hypertensive emergencies -...

Hypertensiveemergencies

The right clinical information, right where it's needed

Last updated: Nov 13, 2017

Table of ContentsSummary 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 11

Diagnostic criteria 11

Treatment 12

Step-by-step treatment approach 12

Treatment details overview 15

Treatment options 18

Emerging 33

Follow up 34

Recommendations 34

Complications 34

Prognosis 34

Guidelines 35

Diagnostic guidelines 35

Treatment guidelines 35

Evidence scores 36

References 38

Images 42

Disclaimer 44

Summary

◊ Defined as elevated BP (usually systolic BP >210 mmHg and diastolic BP >130 mmHg) with rapiddecompensation of vital organ function.

◊ If the clinical suspicion is high, treatment should be initiated immediately without waiting for furthertests.

◊ 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 to1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2 to 6hours. Exceptions to this general rule are patients with intracranial pathology and patients with aorticdissection. Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischaemiashould be avoided.

◊ With appropriate treatment, prognosis is good.

Hypertensive emergencies BasicsBA

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DefinitionHypertensive emergency is elevated BP (usually systolic BP >210 mmHg and diastolic BP >130 mmHg)with rapid 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 acuteend-organ damage.

EpidemiologyThe 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 alsomore 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 isexpected to increase.[1]

AetiologyThere are many causes of hypertensive emergency. By far the most common cause is essentialhypertension that is either undiagnosed or inadequately treated.[4] The next most common cause issecondary to renal disease, such as renal artery stenosis, acute glomerulonephritis, collagen-vasculardiseases, or kidney transplantation.[11] [12]Pregnancy-related eclampsia is also an important cause ofhypertensive emergency. Other rarer causes include hyperaldosteronism and conditions leading to excesscirculating catecholamines (e.g., phaeochromocytoma, sympathomimetic drug intake, autonomic dysfunctionafter spinal cord injury, or inadvertent drug or food interactions with monoamine oxidase inhibitors).[13]

PathophysiologyThe factors that lead to the development of hypertensive emergency are poorly understood. A rise insystemic vascular resistance initiates the cycle. The subsequent increase in BP generates mechanical stressand 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 vasoactivemediators, generating ongoing injury. Volume depletion caused by pressure natriuresis and activation ofthe renin-angiotensin system often leads to further vasoconstriction. Systemic vasoconstriction leads todecreased blood flow to vital organs and the subsequent organ injury that is the hallmark of hypertensiveemergency. 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, aorticdissection, or left ventricular failure with pulmonary oedema. Renal failure may manifest as oliguria andazotaemia.[6] [13] [14] [15]

4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.BMJ Best Practice topics are regularly updated and the most recent versionof 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.

https://bestpractice.bmj.com

Hypertensive emergencies Prevention

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, andmoderation of alcohol consumption.[46] [47]

PREVEN

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This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.BMJ Best Practice topics are regularly updated and the most recent versionof the topics can be found on bestpractice.bmj.com . Use of this content is


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Hypertensive emergencies DiagnosisD

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Case historyCase history #1A 50-year-old black man with a history of untreated hypertension presents to the emergency departmentwith substernal chest pressure. His symptoms started 1 day prior. The pain was initially intermittent innature but has become constant and radiates to his jaw and left shoulder. He also complains of dizzinessand some SOB. Apart from a history of hypertension diagnosed 1 year ago, the patient denies any pastmedical history. He is not taking any antihypertensive medications. The patient denies smoking, or alcoholor drug use. Family history is unremarkable. His BP is 230/130 mmHg with otherwise normal vital signsand 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 presentationsOther 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., aorticdissection, pulmonary oedema), or nephrological symptoms (e.g., decreased or absent urine output).

Step-by-step diagnostic approachThe key to diagnosis of hypertensive emergency is a rapid but thorough evaluation. If hypertensiveemergency is suspected, initiation of treatment should not be delayed while conducting a full diagnosticappraisal.

HistoryAny 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 ofmovement

• Cardiac compromise; for example, chest pain or pressure, SOB, orthopnoea, paroxysmal nocturnaldyspnoea, 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 examinationAn 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 acuff 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 isa more than 20 mmHg pressure difference between arms, aortic dissection should be considered.




Hypertensive emergencies Diagnosis

A fundoscopic examination should be performed, looking for the presence of arteriolar spasm, retinaloedema, 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, motorstrength, 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 evaluationBaseline blood and urine samples must be collected prior to administration of treatment. Laboratoryevaluation 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 patientswith diastolic hypertension with persistent hypokalaemia and metabolic alkalosis)

• Plasma renin activity before and 1 hour after 25-mg captopril is administered if renovascularhypertension is suspected. Renovascular hypertension should be suspected in patients with severehypertension 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., inpatients with hypertension and palpitations, headaches and/or diaphoresis although clinicalpresentation is very variable).

Further investigationCXR and ECG are obtained. If aortic dissection is considered, an urgent thoracic CT scan with contrast ora transoesophageal echocardiogram should also be obtained.

If ischaemic stroke or intracranial haemorrhage is suspected (e.g., in patients with focal neurologicaldefects) urgent non-contrast CT scan (NCCT) of the head and/or an MRI are done, depending on localavailability.

