Hypertensive Emergencies

Hypertensive emergencies
The right clinical information, right where it's needed
Last updated: Mar 13, 2017

Table of Contents
Summary 3
Basics 4
Definition 4
Epidemiology 4
Aetiology 4
Pathophysiology 4
Prevention 5
Primary prevention 5
Secondary prevention 5
Diagnosis 6
Case history 6
Step-by-step diagnostic approach 6
Risk factors 7
History & examination factors 8
Diagnostic tests 9
Differential diagnosis 10
Diagnostic criteria 11
Treatment 12
Step-by-step treatment approach 12

Treatment details overview 15
Treatment options 17
Emerging 31
Follow up 32
Recommendations 32
Complications 32
Prognosis 32
Guidelines 33
Diagnostic guidelines 33
Treatment guidelines 33
Evidence scores 34
References 36
Images 40
Disclaimer 42
Summary
◊ Defined as elevated BP (usually systolic BP >210 mmHg and diastolic BP >130 mmHg) with rapid decompensation
of vital organ function.
◊ If the clinical suspicion is high, treatment should be initiated immediately without waiting for further tests.
◊ BP must be lowered over minutes to hours with parenteral medications in an intensive care setting. Oral
medications should be given shortly thereafter to permit weaning from parenteral agents.
◊ The initial goal of therapy is to reduce mean arterial BP by no more than 25% (within minutes to 1 hour), then,
if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2 to 6 hours. Exceptions to this
general rule are patients with intracranial pathology and patients with aortic dissection. Excessive falls in pressure
that may precipitate renal, cerebral, or coronary ischaemia should be avoided.
◊ With appropriate treatment, prognosis is good.

Hypertensive emergencies Basics
Definition
Hypertensive emergency is elevated BP (usually systolic BP >210 mmHg and diastolic BP >130 mmHg) with rapid
BASICS
deterioration of vital organ function, resulting in symptoms such as encephalopathy, retinopathy, myocardial ischaemia,
or renal failure. The absolute value of the BP is not as vital as the presence of acute end-organ damage.
Epidemiology
The worldwide prevalence of hypertension is around 26%, totalling 1 billion people.[1] Of these, 1% to 2% will suffer a
hypertensive crisis in their lifetime.[2] [3]
Men may be more likely than women to suffer a hypertensive emergency. Hypertensive emergency is also more common
in older patients and in black people.[4] [5] [6]
In the US, 30% of people suffer from hypertension;[7] [8] lack of insurance or a primary care doctor and non-adherence
to treatment all predispose toward development of hypertensive emergency.[9] [10]
As populations age globally, the prevalence of hypertension and therefore hypertensive emergency is expected to
increase.[1]
Aetiology
There are many causes of hypertensive emergency. By far the most common cause is essential hypertension that is
either undiagnosed or inadequately treated.[4] The next most common cause is secondary to renal disease, such as renal
artery stenosis, acute glomerulonephritis, collagen-vascular diseases, or kidney transplantation.[11] [12]Pregnancy-related
eclampsia is also an important cause of hypertensive emergency. Other rarer causes include hyperaldosteronism and
conditions leading to excess circulating catecholamines (e.g., phaeochromocytoma, sympathomimetic drug intake,
autonomic dysfunction after spinal cord injury, or inadvertent drug or food interactions with monoamine oxidase
inhibitors).[13]
Pathophysiology
The factors that lead to the development of hypertensive emergency are poorly understood. A rise in systemic vascular
resistance initiates the cycle. The subsequent increase in BP generates mechanical stress and endothelial injury leading
to increased permeability, activation of the coagulation cascade and platelets, and deposition of fibrin. These processes
result in ischaemia and the release of additional vasoactive mediators, generating ongoing injury. Volume depletion
caused by pressure natriuresis and activation of the renin-angiotensin system often leads to further vasoconstriction.
Systemic vasoconstriction leads to decreased blood flow to vital organs and the subsequent organ injury that is the
hallmark of hypertensive emergency. Neurological injury may manifest as retinopathy, papilloedema, encephalopathy,
stroke, seizures, or coma. Cardiac injury may manifest as chest pains or SOB, signifying impending or actual MI, aortic
dissection, or left ventricular failure with pulmonary oedema. Renal failure may manifest as oliguria and azotaemia.[6]
[13] [14] [15]
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 13, 2017.
4 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com . Use
of this content is subject to our disclaimer. © BMJ Publishing Group Ltd 2017. All rights reserved.
Hypertensive emergencies Prevention
Primary prevention
The mainstay of primary prevention is appropriate screening and treatment of essential hypertension.
Secondary prevention
Major lifestyle modifications shown to lower BP include the Dietary Approaches to Stop Hypertension (DASH) eating plan,
dietary sodium reduction, weight reduction in overweight patients, physical activity, and moderation of alcohol
consumption.[46] [47]
PREVENTION
BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com . Use
5
Hypertensive emergencies Diagnosis
Case history
Case history #1
A 50-year-old black man with a history of untreated hypertension presents to the emergency department with
substernal chest pressure. His symptoms started 1 day prior. The pain was initially intermittent in nature but has
become constant and radiates to his jaw and left shoulder. He also complains of dizziness and some SOB. Apart from
a history of hypertension diagnosed 1 year ago, the patient denies any past medical history. He is not taking any
antihypertensive medications. The patient denies smoking, or alcohol or drug use. Family history is unremarkable.
His BP is 230/130 mmHg with otherwise normal vital signs and no other significant findings. ECG shows diffuse T-wave
inversion and ST depression in lateral leads. Laboratory testing is significant for elevated troponin, signalling MI.
Other presentations
Other ways in which hypertensive emergency can present include neurological symptoms (e.g., stroke, encephalopathy),
chest pain signifying cardiac conditions other than infarction or ischaemia (e.g., aortic dissection, pulmonary oedema),
or nephrological symptoms (e.g., decreased or absent urine output).
Step-by-step diagnostic approach

