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www.elsevier.es/medicinaclinica

Review

Diagnostic and therapeutic approach to the hypertensive crisis夽

Guillermo Arbe a , Irene Pastor b , Jonathan Franco a,∗
a
Servicio de Medicina Interna, Unidad de riesgo cardiovascular, Hospital universitario Quirón Dexeus, Barcelona, Spain
b
Servicio de Enfermería, Unidad de riesgo cardiovascular, Hospital universitario Quirón Dexeus, Barcelona, Spain

a r t i c l e i n f o a b s t r a c t

Article history: High blood pressure is a problem with elevated prevalence in the world population. The acute forms
Received 21 August 2017 of presentation are “hypertensive crises,” which represent a frequent cause for emergency room and
Accepted 14 September 2017 primary care consultations.
Available online xxx
Hypertensive crises are divided into hypertensive emergencies and hypertensive urgencies, depending
on whether or not there is acute damage to the target organ, respectively. Each situation has a different
Keywords: prognosis and treatment. More specifically, hypertensive emergencies are potentially serious and usually
High blood pressure
require rapid reductions in blood pressure, whereas hypertensive urgencies can be treated as outpatients
Hypertensive crises
Hypertensive emergency
by reducing blood pressure in hours or days.
Hypertensive urgency A significant number of patients who consult medical professionals regarding a hypertensive crisis
do not have a prior diagnosis of hypertension; therefore, it is important to periodically monitor blood
pressure levels in the community.
© 2017 Elsevier España, S.L.U. All rights reserved.

Aproximación diagnóstica y terapéutica de las crisis hipertensivas

r e s u m e n

Palabras clave: La hipertensión arterial es un problema de elevada prevalencia en la población mundial. Las crisis
Hipertensión arterial hipertensivas son las formas agudas de presentación y representan un motivo frecuente de consulta
Crisis hipertensiva en urgencias y atención primaria.
Emergencia hipertensiva
Las crisis hipertensivas se dividen en emergencias hipertensivas y urgencias hipertensivas, según exista
Urgencia hipertensiva
o no daño agudo en órgano diana, respectivamente. Cada situación tiene un pronóstico y tratamiento
diferente, siendo las emergencias hipertensivas potencialmente graves, requiriendo por lo general reduc-
ciones rápidas de la presión arterial. Por el contrario, las urgencias hipertensivas podrían ser tratadas
ambulatoriamente, reduciendo la presión arterial en horas o días.
En un número elevado de pacientes que consultan por una crisis hipertensiva no existen antecedentes
de diagnóstico de hipertensión arterial, por lo que es importante incrementar los controles periódicos de
la presión arterial en la comunidad.
© 2017 Elsevier España, S.L.U. Todos los derechos reservados.

Introduction medical consultation, both in primary care and in hospital emer-

High blood pressure (HBP) is a health problem with a high
prevalence around the world. It is considered one of the main car-
diovascular risk factors, being one of the most frequent reasons for
夽 Please cite this article as: Arbe G, Pastor I, Franco J. Aproximación
diagnóstica y terapéutica de las crisis hipertensivas. Med Clin (Barc). 2018.
https://doi.org/10.1016/j.medcli.2017.09.027
∗ Corresponding author.
E-mail address: Jonathan.franco@quironsalud.es (J. Franco).
gency departments.1,2
In Spain, HBP is a highly prevalent disease. Studies such as
ENRICA and DI@BETES estimate prevalence between 33 and 43%,
respectively. In these cohorts, approximately half of the subjects
were not aware of their condition.3,4 These levels are very relevant,
given that today HBP is a disorder that, according to the World
Health Organization, is responsible for 7.1 million deaths a year,
despite being a preventable and treatable disease.5
With respect to hypertensive crises (HC), they are divided into
hypertensive emergencies (HE) and hypertensive urgencies (HU),
depending on whether an acute target organ lesion is present or

2387-0206/© 2017 Elsevier España, S.L.U. All rights reserved.