Risk factorsStronginadequately 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 topredispose to hypertensive emergency.[10]

Weakolder 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 factorsKey diagnostic factorsBP 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 factorsneurological 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 tests1st test to order

Test ResultFBC with smear

• Microangiopathic haemolytic anaemia (MAHA) may occur in patientswith hypertensive emergency and increases the risk of developingacute renal failure.[17]

may reveal schistocytes(red cell fragments)indicating the presence ofhaemolysis

blood chemistry• Renal failure as manifested by elevated creatinine may be the only

sign of hypertensive emergency.

may reveal elevatedcreatinine

urinalysis with microscopy• Renal failure as manifested by haematuria and proteinuria may be the

only sign of hypertensive emergency.

may reveal presence of redcells and protein

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.

may reveal evidence ofischaemia or infarct suchas ST- or T-wave changes

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 type A).[18] If aortic dissectionis suspected, an urgent CT scan with contrast should be ordered.

may reveal evidenceof pulmonary oedemaindicating left ventricularfailure or widenedmediastinum indicatingpossible aortic dissection

head CT without contrast• Indicated if neurological complications are suspected. Although the

non-contrast CT scan (NCCT) is of low sensitivity for acute ischaemicstroke, it is usually ordered to exclude or confirm haemorrhage.

• MRI, although more sensitive than NCCT, may not be widely availablein a timely fashion and should be ordered in follow-up to a NCCT.Further neuroimaging (e.g., CT-angiography, magnetic resonanceangiography, carotid and vertebral Dopplers) should be considered ifinitial tests indicate ischaemia or infarct.[22]

may reveal evidence ofinfarct or haemorrhage

head MRI• More sensitive than non-contrast CT scan, but may not be available

as first-line investigation in all centres.

may reveal evidence ofinfarct or haemorrhage

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Test Resultspot urine or plasma metanephrine

• May be useful before initiation of drug therapy to rule outphaeochromocytoma. 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 orpsychological stress.

may reveal elevatedmetanephrine levels

Other tests to consider

Test Resultthoracic CT scan with contrast

• This test should be ordered only if aortic dissection is suspected,given the risk of contrast-induced nephropathy, especially in thepresence of possible underlying renal abnormality.

• The sensitivity and specificity of standard CT for the diagnosis ofaortic 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 comparableto helical CT and more sensitive than standard CT.[20] [21]

• CT scan may be recommended as the initial test of choice but this isinstitutionally variable and TEE may be substituted if available in atimely fashion.

evidence of 2 separateaortic lumens withdividing intimal flap inaortic dissection

transoesophageal echocardiography (TEE)• May substitute for CT if available in a timely fashion. More sensitive

than standard CT and comparable with helical CT.[20] [21]

evidence of 2 separateaortic lumens withdividing intimal flap inaortic dissection

plasma renin activity and aldosterone level• This test is an indirect measure of the activity of renin through

measurement of the rate of production of angiotensin I, whichincreases as a result of renin stimulation. Aldosterone levelsare usually measured at the same time. High plasma reninactivity suggests hypertension from the vasoconstrictive effects ofangiotensin. Requires renal vein catheterisation and so needs formalconsent from the patient.

in primaryhyperaldosteronism, reninactivity will be decreasedand aldosterone levelsincreased; in secondaryhyperaldosteronism,both renin activity andaldosterone levels will beincreased

single-dose captopril challenge• May be useful where renovascular hypertension is suspected,

particularly in patients who have not received previous medicaltherapy.

• Baseline plasma renin activity is measured and the patient is thengiven 25 to 50 mg of captopril; measurement of plasma renin activityis repeated 60 minutes later.

• Test sensitivity is excellent but specificity is poor. Further testing withrenal arterial Doppler ultrasonography, renal magnetic resonanceangiography, or contrast angiography may be necessary to confirmdiagnosis.

may reveal decrease inrenin plasma activity inresponse to captopril





Differential diagnosis

Condition Differentiating signs /symptoms

Differentiating tests

Hypertensive urgency • Symptomatic elevated BP • History, physicalexamination, laboratorytests, and imaging showno evidence of end-organdamage.

Hypertension • Asymptomatic elevated BP • History, physicalexamination, laboratorytests, and imaging showno evidence of end-organdamage.

Diagnostic criteriaClinical criteriaElevated 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, orimaging), posing an immediate threat to life, is sufficient for diagnosis of hypertensive emergency.[3]

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Hypertensive emergencies TreatmentTR

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Step-by-step treatment approachIf hypertensive emergency is suspected, treatment should not be delayed while conducting a full diagnosticevaluation.

Appropriate facilitiesPatients with hypertensive emergencies should be admitted to an ICU for continuous monitoring ofBP and parenteral administration of appropriate therapeutic agent(s).[23] Other supportive measuresthat may be required include intracranial pressure monitoring (in rare cases of increased intracranialpressure), intubation (in case of respiratory distress), or dialysis (in case of renal failure).

Choice of agents and route of administrationThe specific parenteral agents used for treating a hypertensive emergency should be dictated by theend-organ systems that have been damaged, patient comorbidities, and overall clinical condition. Oraltherapy should begin as soon as possible so that parenteral therapy can be weaned. There are very fewrandomised controlled trials studying different parenteral agents in hypertensive emergency. Publishedguidelines are therefore based on common clinical experience and practice.

Rate of BP reductionThe seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatmentof High Blood Pressure[23] states the initial goal of therapy in hypertensive emergencies is to reducemean arterial BP by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolicand 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 ofhypertensive emergencies or urgency.

