Hipertenz Emergenc

7/27/2019 Hipertenz Emergenc

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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 160/110 to 100 mmHg 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.

Other related conditions

Essential hypertension Gestational hypertension

Subarachnoid haemorrhage

Non-ST-elevation myocardial infarction

ST-elevation myocardial infarction

Acute renal failure

Pre-eclampsia

Aortic dissection

Polycystic kidney disease Email

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Fundus photograph of the right eye with multiple dot-blot haemorrhages typical of hypertensive

retinopathy
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Courtesy Angie Wen MD, Columbia University College of Physicians and Surgeons, New York

Fundus photograph of the left eye with multiple cotton-wool spots typical of hypertensive retinopathy


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


DefinitionHypertensive emergency is elevated BP (usually systolic BP >210 mmHg anddiastolic BP >130 mmHg) with rapid deterioration of vital organ function,

resulting in symptoms such as encephalopathy, retinopathy, myocardialischaemia, or renal failure. The absolute value of the BP is not as vital as thepresence of acute end-organ damage.


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dissection, or left ventricular failure with pulmonary oedema. Renal failuremay manifest as oliguria and azotaemia.[6] [13] [14] [15]

Primary preventionThe mainstay of primary prevention is appropriate screening and treatment of

essential hypertension.

Secondary preventionMajor 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]

History & examinationKey diagnostic factorshide allBP 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 factorshide allneurological 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.

Risk factorshide all

Strong

inadequately treated hypertension

A history of inadequately treated hypertension is commonly seen.[5] [9] [10]
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In the US, lack of medical insurance or access to a primary care doctor have been shown to

predispose to hypertensive emergency.[10]

Weak

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.

Diagnostic tests1st tests to orderhide all

Test

FBC with smear

Microangiopathic haemolytic anaemia (MAHA) may occur in patients with hypertensive emergency and

of developing acute renal failure.[17]

blood chemistry

Renal failure as manifested by elevated creatinine may be the only sign of hypertensive emergency.

urinalysis with microscopy

Renal failure as manifested by haematuria and proteinuria may be the only sign of hypertensive emerge

electrocardiogram

If ECG is abnormal, troponin levels are tested to rule out ongoing ischaemia or infarction.

If ECG is normal, aortic dissection should be considered as an explanation for chest pain.

CXR

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 (56% in type B and 63% in
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aortic dissection is suspected, an urgent CT scan with contrast should be ordered.

head CT without contrast

Indicated if neurological complications are suspected. Although the non-contrast CT scan (NCCT) is of lo

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

up to a NCCT. Further neuroimaging (e.g., CT-angiography, magnetic resonance angiography, carotid a

Dopplers) should be considered if initial tests indicate ischaemia or infarct.[22]

head MRI

More sensitive than non-contrast CT scan, but may not be available as first-line investigation in all centre

spot urine or plasma metanephrine

May be useful before initiation of drug therapy to rule out phaeochromocytoma. However, needs to be in

carefully, with consideration for possible confounding factors such as drugs (e.g., tricyclic antidepressan

phenoxybenzamine, beta-blockers, sympathomimetics, buspirone) or major physiological or psychologic

Tests to considerhide all

Test

thoracic CT scan with contrast

This test should be ordered only if aortic dissection is suspected, given the risk of contrast-induced neph

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 tha

CT.[20] [21]

CT scan may be recommended as the initial test of choice but this is institutionally variable and TEE masubstituted if available in a timely fashion.

transoesophageal echocardiography (TEE)

May be substituted for CT if available in a timely fashion. More sensitive than standard CT and compara

helical CT.[20] [21]

plasma renin activity and aldosterone level
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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

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.

Click to view diagnostic guideline references.

