Introduction

Hypertensive crises are a frequent cause of

emergency department (ED) visits. An isolated
reading of blood pressure (BP) alone does not de-
fine the clinical picture as a hypertensive crisis. In
other words, there are many clinical situations
that are accompanied by an elevation of BP,
which may generate confusion as to whether high
BP (hypertension: HT) in a particular context is
the cause or the consequence of the picture giv-
ing rise to the visit. Although hypertensive crises
usually occur in HT patients who are untreated or
inadequately treated, its definition and clinical
course should not be confined to the magnitude
of the rise in BP value, but also the existence of
specific clinical symptoms that will be discussed
below. Similarly, it should be noted that moder-
ately high BP values can lead to emergency situa-
tions in a previously normotensive person
1
.
In this review we discuss those emergency situ-
ations that require special treatment to achieve
rapid and optimal BP control, and the new criteria
for treatment based primarily on pathophysiologi-
cal mechanisms causing BP elevation.
Definitions
A hypertensive crisis is considered to be any in-
crease of BP generally above 180/120 mmHg. De-
pending on the magnitude and the presence or
absence of target organ damage (TOD) and the
presence of associated symptoms, it is subdivided
into HT emergency (life-threatening), urgent at-
tention HT or pseudocrisis
2
.
Hypertensive emergency
This refers to intense elevation of BP associated
wi th acute i nj ury to vul nerabl e organs. Pro-
nounced increases in BP accompanied by obvious
TOD should be treated immediately (without nec-
essarily waiting for high values to return to nor-
Emergencias 2010; 22: 209-219 209
REVIEW ARTICLE
Hypertension, hypertensive crisis, and hypertensive
emergency: approaches to emergency department care
ELISENDA GMEZ ANGELATS, ERNESTO BRAGULAT BAUR
Seccin de Urgencias Medicina. rea de Urgencias. Hospital Clnic. Barcelona, Spain.
Elevated arterial blood pressure is a frequent reason for seeking emergency care. It is
important to remember that pressure elevation alone does not define whether the
situation should be considered a life-threatening emergency or denotes only a need for
urgent attention. Rather, it is the signs and symptoms accompanying the elevation that
will reveal which patients are in need of emergency treatment. A hypertensive emergency
is characterized by clear signs of acute injury to a target organ, presenting as hypertensive
encephalopathy, intracranial bleeding, acute coronary syndrome, heart failure with acute
pulmonary edema, aortic dissection, eclampsia or preeclampsia, or accelerated
hypertension. These situations require the immediate but not abrupt reduction of arterial
pressures by means of parenteral administration of drugs. A hypertensive patient in need
of urgent care, but not in an emergency situation, on the other hand, has seriously
elevated pressures but no signs of acute or progressive target organ injury. Such a patient
requires gradual reduction of pressures over a period of 24 hours to several days and can
receive oral treatment. A large number of drugs are available for managing hypertension.
No single drug has been reliably shown to be better than others at reducing pressures,
whether administered parenterally or not. However, recommendations can be made
based on the accompanying clinical picture and individual patient characteristics. This
review will outline such recommendations. [Emergencias 2010;22:209-219]
Key words: Hypertension. Hypertensive crisis. Hypertensive emergency.
CORRESPONDENCE:
Dra. Elisenda Gmez Angelats
Seccin de Urgencias Medicina
rea de Urgencias
Hospital Clnic
C/Villarroel, 170
08036 Barcelona. Spain
E-mail: eligomez@clinic.ub.es
RECEIVED:
17-6-2009
ACCEPTED:
29-9-2009
CONFLICT OF INTEREST:
None
Training
accredited
mal BP) to prevent or limit organ damage
3
. Exam-
ples of hypertensive emergencies: hypertensive
encephalopathy, intracranial hemorrhage, acute
coronary syndrome (ACS), heart failure with acute
pulmonary edema, dissecting aorta, eclampsia-
eclampsia and accelerated hypertension. A patient
with a hypertensive emergency usually presents
grade III-IV retinopathy. It is therefore a process
that is identified by the symptoms experienced by
the patient and not by the values of BP.
Urgent attention HT
This denotes elevated BP not accompanied by
progressive TOD, and therefore requires gradual
normalization of BP values in a period of time
ranging from 24 hours to several days with orally
administered drugs. It is therefore important to
note that the difference between urgent attention
HT and hypertensive emergency is not in the val-
ues of BP but rather the existence of TOD. Thus,
patients with long-standing HT may have diastolic
BP between 120-140 mmHg and be asympto-
matic, while patients with preeclampsia, cocaine
users or patients with acute glomerulonephritis
presenting DHT of 105-110 mmHg may consti-
tute a hypertensive emergency.
Hypertensive pseudocrisis or false hypertensive
crisis
This refers to transient elevation of BP appear-
ing in different situations and diseases, and BP el-
evation is a secondary phenomenon associated
with them. We may see this in situations of pain,
emotional stress, peripheral vertigo, spinal cord
injury, acute urinary retention, hypoxia, brain
damage with intracranial hypertension, etc. In
these cases the treatment should be directed to-
ward the underlying disease, since the BP values
usually normalize once the cause of elevation is
resolved.
