Curr Hypertens Rep (2015) 17:5

DOI 10.1007/s11906-014-0515-z

HYPERTENSIVE EMERGENCIES (BM BAUMANN, SECTION EDITOR)

Cardiovascular Hypertensive Emergencies

D. P. Papadopoulos & E. A. Sanidas & N. A. Viniou & V. Gennimata &
V. Chantziara & I. Barbetseas & T. K. Makris

# Springer Science+Business Media New York 2015

Abstract Inevitably, a small proportion of patients with

systematic hypertension will develop hypertensive crisis
at some point. Hypertensive crises can be divided into
hypertensive emergency or hypertensive urgency according
to the presence or lack of acute target organ damage. In
this review, we discuss cardiovascular hypertensive emergencies, including acute coronary syndrome, aortic dissection,
congestive heart failure, and sympathomimetic hypertensive
crises, including those caused by cocaine use. Each presents in
a unique fashion, although some hypertensive emergency
patients report nonspecific symptoms. Treatment includes
several effective and rapid-acting medications to safely reduce
the blood pressure, protect remaining end-organ function,
relieve symptoms, minimize the risk of complications, and
thereby improve patient outcomes.
Keywords Hypertensive emergencies . Myocardial
infarction . Acute coronary syndrome . Congestive heart
failure . Aortic dissection . Sympathomimetic activity

Introduction
Recent data suggest that systematic hypertension is the responsible cause for nearly 7.1 million deaths per year
This article is part of the Topical Collection on Hypertensive Emergencies
D. P. Papadopoulos (*) : E. A. Sanidas : N. A. Viniou :
V. Gennimata : V. Chantziara : I. Barbetseas
ESH Excellent Center of Hypertension, Department of Cardiology,
Laiko General Hospital, Athens, Greece
e-mail: jimpapdoc@yahoo.com
T. K. Makris
ESH Excellent Center of Hypertension, Elena Venizelou Maternity
Hospital, Athens, Greece

worldwide. Approximately 12 % of patients with hypertension will develop a hypertensive crisis which can be further
categorized as either hypertensive emergency or urgency depending on either the presence or absence of acute end-organ
dysfunction, respectively. Hypertensive crises can develop in
patients with or without preexisting chronic hypertension
[13] and the prevalence mirrors the distribution of essential
hypertension in the general population, with men, AfricanAmericans, and the elderly being most commonly affected
[4].
The most common cardiac emergencies associated with
severely elevated blood pressure are acute left ventricular
(LV) dysfunction with pulmonary edema (22 %), acute coronary syndromes (including acute myocardial infarctionMI)
(18 %), and aortic dissection (8 %). In the context of sympathomimetic drug abuse that can cause or mimic the above
clinical conditions, cocaine accounts for almost one third of
all visits to emergency departments [5]. Classical cardiac and
pulmonary symptoms (dyspnea, chest pain, arrhythmias, and
syncope) seem to be less common in patients presenting with
hypertensive crises (28.3 %). The majority present with nonspecific symptoms [6].
The risk of a future cardiovascular event attributable
to hypertension is greater in individuals with established
cardiovascular disease, diabetes mellitus, or chronic kidney disease compared to those without these comorbid
conditions. This increased risk led the 2003 Seventh
Joint National Committee (JNC 7) report on high blood
pressure to list heart disease, heart failure, diabetes,
chronic kidney disease, and cerebrovascular disease as
compelling indications for the treatment of hypertension. Other risk factors include peripheral artery disease
and traditional coronary risk factors such as cigarette smoking
and family history of cardiac disease [7].
Mortality rates of patients with hypertensive emergencies
has decreased significantly over the years (from 80 % in 1928

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to 10 % in 1989) [8], mainly due to the availability of antihypertensive medications. The therapeutic goal is to protect
remaining end-organ function, reduce the risk of complications, and thereby improve patient outcomes [9, 10].
The aim of this review is to summarize the current evaluation and treatment recommendations for the most common
cardiovascular clinical presentations encountered in patients
with hypertensive crisis.