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradualreductions 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 theuse of immediate antihypertensive treatment

• Patients with aortic dissection, who should have their systolic BP lowered to less than 100 mmHg iftolerated

• Patients in whom BP needs to be lowered to enable the use of thrombolytic agents, in which casethe target systolic BP is under 185 mmHg and diastolic BP under 110 mmHg.

Accelerated (malignant) hypertension, hypertensiveencephalopathy or intracranial haemorrhageAccelerated hypertension (also known as malignant hypertension) is severe hypertension occurring withretinopathy of grade III (flame haemorrhages, dot and blot haemorrhages, hard and soft exudates) orgrade IV (papilloedema).




Hypertensive emergencies Treatment

Hypertensive encephalopathy encompasses the transient neurological symptoms that occur withmalignant 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 onindividual factors including: baseline BP, presumed cause of haemorrhage, age, elevated intracranialpressure, and interval since onset.

While elevated BP could in theory increase the risk of ongoing bleeding from ruptured small arteries andarterioles, the relationship between BP, intracranial pressure, and volume of haemorrhage is complex andnot yet fully understood.

The rationale for lowering BP is to minimise further haemorrhage - for example, from a rupturedaneurysm or arteriovenous malformation. However, in primary intracerebral haemorrhage, when a specificvasculopathy is not apparent, the risk from a mildly elevated BP may be lower, so aggressive reductionof 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 goalof maintaining a cerebral perfusion pressure (CPP) above 70 mmHg. Avoid BP dropping to below 110mmHg.

The first-line treatment is labetalol.[13] [14] [15] 1[C]Evidence If patients do not have evidence of raisedintracranial pressure, a second-line treatment choice is nitroprusside.[13] [14] 2[C]Evidence However, ifraised intracranial pressure is present or suspected, nitroprusside is contraindicated and another agentshould be used. Nitroprusside decreases cerebral blood flow while increasing intracranial pressure,effects that are particularly disadvantageous in patients with hypertensive encephalopathy or following astroke.[26] [27] [28] It should also be avoided in patients with renal or hepatic insufficiency. Nicardipine isanother second-line agent which can be used. One RCT found that intravenous nicardipine significantlyincreased the proportion of people who reached physician-specified target range systolic BP within 30minutes compared with intravenous labetalol.[29] Nicardipine is especially useful in the presence ofcardiac disease due to coronary vasodilatory effects.

The third-line treatment choice is fenoldopam, a selective peripheral dopamine-1-receptor agonistwith arterial vasodilator effects.[13] [14] [15] [30] [31] 3[C]Evidence This drug is particularly useful inpatients with renal insufficiency, where the use of nitroprusside is restricted due to the risk of thiocyanatepoisoning.

Acute ischaemic strokeTreating a hypertensive emergency with an associated acute ischaemic stroke warrants greater caution inreducing BP than in other types of hypertensive emergency. Overly rapid or too great a reduction of MAPmay decrease CPP to a level that could theoretically worsen brain injury. The following may be used asguidance.

If systolic BP is below 220 mmHg and diastolic BP below 120 mmHg, then it is reasonable to maintainclose 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

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• There is concurrent intracranial haemorrhage, in which case the goals are a systolic BP of between140 and 160 mmHg and/or a mean arterial pressure (MAP) of 130 mmHg with the CPP maintainedabove 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 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.

If diastolic BP is above 140 mmHg, then nitroprusside[13] [14] is used to achieve a 10% to 15% reductionover 24 hours.[13] [14] [34] 2[C]Evidence

Suspected aortic dissectionIf aortic dissection is suspected in a hypertensive emergency, the BP should be lowered quiteaggressively, typically with a target of reducing systolic BP to between 100 and 120 mmHg within 20minutes.

Medical therapy aims to both lower the BP and decrease the velocity of left ventricular contraction, sodecreasing 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] 5[C]Evidence

Second-line treatment choice would be the combination of nitroprusside and beta-blockers.[13] [14] [15][35] 5[C]Evidence Nitroprusside must be administered with a beta-blocker, as nitroprusside-inducedvasodilation would otherwise induce a compensatory tachycardia and worsen shear stress on the intimalflap.

Myocardial ischaemia/infarctionFirst-line treatment of hypertensive emergency complicated by myocardial ischaemia or infarction is thecombination of esmolol (a selective beta-blocker) plus glyceryl trinitrate (a peripheral vasodilator, whichaffects venous vessels more than arterial).[13] [14] [15] [34] [36] 6[C]Evidence

Esmolol acts to reduce heart rate and glyceryl trinitrate acts to decrease preload and cardiac output andincreases coronary blood flow.

Second-line treatment choice would be labetalol plus glyceryl trinitrate.[13] [14] [15] [34] [36]7[C]Evidence

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

Left ventricular failure and/or pulmonary oedemaFirst-line treatment of hypertensive emergency with left ventricular failure and/or pulmonary oedema isglyceryl trinitrate.[13] [14] [15] [36] 8[C]Evidence

Nitroprusside (a potent arterial and venous vasodilator that decreases afterload and preload) is thesecond-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 failureFenoldopam is the first-line treatment choice of hypertensive emergency complicated by acute renalfailure.[13] [14] [15] [30] [31] 3[C]Evidence This drug (a selective peripheral dopamine-1-receptoragonist with arterial vasodilator effects) is particularly useful in renal insufficiency because it acts toboth decrease afterload and increase renal perfusion. Second-line treatment choice is nicardipine, adihydropyridine calcium-channel blocker, which increases stroke volume and has strong cerebral andcoronary vasodilatory activity.[13] [14] [15] [33] 4[C]Evidence

Hyperadrenergic statesHyperadrenergic 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 arebenzodiazepines, and anti-hypertensive medications are given only if the blood pressure response isinadequate. In all other clinical situations, the first-line treatment choice is phentolamine (which actsby blocking alpha-adrenoceptors).[13] [14] [15] 9[C]Evidence The second-line treatment choice is thecombination of labetalol1[C]Evidence plus nitroprusside.[13] [14] [15] 2[C]Evidence Administration of abeta-blocker alone is contraindicated, since inhibition of beta-adrenoceptor-induced vasodilation results inunopposed alpha-adrenergic vasoconstriction and a further rise in BP.

