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Med Clin (Barc). 2017;xxx(xx):xxx–xxx


Diagnostic and therapeutic approach to the hypertensive crisis夽

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

gency departments.1,2
High blood pressure (HBP) is a health problem with a high In Spain, HBP is a highly prevalent disease. Studies such as
prevalence around the world. It is considered one of the main car- ENRICA and DI@BETES estimate prevalence between 33 and 43%,
diovascular risk factors, being one of the most frequent reasons for 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,
夽 Please cite this article as: Arbe G, Pastor I, Franco J. Aproximación
despite being a preventable and treatable disease.5
diagnóstica y terapéutica de las crisis hipertensivas. Med Clin (Barc). 2018.
With respect to hypertensive crises (HC), they are divided into
∗ Corresponding author. hypertensive emergencies (HE) and hypertensive urgencies (HU),
E-mail address: (J. Franco). 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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2 G. Arbe et al. / Med Clin (Barc). 2017;xxx(xx):xxx–xxx

absent, respectively. The structural and/or physiological alterations organs: preeclampsia, HELLP syndrome (haemolysis, elevated liver
in the target organs can be in heart, brain, kidney, retina and arter- enzymes, thrombocytopenia) and eclampsia.14,15
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%), Diagnosis
highlighting that up to 23% of these patients had no prior history
of HBP or was unknown to them.8 The initial assessment of the patient who comes for HC in many
The objective of this review is to update the clinical and thera- hospitals is performed by nursing staff, either in the triage of an
peutic aspects of HC. In routine clinical practice, hospital emergency emergency service, in a hospital ward or in a primary care clinic,
departments have an increasing demand for care. Health pro- reason why we must work with the medical team in a multidisci-
fessionals need to be able to perform a correct identification, plinary way in terms of learning symptoms and warning signs for
history-taking, physical examination and treatment of HC in a set- early identification, so as to avoid direct target organ damage.
ting where this condition frequently occurs. This would improve History-taking aimed at the possible cause is essential, even in
the global care of this disorder and probably optimize the dynamics, patients who present with levels below the definition of HC, bear-
avoiding long and unnecessary stays in the emergency department. ing in mind that the acute damage to target organs depends on how
quickly the crisis is established and the percentage of BP elevation
Definitions with respect to the baseline, whereby HE could occur with lower BP
values than those proposed by the guidelines. The patient should be
HBP is defined as the chronic elevation of systolic blood asked about episodes of HBP in the past, concomitant or triggering
pressure (SBP) levels ≥140 mmHg and diastolic blood pressure medication, such as non-steroidal anti-inflammatory drugs, recre-
(DBP) ≥ 90 mmHg, and it is classified in different degrees according ational drugs, history of sleep apnoea and the presence of some
to the levels shown at diagnosis (Table 1). other cardiovascular risk factor; likewise, symptoms or signs that
On the other hand, HC is defined as an acute increase in could make us suspect secondary HBP16 (Table 3).
SBP ≥ 180 mmHg and of the DBP ≥ 120 mmHg, capable of causing Symptoms of HC vary widely, from asymptomatic patients or
acute damage to target organs, levels proposed by the committee with nonspecific symptoms such as headache, dizziness, vomiting
for the prevention, detection, assessment and treatment of HBP and palpitations, to acute target organ involvement17 .
(JNC) VII)9 and the guidelines of the European hypertension and Physical examination should be detailed, giving priority to car-
cardiology societies of 2013, still valid today.6 diac, supra-aortic and abdominal trunks auscultation in search
Historically CHs have been divided into 2 groups: HE and HU, of murmurs that suggest arterial damage and/or aneurysms.
and each of them has a different treatment and prognosis. Thus, Likewise, peripheral pulses, neurological deficit or hypertensive
blood pressure (BP) in HU can be controlled in hours or days with encephalopathy (nausea, vomiting, altered state of consciousness)
drugs administered orally and outpatiently.10 On the contrary, HE should be evaluated. Emphasis should be placed on the fundus of
(Table 2) requires strict control in minutes to hours, usually with the eye, perhaps something that has been forgotten, even though is
drugs administered intravenously. one of the most useful examinations in this scenario, since it helps
Within the HC classification we also find the false HC or pseudo to rule out hypertensive retinopathy18 ; in addition, it is impor-
HC, which are defined as transient BP elevations due to exter- tant to assess the rest of vital signs, such as oxygen saturation and
nal stimuli (pain, urinary retention, anxiety, stress, among others), heart rate. Recent studies have shown that HE usually presents with
without evidence of acute damage to target organs. Patients with higher heart rates than HU, with tachycardia being a clinical sign
isolated clinical HBP or “white coat HBP”, and errors in the BP mea- associated with acute left ventricular failure in the context of HE,
surement technique are also classified in this group. Prevalence more specifically a heart rate higher than 100 beats/min.19
studies observe a high percentage of pseudo HC, reaching 24–43% The complementary tests will be aimed at looking for acute
in hospital settings, and up to 91% in outpatient settings.11,12 The damage in target organs and should be individualized according to
symptoms of the trigger usually prevail in their clinical presenta- the patient: electrocardiogram, chest X-ray, pro-natriuretic brain
tion, and their BP levels are generally lower than those observed in peptide, to rule out signs of heart failure and/or acute pulmonary
a true HC. The pseudo HC treatment is based on rest in the supine oedema, urinalysis (haematuria and proteinuria), cardiac enzymes
position and treatment of the precipitating cause, an outpatient in case of suspected acute coronary syndrome, brain computed
follow-up is recommended to confirm or rule out HBP13 . tomography (CT) in case of neurological deficit, thoracic CT angiog-
Within the HC we must take into account a special subgroup raphy and/or Doppler echocardiography if there is suspicion of
such as HE in pregnancy, which are defined as the acute elevation dissecting aneurysm of the aorta. In HE, the most affected organs
of SBP ≥ 160 mmHg and/or DBP ≥ 110 mmHg for a period longer are usually the brain (stroke), acute pulmonary oedema and hyper-
than 15 min and also capable of causing acute damage to target tensive encephalopathy.20