Clinical Manifestations
There are many and varied main reasons for ED
visits or referral among patients with a HT crisis.
They range from the asymptomatic patient re-
ferred after an incidental finding of high BP to a
patient with acute pulmonary edema. As men-
tioned, BP values per se do not determine case
severity, but the accompanying symptoms do, in
which case severity depends on the target organ
affected. However, this does not mean that a pa-
tient with nephritic colic and BP 180/120 mmHg
constitutes hypertensive emergency with renal im-
pairment. Conversely, a patient with rapidly pro-
gressive dyspnea and BP 150/105 mmHg consti-
tutes a hypertensive emergency with cardiac
involvement and acute lung edema, which re-
quires immediate lowering of BP. It is therefore
very important to assess the patient's clinical con-
text when classifying cases as hypertensive crisis or
urgent attention HT, since the approach and thera-
peutic implications are going to be very different.
It should also be noted that patients with
chronic hypertension may tolerate BP levels of
150/100 mmHg well and without symptoms,
while the same levels in younger patients with
acute glomerulonephritis, or after cocaine con-
sumption, may generate severe symptoms.
In the case of a possible hypertensive emer-
gency, the symptoms and physical findings guide
us to the diagnosis. Thus, a patient may consult
for visual disturbances, headache, confusion and
vomiting as a manifestation of hypertensive en-
cephalopathy or with reduced level of conscious-
ness in the case of intracerebral hematoma or
subarachnoid hemorrhage.
Cardiovascular disorders include ACS, rapidly
progressive dyspnea in the case of acute pul-
monary edema and chest pain and/or abdominal
pain in the case of aortic dissection.
I n the case of pregnant women wi th
preeclampsia, the appearance of severe renal im-
pairment with oliguria, anuria and microangio-
pathic anemia indicates eclampsia (Table 1).
The most common presentation of accelerat-
ed-malignant hypertension is headache with visual
alterations, which appear in up to 50% of pa-
tients with this type of hypertensive emergency
4
.
It is characterized pathologically by fibrinoid
necrosis of the arterioles and myointimal prolifera-
tion of small arteries, manifesting in the form of
retinopathy (hypertensive grade III-IV) and renal
disease evidenced by impaired renal function
and/or hematuria and/or proteinuria.
The patient requiring urgent attention for hy-
pertension is one who, despite high BP, does not
exhibit any BP-related symptoms, as shown in
Table 1.
Initial assessment
Patients attending an emergency department
for elevated BP are usually referred or attend
spontaneously due to the appearance of a symp-
tom accompanied by the elevation. So, initially,
E. Gmez Angelats et al.
210 Emergencias 2010; 22: 209-219
rapid triage should assess whether this elevation
involves the possibility of TOD, at least incipient,
and therefore makes the case a hypertensive
emergency. It is important to establish whether
the patient is known to be hypertensive or not,
the regular medication and adherence to treat-
ment, as well as their usual BP values. Many pa-
tients with chronic hypertension have BP values
which range between 150/90-100 mmHg and are
asymptomatic. It is also important, especially in
younger people, to inquire about the possibility of
drug use, such as amphetamines or cocaine. It is
also important to collect information about possi-
ble consumption of medication such as ergot,
non-steroidal anti-inflammatory agents, nasal de-
congestants, and failure to adhere to normal hy-
pertensive medication or abrupt termination of
beta-blockers.
BP must be measured in both arms, if possible,
and take into account that in obese patients the
use of BP arm bands that are not adapted to the
arm circumference causes falsely high readings
4
.
Relevant information should include BP values
before the ED visit, previous or only current caus-
es for concern, and prescribed medication being
taken.
The physical examination should focus on
identifying or excluding evidence of acute TOD. It
is important to check peripheral pulse symmetry.
Auscultation of crackles in a dyspneic patient with
orthopnea and cough as an atypical symptom
should arouse suspicion of acute lung edema, and
the presence of angina suggests ACS. A neurolog-
ical deficit is suggestive of either ischemic or hem-
orrhagi c stroke, and not hypertensi ve en-
cephalopathy, which manifests in the form of
headache and altered level of consciousness.
Fundus examination, mandatory in all hyper-
tensive crises, may reveal the presence of exudate
and hemorrhage (grade III retinopathy), and/or
papilledema (grade IV retinopathy), in which case
the rise in BP should be treated as a hypertensive
emergency (Table 2).
Based on this assessment we should be able to
distinguish between cases requiring urgent atten-
tion and an emergency, with a view to establish-
ing the most appropriate diagnostic and thera-
peutic strategy.
Are complementary tests necessary
in the asymptomatic patient?
This is often asked in the ED. A proper history
and complete physical examination, including
fundus examination, can allow one to detect signs
and symptoms of TOD that were initially not ap-
parent. Thus, in asymptomatic patients, one may
detect grade III-IV retinopathy, or the patient may
present mild confusion, previously not known,
dyspnea or oliguria. The performance of comple-
mentary tests in a patient attending for BP eleva-
tion should be evaluated individually, taking into
account the patients symptoms and clinical find-
ings.