MEDCLE-4313; No. of Pages 6

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absent, respectively. The structural and/or physiological alterations
in the target organs can be in heart, brain, kidney, retina and arter-
ies. Cohorts with an HE prevalence of between 2 and 27% have
been described.6,7 In an Italian multicentre study, 333,407 patients
admitted to the emergency department were included, in which a
total of 1546 were diagnosed with HC and 391 presented HE (25%),
highlighting that up to 23% of these patients had no prior history
of HBP or was unknown to them.8
The objective of this review is to update the clinical and thera-
peutic aspects of HC. In routine clinical practice, hospital emergency
departments have an increasing demand for care. Health pro-
fessionals need to be able to perform a correct identification,
history-taking, physical examination and treatment of HC in a set-
ting where this condition frequently occurs. This would improve
the global care of this disorder and probably optimize the dynamics,
avoiding long and unnecessary stays in the emergency department.
Definitions
HBP is defined as the chronic elevation of systolic blood
pressure (SBP) levels ≥140 mmHg and diastolic blood pressure
(DBP) ≥ 90 mmHg, and it is classified in different degrees according
to the levels shown at diagnosis (Table 1).
On the other hand, HC is defined as an acute increase in
SBP ≥ 180 mmHg and of the DBP ≥ 120 mmHg, capable of causing
acute damage to target organs, levels proposed by the committee
for the prevention, detection, assessment and treatment of HBP
(JNC) VII)9 and the guidelines of the European hypertension and
cardiology societies of 2013, still valid today.6
Historically CHs have been divided into 2 groups: HE and HU,
and each of them has a different treatment and prognosis. Thus,
blood pressure (BP) in HU can be controlled in hours or days with
drugs administered orally and outpatiently.10 On the contrary, HE
(Table 2) requires strict control in minutes to hours, usually with
drugs administered intravenously.
Within the HC classification we also find the false HC or pseudo
HC, which are defined as transient BP elevations due to exter-
nal stimuli (pain, urinary retention, anxiety, stress, among others),
without evidence of acute damage to target organs. Patients with
isolated clinical HBP or “white coat HBP”, and errors in the BP mea-
surement technique are also classified in this group. Prevalence
studies observe a high percentage of pseudo HC, reaching 24–43%
in hospital settings, and up to 91% in outpatient settings.11,12 The
symptoms of the trigger usually prevail in their clinical presenta-
tion, and their BP levels are generally lower than those observed in
a true HC. The pseudo HC treatment is based on rest in the supine
position and treatment of the precipitating cause, an outpatient
follow-up is recommended to confirm or rule out HBP13 .
Within the HC we must take into account a special subgroup
such as HE in pregnancy, which are defined as the acute elevation
of SBP ≥ 160 mmHg and/or DBP ≥ 110 mmHg for a period longer
than 15 min and also capable of causing acute damage to target
Table 1
Classification of arterial hypertension, according to the European Societies of Hypertension and Cardiology.
Category Systolic (mmHg)
Blood pressure level
Optimal <120
Normal 120–129
Normal high 130–139
Arterial hypertension
Grade 1 140–159
Grade 2 160–179
Grade 3 ≥180
Isolated systolic ≥140
mmHg: millimetres of mercury.
organs: preeclampsia, HELLP syndrome (haemolysis, elevated liver
enzymes, thrombocytopenia) and eclampsia.14,15
Diagnosis
The initial assessment of the patient who comes for HC in many
hospitals is performed by nursing staff, either in the triage of an
emergency service, in a hospital ward or in a primary care clinic,
reason why we must work with the medical team in a multidisci-
plinary way in terms of learning symptoms and warning signs for
early identification, so as to avoid direct target organ damage.
History-taking aimed at the possible cause is essential, even in
patients who present with levels below the definition of HC, bear-
ing in mind that the acute damage to target organs depends on how
quickly the crisis is established and the percentage of BP elevation
with respect to the baseline, whereby HE could occur with lower BP
values than those proposed by the guidelines. The patient should be
asked about episodes of HBP in the past, concomitant or triggering
medication, such as non-steroidal anti-inflammatory drugs, recre-
ational drugs, history of sleep apnoea and the presence of some
other cardiovascular risk factor; likewise, symptoms or signs that
could make us suspect secondary HBP16 (Table 3).
Symptoms of HC vary widely, from asymptomatic patients or
with nonspecific symptoms such as headache, dizziness, vomiting
and palpitations, to acute target organ involvement17 .
Physical examination should be detailed, giving priority to car-
diac, supra-aortic and abdominal trunks auscultation in search
of murmurs that suggest arterial damage and/or aneurysms.
Likewise, peripheral pulses, neurological deficit or hypertensive
encephalopathy (nausea, vomiting, altered state of consciousness)
should be evaluated. Emphasis should be placed on the fundus of
the eye, perhaps something that has been forgotten, even though is
one of the most useful examinations in this scenario, since it helps
to rule out hypertensive retinopathy18 ; in addition, it is impor-
tant to assess the rest of vital signs, such as oxygen saturation and
heart rate. Recent studies have shown that HE usually presents with
higher heart rates than HU, with tachycardia being a clinical sign
associated with acute left ventricular failure in the context of HE,
more specifically a heart rate higher than 100 beats/min.19
The complementary tests will be aimed at looking for acute
damage in target organs and should be individualized according to
the patient: electrocardiogram, chest X-ray, pro-natriuretic brain
peptide, to rule out signs of heart failure and/or acute pulmonary
oedema, urinalysis (haematuria and proteinuria), cardiac enzymes
in case of suspected acute coronary syndrome, brain computed