Myocardial Infarction
Epidemiology Published results indicate acute MI as the
leading cause of death and hospital admission in patients with severely elevated blood pressure. Moreover,
nearly 50 % of all patients originally admitted with a
hypertensive emergency died as a result of an acute MI
during long-term follow-up. Of note, no differences
were found in regard to the presence of other cardiovascular risk factors like smoking or prevalence of
diabetes mellitus [11, 12].
Pathophysiology Hypertension is linked to MI as a risk
factor, an atherogenic factor, and a hemodynamic factor
with profound effects on morbidity and mortality. During
a hypertensive emergency, the increase in blood pressure
generates mechanical stress and endothelial injury leading
to increased permeability, activation of the coagulation
cascade and platelets, and deposition of fibrin. This process results in ischemia and release of additional vasoactive mediators generating a vicious cycle of ongoing injury. The renin-angiotensin system is often activated leading
to further vasoconstriction and production of proinflammatory cytokines such as IL-6. Furthermore, NADPH oxidase
activity is increased and generates reactive oxygen species.
These collective mechanisms can culminate in end-organ
hypoperfusion, ischemia, and dysfunction manifested as a
hypertensive emergency [13].
Clinical Presentation and Evaluation Hypertensive crisis
may lead to ischemia and MI causing angina-like chest pain.
Evaluation of cardiovascular risk factors and other comorbidities is essential. An electrocardiogram (ECG) is the gold
standard exam to reveal myocardial ischemia or infarction.
Also, vital signs should be checked carefully during the physical examination of a patient with hypertensive crisis, namely,
blood pressure, oxygen saturation, and heart rate.
Baseline laboratory analyses should be performed rapidly
after the initial evaluation of the patient. These laboratory
analyses include cardiac enzymes and a cardiac troponin-I.
In a retrospective study, patients with hypertensive crises and
elevated cardiac c-troponin-I (cTnI) had 2.7 times higher risk
for the occurrence of major adverse cardiovascular and

Curr Hypertens Rep (2015) 17:5

cerebrovascular events (MACCE) at 2 years follow-up compared to those with normal cTnI values. In patients with
hypertensive crisis, elevated cTnI confers a significantly
greater risk of long-term MACCE and is a strong predictor
of obstructive coronary artery disease [14].
Management Severe hypertension associated with an acute
MI is appropriately treated with intravenous nitroglycerin,
clevidipine, nicardipine, labetalol, or esmolol to reduce the
underlying coronary ischemia and/or increased myocardial
oxygen consumption and to improve prognosis. In addition,
reducing blood pressure improves hemodynamics, ameliorates the risk of pulmonary edema, and decreases the size of
the infarct area. If available, especially in ST-elevation MI,
primary angioplasty is the best option for reperfusion therapy
in patients with high blood pressure since thrombolysis might
increase the risk of cerebral bleeding [1518].
Nitroglycerin is a venodilator that mainly reduces the preload and decreases the cardiac oxygen demands. This agent is
primarily used in acute MI and acute pulmonary edema along
with other antihypertensive regimens [1517].
Labetalol is an alpha1 adrenergic receptor blocker and
nonselective beta-blocker. It reduces the systemic vascular
resistance, but it maintains the cerebral, renal, and coronary
blood flow. Of note, despite the beta-blocking effect, cardiac
output is maintained [1].
Esmolol is an intravenous beta1 cardioselective receptor
blocker with rapid onset and very short duration of action that
can be safely used in most patients treated for acute MI with
relative contraindications to beta-blockers. Tolerance to higher
maintenance doses of esmolol is a good predictor of subsequent outcome with oral beta-blocker therapy [19].
Other agents that can be used in hypertensive emergencies
include nicardipine (dihydropyridine calcium channel
blocker), which is a useful agent for patients with coronary
artery disease due to its beneficial effect on coronary blood
flow or clevidipine, which is a relatively new short-acting,
intravenous dihydropyridine calcium channel blocker with
non-weight-based dosing regimen, allowing prolonged infusion and successful transition to oral therapy [2022].
The optimal blood pressure after an acute coronary syndrome remains controversial. Numerous large studies have
shown an inverse relationship between diastolic pressure and
adverse cardiac ischemic events (i.e., the lower the diastolic
pressure, the greater the risk of coronary heart disease and
adverse outcomes). This effect is defined as the J-curve phenomenon which describes the shape of the relationship between blood pressure and the risk of cardiovascular morbidity
and/or mortality. The aforementioned observation appears to
be even more pronounced in patients with underlying coronary artery disease. Since coronary blood flow mainly occurs
during diastolic phase in patients with coronary heart disease,
a fall in diastolic pressure might lower perfusion pressure