In a recent study
6
, an electrocardiogram and a
chest radiograph changed the diagnostic and
therapeutic decision in only 2 out of 116 patients,
and the authors concluded that it is not necessary
to perform such additional examinations in this
type of patients if they show no symptoms sug-
gestive of TOD.
Generally, in all patients with symptoms and/or
signs of hypertensive emergency, and while treat-
ment is initiated, the following are necessary:
complete blood count and biochemistry, urine
strip test for proteinuria, and electrocardiogram
that will help detect signs of left ventricular hy-
pertrophy and electrical changes in case of chest
pain, as well as chest X-ray to assess the medi-
astinum, the cardiothoracic ratio and signs of
HYPERTENSION, HYPERTENSIVE CRISIS, AND HYPERTENSIVE EMERGENCY: APPROACHES TO EMERGENCY DEPARTMENT CARE
Emergencias 2010; 22: 209-219 211
Table 1. Main forms of presentation of hypertensive emergencies in the emergency department
Hypertensive emergencies Symptoms
Hypertensive encephalopathy Headache, visual disturbances, vomiting, altered level of consciousness.
Severe hypertension with ischemic stroke/cerebral hemorrhage Neurological deficit, altered level of consciousness.
Hypertensive left ventricular failure Cough, dyspnea, orthopnea, rapidly progressive dyspnea.
Accelerated-malignant hypertension Visual changes, headache. Renal failure, oliguria, hematuria.
Hypertension and aortic dissection Chest pain and/or intense abdominal pain. Vegetatism, signs of poor perfusion.
Hypertension with acute coronary syndrome Chest pain.
Use of drugs such as amphetamines, LSD, cocaine or ecstasy Tachycardia, sweating, altered mood and / or level of consciousness.
Severe preeclampsia or eclampsia Oliguria, anuria, microangiopathic anemia.
Table 2. Keith-Wagener-Barker classification of hypotensive
retinal changes
Grade I Mild generalized retinal arteriolar narrowing.
Grade II Definite focal narrowing and aretriovenous nipping.
Grade III The above and retinal hemorrhages, exudates, and cotton
wool spots. Many of these patients present cardiac, brain
or kidney compromise.
Grade IV Severe grade III and papilloedema. Cardiac, brain and
kidney compromise is more severe.
heart failure. In addition, we should proceed to
determine troponin I levels in cases of suspected
ACS or heart failure.
In hypertensive emergency patients with neu-
rological deficit or altered level of consciousness,
CT scan should be requested. Suspected aortic
dissection must be confirmed by contrast CT scan
or chest MRI. If accelerated BP is suspected, schis-
tocyte count must be requested to rule out mi-
croangiopathic hemolytic anemia.
Considerations in the initial management
of PA
The asymptomatic patient
To date, no studies clearly demonstrate the
most appropriate ED approach to the asympto-
matic patient with a hypertensive crisis. Despite
this lack of evidence, it is very common for the at-
tending physician to choose to initiate treatment
in the ED
6
. In this case, and before starting, we
should be aware that at least one third of patients
with DBP increase >95 mmHg in the ED show
spontaneous decrease before they begin follow
up
7
. BP elevation in the absence of symptoms or
signs of TOD rarely requires urgent treatment but
does require deferred monitoring/treatment
3,4
.
Most patients attending the emergency depart-
ment with elevated BP do not present acute TOD
in the initial evaluation. They are usually patients
attending for many different diseases, and there-
fore the elevated BP should be evaluated in the
context of chronic hypertension. In these patients,
either because the finding is coincidental or be-
cause they are asymptomatic and without evi-
dence of acute TOD, treatment should be aimed
at achieving a progressive decrease in BP with oral
drugs within 24-48 hours
8
, and it is not recom-
mended that one should wait for BP values to nor-
malize "pharmacologically" in the ED itself. Rapid
BP reduction, especially in patients with chronic
hypertension, is accompanied by a shift to the
right in the selfregulation pressure/perfusion curve
(Figure 1), in the brain, heart and kidney
9
, which
may lead to cerebral, myocardial or renal ischemia
and infarction, respectively, so this approach is for-
mally disallowed in hypertensive emergencies.
Hypertensive emergency
Given that hypertensive emergency patients
present TOD, a rapid but controlled correction of
BP is necessary. It should be noted that extremely
fast reduction is associated with complications
such as cerebral, myocardial or renal hypoperfu-
sion
2
. That is why the management of these pa-
tients is based on the use of easily titrated drugs
with short half-life in continuous infusion. For the
same reason, the sublingual and intramuscular in-
jection routes should be avoided.
In a hypertensive emergency, the immediate ob-
jective is to reduce DBP by 10-15% or to 110
mmHg over a period of 30 to 60 minutes. In pa-
tients with suspected or confirmed aortic dissection,
the BP must be reduced quickly, in 5-10 min, until
achieving and SBP <120 mmHg, as tolerated
10,11
.