tomography (CT) in case of neurological deficit, thoracic CT angiog-
raphy and/or Doppler echocardiography if there is suspicion of
dissecting aneurysm of the aorta. In HE, the most affected organs
are usually the brain (stroke), acute pulmonary oedema and hyper-
tensive encephalopathy.20
Diastolic (mmHg)
and <80
and/or 80–84
and/or 85–89
and/or 90–99
and/or 100–109
and/or ≥110
and <90
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Table 2
Hypertensive emergencies, according to acute target organ damage.
Organ Type of acute damage
Brain Transient ischaemic attack, ischaemic stroke, haemorrhagic stroke, hypertensive encephalopathy
Heart Acute pulmonary oedema, acute heart failure, acute coronary syndrome
Blood vessels Acute dissecting aneurysm of the aorta, microangiopathic haemolytic anaemia
Kidney Acute renal failure
Retina Haemorrhages and cotton-wool spot, papilledema
Uterus Preeclampsia, eclampsia, HELLP syndrome
HELLP: haemolysis, elevated liver enzymes, low platelets.
Table 3
Causes of secondary arterial hypertension that can trigger hypertensive crises.
Causes
Medication and addictive/recreational drugs
Renal
Endocrine
Neurological
Others
Treatment
Hypertensive urgencies
It should be noted that many of the patients who come to the
emergency department with high BP levels are asymptomatic and
do not require aggressive measures, since the sudden decrease in
BP could generate ischaemia in organs such as heart and brain,
used to high blood pressure levels, a phenomenon known as self-
regulation.5,9 Retrospective studies of patients diagnosed with HU
did not find differences in mortality at 6 months, in A&E revisits
or in cardiovascular episodes between the group treated with oral
medication in A&E and those who were discharged without acute
treatment.21,22
The treatment of HU has not been studied in depth according to
the literature, and there is no consensus nor a strict protocol to fol-
low. In the “ideal scenario”, patients who present with HU should be
kept at rest, preferably in the supine position, for 30–45 min before
administering any drugs. Unfortunately, the emergency depart-
ments in our routine clinical practice are overburdened and in
this environment the above recommendation is difficult to apply;
however, different studies show reductions in SBP ≥ 20 mmHg and
DBP ≥ 10 mmHg in up to 32% of patients with this measure.23,24
The decision to use medications varies greatly depending on the
circumstances; if it is a first episode of HBP, we can use any drug
following the recommendations of the current guidelines, if on the
contrary the patient is known to have HBP, we encourage adherence
to treatment, optimizing the dose or adding a new drug.
In the choice of treatment, short-acting antihypertensive drugs
are recommended, preferably oral versus sublingual, due to hav-
ing a slower action.9 In addition, it must be individualized and
will depend on the characteristics of each patient (concomitant
diseases, age, usual treatment, among others). The pharmacolog-
ical possibilities include loop diuretics, beta-blockers and calcium
antagonists (Table 4).
As a general rule, BP in HU should be reduced by 20–25%
in the first hours or days, considering SBP ≤ 160 mmHg and/or
DBP ≤ 100 mmHg safe levels to continue outpatient management.
3
Symptoms and key history elements
Rebound hypertension after withdrawal of hypotensive agents,
oral contraceptives, nasal vasoconstrictor nebulizers, cocaine,
amphetamines, anabolic steroids, glucocorticoids and
mineralocorticoids
History of kidney disease, urinary tract infection, haematuria,
analgesic abuse (renal parenchymal disease)
Pheochromocytoma, Cushing’s syndrome, primary
hyperaldosteronism, carcinoid syndrome, renin-secreting tumour,
hyperthyroidism
Intracranial hypertension, haemorrhagic or ischaemic stroke, head
injury, sleep apnoea, acute porphyria, familial dysautonomia, lead
poisoning, Guillain–Barre syndrome
Acute stress (including surgery), psychogenic hyperventilation,
burns, alcohol withdrawal, preoperative
It is important to monitor the patient during the following 48–76 h
for progression and to obtain optimal BP levels.
The superiority of one drug over another has not been demon-
strated. In some patients, especially in pseudo HC, anxiolytics can
be used such as benzodiazepines, and also in special situations, such
as hyperadrenergic crises, which benefit from the combination of
antihypertensive agents with benzodiazepines.
The present and the future of cardiovascular health are focused
on primary and secondary prevention. With this premise, profes-
sionals from both medicine and nursing must, from primary care,
encourage the patient to adopt a healthy lifestyle along with self-
care measures; this improves the rapid detection of any indicative
symptom of HU or HE, and better still, it prevents the poor control
of this disorder where a good lifestyle plays an essential role in the
treatment.
Hypertensive emergencies
In HE, the reduction of BP should be done earlier, and intra-
venous drugs are usually the first-line therapy. The drug choice
will depend on each case, but generally fast-acting, short half-life
and easy to use drugs are preferred (Table 5). The patient’s vital
signs and clinical progression must be continuously monitored. The
recommendation, as a general rule, is a BP reduction of 20–25%
from the first minutes to the first 2 h, in order to try to avoid tissue
ischaemia with sharper reductions. The choice of drugs should be
individualized, taking into account the type of acute target organ
damage (Table 6).
Dissecting aneurysm of the aorta
Dissecting aneurysm of the aorta is a serious disorder that
requires immediate control of BP and heart rate. The most com-
mon clinical characteristics depend on the thoracic or abdominal
involvement of the aorta, and should be suspected in the case of
transfixing, chest pain irradiated to the back or non-specific low
back pain with high BP. The therapeutic objective is to achieve lev-
els of SBP < 120 mmHg and/or DBP < 80 mmHg, in the first 10 min
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Table 4
Main drugs used in the treatment of hypertensive emergencies administered orally and their properties.