The key to diagnosis of hypertensive emergency is a rapid but thorough evaluation. If hypertensive emergency is suspected,
initiation of treatment should not be delayed while conducting a full diagnostic appraisal.
History
Any prior history of hypertension and previous treatment should be identified.
Clinical features that may identify specific organ compromise include:
• Neurological compromise; for example, blurry vision, dizziness, loss of sensation, or loss of movement
DIAGNOSIS
• Cardiac compromise; for example, chest pain or pressure, SOB, orthopnoea, paroxysmal nocturnal dyspnoea,
or oedema
• Renal compromise; for example, decrease in urine output.
When appropriate, use of street drugs, particularly sympathomimetics (cocaine, amphetamines, phenylpropanolamine,
phencyclidine, ecstasy, LSD) should be investigated.
Physical examination
An appropriately sized cuff should be used for BP readings. The cuff bladder should encircle at least 80% of the upper
arm. The arm should also be supported at heart level during recordings. Using too large a cuff results in an
underestimation of BP; conversely, too small a cuff will lead to overestimation.
BP readings should be taken from both arms and readings repeated after 5 minutes to confirm. If there is a more than
20 mmHg pressure difference between arms, aortic dissection should be considered.
A fundoscopic examination should be performed, looking for the presence of arteriolar spasm, retinal oedema, retinal
haemorrhages, retinal exudates, papilloedema, or engorged retinal veins. [Fig-1] [Fig-2] [Fig-3]
A rapid bedside neurological examination is also required, including testing cranial nerve function, motor strength,
gross sensory function, and gait.
Cardiopulmonary status should be assessed, examining in particular for the presence of new murmurs, additional
heart sounds, jugular venous distension, rales, and lower extremity oedema.
Laboratory evaluation
Baseline blood and urine samples must be collected prior to administration of treatment. Laboratory evaluation should
include the following:
• FBC, including peripheral blood smear
• Blood chemistry panel, including creatinine and electrolytes
• Urinalysis with microscopy.
In some circumstances, the following may also be indicated:
• Plasma renin activity and aldosterone levels, if primary aldosteronism is suspected (e.g., in patients with diastolic
hypertension with persistent hypokalaemia and metabolic alkalosis)
• Plasma renin activity before and 1 hour after 25-mg captopril is administered if renovascular hypertension is
suspected. Renovascular hypertension should be suspected in patients with severe hypertension who have
abdominal bruits and/or unexplained renal deterioration with angiotensin-converting enzyme (ACE) inhibitor
treatment, although the clinical presentation is variable
• Spot urine or plasma-free metanephrine levels if phaeochromocytoma is suspected (e.g., in patients with
hypertension and palpitations, headaches and/or diaphoresis although clinical presentation is very variable).
Further investigation
DIAGNOSIS
CXR and ECG are obtained. If aortic dissection is considered, an urgent thoracic CT scan with contrast or a
transoesophageal echocardiogram should also be obtained.
If ischaemic stroke or intracranial haemorrhage is suspected (e.g., in patients with focal neurological defects) urgent
non-contrast CT scan (NCCT) of the head and/or an MRI are done, depending on local availability.
Risk factors
Strong
inadequately treated hypertension
• A history of inadequately treated hypertension is commonly seen.[5] [9] [10]
• In the US, lack of medical insurance or access to a primary care doctor have been shown to predispose to hypertensive
emergency.[10]
Weak
7
older age
• Older age predisposes to hypertensive emergency.[4] [5] [6]
black ethnicity
• Black people are predisposed to hypertensive emergency, compared with white people.[4] [5] [6]
male gender
• Men may be more likely than women to suffer a hypertensive emergency.[4] [5] [6]
use of sympathomimetic drugs

• Use of sympathomimetic street drugs (e.g., cocaine, LSD, amphetamines, ecstasy) predisposes to hypertensive
emergency.
use of monoamine oxidase inhibitors (MAOIs)

• Inadvertent ingestion of food containing tyramine in patients taking MAOIs can precipitate a hypertensive emergency.
History & examination factors

Key diagnostic factors
BP above 210/130 mmHg (common)

• BP is usually above 210/130 mmHg in hypertensive emergencies.
presence of risk factors (common)

• Risk factors include: inadequately treated hypertension, older age, black ethnicity, male gender, use of
sympathomimetic drugs, and use of monoamine oxidase inhibitors.
Other diagnostic factors

DIAGNOSIS
neurological symptoms (common)

• Neurological abnormalities such as dizziness, headaches, mental status changes, and loss of sensation or motor
strength are symptoms often associated with hypertensive emergency.[6]
cardiac symptoms (common)

• Cardiac abnormalities (e.g., chest pain or pressure, SOB, oedema) are frequently associated with hypertensive
emergency.[6]
abnormal cardiopulmonary examination (common)

• The presence of new murmurs, S3, jugular venous distension, rales, or lower extremity oedema may be found.
oliguria or polyuria (common)

• Any changes in renal output can be indicative of renal damage.[11]
abnormal fundoscopic examination (common)

• The following signs are indicative of hypertensive retinopathy: arteriolar spasm, retinal oedema, retinal haemorrhages,
retinal exudates, papilloedema, engorged retinal veins.[16]
abnormal neurological examination (common)
• Abnormal findings in cranial nerve function, motor strength, gross sensory function, and gait can frequently result
from hypertensive crisis.
Diagnostic tests
1st test to order
Test Result
FBC with smear may reveal schistocytes (red
cell fragments) indicating the
• Microangiopathic haemolytic anaemia (MAHA) may occur in patients with
presence of haemolysis
hypertensive emergency and increases the risk of developing acute renal
failure.[17]
blood chemistry may reveal elevated creatinine
• Renal failure as manifested by elevated creatinine may be the only sign of
hypertensive emergency.
urinalysis with microscopy may reveal presence of red
cells and protein
• Renal failure as manifested by haematuria and proteinuria may be the only sign
of hypertensive emergency.
electrocardiogram may reveal evidence of
• If ECG is abnormal, troponin levels are tested to rule out ongoing ischaemia or ischaemia or infarct such as ST-
or T-wave changes
infarction.
• If ECG is normal, aortic dissection should be considered as an explanation for
chest pain.
CXR may reveal evidence of
pulmonary oedema indicating
• CXR is useful to assess for pulmonary oedema, LVH, and aortic dissection.
• Note, however, that a CXR has low sensitivity in detection of aortic dissection left ventricular failure or
widened mediastinum
(56% in type B and 63% in type A).[18] If aortic dissection is suspected, an
indicating possible aortic
DIAGNOSIS
urgent CT scan with contrast should be ordered.
dissection
head CT without contrast may reveal evidence of infarct

or haemorrhage
• Indicated if neurological complications are suspected. Although the
non-contrast CT scan (NCCT) is of low sensitivity for acute ischaemic stroke, it
is usually ordered to exclude or confirm haemorrhage.
• MRI, although more sensitive than NCCT, may not be widely available in a timely
fashion and should be ordered in follow-up to a NCCT. Further neuroimaging
(e.g., CT-angiography, magnetic resonance angiography, carotid and vertebral
Dopplers) should be considered if initial tests indicate ischaemia or infarct.[22]
head MRI may reveal evidence of infarct
• More sensitive than non-contrast CT scan, but may not be available as first-line or haemorrhage
investigation in all centres.
spot urine or plasma metanephrine may reveal elevated
• May be useful before initiation of drug therapy to rule out phaeochromocytoma. metanephrine levels
However, needs to be interpreted carefully, with consideration for possible
confounding factors such as drugs (e.g., tricyclic antidepressants, clozapine,
phenoxybenzamine, beta-blockers, sympathomimetics, buspirone) or major
physiological or psychological stress.
9
Other tests to consider
Test Result
thoracic CT scan with contrast evidence of 2 separate aortic
• This test should be ordered only if aortic dissection is suspected, given the risk lumens with dividing intimal
flap in aortic dissection
of contrast-induced nephropathy, especially in the presence of possible
underlying renal abnormality.
• The sensitivity and specificity of standard CT for the diagnosis of aortic
dissection is around 90% and 95%, respectively.
• Newer imaging techniques such as helical CT approach 100% sensitivity and
specificity.[19] [20]
• Transoesophageal echocardiogram (TEE) and MRI are comparable to helical
CT and more sensitive than standard CT.[20] [21]
• CT scan may be recommended as the initial test of choice but this is
institutionally variable and TEE may be substituted if available in a timely fashion.
transoesophageal echocardiography (TEE) evidence of 2 separate aortic
lumens with dividing intimal
• May substitute for CT if available in a timely fashion. More sensitive than
flap in aortic dissection
standard CT and comparable with helical CT.[20] [21]
plasma renin activity and aldosterone level in primary hyperaldosteronism,
renin activity will be decreased
• This test is an indirect measure of the activity of renin through measurement
and aldosterone levels
of the rate of production of angiotensin I, which increases as a result of renin
increased; in secondary
stimulation. Aldosterone levels are usually measured at the same time. High
hyperaldosteronism, both renin
plasma renin activity suggests hypertension from the vasoconstrictive effects
activity and aldosterone levels
of angiotensin. Requires renal vein catheterisation and so needs formal consent
will be increased
from the patient.
single-dose captopril challenge may reveal decrease in renin
plasma activity in response to
• May be useful where renovascular hypertension is suspected, particularly in
captopril
patients who have not received previous medical therapy.
• Baseline plasma renin activity is measured and the patient is then given 25 to
50 mg of captopril; measurement of plasma renin activity is repeated 60
minutes later.
• Test sensitivity is excellent but specificity is poor. Further testing with renal
DIAGNOSIS
arterial Doppler ultrasonography, renal magnetic resonance angiography, or