EclampsiaThe first-line treatment choices in this situation are hydralazine,[13] [14] [15] [37] [38] [39] 10[C]Evidencelabetalol,[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 fetalcyanide poisoning.

A guide target in these patients is to maintain a systolic BP of 130 to 150 mmHg and a diastolic BP of 80to 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 asan adjunctive therapy,[13] [14] [15] [37] [42] 13[B]Evidence although there is no consensus on the optimalregimen, when it should be started and terminated, or the optimal route of administration. The drug isusually initiated at the onset of labour.

Treatment details overviewConsult your local pharmaceutical database for comprehensive drug information including contraindications,drug interactions, and alternative dosing. ( see Disclaimer )

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Acute ( summary )Patient group Tx line Treatment

increased intracranialpressure or renal disease

1st labetalol


2nd nicardipine


3rd fenoldopam

normal intracranialpressure and renalfunction

1st labetalol


2nd nitroprusside or nicardipine


3rd fenoldopam

SBP ≤220 mmHg and DBP≤120 mmHg

1st close observation ± BP reduction

SBP >220 mmHg or DBP121 to 140 mmHg

1st labetalol


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/orpulmonary oedema

1st glyceryl trinitrate + furosemide

2nd nitroprusside + furosemide

aortic dissection 1st labetalol or esmolol

2nd nitroprusside

plus labetalol or esmolol

acute renal failure 1st fenoldopam





Acute ( summary )2nd nicardipine

sympathomimetic druguse

1st benzodiazepines


2nd phentolamine


3rd labetalol and nitroprusside

no sympathomimeticdrug use

1st phentolamine


2nd labetalol and nitroprusside

eclampsia 1st hydralazine, labetalol, or nicardipine

adjunct magnesium

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Treatment options

Acute

Patient group Tx line Treatment


1st labetalol

» Labetalol is drug of choice in situationscharacterised by markedly elevated intracranialpressure.

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

» In cases of intracranial haemorrhage, goalmean arterial pressure (MAP) is 130 mmHg andgoal cerebral perfusion pressure is above 70mmHg. MAP should not be dropped below 110mmHg.

» Encephalopathy should improve once BP islowered. If there is no improvement despite adecrease in BP, an alternative diagnosis shouldbe considered.

» Dose should be adjusted to maintain BPin desired range and is continued until BPcontrolled on oral agents.

Primary options

» labetalol: 20 mg intravenously every 10minutes according to response, maximum300 mg total dose; or 0.5 to 2 mg/minuteintravenous infusion


2nd nicardipine

» Nicardipine is a second-generationdihydropyridine derivative calcium-channelblocker with high vascular selectivity and strongcerebral and coronary vasodilatory activity. Theonset of action of IV nicardipine is from 5 to 15minutes, with a duration of action of 4 to 6 hours.

» Nicardipine is especially useful in the presenceof cardiac disease due to coronary vasodilatoryeffects.

Primary options

» nicardipine: 5 mg/hour intravenouslyinitially, increase by 2.5 mg/hour incrementsevery 15 minutes according to response,maximum 15 mg/hour


3rd fenoldopam





Acute

Patient group Tx line Treatment» Fenoldopam is especially useful in renalinsufficiency, where the use of nitroprussideis restricted because of the risk of thiocyanatepoisoning.

» It acts as a selective peripheral dopamine-1-receptor agonist with arterial vasodilator effects.Its haemodynamic effects are a decrease inafterload and an increase in renal perfusion.

» Onset of action: 5 minutes. Duration of action:30 minutes.

» In cases of intracranial haemorrhage, goalmean arterial pressure (MAP) is 130 mmHg andgoal cerebral perfusion pressure is above 70mmHg. MAP should not be dropped to below110 mmHg.


» Continue until BP controlled on oral agents

Primary options

» fenoldopam: 0.1 to 0.3 micrograms/kg/minute intravenously initially, increase by0.05 to 0.1 micrograms/kg/minute incrementsevery 15 minutes according to response,maximum 1.6 micrograms/kg/minute


1st labetalol


» In cases of intracranial haemorrhage, goalmean arterial pressure (MAP) is 130 mmHg andgoal cerebral perfusion pressure is above 70mmHg. MAP should not be dropped below 110mmHg.


» Dose should be adjusted to maintain BPin desired range and is continued until BPcontrolled on oral agents.

Primary options

» labetalol: 20 mg intravenously every 10minutes according to response, maximum

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Acute

Patient group Tx line Treatment300 mg total dose; or 0.5 to 2 mg/minuteintravenous infusion


2nd nitroprusside or nicardipine

» Sodium nitroprusside acts as a potent arterialand venous vasodilator, thereby reducingafterload and preload. Its haemodynamic effectsare to decrease mean arterial pressure (MAP),with a modest increase or no change in cardiacoutput. Onset of action: immediate. Duration ofaction: 3 to 5 minutes.