Table 1
Classification of arterial hypertension, according to the European Societies of Hypertension and Cardiology.

Category Systolic (mmHg) Diastolic (mmHg)

Blood pressure level

Optimal <120 and <80
Normal 120–129 and/or 80–84
Normal high 130–139 and/or 85–89

Arterial hypertension
Grade 1 140–159 and/or 90–99
Grade 2 160–179 and/or 100–109
Grade 3 ≥180 and/or ≥110
Isolated systolic ≥140 and <90

mmHg: millimetres of mercury.

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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 Symptoms and key history elements

Medication and addictive/recreational drugs Rebound hypertension after withdrawal of hypotensive agents,
oral contraceptives, nasal vasoconstrictor nebulizers, cocaine,
amphetamines, anabolic steroids, glucocorticoids and
Renal History of kidney disease, urinary tract infection, haematuria,
analgesic abuse (renal parenchymal disease)
Endocrine Pheochromocytoma, Cushing’s syndrome, primary
hyperaldosteronism, carcinoid syndrome, renin-secreting tumour,
Neurological Intracranial hypertension, haemorrhagic or ischaemic stroke, head
injury, sleep apnoea, acute porphyria, familial dysautonomia, lead
poisoning, Guillain–Barre syndrome
Others Acute stress (including surgery), psychogenic hyperventilation,
burns, alcohol withdrawal, preoperative

