldo-
wall thickening can be early signs of poorly
pam, a selective dopamine-1 receptor agonist,
controlled BP.25 Retinopathy with bilateral flame-
which activates dopamine at the level of the kidney,
shaped hemorrhages and exudates (cotton-wool
is a recommended agent for patients with acute
spots) usually indicates severe hypertension and
renal insufficiency because it increases renal perfu-
is classified as grade III retinopathy. More ad-
sion. Calcium-channel blockers and b-blockers
vanced, grade IV retinopathy includes papillede-
can also be used for lowering BP, although they
ma, which can be seen with hypertensive
have no effect on glomerular filtration.3
encephalopathy.26 These fundoscopic findings of
retinopathy in patients with hypertension have
Hypertension in Pregnancy
a low sensitivity. Also, there is a high rate of intra-
observer and interobserver variability when it Hypertension complicates 5% to 7% of all preg-
comes to identifying arteriolar narrowing through nancies, and unfortunately is still a leading cause
540 Johnson et al

of maternal and fetal morbidity and, rarely, clinical trials found that compared with labetalol
mortality.33–36 ED physicians and obstetricians or nifedipine, hydralazine was associated with
often have to consider preterm delivery as the more cesarean sections, more placental abrup-
only viable option in the management of severe tion, more maternal oliguria, more adverse effects
preeclampsia. on fetal heart rate, and more maternal hypoten-
The hypertension of pregnancy is defined as sion.41 Nifedipine and magnesium sulfate have
a BP greater than 140 mm Hg systolic and/or both been found to be effective in the treatment
greater than 90 mm Hg diastolic according to of hypertension associated with pregnancy, but it
National High Blood Pressure Education Pro- is important to remember that severe reductions
gram.37 Preeclampsia is a condition that needs in BP can occur when these agents are given
to be distinguished from chronic hypertension, together.
which usually is without complications and can
be treated similarly to hypertension without preg- Postoperative Hypertension
nancy with treatment plans that are safe for the
Postoperative hypertension is defined as signifi-
mother and fetus. Preeclampsia is primarily char-
cantly elevated BP within the first 2 hours after
acterized by hypertension and proteinuria, but
surgery. The most common cause of postopera-
can also involve multiple organ systems. The
tive hypertension is sympathetic activation and
proteinuria is defined by excretion of 300 mg per
adrenergic surge. Reversible contributors to this
24 hours, a urine protein/creatinine ratio of greater
sympathetic activation such as pain, hypoxemia,
than 0.3, or a qualitative dipstick reading of 11.38
hypercarbia, hypothermia, volume overload, and
One potentially life-threatening complication of
anxiety should be treated first before ad-
preeclampsia is the HELLP syndrome, character-
ministering antihypertensives unless end-organ
ized by some or all of the following signs: Hemo-
damage is present.42 Urinary retention after
lysis, abnormal Elevation of Liver enzyme levels
surgery is also thought to cause markedly elevated
(aspartate aminotransferase and lactate dehydro-
BP. Moreover, withdrawal from holding antihyper-
genase), and Low Platelets (often <40,000/mL).39
tensives should be considered. In general,
There are multiple controversies related to
patients should not stop taking their home antihy-
both the pathophysiology and management of
pertensive medications on the day of surgery,
preeclampsia, but there is a general consensus
especially centrally acting agents such as cloni-
that only delivery results in a true “cure”.34 De
dine and b-blockers. Patients with or without pre-
novo hypertension alone occurring after the 20th
existing hypertension can develop postoperative
week of gestation in a nulliparous woman should,
hypertension. Patients with poorly controlled
as a precaution, initially be treated as pre-
hypertension are more likely to have postoperative
eclampsia.7 Preeclampsia has also been found to
hypertension.43 Treatment should be focused on
be a risk marker for future cardiovascular disease,
the cause of the hypertension and on whether
so close postpartum risk-factor monitoring is
the patient is able to take oral medications after
strongly recommended.
the procedure. If possible, the patient’s home
Regarding treatment, there is a consensus that
medication can be given if there are no contraindi-
antihypertensive therapy should be given to lower
cations. b-Blockers should be avoided in certain
the maternal risk of central nervous system
instances such as profound bradycardia, heart
complications in pregnant women with a sustained
block, severe chronic obstructive pulmonary
systolic BP greater than 160 mm Hg and/or dia-
disease, or acute heart failure.
stolic BP greater than 110 mm Hg.40 At lower BP
levels between 140 and 159 mm Hg systolic and
Hyperadrenergic States
90 and 105 mm Hg diastolic, there is no consensus
on when and how to treat these levels of blood The hyperadrenergic states include pheochro-
pressure. The antihypertensive drugs frequently mocytoma; cocaine, amphetamine, and phency-
used to treat severe hypertension in pregnancy clidine overdose; clonidine withdrawal; and
include labetalol, hydralazine, nifedipine, and ni- monoamine oxidase (MAO) inhibitor–tyramine
troprusside only as a last resort.33,34 Methyldopa, reaction. In these conditions there is a surge in
a central adrenergic inhibitor, is the oral drug of catecholamine levels.31 In a pheochromocytoma
choice.34,36 Labetalol is an adrenergic blocking crisis and MAO inhibitor–tyramine reaction, phen-
agent that has an oral and parental formulation tolamine, phenoxybenzamine, or nitroprusside
with the extra advantage of being safe to use in can be used to control BP. The use of b-blockers
breastfeeding women. Hydralazine was once alone is not recommended for these conditions
considered the drug of choice in hypertensive because it would result in an unopposed periph-
emergencies, but a meta-analysis of multiple eral a-adrenergic vasoconstriction, which further
 Hypertension Crisis in the ED 541

Table 3
Target blood pressure goals

Hypertensive Emergency Target Blood Pressure

Hypertensive encephalopathy MAP lowered by maximum 20% or to DBP 100–110 mm Hg within
first hour then gradual reduction in BP to normal range over
48–72 h
Ischemic stroke MAP lowered no more than 15%–20%, DBP not less than
100–110 mm Hg in first 24 h (thrombolytic protocols in stroke may
allow slightly more aggressive management)
Ischemic stroke post-tPA SBP <185 mm Hg or DBP <110 mm Hg
Intracerebral hemorrhage MAP lowered by 20%–25%
Hypertensive retinopathy MAP lowered by 20%–25%
Left ventricular failure MAP to 60–100 mm Hg
Aortic dissection SBP 100–120 mm Hg
Acute renal insufficiency MAP lowered by 20%–25%
Pregnancy-induced hypertension SBP 130–150 mm Hg and DBP 80–100 mm Hg
Postoperative hypertension MAP lowered by 20%–25% (not based on published guidelines)
Myocardial ischemia/infarct MAP to 60–100 mm Hg
Hyperadrenergic states MAP lowered by 20%–25% (not based on published guidelines)

Abbreviations: DBP, diastolic blood pressure; MAP, mean arterial pressure; SBP, systolic blood pressure; tPA, tissue plasmin-
ogen activator.

increases BP.19 Labetalol, which has both an a- stabilized with parenteral therapy, the transition
and b-receptor antagonist effect, can also be to oral therapy can begin within 6 to 12 hours.
used in a pheochromocytoma crisis; however,
paradoxic hypertension may occur.31 In the case REFERENCES
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