» Patients should be monitored by drawingthiocyanate levels after 48 hours of therapy(levels kept at <2064 micromol/L (<12 mg/dL or120 mg/L)). Maximum dose should be deliveredfor less than 10 minutes to decrease chance ofcyanide toxicity.

» Nicardipine is a second-generationdihydropyridine derivative calcium-channelblocker with high vascular selectivity and strongcerebral and coronary vasodilatory activity. Theonset of action of IV nicardipine is from 5 to 15minutes, with a duration of action of 4 to 6 hours.It is especially useful in the presence of cardiacdisease due to coronary vasodilatory effects.

» In cases of intracranial haemorrhage, goalMAP is 130 mmHg and goal cerebral perfusionpressure is above 70 mmHg. MAP should not bedropped to below 110 mmHg. Encephalopathyshould improve once BP is lowered. If there isno improvement despite a decrease in BP, analternative 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 0.5micrograms/kg/minute increments accordingto response, maximum 10 micrograms/kg/minute

OR

Primary options






Acute

Patient group Tx line Treatmentnormal intracranialpressure and renalfunction

3rd fenoldopam

» Fenoldopam acts as a selective peripheraldopamine-1-receptor agonist with arterialvasodilator effects. Its haemodynamic effects area decrease in afterload and an increase in renalperfusion.

» Onset of action: 5 minutes. Duration of action:30 minutes.

» In cases of intracranial haemorrhage, goalmean arterial pressure (MAP) is 130 mmHg andgoal cerebral perfusion pressure is above 70mmHg. MAP should not be dropped to below110 mmHg.


» Continue until BP controlled on oral agents

Primary options


SBP ≤220 mmHg and DBP≤120 mmHg

1st close observation ± BP reduction

» Treatment of a hypertensive emergency withan associated acute ischaemic stroke warrantsgreater caution in reducing BP than with othertypes of hypertensive emergency. Overly rapid ortoo great a reduction of mean arterial pressure(MAP) may decrease cerebral perfusionpressure to a level that could theoreticallyworsen brain injury. The following may be usedas guidance:

» If the systolic BP is below 220 mmHg andthe diastolic BP is below 120 mmHg, thereis no evidence of end organ involvement orintracranial haemorrhage and thrombolytictreatment is not proposed, then it is reasonableto maintain close observation without directintervention to reduce BP.

» If there is other end-organ involvement suchas aortic dissection, renal failure, or acute MI, orthe patient is to receive thrombolytics, the target

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Patient group Tx line Treatmentsystolic BP is below 185 mmHg and diastolic BPis below 110 mmHg.

» If there is intracranial haemorrhage, the targetsystolic BP is 140 to 160 mmHg and/or a meanarterial pressure (MAP) of 130 mmHg and acerebral perfusion pressure maintained above 70mmHg.

» MAP should not be dropped below 110 mmHg.

» The choice of agent to reduce bloodpressure depends on the associated end-organinvolvement.


1st labetalol

» If the systolic BP is above 220 mmHg or thediastolic BP is between 121 and 140 mmHg,then labetalol[13] [14] [15] 1[C]Evidence ornicardipine[13] [14] [15] [33] 4[C]Evidenceshould 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 vascularresistance, MAP, and heart rate, accompaniedby a slight decrease or minimal change incardiac output.



Primary options



2nd nicardipine

» If systolic BP is above 220 mmHg ordiastolic BP is between 121 and 140 mmHg,then labetalol[13] [14] [15] 1[C]Evidence ornicardipine[13] [14] [15] [33] 4[C]Evidenceshould be used to achieve a 10% to 15%reduction in 24 hours.

» Nicardipine is a dihydropyridine calcium-channel blocker, which increases strokevolume and has strong cerebral and coronaryvasodilatory activity.





Acute

Patient group Tx line Treatment» Onset of action: 5 to 10 minutes. Duration ofaction: 2 to 4 hours.


Primary options


DBP >140 mmHg 1st nitroprusside

» If diastolic BP is above 140 mmHg, thennitroprusside[13] [14] 2[C]Evidence may beused to achieve a 10% to 15% reduction over 24hours.

» It acts as a potent arterial and venousvasodilator thereby reducing afterload andpreload. Its haemodynamic effects are todecrease MAP, with a modest increase or nochange in cardiac output.

» Onset of action: immediate. Duration of action:3 to 5 minutes.

» Patients should be monitored by drawingthiocyanate levels after 48 hours of therapy(levels maintained <2064 micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose should bedelivered for less than 10 minutes to decreasechance 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 peripheralvasodilator, with greater action on the venousvessels than on arterial vessels. It causes adecrease in preload and cardiac output andincreases coronary blood flow. Onset of action:immediate. Duration of action: 3 to 5 minutes.

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Patient group Tx line Treatment» Continue until BP controlled on oral agents.

Primary options

» esmolol: 50-100 micrograms/kg/minuteintravenously-and-» glyceryl trinitrate: 5-100 micrograms/minuteintravenously

2nd labetalol and glyceryl trinitrate

» Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemicvascular resistance, mean arterial pressure(MAP) and heart rate, and causes a decrease orno change in cardiac output. Onset of action: 5to 10 minutes. Duration of action: 3 to 8 hours.