contrast angiography may be necessary to confirm diagnosis.
Differential diagnosis
Condition Differentiating signs / Differentiating tests

symptoms
Hypertensive urgency • Symptomatic elevated BP • History, physical examination,
laboratory tests, and imaging
show no evidence of end-organ
damage.
Hypertension • Asymptomatic elevated BP • History, physical examination,

laboratory tests, and imaging
show no evidence of end-organ
damage.
Diagnostic criteria
Clinical criteria
Elevated BP in the presence of acute or rapidly deteriorating end-organ damage (e.g., neurological, cardiac, or renal
compromise) based on historical or clinical criteria (physical examination, laboratory tests, or imaging), posing an immediate
threat to life, is sufficient for diagnosis of hypertensive emergency.[3]
DIAGNOSIS
11
Hypertensive emergencies Treatment
Step-by-step treatment approach

If hypertensive emergency is suspected, treatment should not be delayed while conducting a full diagnostic evaluation.
Appropriate facilities
Patients with hypertensive emergencies should be admitted to an ICU for continuous monitoring of BP and parenteral
administration of appropriate therapeutic agent(s).[23] Other supportive measures that may be required include
intracranial pressure monitoring (in rare cases of increased intracranial pressure), intubation (in case of respiratory
distress), or dialysis (in case of renal failure).
Choice of agents and route of administration

The specific parenteral agents used for treating a hypertensive emergency should be dictated by the end-organ
systems that have been damaged, patient comorbidities, and overall clinical condition. Oral therapy should begin as
soon as possible so that parenteral therapy can be weaned. There are very few randomised controlled trials studying
different parenteral agents in hypertensive emergency. Published guidelines are therefore based on common clinical
experience and practice.
Rate of BP reduction
The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure[23] states the initial goal of therapy in hypertensive emergencies is to reduce mean arterial BP by no
more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within
the next 2 to 6 hours.
Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischaemia should be avoided. For this
reason, short-acting nifedipine is no longer considered acceptable in the initial treatment of hypertensive emergencies
or urgency.
If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions towards
a normal BP can be implemented over the next 24 to 48 hours.
Exceptions to the above recommendation include:
• Patients with an ischaemic stroke, as there is no clear evidence from clinical trials to support the use of immediate
antihypertensive treatment
• Patients with aortic dissection, who should have their systolic BP lowered to less than 100 mmHg if tolerated
• Patients in whom BP needs to be lowered to enable the use of thrombolytic agents, in which case the target
systolic BP is under 185 mmHg and diastolic BP under 110 mmHg.
Accelerated (malignant) hypertension, hypertensive encephalopathy or

intracranial haemorrhage
TREATMENT
Accelerated hypertension (also known as malignant hypertension) is severe hypertension occurring with retinopathy
of grade III (flame haemorrhages, dot and blot haemorrhages, hard and soft exudates) or grade IV (papilloedema).
Hypertensive encephalopathy encompasses the transient neurological symptoms that occur with malignant
hypertension, which are usually reversed by prompt treatment and lowering of BP.
In the management of intracerebral haemorrhage, the ideal level of a patient's BP should be based on individual
factors including: baseline BP, presumed cause of haemorrhage, age, elevated intracranial pressure, and interval since
onset.
While elevated BP could in theory increase the risk of ongoing bleeding from ruptured small arteries and arterioles,
the relationship between BP, intracranial pressure, and volume of haemorrhage is complex and not yet fully understood.
The rationale for lowering BP is to minimise further haemorrhage - for example, from a ruptured aneurysm or
arteriovenous malformation. However, in primary intracerebral haemorrhage, when a specific vasculopathy is not
apparent, the risk from a mildly elevated BP may be lower, so aggressive reduction of BP must be balanced against
the possible risk of inducing cerebral ischaemia in other brain areas.[24] [25]
In cases of intracranial haemorrhage, target mean arterial pressure (MAP) is 130 mmHg, with a goal of maintaining a
cerebral perfusion pressure (CPP) above 70 mmHg. Avoid BP dropping to below 110 mmHg.
The first-line treatment is labetalol.[13] [14] [15] 1[C]Evidence If patients do not have evidence of raised intracranial
pressure, a second-line treatment choice is nitroprusside.[13] [14] 2[C]Evidence However, if raised intracranial
pressure is present or suspected, nitroprusside is contraindicated and another agent should be used. Nitroprusside
decreases cerebral blood flow while increasing intracranial pressure, effects that are particularly disadvantageous in
patients with hypertensive encephalopathy or following a stroke.[26] [27] [28] It should also be avoided in patients
with renal or hepatic insufficiency. Nicardipine is another second-line agent which can be used. One RCT found that
intravenous nicardipine significantly increased the proportion of people who reached physician-specified target range
systolic BP within 30 minutes compared with intravenous labetalol.[29] Nicardipine is especially useful in the presence
of cardiac disease due to coronary vasodilatory effects.
The third-line treatment choice is fenoldopam, a selective peripheral dopamine-1-receptor agonist with arterial
vasodilator effects.[13] [14] [15] [30] [31] 3[C]Evidence This drug is particularly useful in patients with renal
insufficiency, where the use of nitroprusside is restricted due to the risk of thiocyanate poisoning.
Acute ischaemic stroke

Treating a hypertensive emergency with an associated acute ischaemic stroke warrants greater caution in reducing
BP than in other types of hypertensive emergency. Overly rapid or too great a reduction of MAP may decrease CPP
to a level that could theoretically worsen brain injury. The following may be used as guidance.
If systolic BP is below 220 mmHg and diastolic BP below 120 mmHg, then it is reasonable to maintain close observation
without direct intervention to reduce BP,[32] unless:
• There is other end-organ involvement such as aortic dissection, renal failure, or acute MI
• The patient is to receive thrombolytics, in which case the target systolic BP is below 185 mmHg and diastolic
BP below 110 mmHg
• There is concurrent intracranial haemorrhage, in which case the goals are a systolic BP of between 140 and
160 mmHg and/or a mean arterial pressure (MAP) of 130 mmHg with the CPP maintained above 70 mmHg.
Additionally, MAP should not be dropped to below 110 mmHg.
TREATMENT
If systolic BP is above 220 mmHg or diastolic BP is between 121 to 140 mmHg, then labetalol[13] [14] [15]
1[C]Evidence or nicardipine[13] [14] [15] [33] 4[C]Evidence should be used to achieve a 10% to 15% reduction in
24 hours.
13
If diastolic BP is above 140 mmHg, then nitroprusside[13] [14] is used to achieve a 10% to 15% reduction over 24
hours.[13] [14] [34] 2[C]Evidence
Suspected aortic dissection