Curr Hypertens Rep (2015) 17:5

distal to a stenosis below the critical level at which autoregulation is effective. Hence, reducing systolic blood pressure to
values close or below 120125 mmHg and diastolic pressure
below 7075 mmHg in patients at high cardiovascular risk
might be accompanied by an increase in the incidence of
coronary events [2325].

Congestive Heart Failure

Epidemiology The most common clinical manifestations of
hypertensive crises include pulmonary edema (22.5 %) and
congestive heart failure (12 %) [26].
Pathophysiology Acute congestive heart failure is most commonly related to systolic or diastolic dysfunction, with or
without additional cardiac pathology, such as coronary artery
disease or valve abnormalities. Nonetheless, a variety of conditions or events can cause cardiogenic pulmonary edema in
the absence of heart disease including severe hypertension.
Patients presenting with cardiogenic pulmonary edema frequently suffer from uncontrolled severe hypertension. Many
of these patients have a preserved (normal or near normal) LV
ejection fraction. Increased afterload, instead of or in addition
to fluid overload, may precipitate decompensation in these
patients [27].
Clinical Presentation and Evaluation Cardiac decompensation may lead to symptoms like dyspnea, orthopnea, cough,
fatigue, or pulmonary edema. In a recent study of 189 patients,
normal heart rate was associated with hypertensive urgency,
whereas tachycardia denoted a hypertensive complication in
the setting of LV failure [28]. Imaging may include radiography or echocardiography. A plain chest radiograph is extremely helpful for documentation of cardiomegaly or pulmonary
edema. Although newer echocardiography techniques are not
extensively used in daily clinical practice, speckle tracking
echocardiography may detect depression of global longitudinal LV systolic strain and global systolic strain rate during
hypertensive crisis and improvement after medical therapy
[29].
Management It has been reported that most patients with
elevated blood pressure, particularly the elderly, experience
acute pulmonary edema with normal LV systolic function,
presumably due to diastolic dysfunction. However, it has also
been reported that uncontrolled hypertension may be responsible for the development of LV systolic dysfunction and heart
failure with consequent functional mitral regurgitation and
subendocardial myocardial ischemia [30]. For patients with
heart failure due to systolic dysfunction, the goal of therapy
is the lowest blood pressure not associated with symptoms of

Page 3 of 6 5

hypotension or evidence of hypoperfusion (i.e., worsening

prerenal azotemia). In some patients with severe heart failure,
this may be a systolic pressure as low as 90 mmHg [7, 27].
Although related data are not convincing, there may be a
threshold diastolic pressure below which adverse cardiovascular outcomes might increase in elderly patients with isolated
systolic hypertension. When treating such patients, a minimum posttreatment diastolic pressure of 60 mmHg overall or
perhaps 65 mmHg in those with known coronary artery disease is suggested unless there are symptoms attributable to
hypoperfusion that occur at higher pressures [7, 27].
Most patients with systolic heart failure are treated with
inhibition of the renin-angiotensin system (i.e., angiotensin
converting enzyme inhibitors or angiotensin II receptor
blockers), beta-blockers, and, in selected patients, an aldosterone antagonist. These agents have favorable effects on
survival in heart failure that are independent of their effects
on blood pressure [31].
Patients with acute LV dysfunction and pulmonary edema
should usually receive loop diuretics. Diuretics are not generally recommended agents for the treatment of hypertensive
emergencies with the exception of acute pulmonary edema.
However, in a recent small controlled trial, 59 patients with
acute pulmonary edema due to hypertensive crisis were randomized to either furosemide or placebo. The investigators
concluded that the subjective perception of dyspnea in patients with hypertensive pulmonary edema was not influenced
by the administration of a loop diuretic. This is probably
related to the fact that patients with hypertensive heart failure
are often euvolemic or only mildly hypervolemic [32].
An easily titratable vasodilator (i.e., sodium nitroprusside,
nitroglycerin) is often added to reduce afterload. However,
drugs that increase cardiac work (i.e., hydralazine) or acutely
decrease cardiac contractility (i.e., labetalol) should be
avoided [33].
Treatment of hypertension in patients with heart failure
must take into account the type of heart failure that is present:
systolic dysfunction, in which impaired cardiac contractility is
the primary abnormality, or diastolic dysfunction, in which
there is a limitation to diastolic filling and therefore in forward
output due to increased ventricular stiffness. All the above
therapies aim to ameliorate heart failure which can often be
achieved with a 1015 % reduction in blood pressure [31].