» Glyceryl trinitrate acts as a peripheralvasodilator, with greater action on the venousvessels than on arterial vessels. It causes adecrease in preload and cardiac output andincreases coronary blood flow. Onset of action:immediate. Duration of action: 3 to 5 minutes.


Primary options

» glyceryl trinitrate: 5-100 micrograms/minuteintravenously

3rd nitroprusside

» Sodium nitroprusside acts as a potent arterialand venous vasodilator thereby reducingafterload and preload. Its haemodynamic effectsare to decrease mean arterial pressure, with amodest increase or no change in cardiac output.




Primary options

» nitroprusside: 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5micrograms/kg/minute increments according





Acute

Patient group Tx line Treatmentto response, maximum 10 micrograms/kg/minute

left ventricular failure and/orpulmonary oedema

1st glyceryl trinitrate + furosemide

» Glyceryl trinitrate acts as a peripheralvasodilator, with greater action on the venousvessels than on arterial vessels.

» It causes a decrease in preload and cardiacoutput and increases coronary blood flow.



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

Primary options

» glyceryl trinitrate: 5-100 micrograms/minuteintravenously-and-» furosemide: 40-80 mg intravenously initially,increase according to response

2nd nitroprusside + furosemide

» Sodium nitroprusside acts as a potent arterialand venous vasodilator thereby reducingafterload and preload. Its haemodynamic effectsare to decrease mean arterial pressure, with amodest increase or no change in cardiac output.



Primary options

» nitroprusside: 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5micrograms/kg/minute increments accordingto response, maximum 10 micrograms/kg/minute-and-» furosemide: 40-80 mg intravenously initially,increase according to response

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Acute

Patient group Tx line Treatmentaortic dissection 1st labetalol or esmolol

» Medical therapy of aortic dissection involveslowering the BP and decreasing the velocity ofleft ventricular contraction, which decreasesaortic shear stress and minimises the tendencyfor propagation of the dissection.

» Systolic BP should be reduced to 100 to 120mmHg in the first 20 minutes or as tolerated bythe patient.

» Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemicvascular resistance, mean arterial pressure,and heart rate, and causes a decrease or nochange in cardiac output. Onset of action: 5 to10 minutes. Duration of action: 3 to 8 hours.

» The mechanism of action of esmolol is as aselective beta-blocker, producing a decreasein heart rate. Onset of action: 1 to 5 minutes.Duration of action: 5 minutes.

» Dose adjusted to maintain BP in desiredrange; continue until patient has undergonesurgical repair/evaluation and is stable on oraltherapy.

Primary options


OR

Primary options

» esmolol: 50-100 micrograms/kg/minuteintravenously

2nd nitroprusside

» Medical therapy of aortic dissection involveslowering the BP and decreasing the velocity ofleft ventricular contraction, both of which willdecrease aortic shear stress and minimise thetendency for propagation of the dissection.

» Systolic BP should be reduced to 100 to 120mmHg in the first 20 minutes or as tolerated bypatient.

» Sodium nitroprusside must be administeredwith a beta-blocker as nitroprusside-inducedvasodilation would otherwise induce a





Acute

Patient group Tx line Treatmentcompensatory tachycardia and worsen shearstress.

» Nitroprusside acts as a potent arterial andvenous vasodilator thereby reducing afterloadand preload. Its haemodynamic effects are todecrease mean arterial pressure (MAP), with amodest increase or no change in cardiac output.Onset of action: immediate. Duration of action: 3to 5 minutes.


Primary options


plus labetalol or esmolol

» Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemicvascular resistance, MAP and heart rate, andcauses a decrease or no change in cardiacoutput. Onset of action: 5 to 10 minutes.Duration of action: 3 to 8 hours.

» The mechanism of action of esmolol is as aselective beta-blocker, producing a decreasein heart rate. Onset of action: 1 to 5 minutes.Duration of action: 5 minutes.

» Dose adjusted to maintain BP in desiredrange; continue until patient has undergonesurgical repair/evaluation and is stable on oraltherapy

Primary options


OR

Primary options

» esmolol: 50-100 micrograms/kg/minuteintravenously

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Patient group Tx line Treatment

acute renal failure 1st fenoldopam

» Fenoldopam is useful in renal insufficiencybecause it causes an increase in blood flow tothe kidneys.

» It acts as a selective peripheral dopamine-1-receptor agonist with arterial vasodilator effects.Its haemodynamic effects are a decrease inafterload and an increase in renal perfusion.

Primary options


2nd nicardipine

» Nicardipine is a dihydropyridine calcium-channel blocker that increases stroke volumeand has strong cerebral and coronaryvasodilatory activity.


Primary options



1st benzodiazepines

» Sympathomimetic drug use includes cocaine,amphetamines, phenylpropanolamine,phencyclidine, or the combination of amonoamine oxidase inhibitor with foods rich intyramine.

» If the patient is agitated, benzodiazepines canbe given first.

» Lorazepam should be used with cautionin patients with renal or hepatic impairment,myasthenia gravis, organic brain syndrome, orParkinson disease. Excess CNS or respiratorydepression can occur with higher doses andshould be watched for.





Acute

Patient group Tx line Treatment» Anti-hypertensive agents can be given if theblood pressure response to benzodiazepines isinadequate.