Drug Dose Maximum action time Duration Adverse reaction

Calcium channel blockers

Amlodipine 5–10 mg 6–12 h 35–50 h Headache, oedema, digestive intolerance,
Lacidipine 2–4 mg 0.5–3 h 13–19 h palpitations

Beta-blockers
Labetalol 100–200 mg 0.5–4 h 8–14 h Headache, nausea, hypotension,
Bisoprolol 2.5–5 mg 2–4 h 9–12 h bradycardia, diarrhoea
Carvedilol 12.5–200 mg 1–2 h 16–20 h

Angiotensin-converting enzyme inhibitors

Captopril 25–50 mg 0.5–1 h 3–6 h Hypotension, angioedema, hyperkalaemia,
Enalapril 10–20 mg 2–4 h 12–16 h cough

Loop diuretics
Furosemide 20–40 mg 0.5–1 h 2–4 h Polyuria,
Torasemide 5–10 mg 0.5–1 h 6h hyperuricemia

Table 5
Main drugs administered intravenously and their properties, used in the treatment of hypertensive emergencies.

Drug Dose Action onset Duration Adverse reaction

Calcium receptor antagonists

Nicardipine 5–8 mg/h 5–15 min 1.5–4 h Tachycardia, headache, dizziness, flushing,
Clevedipine 1–2 mg/h 2–4 min 5–10 min nausea

Beta-blockers
Esmolol Bolus 250–500 ␮g/kg, 1–2 min 10–30 min
Nausea, paraesthesia, bronchospasm,
followed by
dizziness, atrioventricular block
150 ␮g/kg/min
Labetalol Bolus 20 mg every 5–10 min 3–6 h
15 min (max 80 mg), or
2 mg/min in infusion
Metoprolol Bolus 5 mg, followed by 20 min 5–8 h
5–15 mg every 3–6 h
Angiotensin-converting enzyme inhibitor
Enalaprilat 1.25–5 mg every 6 h 15–60 min 4–6 h Headache, dizziness