Once BP has been controlled and accompany-
ing organ damage has ceased, oral antihyperten-
sive drugs should be started, and the dose of the
continuous infusion progressively reduced.
Drugs used in hypertensive crises
Habitually, intravenous drugs are used in hyper-
tensive emergencies and oral drugs in cases of ur-
gent attention
12
. A great variety of antihypertensive
agents are used in hypertensive crisis. The choice
of drug depends on the patient's clinical condition
and symptom presentation. The most commonly
used in emergencies are: labetalol, fenoldopam,
nitroglycerin and nitroprusside, because they are
easily titratable, and their effect is rapid.
Cases requiring urgent attention
It is important to remember that sublingual
nifedipine is not recommended in any type of hy-
pertensive crisis
3
. The recommended drugs are
those with long half-life (Table 3), since the aim is
to normalize BP values in about 48-72 hours
3
. An-
giotensin converting enzyme inhibitors (ACEI) are
most commonly used in cases requiring urgent at-
E. Gmez Angelats et al.
212 Emergencias 2010; 22: 209-219
70
60
50
40
30
20
10
0
0 25 50 75 100 125 150 175 200
Normotensive
Hypertensive
Figure 1. Diagram showing the limits of cerebral blood flow
self-regulation in relation to changes in blood pressure. X axis:
cerebral blood flow (ml/100 g per min) and Y axis: values of
blood pressure in mmHg (Adapted from Strangaard et al, Br
Med J.).
tention, especially captopril, which has faster on-
set of action (between 30 and 60 minutes)
13
, al-
though, as said, BP should not be reduced too
rapidly. Any drug with a relatively fast onset of ac-
tion can be used, including loop diuretics, -
blockers,
2
-adrenergic agonists or calcium antag-
onists (except short-acting nifedipine). The most
significant change in recent years in pharmaco-
logic management of hypertension has been the
development of type 1 angiotensin II receptor an-
tagonists (ARA II), of which Losartan is the most
used. The use of these drugs in hypertensive
crises is poorly documented but possibly the de-
crease in BP is comparable to that obtained with
ACE inhibitors, although the onset of its action
may be slower.
Hypertensive Emergencies
Labetalol
This is a combined selective blocker of
1
and non-selective blocker of -adrenergic recep-
tors, with an - blocker ratio of 1:7. Its hy-
potensive action begins at 2-5 minutes after in-
travenous administration, reaching a peak at
5-15 minutes, with a duration of between 2 and
4 hours
14
. Unlike selective beta-blockers, it does
not have a negative inotropic effect
15
. It decreas-
es peripheral resistance without reducing pe-
ripheral flow, whereas renal, cerebral and coro-
nary blood flow remain constant. It can be used
in cases of eclampsia and preeclampsia because
passage through the pl acental barri er i s
minimal
15-18
.
It is administered with an initial loading dose
of 20 mg, followed by progreesively larger doses
of 20 to 80 mg in 10 minute intervals. After the
l oadi ng dose, one can start i nfusi on of 1-2
mg/min titrated on the basis of the hypotensive
effect desired. A bolus of 1-2 mg/kg should be
avoided because of the risk of sudden hypoten-
sion (Table 4).
Esmolol
This is a cardioselective blocker with extremely
short-acting effect. Onset of action occurs in 1
minute, with a duration of 10-20 minutes. A bolus
of 0.5 mg/kg is recommended followed by con-
tinuous infusion of 25-300 mg/kg/min. This drug
is safe in ischemic heart disease, and given its
pharmacokinetic properties, some authors consid-
er it to be the beta-blocker of choice in critically
ill patients
19
(Table 4).
HYPERTENSION, HYPERTENSIVE CRISIS, AND HYPERTENSIVE EMERGENCY: APPROACHES TO EMERGENCY DEPARTMENT CARE
Emergencias 2010; 22: 209-219 213
Table 3. Main drugs used in the treatment of hypertensive
patients requiring urgent attention
Drug Initial Dose
Calcium antagonists (long-acting dihydropyridines)
Amlodipine 5-10 mg
Lacidipine 4 mg
Betablockers
Bisoprolol 2,5-5 mg
Carvedilol 12,5-25 mg
Atenolol 25-50 mg
Diuretics
Furosemide 20-40 mg
Torasemide 5-10 mg
Angiotensin-converting enzyme inhibitors
Captopril 12,5-25 mg
Enalapril 5-20 mg
Angiotensin II receptor antagonists
Losartan 50 mg
Irbesartan 75-150 mg
Candesartan 8-16 mg
Alpha blockers
Doxazosin 1-4 mg
Table 4. Major drugs administered for the treatment of hypertensive emergency
Drug Mechanism Dosage Effect Duration Specific indications
Labetalol --blocker Bolus 20 mg and repeat bolus with doses 5-10 min 3-6 h Most hypertensive
(not cardioselective) of 20-80 mg at 10 min intervals emergencies.
(Max. 300 mg) Stroke.
Perfusion: 1-2 mg/min
Esmolol -blocker Bolus 0,5 mg/Kg 1-2 min 10-20 min ACS.