Treatment It is important to monitor the patient during the following 48–76 h

for progression and to obtain optimal BP levels.
Hypertensive urgencies The superiority of one drug over another has not been demon-
strated. In some patients, especially in pseudo HC, anxiolytics can
It should be noted that many of the patients who come to the be used such as benzodiazepines, and also in special situations, such
emergency department with high BP levels are asymptomatic and as hyperadrenergic crises, which benefit from the combination of
do not require aggressive measures, since the sudden decrease in antihypertensive agents with benzodiazepines.
BP could generate ischaemia in organs such as heart and brain, The present and the future of cardiovascular health are focused
used to high blood pressure levels, a phenomenon known as self- on primary and secondary prevention. With this premise, profes-
regulation.5,9 Retrospective studies of patients diagnosed with HU sionals from both medicine and nursing must, from primary care,
did not find differences in mortality at 6 months, in A&E revisits encourage the patient to adopt a healthy lifestyle along with self-
or in cardiovascular episodes between the group treated with oral care measures; this improves the rapid detection of any indicative
medication in A&E and those who were discharged without acute symptom of HU or HE, and better still, it prevents the poor control
treatment.21,22 of this disorder where a good lifestyle plays an essential role in the
The treatment of HU has not been studied in depth according to treatment.
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 Hypertensive emergencies
kept at rest, preferably in the supine position, for 30–45 min before
administering any drugs. Unfortunately, the emergency depart- In HE, the reduction of BP should be done earlier, and intra-
ments in our routine clinical practice are overburdened and in venous drugs are usually the first-line therapy. The drug choice
this environment the above recommendation is difficult to apply; will depend on each case, but generally fast-acting, short half-life
however, different studies show reductions in SBP ≥ 20 mmHg and and easy to use drugs are preferred (Table 5). The patient’s vital
DBP ≥ 10 mmHg in up to 32% of patients with this measure.23,24 signs and clinical progression must be continuously monitored. The
The decision to use medications varies greatly depending on the recommendation, as a general rule, is a BP reduction of 20–25%
circumstances; if it is a first episode of HBP, we can use any drug from the first minutes to the first 2 h, in order to try to avoid tissue
following the recommendations of the current guidelines, if on the ischaemia with sharper reductions. The choice of drugs should be
contrary the patient is known to have HBP, we encourage adherence individualized, taking into account the type of acute target organ
to treatment, optimizing the dose or adding a new drug. damage (Table 6).
In the choice of treatment, short-acting antihypertensive drugs
are recommended, preferably oral versus sublingual, due to hav-
Dissecting aneurysm of the aorta
ing a slower action.9 In addition, it must be individualized and
will depend on the characteristics of each patient (concomitant
Dissecting aneurysm of the aorta is a serious disorder that
diseases, age, usual treatment, among others). The pharmacolog-
requires immediate control of BP and heart rate. The most com-
ical possibilities include loop diuretics, beta-blockers and calcium
mon clinical characteristics depend on the thoracic or abdominal
antagonists (Table 4).
involvement of the aorta, and should be suspected in the case of
As a general rule, BP in HU should be reduced by 20–25%
transfixing, chest pain irradiated to the back or non-specific low
in the first hours or days, considering SBP ≤ 160 mmHg and/or
back pain with high BP. The therapeutic objective is to achieve lev-
DBP ≤ 100 mmHg safe levels to continue outpatient management.
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

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

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

Haemorrhagic stroke
Ischaemic stroke
The management of HBP in this disorder represents a challenge,
In this frequent disorder it is necessary to take into account since on the one hand it can reduce cerebral perfusion and worsen
the time of establishment and if the patient is a candidate for the initial clinical symptoms, but on the other hand it reduces
fibrinolytic treatment. In the acute phase (<4, 5–6 h) antihy- serious complications, such as future haemorrhages. Therefore,
pertensive medication should not be administered, as it could each case must be individualized, acting according to a risk-benefit
worsen brain perfusion and perfusion of the tissue surrounding assessment. There are different studies in which BP was compared
the ischaemic lesion (penumbra area). The American Heart Asso- to SBP levels ≤140 mmHg versus SBP levels ≤180 mmHg during the
ciation guidelines recommend treatment if the SBP ≥ 220 and/or first hour, and as a conclusion there were no differences in general
the DBP ≥ 120 mmHg, and the aim is to reduce BP by 15% in the prognosis and mortality, but there was an improvement in the short
first 24 h. In the case of fibrinolysis-candidate patients (stroke and long term functional prognosis with the most significant reduc-
code meeting specific clinical-radiological criteria), the treatment 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,
Ischaemic stroke • Fibrinolysis: ≤180/110 Labetalol, esmolol,
• No fibrinolysis: reduce if nicardipine, urapidil
BP ≥ 220/120
Haemorrhagic stroke • BP ≤ 180/105 Labetalol, esmolol,
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

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

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

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

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

bidity and mortality, despite therapeutic advances. The first-choice Acute renal failure
treatment in the acute phase are venous and arterial vasodila-
tors, such as nitro-glycerine and/or sodium nitroprusside. It should Severe HBP can occasionally cause kidney damage (hyperten-
be noted that few therapeutic measures have shown a prognostic sive nephrosclerosis or malignant nephrosclerosis), or this may be
impact in acute heart failure; however, a Spanish study showed an a consequence of an underlying process such as acute glomeru-
increase in short-term survival with the use of vasodilators in acute lonephritis, vasculitis, or renal artery stenosis. This process is
pulmonary oedema secondary to hypertension.34 Other drugs to be characterized by the presence of haematuria in 75% of cases, in
associated are loop diuretics in order to rapidly reduce BP, myocar- addition to altered glomerular filtration and elevation of creati-
dial oxygen consumption and preload. Acute pulmonary oedema nine levels. Sometimes it is difficult to differentiate whether kidney
is within this scenario, which can be triggered by left ventricu- damage is due to chronic HBP or an acute process. The most com-
lar dysfunction secondary to HE. A reduction of 10 to 15% of the monly used drugs are labetalol or nicardipine. A BP reduction
average BP improves the patient’s symptoms35 . Beta-blockers or between 10 and 20% should be the goal in the first 24 h.
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