Primary options

» lorazepam: 1 mg intravenous bolus initially,repeated every 10-15 minutes according toresponse, maximum 8 mg

OR

Primary options

» diazepam: 5 mg intravenous bolus initially,repeated every 5-10 minutes according toresponse, maximum 50 mg


2nd phentolamine

» Phentolamine acts to block alpha-adrenoceptors. Its main haemodynamic effectsare to increase heart rate and contractility.

» Onset of action: 1 to 2 minutes. Duration ofaction: 3 to 10 minutes.

Primary options

» phentolamine: 2-5 mg intravenous bolussympathomimetic druguse

3rd labetalol and nitroprusside

» Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemicvascular resistance, mean arterial pressure(MAP), and heart rate, and causes a decrease orno change in cardiac output. Onset of action: 5to 10 minutes. Duration of action: 3 to 8 hours.

» Sodium nitroprusside must be administeredwith a beta-blocker as nitroprusside-inducedvasodilation would otherwise induce acompensatory tachycardia and worsen shearstress.

» Nitroprusside acts as a potent arterial andvenous vasodilator thereby reducing afterloadand preload. Its haemodynamic effects areto decrease MAP, with a modest increase orno change in cardiac output. Onset of action:immediate. Duration of action: 3 to 5 minutes.


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Acute

Patient group Tx line Treatment» Continue until BP controlled on oral agents.

Primary options

» labetalol: 20 mg intravenously every 10minutes according to response, maximum300 mg total dose; or 0.5 to 2 mg/minuteintravenous infusion-and-» nitroprusside: 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5micrograms/kg/minute increments accordingto response, maximum 10 micrograms/kg/minute


1st phentolamine

» Causes of hyperadrenergic states includephaeochromocytoma and abrupt discontinuationof a short-acting sympathetic blocker.

» Phentolamine acts to block alpha-adrenoceptors. Its main haemodynamic effectsare to increase heart rate and contractility.

» Onset of action: 1 to 2 minutes. Duration ofaction: 3 to 10 minutes.

Primary options

» phentolamine: 2-5 mg intravenous bolusno sympathomimeticdrug use

2nd labetalol and nitroprusside

» Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemicvascular resistance, mean arterial pressure(MAP), and heart rate, and causes a decrease orno change in cardiac output. Onset of action: 5to 10 minutes. Duration of action: 3 to 8 hours.

» Sodium nitroprusside must be administeredwith a beta-blocker as nitroprusside-inducedvasodilation would otherwise induce acompensatory tachycardia and worsen shearstress.

» Nitroprusside acts as a potent arterial andvenous vasodilator thereby reducing afterloadand preload. Its haemodynamic effects areto decrease MAP, with a modest increase orno change in cardiac output. Onset of action:immediate. Duration of action: 3 to 5 minutes.

» Patients should be monitored by drawingthiocyanate levels after 48 hours of therapy(levels maintained <2064 micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose should be





Acute

Patient group Tx line Treatmentdelivered for less than 10 minutes to decreasechance of cyanide toxicity.


Primary options

» labetalol: 20 mg intravenously every 10minutes according to response, maximum300 mg total dose; or 0.5 to 2 mg/minuteintravenous infusion-and-» nitroprusside: 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5micrograms/kg/minute increments accordingto response, maximum 10 micrograms/kg/minute

eclampsia 1st hydralazine, labetalol, or nicardipine

» A guide target in these patients is to maintain asystolic BP of 130 to 150 mmHg and a diastolicBP of 80 to 100 mmHg. However, it should benoted that there are no trials supporting thesesuggested thresholds, and treatments should betailored to individual patient circumstances.

» Hydralazine, labetalol, or nicardipine can beused first-line.

» Hydralazine is an arterial vasodilator withminimal effects on the fetus. Onset of action: 10to 20 minutes. Duration of action: 3 to 8 hours.Its main haemodynamic effects are a decreasein systemic vascular resistance, an increasein heart rate and an increase in intracranialpressure.

» Labetalol acts as an alpha-1-blocker and non-selective beta-blocker and its haemodynamiceffects include decreasing systemic vascularresistance, mean arterial pressure, and heartrate, accompanied by a slight decrease orminimal change in cardiac output. Onset ofaction: 5 to 10 minutes. Duration of action: 3 to 8hours.

» Nicardipine is a dihydropyridine calcium-channel blocker that increases stroke volumeand has strong cerebral and coronaryvasodilatory activity. Onset of action: 5 to 10minutes. Duration of action: 2 to 4 hours.

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Acute

Patient group Tx line Treatment» Therapy should be continued until the fetushas been delivered and the patient is stable onoral therapy.

Primary options

» hydralazine: 5-10 mg intravenously every30 minutes according to response

OR

Primary options


OR

Primary options


adjunct magnesium

» There is no consensus on the optimalmagnesium regimen, when it should be startedand terminated, or route of administration.

» Usually initiated at the onset of labour.

» Therapeutic levels: 2.0 to 3.5 mmol/L (4.8 to8.4 mg/dL).

» Continued for 24 hours after delivery.

» Discontinue if patellar reflex absent, respiratoryrate below 12/minute, or urine output above 25mL/hour.

Primary options

» magnesium sulphate: 6 g intravenouslyover 20 minutes as a loading dose at onset oflabour, followed by 2 mg/hour infusion





EmergingClevidipineClevidipine is a third-generation dihydropyridine calcium-channel blocker that appears promising for thetreatment of hypertensive emergency.[43] It is a potent and short-acting selective arteriolar vasodilator. Ithas been shown to be effective in postoperative hypertension but has not been studied in hypertensiveemergency.