Diagnostic criteria

Clinical criteria

Elevated BP in the presence of acute or rapidly deteriorating end-organdamage (e.g., neurological, cardiac, or renal compromise) based on historicalor clinical criteria (physical examination, laboratory tests, or imaging), posingan immediate threat to life, is sufficient for diagnosis of hypertensiveemergency.[3]

Case historyA 50-year-old black man with a history of untreated hypertension presents tothe emergency department with substernal chest pressure. His symptomsstarted 1 day prior. The pain was initially intermittent in nature but hasbecome constant and radiates to his jaw and left shoulder. He also complainsof dizziness and some SOB. Apart from a history of hypertension diagnosed1 year ago, the patient denies any past medical history. He is not taking anyantihypertensive medications. The patient denies smoking, or alcohol or druguse. Family history is unremarkable. His BP is 230/130 mmHg with otherwisenormal vital signs and no other significant findings. ECG shows diffuse T-wave inversion and ST depression in lateral leads. Laboratory testing issignificant for elevated troponin, signalling MI.

Other presentationsOther ways in which hypertensive emergency can present includeneurological symptoms (e.g., cerebrovascular accidents, 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).
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Treatment Options

Patient group

Treatment

line Treatmenthide all

accelerated (malignant)hypertension or hypertensive

encephalopathy or intracranial

haemorrhage

increased intracranial pressure or

renal disease

1st labetalol

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.
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Patient group

Treatment


accelerated (malignant)

hypertension or hypertensive


haemorrhage

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

minutes according to response, maximum 15

mg/hour

3rd fenoldopam

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.




MAP should not be dropped to below 110 mmHg.



decrease in BP, an alternative diagnosis should be

considered.

Continue until BP controlled on oral agents

Primary Options
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Patient group

Treatment





haemorrhage

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 andrenal function

1st labetalol









decrease in BP, an alternative diagnosis should beconsidered.

Dose should be adjusted to maintain BP in desired

range and is continued until BP controlled on oral

agents.

Primary Options




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
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Patient group

Treatment





haemorrhage

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


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Patient group

Treatment





haemorrhage

SBP 220 mmHg and DBP 120

mmHg

1st close observation BP reduction

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.


The choice of agent to reduce blood pressure

depends on the associated end-organ involvement.

SBP >220 mmHg or DBP 121 to

140 mmHg

1st labetalol

If the systolic BP is above 220 mmHg or the


16/37

Patient group

Treatment





haemorrhage

diastolic BP is between 121 and 140 mmHg, then

labetalol[13] [14] [15] [C Evidence] or

nicardipine[13] [14][15] [33] [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 haemodynamiceffects include decreasing systemic vascular

resistance, MAP, and heart rate, accompanied by

a slight decrease or minimal change in cardiac

output.



Continue until BP controlled on oral agents.

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] [C Evidence] or

nicardipine[13] [14] [15][33] [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.


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Patient group

Treatment





haemorrhage


Primary Options




mg/hour

DBP >140 mmHg1st nitroprusside

If diastolic BP is above 140 mmHg, then

nitroprusside[13] [14] [C Evidence]may be used to

achieve a 10% to 15% reduction over 24 hours.

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.



maintained


18/37

Patient group

Treatment





haemorrhage

myocardial ischaemia/infarction1st 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

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 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

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Patient group

Treatment





haemorrhage


Primary Options


intravenously

3rd nitroprusside


venous vasodilator thereby reducing afterload and


mean arterial pressure, with a modest increase or

no change in cardiac output.


5 minutes.



maintained


20/37

Patient group

Treatment





haemorrhage

arterial vessels.

It causes a decrease in preload and cardiac output

and increases coronary blood flow.


5 minutes.


If patient is not already on one, a loop diuretic

should be started (e.g., furosemide).

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 change in cardiac output.


thiocyanate levels after 48 hours of therapy (levelsmaintained


21/37

Patient group

Treatment





haemorrhage

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

and

furosemide: 40-80 mg intravenously initially,

increase according to response

aortic dissection1st 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 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;


22/37

Patient group

Treatment





haemorrhage

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.