Arterial and venous vasodilators

Nitro-glycerine 5–100 ␮g/min 2–5 min 5–15 min Headache, tachycardia
Nitropionate 0.25–10 ␮g/kg/min 1–2 min 5–10 min Increase in ICP, thiocyanate and cyanide toxicity in renal failure
sodium
Hydralazine Bolus 5–20 mg every 10–20 min 4–6 h Headache, tachycardia, hypotension
20 min
Other mechanisms of action
Fenoldopam 005–1.6 ␮g/kg/min 5–10 min 30–60 min
Tachycardia, headache, flushing
Phentolamine 5–15 mg every 1–2 min 10–30 min
5–15 min
Urapidil Bolus of 10–25 mg, 3–5 min 4–6 h Headache, tachycardia
followed by 5–40 mg/h
in infusion

ICP: intracranial pressure.

and heart rate below 60 beats/min. An arterial vasodilator plus
a beta-blocker drug, such as sodium nitroprusside plus labetalol
or esmolol, are recommended as first-line drugs.25 As an alterna-
tive, clevedipine and/or nicardipine could be used, which have also
shown great efficacy in the control of BP in dissecting aneurysm of
the aorta.26
indicated is to maintain BP ≤ 180/110 mmHg and thus avoid haem-
orrhagic fibrinolytic treatment complications.27
The recommended drug is labetalol. In cases of difficult BP con-
trol and at risk of cerebral oedema, sodium nitroprusside could be
used, especially if the DBP is >140 mmHg.

Ischaemic stroke
In this frequent disorder it is necessary to take into account
the time of establishment and if the patient is a candidate for
fibrinolytic treatment. In the acute phase (<4, 5–6 h) antihy-
pertensive medication should not be administered, as it could
worsen brain perfusion and perfusion of the tissue surrounding
the ischaemic lesion (penumbra area). The American Heart Asso-
ciation guidelines recommend treatment if the SBP ≥ 220 and/or
the DBP ≥ 120 mmHg, and the aim is to reduce BP by 15% in the
first 24 h. In the case of fibrinolysis-candidate patients (stroke
code meeting specific clinical-radiological criteria), the treatment
Haemorrhagic stroke
The management of HBP in this disorder represents a challenge,
since on the one hand it can reduce cerebral perfusion and worsen
the initial clinical symptoms, but on the other hand it reduces
serious complications, such as future haemorrhages. Therefore,
each case must be individualized, acting according to a risk-benefit
assessment. There are different studies in which BP was compared
to SBP levels ≤140 mmHg versus SBP levels ≤180 mmHg during the
first hour, and as a conclusion there were no differences in general
prognosis and mortality, but there was an improvement in the short
and long term functional prognosis with the most significant reduc-
tions (SBP ≤ 140 mmHg).28,29 As drugs, beta-blockers are used as
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Table 6
Main hypertensive emergencies and their therapeutic approach.

Type of hypertensive Blood pressure target Drugs

emergency (mmHg)

Acute dissecting aneurysm • BP ≤ 120/80 Labetalol, sodium

of the aorta • HR ≤ 60 beats/min nitroprusside, nicardipine,
clevedipine
Ischaemic stroke • Fibrinolysis: ≤180/110 Labetalol, esmolol,
• No fibrinolysis: reduce if nicardipine, urapidil
BP ≥ 220/120
Haemorrhagic stroke • BP ≤ 180/105 Labetalol, esmolol,
nicardipine
Hypertensive • Reduce BP 10–15% in 2 h Labetalol, esmolol,
encephalopathy up to 25% in 24 h nicardipine
Acute heart failure and/or • Reduce BP 10–15%, Nitro-glycerine,
acute pulmonary oedema continue according to nitroprusside, furosemide
clinical response
Acute coronary syndrome • Reduce 20% in 2 h, Nitro-glycerine, sodium
continue according to nitroprusside,
response beta-blockers, nicardipine
Acute renal failure • Reduce BP 10–20% in 24 h Sodium Nitroprusside,
Nicardipine, Fenoldopam
Eclampsia • Reduce BP 20% in 2–6 h Labetalol, hydralazine
Excess catecholamines, • Reduce BP 20% by 2–3 h Phentolamine, nicardipine,
cocaine, amphetamines • In pheochromocytoma sodium nitroprusside,
reduce to resolution of labetalol (do not use
symptoms beta-blockers in
monotherapy)

CVA: cerebrovascular accident, stroke; HR: heart rate; BP: blood pressure.