Aortic Dissection
Epidemiology Aortic dissection has an estimated incidence of
3/100,000 per year. Seventy percent of these patients are
hypertensive and most of them are over 50 years of age, as
there is reduced resistance of arterial walls with age [34, 35].

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Curr Hypertens Rep (2015) 17:5

Pathophysiology In aortic dissection, target organ damage

occurs in the form of retrograde dissection into the heart with
involvement of aortic branches accompanied by endothelial
injury. Of note, the propagation of the dissection is dependent
not only on the elevation in blood pressure itself but also on
the velocity of LV ejection [34, 35].

arterial pressure <80 mmHg is crucial for the patient). Blood

pressure should be maintained as low in this range as can be
achieved without compromising mentation or urine output
[20, 39].

Clinical Presentation and Evaluation Patients frequently

present with sudden onset of chest pain radiating to the back
and elevated blood pressure. Pulse deficit occurs in 20 % of
patients with type A dissection, while hypertension at initial
presentation is more common in patients with type B dissection [36]. Clinical presentation, however, sometimes varies
and diagnosis may be elusive if not initially considered in
the differential. Physical examination should include auscultation of the abdomen for murmur and blood pressure measurements in both arms to determine if they are symmetric.
Confirmation of aortic dissection is usually obtained by using
contrast-enhanced computed tomography or transesophageal
echocardiogram. Timely recognition of this disease entity
coupled with urgent and appropriate management is the key
to a successful outcome in a majority of patients [35, 37].

Increased Sympathomimetic Activity

Management Antihypertensive therapy in acute aortic dissection aims specifically to lessen pulsatile load or aortic stress
(dp/dt) by lowering the blood pressure in order to retard the
propagation of the dissection and prevent aortic rupture. Pharmacological treatment aims to prevent myocardial ischemia
and decrease LV afterload and myocardial oxygen consumption. Still, only few comparative studies or randomized controlled trials provide definitive conclusions and recommendations regarding the efficacy and safety of comparative agents
[30, 38].
Hypertensive emergencies mainly require rapid blood pressure control with a parenteral antihypertensive medication
while the patient is usually admitted to the intensive care unit.
Typically, blood pressure should be reduced within minutes
to an hour approximately 2025 % and then gradually to
160/100 or 160/110 mmHg within the next 2 to 6 h. An abrupt
fall in blood pressure in patients with preexisting hypertension
may induce severe ischemic injury in major organs as a result
of the chronic adaptation of autoregulation mechanisms [20].
Unlike other hypertensive emergencies, aortic dissection is an
exception, where the rapid and immediate reduction of blood
pressure within 5 to 10 min is required. Management includes
primarily a parenteral beta-blocker. Esmolol is the drug of
choice, but labetalol, propranolol, and metoprolol can also
be used to reduce the heart rate below 60 beats per minute
and decrease the shear stress on the aortic wall. If the blood
pressure remains elevated after beta blockade administration,
a vasodilator such as nitroglycerin can be added to achieve a
systolic blood pressure of 100 to 120 mmHg (blood pressure
target: systolic blood pressure <120 mmHg and a mean