(cardioselective) Perfusion 25-300 g/Kg/min
Enalapril ACEI Bolus de 1 mg 15-60 min 4-6 h Hypertensive encephalopathy.
Fenoldopam Dopamine agonist Perfusion 0,1 g/Kg/min < 5 min 30 min Most emergencies
Nitroprusside Arterial and venous Perfusion 0,25-0,5 g/Kg/min; Instant < 2 min Acute pulmonary edema.
vasodilator Max. dose 8-10 g/Kg/min
(Max. 10 min)
Nitroglycerin Venodilator Perfusion 5-100 g/min 2-5 min 5-10 min ACS.
Nicardipino Dihydropyridine Perfusion 5 mg/h 5-10 min 4-6 h Hyperadrenergic crisis.
calcium antagonist Increase 2,5 mg/h cada 5 min
(Max. 15 mg/h)
Urapidilo Selective -adrenergic Boluses 25-100 mg 3-5 min 4-6 h Perioperative
antagonist at 5 min intervals hypertension.
Phentolamine -adrenergic blocker Boluses 1-5 mg 1-2 min 10-30 min Pheochromocytoma
ACEI: angiotensin converting enzyme inhibitors; ACS: acute coronary syndrome.
Enalapril
This is an ACE inhibitor that is available for
parenteral administration. It is used in doses of 1
mg and its effect starts after 15 minutes, lasting
12 to 24 hours. It has few side effects and only
causes very slight symptomatic hypotension. It is
not recommended i n cases of ecl ampsi a or
preeclampsia (Table 4).
Fenoldopam
This is an antihypertensive drug for parenteral
administration. It is a dopamine agonist with po-
tent vasodilator action, especially renal. It causes
vasodilation which acts at the level of peripheral
dopamine receptors. Its effect starts at 5 minutes
and maximum response is reached at 15 minutes;
action lasts between 30 and 60 minutes, and it
has no rebound effect
20-22
. Studies comparing
fenoldopam with nitroprusside have demonstrated
similar effectiveness but with fewer side effects
23
.
The recommended starti ng dose i s 0.1
g/kg/min. It improves creatinine clearance and
sodium excretion in patients with severe hyper-
tension with or without impaired renal function
24-26
.
Its main contraindications are patients with glau-
coma (Table 4).
Nitroprusside
This is an arterial and venous vasodilator that
decreases both preload and afterload
27,28
. It de-
creases cerebral blood flow and increases intracra-
nial pressure so it is not recommended in cases of
hypertensive emergency with the brain as the tar-
get organ
29-32
or in patients with ACS because it
causes coronary steal
33
. It is a very powerful agent,
with very fast onset of action within seconds, and
a duration of 1-2 minutes with a half-life of 3-4
minutes. It should only be used in patients with
normal liver and right kidney function, due to the
risk of thiocyanite accumulation (Table 4). The du-
ration of treatment should be as short as possible
and perfusi on dose shoul d not exceed 2
g/kg/min (Table 4).
Nitroglycerine
This is a very potent venous vasodilator, and
only affects arterial bed tone at high doses
34
. It
causes hypotension and reflex tachycardia, exacer-
bated with volume depletion which is characteris-
tic of hypertensive emergencies. Nitroglycerin re-
duces BP and reduces preload and cardiac output,
so it can have deleterious effects in patients with
altered cerebral or renal perfusion. It is the drug
of choice to reduce the BP and ischemic symp-
toms in patients with ACS
35
. Its onset of action oc-
curs within 1-2 minutes, lasting 3-10 minutes. The
recommended dose is 500-100 g/min, depend-
ing on the desired effect (Table 4).
Nicardipine
This is a dihydropyridine-derivative calcium an-
tagonist, with high cardiovascular selectivity and
great cerebral and coronary vasodilatory activity.
Onset of action is 5-10 minutes, and it has
been shown to reduce cerebral and cardiac is-
chemia. Initial infusion of 5 mg/h, which can be
stepped up by 2.5 mg/h every 5 minutes to a
maximum of 15 mg/h, or until the target BP is
achieved
19
.
It is a good choice of drug in patients with
ACS and congestive heart failure because in addi-
tion to being a coronary artery vasodilator, it in-
creases stroke volume, thus favoring the correct
myocardial oxygen balance. It is also indicated in
hyperadrenergic crisis, and considered a good
choice in eclampsia/preeclampsia. Its main draw-
back is its long half-life (4-6 h) (Table 4).
Urapidilo
This is a new selective -blocker. It produces
reactive vasodilation without tachycardia, and acts
centrally. It is used intravenously at doses of 25
mg, and may be stepped up to 100 mg at inter-
vals of five minutes. It is not often used, but stud-
ies support its use in the treatment of prehospital
hypertensive emergencies and in perioperative hy-
pertension
36
(Table 4).
Phentolamine
This is an -adrenergic blocker used in hyper-
tensi ve cri ses i nduced by catechol ami nes
(Pheochromocytoma). Its effect is immediate, and
may cause angina and tachyarrhythmia (Table 4).