If aortic dissection is suspected in a hypertensive emergency, the BP should be lowered quite aggressively, typically
with a target of reducing systolic BP to between 100 and 120 mmHg within 20 minutes.
Medical therapy aims to both lower the BP and decrease the velocity of left ventricular contraction, so decreasing
aortic shear stress and minimising the tendency for propagation of the dissection.
First-line treatment choice is beta-blockers, either labetalol or esmolol, administered intravenously.[13] [14] [15] [35]
8[C]Evidence
Second-line treatment choice would be the combination of nitroprusside and beta-blockers.[13] [14] [15] [35]
8[C]Evidence Nitroprusside must be administered with a beta-blocker, as nitroprusside-induced vasodilation would
otherwise induce a compensatory tachycardia and worsen shear stress on the intimal flap.
Myocardial ischaemia/infarction
First-line treatment of hypertensive emergency complicated by myocardial ischaemia or infarction is the combination
of esmolol (a selective beta-blocker) plus glyceryl trinitrate (a peripheral vasodilator, which affects venous vessels
more than arterial).[13] [14] [15] [34] [36] 5[C]Evidence
Esmolol acts to reduce heart rate and glyceryl trinitrate acts to decrease preload and cardiac output and increases
coronary blood flow.
Second-line treatment choice would be labetalol plus glyceryl trinitrate.[13] [14] [15] [34] [36] 6[C]Evidence
The third-line treatment choice would be nitroprusside.[13] [14] [34] 2[C]Evidence
Left ventricular failure and/or pulmonary oedema

First-line treatment of hypertensive emergency with left ventricular failure and/or pulmonary oedema is glyceryl
trinitrate.[13] [14] [15] [36] 7[C]Evidence
Nitroprusside (a potent arterial and venous vasodilator that decreases afterload and preload) is the second-line
treatment choice in this situation.[13] [14] [34] 2[C]Evidence
If patient is not already on one, a loop diuretic should be started (e.g., furosemide).
Acute renal failure

Fenoldopam is the first-line treatment choice of hypertensive emergency complicated by acute renal failure.[13] [14]
[15] [30] [31] 3[C]Evidence This drug (a selective peripheral dopamine-1-receptor agonist with arterial vasodilator
effects) is particularly useful in renal insufficiency because it acts to both decrease afterload and increase renal
perfusion. Second-line treatment choice is nicardipine, a dihydropyridine calcium-channel blocker, which increases
stroke volume and has strong cerebral and coronary vasodilatory activity.[13] [14] [15] [33] 4[C]Evidence
TREATMENT
Hyperadrenergic states
Hyperadrenergic states include:
• Phaeochromocytoma
• Sympathomimetic drug use - for example, cocaine, amphetamines, phenylpropanolamine, phencyclidine, or

the combination of monoamine oxidase inhibitors with foods rich in tyramine
• Following abrupt discontinuation of a short-acting sympathetic blocker.
If the hyperadrenergic state is due to sympathomimetic drug use, the first-line agents are benzodiazepines, and
anti-hypertensive medications are given only if the blood pressure response is inadequate. In all other clinical situations,
the first-line treatment choice is phentolamine (which acts by blocking alpha-adrenoceptors).[13] [14] [15]
9[C]Evidence The second-line treatment choice is the combination of labetalol1[C]Evidence plus nitroprusside.[13]
[14] [15] 2[C]Evidence Administration of a beta-blocker alone is contraindicated, since inhibition of
beta-adrenoceptor-induced vasodilation results in unopposed alpha-adrenergic vasoconstriction and a further rise
in BP.
Eclampsia
The first-line treatment choices in this situation are hydralazine,[13] [14] [15] [37] [38] [39] 10[C]Evidence labetalol,[13]
[14] [15] [37] [39] [40] 11[C]Evidence or nicardipine.[13] [14] [15] [37] [40] [41] 12[C]Evidence
In pregnancy, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are avoided
due to potential teratogenic effects, and nitroprusside is avoided due to its potential for fetal cyanide poisoning.
A guide target in these patients is to maintain a systolic BP of 130 to 150 mmHg and a diastolic BP of 80 to 100 mmHg.
It should be noted, however, that there are no trials supporting these suggested thresholds, and treatments should
be tailored to individual patient circumstances.
In addition to the first-line treatments mentioned, it has been proposed that magnesium may be useful as an adjunctive
therapy,[13] [14] [15] [37] [42] although there is no consensus on the optimal regimen, when it should be started
and terminated, or the optimal route of administration. The drug is usually initiated at the onset of labour.
Treatment details overview

Consult your local pharmaceutical database for comprehensive drug information including contraindications, drug
interactions, and alternative dosing. ( see Disclaimer )
Acute ( summary )
Patient group Tx line Treatment
accelerated (malignant) hypertension or

hypertensive encephalopathy or
increased intracranial pressure or 1st labetalol

renal disease
2nd nicardipine
3rd fenoldopam
TREATMENT
normal intracranial pressure and 1st labetalol

renal function
2nd nitroprusside or nicardipine
15
Acute ( summary )
3rd fenoldopam
acute ischaemic stroke
SBP ≤220 mmHg and DBP ≤120 1st close observation ± BP reduction
mmHg
SBP >220 mmHg or DBP 121 to 1st labetalol

140 mmHg
2nd nicardipine
DBP >140 mmHg 1st nitroprusside
myocardial ischaemia/infarction 1st esmolol and glyceryl trinitrate
2nd labetalol and glyceryl trinitrate
3rd nitroprusside
left ventricular failure and/or pulmonary 1st glyceryl trinitrate + furosemide

oedema
2nd nitroprusside + furosemide
aortic dissection 1st labetalol or esmolol
2nd nitroprusside
plus labetalol or esmolol
acute renal failure 1st fenoldopam
2nd nicardipine
hyperadrenergic state
sympathomimetic drug use 1st benzodiazepines
2nd phentolamine
3rd labetalol and nitroprusside
no sympathomimetic drug use 1st phentolamine
2nd labetalol and nitroprusside
eclampsia 1st hydralazine, labetalol, or nicardipine

TREATMENT
adjunct magnesium
Treatment options
Acute
accelerated (malignant) hypertension or
hypertensive encephalopathy or
increased intracranial pressure or 1st labetalol

renal disease » Labetalol is drug of choice in situations characterised
by markedly elevated intracranial pressure.
» Onset of action: 5 to 10 minutes. Duration of action:

3 to 8 hours.
» In cases of intracranial haemorrhage, goal mean

arterial pressure (MAP) is 130 mmHg and goal cerebral
perfusion pressure is above 70 mmHg. MAP should not
be dropped below 110 mmHg.
» Encephalopathy should improve once BP is lowered.

If there is no improvement despite a decrease in BP,
an alternative diagnosis should be considered.
» Dose should be adjusted to maintain BP in desired

range and is continued until BP controlled on oral
agents.
Primary options
» labetalol: 20 mg intravenously every 10 minutes

according to response, maximum 300 mg total
dose; or 0.5 to 2 mg/minute intravenous infusion
2nd nicardipine
» Nicardipine is a second-generation dihydropyridine
derivative calcium-channel blocker with high vascular
selectivity and strong cerebral and coronary
vasodilatory activity. The onset of action of IV
nicardipine is from 5 to 15 minutes, with a duration of
action of 4 to 6 hours.
» Nicardipine is especially useful in the presence of

cardiac disease due to coronary vasodilatory effects.
Primary options
» nicardipine: 5 mg/hour intravenously initially,

increase by 2.5 mg/hour increments every 15
TREATMENT
minutes according to response, maximum 15

mg/hour
3rd fenoldopam
17
Acute
» Fenoldopam is especially useful in renal insufficiency,
where the use of nitroprusside is restricted because of
the risk of thiocyanate poisoning.
» It acts as a selective peripheral dopamine-1-receptor

agonist with arterial vasodilator effects. Its
haemodynamic effects are a decrease in afterload and
an increase in renal perfusion.
» Onset of action: 5 minutes. Duration of action: 30

minutes.

be dropped to below 110 mmHg.