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Patient group

Treatment





haemorrhage


maintained


24/37

Patient group

Treatment





haemorrhage

OR


intravenously

acute renal failure1st 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

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

2nd nicardipine


blocker that increases stroke volume and has




Primary Options

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Patient group

Treatment





haemorrhage



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


26/37

Patient group

Treatment





haemorrhage

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.

Primary Options

phentolamine: 2-5 mg intravenous bolus

3rd labetalol and nitroprusside



resistance, mean arterial pressure (MAP), and






would otherwise induce a compensatory

tachycardia and worsen shear stress.



Its haemodynamic effects are to decrease MAP,

with a modest increase or no change in cardiac

output. Onset of action: immediate. Duration of




maintained


27/37

Patient group

Treatment





haemorrhage

mg/L)). Maximum dose should be delivered for less

than 10 minutes to decrease chance of cyanide

toxicity.


Primary Options




and

nitroprusside : 0.3 to 0.5 micrograms/kg/minute

intravenously initially, increase by 0.5

micrograms/kg/minute increments according to


no sympathomimetic drug use1st 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.

Primary Options

phentolamine: 2-5 mg intravenous bolus

2nd labetalol and nitroprusside


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Patient group

Treatment





haemorrhage

resistance, mean arterial pressure (MAP), and






would otherwise induce a compensatorytachycardia and worsen shear stress.



Its haemodynamic effects are to decrease MAP,

with a modest increase or no change in cardiac

output. Onset of action: immediate. Duration of



thiocyanate levels after 48 hours of therapy (levelsmaintained


29/37

Patient group

Treatment





haemorrhage


eclampsia1st 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.

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.

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




Therapy should be continued until the fetus has


30/37

Patient group

Treatment





haemorrhage

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.

Primary Options

magnesium sulphate: 6 g intravenously over 20
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more than 25% (within minutes to 1 hour), then, if stable, to 160/100 to 110mmHg within the next 2 to 6 hours.

Excessive falls in pressure that may precipitate renal, cerebral, or coronaryischaemia should be avoided. For this reason, short-acting nifedipine is nolonger 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 clinicallystable, further gradual reductions towards a normal BP can be implementedover 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 intracranialhaemorrhage

Accelerated hypertension (also known as malignant hypertension) is severehypertension occurring with retinopathy of grade III (flame haemorrhages, dotand blot haemorrhages, hard and soft exudates) or grade IV (papilloedema).

Hypertensive encephalopathy encompasses the transient neurologicalsymptoms that occur with malignant hypertension, which are usually reversedby prompt treatment and lowering of BP.

In the management of intracerebral haemorrhage, the ideal level of a patient'sBP should be based on individual factors including: baseline BP, presumedcause of haemorrhage, age, elevated intracranial pressure, and interval sinceonset.

While elevated BP could in theory increase the risk of ongoing bleeding fromruptured small arteries and arterioles, the relationship between BP,


33/37

intracranial pressure, and volume of haemorrhage is complex and not yetfully understood.

The rationale for lowering BP is to minimise further haemorrhage - forexample, from a ruptured aneurysm or arteriovenous malformation. However,

in primary intracerebral haemorrhage, when a specific vasculopathy is notapparent, the risk from a mildly elevated BP may be lower, so aggressivereduction of BP must be balanced against the possible risk of inducingcerebral ischaemia in other brain areas.[24] [25]

In cases of intracranial haemorrhage, target mean arterial pressure (MAP) is130 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] [C Evidence] If patients donot have evidence of raised intracranial pressure, a second-line treatmentchoice is nitroprusside.[13] [14] [C Evidence] However, if raised intracranialpressure is present or suspected, nitroprusside is contraindicated andanother agent should be used. Nitroprusside decreases cerebral blood flowwhile increasing intracranial pressure, effects that are particularlydisadvantageous in patients with hypertensive encephalopathy or following acerebrovascular accident.[26] [27][28] It should also be avoided in patientswith renal or hepatic insufficiency. Nicardipine is another second-line agentwhich can be used. One RCT found that intravenous nicardipine significantlyincreased the proportion of people who reached physician-specified target

range systolic BP within 30 minutes compared with intravenouslabetalol.[29] Nicardipine is especially useful in the presence of cardiacdisease due to coronary vasodilatory effects.The third-line treatment choice is fenoldopam, a selective peripheraldopamine-1-receptor agonist with arterial vasodilatoreffects.[13] [14] [15] [30] [31] [C Evidence] This drug is particularly useful inpatients with renal insufficiency, where the use of nitroprusside is restricteddue to the risk of thiocyanate poisoning.