Specific situations
Hypertension and aortic dissection
This constitutes a differential diagnosis to be
considered in every patient consulting the ED
with persistent chest pain accompanied by BP ele-
vation. Three-quarters of patients with aortic dis-
section that is not diagnosed and not treated
properl y di e wi thi n two weeks of the acute
episode; otherwise, survival at 5 years is 75%
37
.
The recommendations in terms of BP values to
be achieved in the treatment of hypertension and
aortic dissection range from SBP <140 and 110
mmHg
38,39
.
E. Gmez Angelats et al.
214 Emergencias 2010; 22: 209-219
While it is true that there are few randomized
controlled trials that can provide clear guidance
on how to treat hypertension in cases of aortic
dissection
40
, a recommendation that should be
borne in mind is that one should not employ a
vasodilator alone, because it promotes reflex
tachycardia, increases speed of aortic ejection,
and therefore propagation of the dissection, since
the dissection depends not only on raised BP, but
also the speed of ventricular ejection. The best
option for these patients is the combination of a
beta blocker and a vasodilator
41
. As beta-blockers,
labetalol and esmolol are used, and the vasodila-
tor traditionally used is sodium nitroprusside, al-
though fenoldopam is less toxic and improves re-
nal perfusion (Table 5).
Severe hypertension with ischemic stroke
Most patients with acute ischemic stroke pres-
ent high BP on ED consultation, regardless of the
etiology or whether they are hypertensive or
not
42,43
. High BP does not per se constitute a hy-
pertensive emergency, but is rather a physiologi-
cal mechanism designed to maintain perfusion
pressure in the area affected by cerebral ischemia.
This increase in BP normalizes progressively and
spontaneously. For this reason, these patients
should be assessed with caution, because rapid BP
reduction may worsen the ischemic area. The
common practice of "normalizing" BP in acute is-
chemic stroke patients is potentially dangerous, as
shown by some studies
44
. Hypertension in the
acute phase of stroke has not been shown to have
a deleterious effect and some studies suggest a
protective role
45
. Depending on the upper limit of
BP self regulation by the brain, it is advisable not
to initiate antihypertensive treatment in these pa-
tients unless TOD has been established or throm-
bolytic treatment is being evaluated or SBP >220
mmHg or DBP >120 mmHg
46,47
. In this context, it
is recommended not to allow more than a 15%
decrease of BP values in the first 24 hours. In the
event that the patient is a candidate for throm-
bolytic therapy, blood pressure should be reduced
below 185/110 mmHg, to 180/105 mmHg
47
. The
drug of choice is labetalol, and fenoldopam is the
main alternative. Nitroprusside is not recommend-
ed due to its well-known side effect of reducing
cerebral blood flow and increasing intracranial
pressure
29-32
(Table 5).
Hypertension and cerebral hemorrhage
Intracerebral hemorrhage (ICH) frequently pro-
duces reflex hypertension, but unlike ischemic
stroke, this increase in BP does not usually im-
prove spontaneously during the days immediately
after the onset of sympyoms
48
.
Unlike ICH secondary to rupture of an arteri-
ovenous malformation or to an intracerebral
aneurysm, there is no clear evidence that in-
creased BP causes more bleeding in patients with
spontaneous ICH, and a sharp decrease of BP may
compromise brain perfusion
49
.
There are no specific recommendations on
what specific level of BP is most beneficial for a
patient with ICH, although the following evidence
is relevant:
Increased bleeding has been shown to be
more common in patients with isolated systolic
BP, but it is not known whether this increase is
due to increased ICH itself, leading to increased
intracranial pressure
49
. However, we do know that:
Isolated systolic pressure 210 mmHg has
not been clearly linked with increased bleeding or
neurological deterioration
50
.
A 15% reduction in MAP does not affect
cerebral blood flow
51
.
Reducing SBP to <160/90 mmHg during the
first 6 hours of onset of ICH is associated with
better functional outcome
52
.
It is important, likewise, to individualize BP
treatment based on the patient's prior baseline,
assess the cause of bleeding, age and the signs of
intracranial hypertension
53
. The drug of choice in
these cases is also labetalol, and the second op-
tion is fenoldopam (Table 5).
HYPERTENSION, HYPERTENSIVE CRISIS, AND HYPERTENSIVE EMERGENCY: APPROACHES TO EMERGENCY DEPARTMENT CARE
Emergencias 2010; 22: 209-219 215
Table 5. Therapeutic considerations depending on the type of hypertensive emergency
Affected organ Complications Therapeutic considerations Contraindicated
Aorta Dissection Labetalol/Esmolol + Fenoldopam/Nitroprusside
Brain Ischemic stroke Labetalol/Fenoldopam Nitroprusside
Brain Intraparenchymal hemorrhage Labetalol/Fenoldopam Nitroprusside
Brain Hypertensive encephalopathy ACEI and/or labetalol Nitroprusside
Heart Acute coronary syndrome Nitroglycerin + labetalol/esmolol/ACEI Nitroprusside
Heart Heart failure/pulmonary edema Nitroglycerin/nitroprusside + loop diuretic Labetalol
Placenta Eclampsia/preeclampsia Magnesium sulfate + Labetalol/Nicardipine ACEI/Nitroprusside
Kidney Acute renal failure/hematuria/proteinuria ACEI?/Boluses Labetalol/fenoldopam perfusion ACEI?/Nitroprusside
ACEI: angiotensin converting enzyme inhibitor.