» Continue until BP controlled on oral agents
Primary options
» fenoldopam: 0.1 to 0.3 micrograms/kg/minute

intravenously initially, increase by 0.05 to 0.1
micrograms/kg/minute increments every 15
minutes according to response, maximum 1.6
micrograms/kg/minute
normal intracranial pressure and 1st labetalol

renal function » Onset of action: 5 to 10 minutes. Duration of action:
3 to 8 hours.

be dropped below 110 mmHg.

» Dose should be adjusted to maintain BP in desired

range and is continued until BP controlled on oral
agents.
TREATMENT
Primary options

Acute
2nd nitroprusside or nicardipine
» Sodium nitroprusside acts as a potent arterial and
venous vasodilator, thereby reducing afterload and
preload. Its haemodynamic effects are to decrease
mean arterial pressure (MAP), with a modest increase
or no change in cardiac output. Onset of action:
immediate. Duration of action: 3 to 5 minutes.
» Patients should be monitored by drawing thiocyanate

levels after 48 hours of therapy (levels kept at <2064
micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose
should be delivered for less than 10 minutes to
decrease chance of cyanide toxicity.
» Nicardipine is a second-generation dihydropyridine

derivative calcium-channel blocker with high vascular
selectivity and strong cerebral and coronary
vasodilatory activity. The onset of action of IV
nicardipine is from 5 to 15 minutes, with a duration of
action of 4 to 6 hours. It is especially useful in the
presence of cardiac disease due to coronary
vasodilatory effects.
» In cases of intracranial haemorrhage, goal MAP is 130

mmHg and goal cerebral perfusion pressure is above
70 mmHg. MAP should not be dropped to below 110
mmHg. Encephalopathy should improve once BP is
lowered. If there is no improvement despite a decrease
in BP, an alternative diagnosis should be considered.
» Continue until BP controlled on oral agents.
Primary options
» nitroprusside: 0.3 to 0.5 micrograms/kg/minute

intravenously initially, increase by 0.5
micrograms/kg/minute increments according to
response, maximum 10 micrograms/kg/minute
OR
mg/hour
3rd fenoldopam
» Fenoldopam acts as a selective peripheral
TREATMENT
dopamine-1-receptor agonist with arterial vasodilator

effects. Its haemodynamic effects are a decrease in
afterload and an increase in renal perfusion.
» Onset of action: 5 minutes. Duration of action: 30

minutes.
19
Acute
be dropped to below 110 mmHg.

» Continue until BP controlled on oral agents
Primary options

acute ischaemic stroke
SBP ≤220 mmHg and DBP ≤120 1st close observation ± BP reduction
mmHg » Treatment of a hypertensive emergency with an
associated acute ischaemic stroke warrants greater
caution in reducing BP than with other types of
hypertensive emergency. Overly rapid or too great a
reduction of mean arterial pressure (MAP) may
decrease cerebral perfusion pressure to a level that
could theoretically worsen brain injury. The following
may be used as guidance:
» If the systolic BP is below 220 mmHg and the diastolic

BP is below 120 mmHg, there is no evidence of end
organ involvement or intracranial haemorrhage and
thrombolytic treatment is not proposed, then it is
reasonable to maintain close observation without direct
intervention to reduce BP.
» If there is other end-organ involvement such as aortic

dissection, renal failure, or acute MI, or the patient is
to receive thrombolytics, the target systolic BP is below
185 mmHg and diastolic BP is below 110 mmHg.
» If there is intracranial haemorrhage, the target systolic

BP is 140 to 160 mmHg and/or a mean arterial pressure
(MAP) of 130 mmHg and a cerebral perfusion pressure
maintained above 70 mmHg.
TREATMENT
» MAP should not be dropped below 110 mmHg.
» The choice of agent to reduce blood pressure

depends on the associated end-organ involvement.
Acute
SBP >220 mmHg or DBP 121 to 1st labetalol
140 mmHg » If the systolic BP is above 220 mmHg or the diastolic
BP is between 121 and 140 mmHg, then labetalol[13]
[14] [15] 1[C]Evidence or nicardipine[13] [14] [15]
[33] 4[C]Evidence should be used to achieve a 10%
to 15% reduction in 24 hours.
» Labetalol acts as an alpha-1-blocker and non-selective

beta-blocker, and its haemodynamic effects include
decreasing systemic vascular resistance, MAP, and
heart rate, accompanied by a slight decrease or minimal
change in cardiac output.

3 to 8 hours.
Primary options

2nd nicardipine
» If systolic BP is above 220 mmHg or diastolic BP is
between 121 and 140 mmHg, then labetalol[13] [14]
[15] 1[C]Evidence or nicardipine[13] [14] [15] [33]
4[C]Evidence should be used to achieve a 10% to 15%
reduction in 24 hours.
» Nicardipine is a dihydropyridine calcium-channel

blocker, which increases stroke volume and has strong
cerebral and coronary vasodilatory activity.

2 to 4 hours.
Primary options

mg/hour
TREATMENT
DBP >140 mmHg 1st nitroprusside

» If diastolic BP is above 140 mmHg, then
nitroprusside[13] [14] 2[C]Evidence may be used to
achieve a 10% to 15% reduction over 24 hours.
21
Acute
» It acts as a potent arterial and venous vasodilator
thereby reducing afterload and preload. Its
haemodynamic effects are to decrease MAP, with a
modest increase or no change in cardiac output.
» Onset of action: immediate. Duration of action: 3 to

5 minutes.

levels after 48 hours of therapy (levels maintained
<2064 micromol/L (<12 mg/dL or 120 mg/L)).
Maximum dose should be delivered for less than 10
minutes to decrease chance of cyanide toxicity.
Primary options

myocardial ischaemia/infarction 1st esmolol and glyceryl trinitrate

» Esmolol onset of action: 1 to 5 minutes. Duration of
action: 5 minutes.
» Glyceryl trinitrate acts as a peripheral vasodilator, with

greater action on the venous vessels than on arterial
vessels. It causes a decrease in preload and cardiac
output and increases coronary blood flow. Onset of
action: immediate. Duration of action: 3 to 5 minutes.
Primary options
» esmolol: 50-100 micrograms/kg/minute

intravenously
-and-
» glyceryl trinitrate: 5-100 micrograms/minute
intravenously
2nd labetalol and glyceryl trinitrate

» Labetalol is an alpha-1-blocker and non-selective
beta-blocker that decreases systemic vascular
TREATMENT
resistance, mean arterial pressure (MAP) and heart rate,

and causes a decrease or no change in cardiac output.
Onset of action: 5 to 10 minutes. Duration of action: 3
to 8 hours.
» Glyceryl trinitrate acts as a peripheral vasodilator, with

Acute
vessels. It causes a decrease in preload and cardiac
output and increases coronary blood flow. Onset of
action: immediate. Duration of action: 3 to 5 minutes.
Primary options

intravenously
3rd nitroprusside
venous vasodilator thereby reducing afterload and
mean arterial pressure, with a modest increase or no

5 minutes.