Epidemiology Hyperadrenergic states can be produced by the

use of drugs such as cocaine, amphetamines, phencyclidine,
or monoamine oxidase inhibitors or recent discontinuation of
clonidine or other sympatholytic agents. Pheochromocytoma
and severe autonomic dysfunction (i.e., Guillain-Barr and
Shy-Drager syndromes or acute spinal cord injury) are associated with hypertensive emergencies as well. Recent data
showed that the number of individuals with cocaine dependence or abuse visiting an emergency department is growing
[5].
Pathophysiology Sympathomimetic agents can cause severe
hypertension and end-organ damage. In particular, cocaine
and other sympathomimetic drugs have various physiological
actions in peripheral circulation including stimulation of heart
rate and vasoconstriction. Although the majority of cocainedependent individuals are normotensive, cocaine may precipitate hypertensive emergency due to central nervous system
stimulation and peripheral alpha-agonist effects. The influence of cocaine on heart rate and blood pressure is dosedependent and is mediated through a-adrenergic stimulation
[5].
Clinical Presentation and Evaluation Such conditions may
cause chest pain either due to increased oxygen demand or
decreased oxygen delivery. Symptoms involve the presence of
chest pain, tachycardia, dilated pupils, combativeness, altered
mental status, and seizures.
The differential diagnosis of chest pain in patients that
have used cocaine is similar to the general population;
however, the likelihood of the patient having a serious
event is increased. In a consecutive series of 233 emergency visits by cocaine-using patients, 56 % presented
with cardiovascular complaints, including 40 % with
chest pain. The minority of these patients suffered from
an acute MI (6 %) but the overall mortality was low
(<1 %). Other known complications of cocaine intoxication include arrhythmias, myocarditis, pneumothorax, pulmonary hypertension, acute pulmonary edema, aortic dissection, and bronchospasm [40, 41].
Methamphetamine intoxication may mimic cocaine
intoxication and cause similar cardiac complications. In
one study of patients presenting to the emergency department with chest pain after methamphetamine use,

Curr Hypertens Rep (2015) 17:5

25 % of patients suffered acute coronary syndromes,

and 8 % had other cardiac complications such as tachyarrhythmias [42].
Management Stress testing and myocardial imaging have
been suggested to facilitate safe, rapid discharge of patients
with cocaine-associated chest pain.
Toxicity may be superimposed on preexisting hypertension in patients that have become dependent on elevated blood pressure to maintain cerebral perfusion.
Hypertension secondary to cocaine is mainly responsive
to intravenous benzodiazepines because benzodiazepines
minimize the stimulant effects of cocaine on the central
nervous system.
A vasodilator, such as nitroglycerin or nitroprusside,
may be titrated to effect if further therapy is indicated.
Nitroglycerin is the drug of choice in patients with chest
pain. The use of nitroprusside to control hypertension has
the additional advantage of aiding heat loss by peripheral
vasodilatation. However, frequent monitoring is required
since this drug can produce a sudden and drastic drop in
blood pressure [43, 44].
Nonselective beta-blockers such as propranolol
should generally be avoided because of the risk of an
abrupt rise in blood pressure as well as coronary vasoconstriction due to the exaggerated effect of catecholamines on unblocked alpha-receptors [5].

Page 5 of 6 5

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Conclusions
Cardiovascular events related to hypertensive emergencies are life-threatening situations requiring immediate
evaluation and management to prevent end-organ damage. Several regimens have proven to be effective
enough but the choice of treatment depends on the
clinical presentation of the patient. A very important
aspect of care for these patients is to assure highquality outpatient follow-up since a large proportion of
them will return to the hospital with a recurrent hypertensive emergency. Adequate control of blood pressure
should be pursued as a way to avoid this severe complication of hypertension.
Compliance with Ethics Guidelines
Conflict of Interest D.P. Papadopoulos, E.A. Sanidas, N.A. Viniou, V.
Chantziara, I. Barbetseas, and T.K. Makris declare that they have no
conflicts of interest.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.

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