Hypertensive encephalopathy
This diagnosis is made by exclusion, after cere-
bral hemorrhage and ischemic stroke have been
reasonably ruled out. It is characterized by signs
and symptoms such as severe headache, altered
state of consciousness, seizures, and papilledema,
without neurological deficit. The mechanism re-
sponsible has been attributed to a sudden in-
crease in pressure of cerebral perfusion, secondary
to a rapid, abrupt increase in BP, resulting in ede-
ma and reduced cerebral blood flow. This entity is
usually found in patients with untreated primary
hypertension and a rapid, abrupt increase of BP,
but also in patients with other predisposing con-
di ti ons, such as renovascul ar hypertensi on,
glomerulonephritis, pheochromocytoma and
eclampsia. It has been known for years that the
cause of this rise in BP is due, in most cases, to
overproduction of renin and angiotensin II in re-
sponse to renal ischemia, although other mecha-
nisms have been identified, such as sympathetic
vasoconstriction, blood-brain barrier disruption
due to alterations in cerebral blood flow and over-
production of angiotensin II, which promotes ox-
idative stress in brain vessels
54
.
The etiologic role of overstimulation of the
renin-angiotensin system underlies focus of treat-
ment, so drugs that block this axis are used. The
drugs of choice are oral or intravenous ACE in-
hibitors, such as captopril and enalapril, respec-
tively. Likewise, an ACE inhibitor with a beta-
adrenergic blocker, such as labetalol, interrupt the
renin angiotensin axis at various points and help
to maintain cerebral blood flow while decreasing
systemic BP. Diuretics and vasodilators are not ad-
visable for this reason (Table 5).
Hypertensive left ventricular failure
This is characterized by the presence of signs
and symptoms of intravascular volume overload
and interstitial or secondary manifestations of tis-
sue hypoperfusion, such as dyspnea. Elevated BP
in these cases can be both the cause and the re-
sult of acute pulmonary edema. The treatment of
choice is based on the use of vasodilators such as
nitroglycerin or nitroprusside with an intravenous
loop diuretic
55
. Drugs that decrease contractility,
such as beta-blockers, should be avoided (Table 5).
Hypertension with acute coronary syndrome
Like acute pulmonary edema, ACS can develop
in the context of a peak in hypertension. Experi-
mental studies have shown that, in the early
stages of ACS, excessive renin-angiotensin axis ac-
tivation occurs, and some studies ascribe increas-
ing importance to this finding
56
. The treatment
goal in a hypertensive emergency with ACS is,
firstly, to reduce myocardial oxygen demand, and
secondly, to block neurohumoral action. For the
former, the use of intravenous nitroglycerin is in-
dicated. Nitroprusside is contraindicated because
it may cause a decrease in transmural flow. Block-
ing the neurohumoral system may be achieved
with beta-blockers, such as labetalol (alpha and
beta adrenergic receptor blocker) and esmolol
(cardioselective beta blocker), or intravenous
enalapril.
ACS arising from cocaine use is characterized
by adrenergic receptor stimulation, so the treat-
ment of choice is alpha-adrenergic blockers. Beta-
blockers are formally contraindicated since they
may give rise to a alpha-adrenergic storm and en-
hance the toxicity of cocaine (Table 5).
Crisis mediated by excessive secretion or release
of catecholamines
This is the case of hypertensive crisis related
with the consumption of recreational drugs of
abuse such as cocaine, amphetamines, LSD or Ec-
stasy, and more rarely in the context of pheochro-
mocytoma, consumption of monoamine oxidase
or abrupt cessation of treatment with beta-adren-
ergic agonists.
Patients with pheochromocytoma present
headache, alternating periods of elevated BP,
tachycardia and flushing that follow periods of
normotension, while subjects that have taken
recreational drugs show tachycardia, diaphoresis,
hypertension and changes in mood and level of
consciousness. The treatment drug of choice is
phentolamine, to which calcium channel blockers
can be added.
In clinical situations characterized by sympa-
thetic overstimulation, beta-adrenergic antago-
nists should be avoided to prevent beta-receptor
antagonism, which would result in response acti-
vation of alpha adrenergic activity, with a sec-
ondary effect of increasing BP level. Although la-
betalol has a beta and alfha blocking effect, it is
not recommended for use in these cases. The
drugs that should be used in this circumstance
include nitroglycerin, nicardipine or verapamil in
combination with intravenous benzodiazepine
57
.
Also, fenoldopam, nitroprusside, nitroglycerin
and phentolamine can be used as alternatives
58
(Table 5).