Primary options

left ventricular failure and/or pulmonary 1st glyceryl trinitrate + furosemide

oedema » Glyceryl trinitrate acts as a peripheral vasodilator, with
vessels.
» It causes a decrease in preload and cardiac output

and increases coronary blood flow.

5 minutes.
TREATMENT
» If patient is not already on one, a loop diuretic should

be started (e.g., furosemide).
23
Acute
Primary options

intravenously
-and-
» furosemide: 40-80 mg intravenously initially,
increase according to response
2nd nitroprusside + furosemide

venous vasodilator thereby reducing afterload and
mean arterial pressure, with a modest increase or no

Primary options

-and-
» furosemide: 40-80 mg intravenously initially,
increase according to response
aortic dissection 1st labetalol or esmolol

» Medical therapy of aortic dissection involves lowering
the BP and decreasing the velocity of left ventricular
contraction, which decreases aortic shear stress and
minimises the tendency for propagation of the
dissection.
» Systolic BP should be reduced to 100 to 120 mmHg

in the first 20 minutes or as tolerated by the patient.

resistance, mean arterial pressure, and heart rate, and
TREATMENT
causes a decrease or no change in cardiac output.

Onset of action: 5 to 10 minutes. Duration of action: 3
to 8 hours.
Acute
» The mechanism of action of esmolol is as a selective
beta-blocker, producing a decrease in heart rate. Onset
of action: 1 to 5 minutes. Duration of action: 5 minutes.
» Dose adjusted to maintain BP in desired range;

continue until patient has undergone surgical
repair/evaluation and is stable on oral therapy.
Primary options

OR
intravenously
2nd nitroprusside
» Medical therapy of aortic dissection involves lowering
the BP and decreasing the velocity of left ventricular
contraction, both of which will decrease aortic shear
stress and minimise the tendency for propagation of
the dissection.
» Systolic BP should be reduced to 100 to 120 mmHg

in the first 20 minutes or as tolerated by patient.
» Sodium nitroprusside must be administered with a

beta-blocker as nitroprusside-induced vasodilation
would otherwise induce a compensatory tachycardia
and worsen shear stress.
» Nitroprusside acts as a potent arterial and venous

vasodilator thereby reducing afterload and preload. Its
haemodynamic effects are to decrease mean arterial
pressure (MAP), with a modest increase or no change
in cardiac output. Onset of action: immediate. Duration
of action: 3 to 5 minutes.

Primary options
TREATMENT

25
Acute
plus labetalol or esmolol
resistance, MAP and heart rate, and causes a decrease
or no change in cardiac output. Onset of action: 5 to
10 minutes. Duration of action: 3 to 8 hours.
» The mechanism of action of esmolol is as a selective

beta-blocker, producing a decrease in heart rate. Onset
of action: 1 to 5 minutes. Duration of action: 5 minutes.
» Dose adjusted to maintain BP in desired range;

continue until patient has undergone surgical
repair/evaluation and is stable on oral therapy
Primary options

OR
intravenously
acute renal failure 1st fenoldopam

» Fenoldopam is useful in renal insufficiency because
it causes an increase in blood flow to the kidneys.
» It acts as a selective peripheral dopamine-1-receptor

agonist with arterial vasodilator effects. Its
haemodynamic effects are a decrease in afterload and
an increase in renal perfusion.
Primary options

2nd nicardipine
blocker that increases stroke volume and has strong
TREATMENT
cerebral and coronary vasodilatory activity.

2 to 4 hours.
Acute
Primary options

mg/hour
hyperadrenergic state
sympathomimetic drug use 1st benzodiazepines

» Sympathomimetic drug use includes cocaine,
amphetamines, phenylpropanolamine, phencyclidine,
or the combination of a monoamine oxidase inhibitor
with foods rich in tyramine.
» If the patient is agitated, benzodiazepines can be

given first.
» Lorazepam should be used with caution in patients

with renal or hepatic impairment, myasthenia gravis,
organic brain syndrome, or Parkinson disease. Excess
CNS or respiratory depression can occur with higher
doses and should be watched for.
» Anti-hypertensive agents can be given if the blood

pressure response to benzodiazepines is inadequate.
Primary options
» lorazepam: 1 mg intravenous bolus initially,

repeated every 10-15 minutes according to
response, maximum 8 mg
OR
» diazepam: 5 mg intravenous bolus initially,
repeated every 5-10 minutes according to
response, maximum 50 mg
2nd phentolamine
» Phentolamine acts to block alpha-adrenoceptors. Its
main haemodynamic effects are to increase heart rate
and contractility.
» Onset of action: 1 to 2 minutes. Duration of action: 3

to 10 minutes.
TREATMENT
Primary options
» phentolamine: 2-5 mg intravenous bolus
3rd labetalol and nitroprusside
27
Acute
resistance, mean arterial pressure (MAP), and heart
rate, and causes a decrease or no change in cardiac
output. Onset of action: 5 to 10 minutes. Duration of
action: 3 to 8 hours.


modest increase or no change in cardiac output. Onset
of action: immediate. Duration of action: 3 to 5 minutes.

Primary options

-and-
no sympathomimetic drug use 1st phentolamine

» Causes of hyperadrenergic states include
phaeochromocytoma and abrupt discontinuation of a
short-acting sympathetic blocker.
» Phentolamine acts to block alpha-adrenoceptors. Its

main haemodynamic effects are to increase heart rate
and contractility.
» Onset of action: 1 to 2 minutes. Duration of action: 3

to 10 minutes.
TREATMENT
Primary options
» phentolamine: 2-5 mg intravenous bolus
2nd labetalol and nitroprusside
Acute
resistance, mean arterial pressure (MAP), and heart
rate, and causes a decrease or no change in cardiac
output. Onset of action: 5 to 10 minutes. Duration of
action: 3 to 8 hours.


modest increase or no change in cardiac output. Onset
of action: immediate. Duration of action: 3 to 5 minutes.

Primary options

-and-
eclampsia 1st hydralazine, labetalol, or nicardipine

» A guide target in these patients is to maintain a
systolic BP of 130 to 150 mmHg and a diastolic BP of
80 to 100 mmHg. However, it should be noted that
there are no trials supporting these suggested
thresholds, and treatments should be tailored to
individual patient circumstances.
» Hydralazine, labetalol, or nicardipine can be used

first-line.
TREATMENT
» Hydralazine is an arterial vasodilator with minimal

effects on the fetus. Onset of action: 10 to 20 minutes.
Duration of action: 3 to 8 hours. Its main
haemodynamic effects are a decrease in systemic
vascular resistance, an increase in heart rate and an
increase in intracranial pressure.
29
Acute
» Labetalol acts as an alpha-1-blocker and non-selective
beta-blocker and its haemodynamic effects include
decreasing systemic vascular resistance, mean arterial
pressure, and heart rate, accompanied by a slight
decrease or minimal change in cardiac output. Onset
of action: 5 to 10 minutes. Duration of action: 3 to 8
hours.