Acute ischaemic strokeTreating a hypertensive emergency with an associated acute ischaemicstroke warrants greater caution in reducing BP than in other types ofhypertensive emergency. Overly rapid or too great a reduction of MAP maydecrease CPP to a level that could theoretically worsen brain injury. Thefollowing may be used as guidance.
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If systolic BP is below 220 mmHg and diastolic BP below 120 mmHg, then itis reasonable to maintain close observation without direct intervention toreduce 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 anddiastolic 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.

If systolic BP is above 220 mmHg or diastolic BP is between 121 to 140mmHg, then labetalol[13] [14] [15] [C Evidence] ornicardipine[13] [14] [15] [33] [C Evidence] should be used to achieve a 10%

to 15% reduction in 24 hours.If diastolic BP is above 140 mmHg, then nitroprusside[13] [14] is used toachieve a 10% to 15% reduction over 24 hours.[13] [14] [34] [C Evidence]

Suspected aortic dissectionIf aortic dissection is suspected in a hypertensive emergency, the BP shouldbe lowered quite aggressively, typically with a target of reducing systolic BPto between 100 and 120 mmHg within 20 minutes.

Medical therapy aims to both lower the BP and decrease the velocity of leftventricular contraction, so decreasing aortic shear stress and minimising thetendency for propagation of the dissection.

First-line treatment choice is beta-blockers, either labetalol or esmolol,administered intravenously.[13] [14] [15] [35] [C Evidence]Second-line treatment choice would be the combination of nitroprusside andbeta-blockers.[13] [14] [15] [35] [C Evidence] Nitroprusside must beadministered with a beta-blocker, as nitroprusside-induced vasodilation would

otherwise induce a compensatory tachycardia and worsen shear stress onthe intimal flap.

Myocardial ischaemia/infarctionFirst-line treatment of hypertensive emergency complicated by myocardialischaemia or infarction is the combination of esmolol (a selective beta-
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blocker) plus glyceryl trinitrate (a peripheral vasodilator, which affects venousvessels more than arterial).[13] [14] [15] [34][36] [C Evidence]

Esmolol acts to reduce heart rate and glyceryl trinitrate acts to decreasepreload and cardiac output and increases coronary blood flow.

Second-line treatment choice would be labetalol plus glyceryltrinitrate.[13] [14] [15] [34] [36][C Evidence]The third-line treatment choice would be nitroprusside.[13] [14] [34] [CEvidence]

Left ventricular failure and/or pulmonaryoedema

First-line treatment of hypertensive emergency with left ventricular failureand/or pulmonary oedema is glyceryl trinitrate.[13] [14] [15] [36] [C Evidence]Nitroprusside (a potent arterial and venous vasodilator that decreasesafterload and preload) is the second-line treatment choice in thissituation.[13] [14] [34] [C Evidence]

If patient is not already on one, a loop diuretic should be started (e.g.,furosemide).

Acute renal failureFenoldopam is the first-line treatment choice of hypertensive emergency

complicated by acute renal failure.[13] [14] [15] [30] [31] [C Evidence] Thisdrug (a selective peripheral dopamine-1-receptor agonist with arterialvasodilator effects) is particularly useful in renal insufficiency because it actsto both decrease afterload and increase renal perfusion. Second-linetreatment choice is nicardipine, a dihydropyridine calcium-channel blocker,which increases stroke volume and has strong cerebral and coronaryvasodilatory activity.[13] [14] [15] [33] [C Evidence]

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.
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