E. Gmez Angelats et al.
216 Emergencias 2010; 22: 209-219
Accelerated-malignant hypertension
The picture of severe hypertension associated
with edema of the papilla (Hypertensive retinopa-
thy grade-IV Keith-Wagener) is called accelerated-
malignant hypertension. If retinopathy is of grade-
III (bleeding and exudates) it is called accelerated
hypertension. In this case, as in hypertensive en-
cephalopathy, the rapid increase in BP is mostly
caused by overproducti on of reni n and an-
giotensin II in response to renal ischemia
59
. This
situation very rarely presents as de novo hyperten-
sion, and generally presents in the context of
long-standing hypertension or, more often, hyper-
tension secondary to renovascular hypertension,
scleroderma, or vasculitis. Its incidence before the
advent of antihypertensive drugs was 7%, where-
as currently this is 1% of hypertensive patients,
characteristically those of a relatively young age
60
.
Unless treated with antihypertensive drugs, medi-
um-term mortality is high, associated with long-
term cardiac and renal sequelae in most patients.
In these patients the objective is to reduce BP
by less than 25% of initial BP or to achieve a DBP
of 100-105 mmHg
61
.
The etiologic role of overstimulation of the
renin-angiotensin axis conditions treatment and
the use of drugs that block this axis, and although
the use of ACE inhibitors is recommended by
some authors, others claim otherwise
61
. Captopril
has an onset of action between 30-60 minutes.
Intravenous enalapril has a rapid effect and there-
fore should be avoided (Table 5). Boluses of la-
betalol are recommended, and continuous infu-
sion of enoldopam is a very good alternative,
since for cases of hypotension its half-life is 30
minutes.
Preeclampsia and eclampsia
Hypertension is one of the processes that can
complicate a pregnancy. This syndrome, charac-
terized by BP >140/90 mm Hg and proteinuria
>300 mg/24 h, usually occurs after 20 weeks of
gestation
62
. Depending on the series of patients, it
may affect up to 12% of pregnancies, and is esti-
mated to be involved in 18% of maternal deaths,
so pregnancy-induced hypertension can be life-
threatening
63
.
Accompani ed by headache, vi sual di stur-
bances, increased serum creatinine, thrombocy-
topenia, hemolytic microangiopathic anemia, in-
creased dehydrogenase lactate and liver enzymes.
Del i very i s the defi ni ti ve treatment for
preeclampsia and eclampsia. Initial treatment of
pre-eclampsia includes volume expansion, magne-
sium sulfate (MgSO
4
) for seizure prophylaxis and
BP control
62
. Magnesium sulphate is administered
with a loading dose of 4-6 g in 5% dextrose solu-
tion during 15-20 minutes followed by a continu-
ous infusion of 1-2 g/h. The objective, in addition
to treating severe hypertension, is not to compro-
mise cerebral and placental blood flow, since in
this situation BP is most labile. The drug of choice
for these patients is labetalol since it is safe and ef-
fective, easily titrated and has a short half-life
63
.
Nicardipine is a good alternative, while nitroprus-
side and ACE inhibitors are formally contraindicat-
ed in pregnancy. Classically hydralazine used to be
recommended, but it is associated with side effects
such as headache, nausea and vomiting, which
mimic the picture, so in these situations it is not
recommended as a first-line option
64
(Table 5).
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218 Emergencias 2010; 22: 209-219
HYPERTENSION, HYPERTENSIVE CRISIS, AND HYPERTENSIVE EMERGENCY: APPROACHES TO EMERGENCY DEPARTMENT CARE
Emergencias 2010; 22: 209-219 219
Hipertensin arterial, crisis hipertensiva y emergencia hipertensiva: actitud en urgencias
Gmez Angelats E, Bragulat Baur E
La elevacin de las cifras de presin arterial (PA) constituye un motivo de consulta frecuente en los servicios de urgen-
cias. Es importante tener en cuenta que esta elevacin por si sola no define si se trata de una urgencia o de una emer-
gencia, sino el cuadro que acompaa a dicha elevacin, por lo que es primordial diferenciar, de entrada, ambas situa-
ciones. La emergencia hipertensiva se caracteriza por la existencia de una lesin aguda evidente de rgano diana, y
que se presenta en forma de la encefalopata hipertensiva, hemorragia intracraneal, sndrome coronario agudo, insufi-
ciencia cardiaca con edema agudo de pulmn, diseccin de aorta, eclampsia-preeclampsia o hipertensin acelerada.
Requiere una reduccin inmediata aunque no brusca de las cifras de PA por va parenteral. En contraposicin, la ur-
gencia hipertensiva es aquel cuadro caracterizado por un aumento severo de las cifras de PA sin evidencia de lesin
aguda o progresiva de rgano diana y que require una reduccin progresiva de dichas cifras en el plazo de 24 horas a
varios das con frmacos administrados por va oral. Existe un gran nmero de frmacos para el manejo de esta patolo-
ga, y no se ha demostrado de forma fehaciente que un frmaco, ya sea parenteral o no, sea mejor que otro para re-
ducir las cifras de PA. Sin embargo, en funcin del cuadro acompaante y de las caractersticas individuales de cada
paciente, se pueden hacer recomendaciones particulares, como se muestra en la presente revisin. [Emergencias
2010;22:209-219]
Palabras clave: Hipertensin arterial. Crisis hipertensiva. Emergencia hipertensiva.