blocker that increases stroke volume and has strong
cerebral and coronary vasodilatory activity. Onset of
action: 5 to 10 minutes. Duration of action: 2 to 4 hours.
» Therapy should be continued until the fetus has been

delivered and the patient is stable on oral therapy.
Primary options
» hydralazine: 5-10 mg intravenously every 30

minutes according to response
OR
OR
mg/hour
adjunct magnesium
» There is no consensus on the optimal magnesium
regimen, when it should be started and terminated, or
route of administration.
» Usually initiated at the onset of labour.
» Therapeutic levels: 2.0 to 3.5 mmol/L (4.8 to 8.4

mg/dL).
» Continued for 24 hours after delivery.
» Discontinue if patellar reflex absent, respiratory rate

below 12/minute, or urine output above 25 mL/hour.
TREATMENT
Primary options
» magnesium sulphate: 6 g intravenously over 20

minutes as a loading dose at onset of labour,
followed by 2 mg/hour infusion
Emerging
Clevidipine
Clevidipine is a third-generation dihydropyridine calcium-channel blocker that appears promising for the treatment of
hypertensive emergency.[43] It is a potent and short-acting selective arteriolar vasodilator. It has been shown to be
effective in postoperative hypertension but has not been studied in hypertensive emergency.
TREATMENT
31
Hypertensive emergencies Follow up
Recommendations
Monitoring
FOLLOW UP
The patient should return for a follow-up visit and BP check within 1 week of discharge. During the follow-up visit, BP
should be checked by a medical professional in both arms and with the appropriate cuff size. The goal BP is below
140/90 mmHg. In patients with hypertension and diabetes or renal disease, the BP goal is below 130/80 mmHg.
Patients should return for follow-up visits once a month, or more frequently, until goal BP is achieved. Once goal BP
is achieved, patient should be monitored every 3 to 6 months (or more frequently based on comorbidities). Serum
potassium and creatinine should be measured twice a year.
Patient instructions
Patients should be reminded of the importance of taking medications as directed and not missing doses. Patients
are advised to call their doctor or an ambulance immediately if they experience any dizziness, loss of sensation or
mobility, blurred vision, chest pain, SOB, or any other relevant symptoms.
Complications
Complications Timeframe Likelihood

cardiac impairment variable high
Myocardial damage and subsequent heart failure is a frequent complication and cause of death in hypertensive
emergency.[44] [45]
neurological deficit variable medium
Permanent neurological compromise may occur after stroke, haemorrhage, or hypertensive encephalopathy and is
a frequent cause of death.[44] [45]
renal impairment variable medium
Renal insufficiency and failure is both a frequent cause and complication of hypertensive emergency.[44] [45]
Prognosis
Without therapy, the prognosis of hypertensive emergencies is grim, with 1-year survival rates of 10% to 20%. However,
current antihypertensive therapy has greatly improved survival, with 5-year survival rates around 70% in patients who
receive appropriate treatment. The presence of renal failure on diagnosis of hypertensive emergency increases mortality
rate.[44] [45]
Hypertensive emergencies Guidelines
Diagnostic guidelines
Europe
Risk estimation and the prevention of cardiovascular disease: a national clinical guideline
Published by: Scottish Intercollegiate Guidelines Network Last published: 2007
Treatment guidelines
Europe
2013 ESH/ESC guidelines for the management of arterial hypertension

Published by: European Society of Cardiology Last published: 2013
GUIDELINES
Summary: The main difference is that the ESC guidelines group malignant hypertension and hypertensive emergency
under different entities. Like the JNC 7, the ESC emphasises rapid but controlled management of hypertensive emergency
without specifying rates of BP decrease. The ESC also accepts the use of oral agents for malignant hypertension.
Risk estimation and the prevention of cardiovascular disease: a national clinical guideline
Published by: Scottish Intercollegiate Guidelines Network Last published: 2007
North America
Seventh report of the Joint National Committee on prevention, detection, evaluation, and
treatment of high blood pressure (JNC 7)
Published by: National Heart, Lung, and Blood Institute Last published: 2004
Summary: Hypertensive emergency is defined as elevated BP (>180/120 mmHg) complicated by impending or

progressive target organ dysfunction. Goal of therapy is to reduce mean arterial pressure by no more than 25% (within
minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic over 2 to 6 hours. Exceptions
to this rule are patients with ischaemic stroke or aortic dissection, and patients undergoing thrombolysis.
Africa
South African hypertension practice guideline 2014