first-line or arterial vasodilators as an alternative, such as labetalol
or sodium nitroprusside, respectively. It is essential to monitor the
signs of cerebral hypoperfusion, secondary to the decrease in BP.
It is preferable to avoid drugs such as nitro-glycerine, except if
the BP is not controlled with other drugs or in those that present
other concomitant processes, such as acute coronary syndrome or
dissecting aneurysm of the aorta, since these produce increased
blood volume, cerebral oedema and, therefore, increased intracra-
nial pressure.30,31
calcium antagonists should be avoided during the acute phase, as
they would be counterproductive in reducing cardiac contractility
and, consequently, worsen the condition. However, once stabilized,
the initiation of beta-blockers before hospital discharge has shown
improvements in the survival of patients with heart failure.36
Acute coronary syndrome

Hypertensive encephalopathy
It is a disorder characterized by the rapid onset of nonspe-
cific neurological symptoms, such as altered state of consciousness,
headache, dizziness, confusion, nausea and vomiting, but without
a clear neurological focus, all secondary to a sudden and sustained
rise in BP. There may be involvement of the retina. These symp-
toms improve when BP is reduced. The reduction must be between
10 and 15% within the first 2 h of treatment, without exceeding
25% during the first 24 h.32 The most commonly used drugs are
labetalol, sodium nitroprusside and nicardipine; for some authors,
nicardipine is the first-line drug because of its potency and its easy
titration.33
Acute heart failure and/or acute pulmonary oedema
Acute coronary syndrome requires strict and immediate con-
trol of BP and heart rate, as this improves coronary perfusion. The
purpose is to reduce cardiac workload and, consequently, its oxy-
gen consumption. We must also bear in mind that the elevation
of BP can be multifactorial, including factors such as anxiety and
pain. The most commonly used drugs are nitro-glycerine in com-
bination with beta-blockers; nicardipine or clevedipine can be also
used. It is recommended to reduce BP by 20% during the first 2 h, to
subsequently reach levels below 160/100 mmHg in the next 4–6 h.
The associated therapeutic measures -like opiates, because of their
anxiolytic and analgesic effects- play an essential role. More specific
interventions will depend on the type of acute coronary syndrome;
these are not the objective of this review, and should be consulted
in the corresponding European guidelines.37,38

This disorder is a “modern epidemic”, with high rates of mor-

bidity and mortality, despite therapeutic advances. The first-choice
treatment in the acute phase are venous and arterial vasodila-
tors, such as nitro-glycerine and/or sodium nitroprusside. It should
be noted that few therapeutic measures have shown a prognostic
impact in acute heart failure; however, a Spanish study showed an
increase in short-term survival with the use of vasodilators in acute
pulmonary oedema secondary to hypertension.34 Other drugs to be
associated are loop diuretics in order to rapidly reduce BP, myocar-
dial oxygen consumption and preload. Acute pulmonary oedema
is within this scenario, which can be triggered by left ventricu-
lar dysfunction secondary to HE. A reduction of 10 to 15% of the
average BP improves the patient’s symptoms35 . Beta-blockers or
Acute renal failure
Severe HBP can occasionally cause kidney damage (hyperten-
sive nephrosclerosis or malignant nephrosclerosis), or this may be
a consequence of an underlying process such as acute glomeru-
lonephritis, vasculitis, or renal artery stenosis. This process is
characterized by the presence of haematuria in 75% of cases, in
addition to altered glomerular filtration and elevation of creati-
nine levels. Sometimes it is difficult to differentiate whether kidney
damage is due to chronic HBP or an acute process. The most com-
monly used drugs are labetalol or nicardipine. A BP reduction
between 10 and 20% should be the goal in the first 24 h.
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High blood pressure in pregnancy
Preeclampsia and eclampsia are serious situations of pregnancy
with elevation of SBP ≥ 160 and/or the DBP ≥ 110 mmHg, and usu-
ally they are associated with proteinuria, occurring from week 32
of pregnancy (some women develop it since week 20). The treat-
ment is aimed at reducing BP and maintaining adequate placental
perfusion pressure. The definitive treatment would be delivery or
caesarean section. The intravenous drugs used are labetalol and
hydralazine.14,15
Conclusions
Acute elevation of blood pressure is a frequent reason for med-
ical consultation in the emergency departments. It is important
to perform a comprehensive assessment of the patient and early
recognition of the scenarios that require immediate attention, that
is, hypertensive emergencies. In some cases of hypertensive emer-
gencies, treatment could be performed on an outpatient basis. In
all patients who come with high blood pressure levels, monitor-
ing and follow-up by their doctor should be optimized to prevent
future cardiovascular complications.
Conflict of interests
The authors declare no conflict of interest.
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