Published by: Joint National Hypertension Guideline Working Group; Southern Last published: 2014
African Hypertension Society
33
Hypertensive emergencies Evidence scores
Evidence scores
1. Reduction of BP: there is poor-quality evidence that labetalol may reduce BP in people with hypertensive
emergencies.[13] [14]
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized controlled
trials (RCTs) of <200 participants.
2. Reduction of BP: there is poor-quality evidence that sodium nitroprusside may reduce BP in people with hypertensive
emergencies.[13] [14] [15]
3. Reduction of BP: there is poor-quality evidence that fenoldopam may reduce BP in people with hypertensive
emergencies.[13] [14] [15] [30] [31]
4. Reduction of BP: there is poor-quality evidence that nicardipine may reduce BP in people with hypertensive
emergencies.[13] [14] [15] [33]
5. Reduction of BP: there is poor-quality evidence that esmolol and glyceryl trinitrate may reduce BP in people with
hypertensive emergencies and myocardial injury.[13] [14] [15] [34] [36]
6. Reduction of BP: there is poor-quality evidence that labetalol and glyceryl trinitrate may reduce BP in people with
hypertensive emergencies.[13] [14] [15] [34] [36]
7. Reduction of BP: there is poor-quality evidence that glyceryl trinitrate may reduce BP in people with hypertensive
emergencies and myocardial injury.[13] [14] [15] [34] [36]
EVIDENCE SCORES
8. Reduction of BP: there is poor-quality evidence that beta-blockers may be effective in people with hypertensive
emergencies and aortic dissection.[13] [14] [15] [35]
Hypertensive emergencies Evidence scores
9. Reduction of BP: there is poor-quality evidence that phentolamine may reduce BP in people with hypertensive
emergencies.[13] [14] [15]
10. Reduction of BP: there is poor-quality evidence that hydralazine may reduce BP in pregnant women with hypertensive
emergencies.[13] [14] [15] [37] [38] [39]
11. Reduction of BP: there is poor-quality evidence that labetalol may reduce BP in pregnant women with hypertensive
emergencies.[13] [14] [15] [37] [39] [40]
12. Reduction of BP: there is poor-quality evidence that nicardipine may reduce BP in pregnant women with hypertensive
emergencies.[13] [14] [15] [37] [40]
EVIDENCE SCORES
35
Hypertensive emergencies References
Key articles
REFERENCES
• Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet. 2000;356:411-417. Abstract
• Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral hemorrhage
in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke
Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary
Working Group. Stroke. 2007;38:2001-2023. Full text Abstract
• ACOG Committee on Obstetric Practice. ACOG practice bulletin. Diagnosis and management of preeclampsia and
eclampsia. Number 33, January 2002. American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet.
2002;77:67-75. Abstract
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Hum Hypertens. 1995;9:547-551. Abstract
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magnetic resonance imaging, and aortography in acute aortic dissection: International Registry of Acute Aortic
Dissection (IRAD). Am J Cardiol. 2002;89:1235-1238. Abstract
22. Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke.
Stroke. 2007;38:1655-1711. Full text Abstract
23. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection,
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24. Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral hemorrhage
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labetalol use in the emergency department. Crit Care. 2011;15:R157. Full text Abstract
30. Tumlin JA, Dunbar LM, Oparil S, et al. Fenoldopam, a dopamine agonist, for hypertensive emergency: a multicenter
randomized trial. Acad Emerg Med. 2000;7:653-662. Abstract
31. Devlin JW, Seta ML, Kanji S, Somerville AL. Fenoldopam versus nitroprusside for the treatment of hypertensive
emergency. Ann Pharmacother. 2004;38:755-759. Abstract
32. Bath PM, Krishnan K. Interventions for deliberately altering blood pressure in acute stroke. Cochrane Database Syst
Rev. 2014;(10):CD000039. Full text Abstract
33. Neutel JM, Smith DHG, Wallin D, et al. A comparison of intravenous nicardipine and sodium nitroprusside in the
immediate treatment of severe hypertension. Am J Hypertens. 1994;7:623-628. Abstract
34. Lau J, Antman EM, Jimenez-Silva J, Kupelnick B. Cumulative meta-analysis of therapeutic trials for MI. N Engl J Med.
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Full text Abstract
36. Bussmann WD, Kenedi P, von Mengden HJ, et al. Comparison of nitroglycerin with nifedipine in patients with
hypertensive crisis or severe hypertension. Clin Investig. 1992;70:1085-1088. Abstract
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eclampsia. Number 33, January 2002. American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet.
2002;77:67-75. Abstract
38. Magee LA, Cham C, Waterman EJ, et al. Hydralazine for treatment of severe hypertension in pregnancy: meta-analysis.
BMJ. 2003;327:955-960. Full text Abstract
39. Mabie WC, Gonzalez AR, Sibai BM, et al. A comparative trial of labetalol and hydralazine in the acute management
of severe hypertension complicating pregnancy. Obstet Gynecol. 1987;70:328-333. Abstract
40. Elatrous S, Nouira S, Ouanes Besbes L, et al. Short-term treatment of severe hypertension of pregnancy: prospective
comparison of nicardipine and labetalol. Intensive Care Med. 2002;28:1281-1286. Abstract
41. Nij Bijvank SW, Duvekot JJ. Nicardipine for the treatment of severe hypertension in pregnancy: a review of the
literature. Obstet Gynecol Surv. 2010;65:341-347. Abstract
42. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of
eclampsia. N Engl J Med. 1995;333:201-205. Full text Abstract
43. Bailey JM, Lu W, Levy JH, et al. Clevidipine: a unique agent for the critical care practitioner. Crit Care Shock. 2006;9:9-15.
44. Lip GY, Beevers M, Beevers DG. Complications and survival of 315 patients with malignant-phase hypertension. J
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45. Webster J, Petrie JC, Jeffers TA, et al. Accelerated hypertension patterns or mortality and clinical factors affecting
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46. Midgley JP, Matthew AG, Greenwood CM, et al. Effect of reduced dietary sodium on blood pressure: a meta-analysis
of randomized controlled trials. JAMA. 1996;275:1590-1597. Abstract
47. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement
from the American Heart Association Nutrition Committee. Circulation. 2006;114:82-96. Full text Abstract
39
Hypertensive emergencies Images
Images
Figure 1: Fundus photograph of the right eye with multiple dot-blot haemorrhages typical of hypertensive retinopathy
IMAGES
Courtesy Angie Wen MD, Attending Faculty, New York Eye and Ear Infirmary, New York
Figure 2: Fundus photograph of the left eye with multiple cotton-wool spots typical of hypertensive retinopathy
Hypertensive emergencies Images
Figure 3: Fundus photograph of the right eye centred on the optic nerve, showing multiple cotton-wool spots and macular
exudates in a radiating star configuration around the fovea
IMAGES
41
Hypertensive emergencies Disclaimer
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DISCLAIMER
Contributors:
// Authors:
Hector Ventura, MD
Head
Section of Cardiomyopathy and Heart Transplantation, Ochsner Clinic Foundation, New Orleans, LA
DISCLOSURES: HV declares that he has no competing interests.
Madhavi T. Reddy, MD
Assistant Professor
University of Pennsylvania, Philadelphia, PA
DISCLOSURES: MR is employed by Merck and owns stocks in Merck, and Johnson & Johnson.
// Peer Reviewers:
Aparna Sundaram, DO, MBA, MPH

Physician Consultant
Preventive Medicine, Private Practice, Atlanta, GA
DISCLOSURES: AS declares that she has no competing interests.
Ethan Cumbler, MD
Assistant Professor
Department of Internal Medicine, University of Colorado Health Sciences Center, Denver, CO
DISCLOSURES: EC declares that he has no competing interests.
Michael Schachter, MB, BSc, FRCP

Department of Clinical Pharmacology
St Mary’s Hospital, Imperial College, London, UK
DISCLOSURES: MS declares that he has no competing interests.

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Hypertensive emergencies

The right clinical information, right where it's needed

Last updated: Mar 13, 2017

Step-by-step treatment approach 12

◊ With appropriate treatment, prognosis is good.

Step-by-step diagnostic approach

Clinical features that may identify specific organ compromise include:

• Renal compromise; for example, decrease in urine output.

• FBC, including peripheral blood smear

• Blood chemistry panel, including creatinine and electrolytes

• Urinalysis with microscopy.

In some circumstances, the following may also be indicated:

use of sympathomimetic drugs

use of monoamine oxidase inhibitors (MAOIs)

History & examination factors

BP above 210/130 mmHg (common)

presence of risk factors (common)

Other diagnostic factors

neurological symptoms (common)

cardiac symptoms (common)

abnormal cardiopulmonary examination (common)

oliguria or polyuria (common)

abnormal fundoscopic examination (common)

head CT without contrast may reveal evidence of infarct

Other tests to consider

arterial Doppler ultrasonography, renal magnetic resonance angiography, or

Condition Differentiating signs / Differentiating tests

Hypertension • Asymptomatic elevated BP • History, physical examination,

Step-by-step treatment approach

Choice of agents and route of administration

Exceptions to the above recommendation include:

Accelerated (malignant) hypertension, hypertensive encephalopathy or

Acute ischaemic stroke

Suspected aortic dissection

The third-line treatment choice would be nitroprusside.[13] [14] [34] 2[C]Evidence

Left ventricular failure and/or pulmonary oedema

Acute renal failure

• Sympathomimetic drug use - for example, cocaine, amphetamines, phenylpropanolamine, phencyclidine, or

• Following abrupt discontinuation of a short-acting sympathetic blocker.

Treatment details overview

accelerated (malignant) hypertension or

increased intracranial pressure or 1st labetalol

normal intracranial pressure and 1st labetalol

2nd nitroprusside or nicardipine

acute ischaemic stroke

SBP >220 mmHg or DBP 121 to 1st labetalol

DBP >140 mmHg 1st nitroprusside

myocardial ischaemia/infarction 1st esmolol and glyceryl trinitrate

2nd labetalol and glyceryl trinitrate

left ventricular failure and/or pulmonary 1st glyceryl trinitrate + furosemide

2nd nitroprusside + furosemide

aortic dissection 1st labetalol or esmolol

plus labetalol or esmolol

acute renal failure 1st fenoldopam

sympathomimetic drug use 1st benzodiazepines

3rd labetalol and nitroprusside

no sympathomimetic drug use 1st phentolamine

2nd labetalol and nitroprusside

eclampsia 1st hydralazine, labetalol, or nicardipine

increased intracranial pressure or 1st labetalol

» Onset of action: 5 to 10 minutes. Duration of action:

» In cases of intracranial haemorrhage, goal mean

» Encephalopathy should improve once BP is lowered.

» Dose should be adjusted to maintain BP in desired