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Hypertensive emergencies Follow upFO

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RecommendationsMonitoringThe 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 BPgoal 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 (ormore frequently based on comorbidities). Serum potassium and creatinine should be measured twice ayear.

Patient instructionsPatients 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 Likelihoodcardiac impairment variable high

Myocardial damage and subsequent heart failure is a frequent complication and cause of death inhypertensive emergency.[44] [45]

neurological deficit variable medium

Permanent neurological compromise may occur after stroke, haemorrhage, or hypertensiveencephalopathy 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% to20%. However, current antihypertensive therapy has greatly improved survival, with 5-year survival ratesaround 70% in patients who receive appropriate treatment. The presence of renal failure on diagnosis ofhypertensive emergency increases mortality rate.[44] [45]




Hypertensive emergencies Guidelines

Diagnostic guidelines

Europe

Risk estimation and the prevention of cardiovascular disease: a nationalclinical guidelinePublished by: Scottish Intercollegiate Guidelines Network Last published: 2007

Treatment guidelines

Europe

2013 ESH/ESC guidelines for the management of arterial hypertensionPublished by: European Society of Cardiology Last published: 2013Summary: The main difference is that the ESC guidelines group malignant hypertension andhypertensive emergency under different entities. Like the JNC 7, the ESC emphasises rapid but controlledmanagement of hypertensive emergency without specifying rates of BP decrease. The ESC also acceptsthe use of oral agents for malignant hypertension.

Risk estimation and the prevention of cardiovascular disease: a nationalclinical guidelinePublished 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: 2004Summary: Hypertensive emergency is defined as elevated BP (>180/120 mmHg) complicated byimpending or progressive target organ dysfunction. Goal of therapy is to reduce mean arterial pressure byno more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHgdiastolic 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 2014Published by: Joint National Hypertension Guideline Working Group;Southern African Hypertension Society

Last published: 2014

GU

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35

http://www.sign.ac.uk/guidelines/published/index.html#CHD


http://www.escardio.org/guidelines-surveys/esc-guidelines/Pages/GuidelinesList.aspx



http://www.nhlbi.nih.gov/guidelines/index.htm

http://www.nhlbi.nih.gov/guidelines/index.htm

http://www.hypertension.org.za/#Guidelines


Hypertensive emergencies Evidence scoresEV

IDEN

CE

SCO

RES

Evidence scores

1. Reduction of BP: there is poor-quality evidence that labetalol may reduce BP in people withhypertensive emergencies.[13] [14]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

2. Reduction of BP: there is poor-quality evidence that sodium nitroprusside may reduce BP in peoplewith hypertensive emergencies.[13] [14] [15]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

3. Reduction of BP: there is poor-quality evidence that fenoldopam may reduce BP in people withhypertensive emergencies.[13] [14] [15] [30] [31]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

4. Reduction of BP: there is poor-quality evidence that nicardipine may reduce BP in people withhypertensive emergencies.[13] [14] [15] [33]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

5. Reduction of BP: there is poor-quality evidence that beta-blockers may be effective in people withhypertensive emergencies and aortic dissection.[13] [14] [15] [35]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

6. Reduction of BP: there is poor-quality evidence that esmolol and glyceryl trinitrate may reduce BP inpeople with hypertensive emergencies and myocardial injury.[13] [14] [15] [34] [36]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

7. Reduction of BP: there is poor-quality evidence that labetalol and glyceryl trinitrate may reduce BP inpeople with hypertensive emergencies.[13] [14] [15] [34] [36]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

8. Reduction of BP: there is poor-quality evidence that glyceryl trinitrate may reduce BP in people withhypertensive emergencies and myocardial injury.[13] [14] [15] [34] [36]




Hypertensive emergencies Evidence scores

Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

9. Reduction of BP: there is poor-quality evidence that phentolamine may reduce BP in people withhypertensive emergencies.[13] [14] [15]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

10. Reduction of BP: there is poor-quality evidence that hydralazine may reduce BP in pregnant womenwith hypertensive emergencies.[13] [14] [15] [37] [38] [39]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

11. Reduction of BP: there is poor-quality evidence that labetalol may reduce BP in pregnant women withhypertensive emergencies.[13] [14] [15] [37] [39] [40]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

12. Reduction of BP: there is poor-quality evidence that nicardipine may reduce BP in pregnant womenwith hypertensive emergencies.[13] [14] [15] [37] [40]Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomizedcontrolled trials (RCTs) of <200 participants.

13. Reduction of BP: there is poor-quality evidence that magnesium may reduce BP in pregnant womenwith hypertensive emergencies.[13] [14] [15] [37] [42]Evidence level B: Randomized controlled trials (RCTs) of <200 participants, methodologicallyflawed RCTs of >200 participants, methodologically flawed systematic reviews (SRs) or good qualityobservational (cohort) studies.

EVIDEN

CE SCO

RES



37


Hypertensive emergencies ReferencesR

EFER

ENC

ES

Key articles

• 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 spontaneousintracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Qualityof Care and Outcomes in Research Interdisciplinary Working Group. Stroke. 2007;38:2001-2023. Fulltext Abstract

• ACOG Committee on Obstetric Practice. ACOG practice bulletin. Diagnosis and management ofpreeclampsia and eclampsia. Number 33, January 2002. American College of Obstetricians andGynecologists. Int J Gynaecol Obstet. 2002;77:67-75. Abstract

References

1. Kearney PM, Whelton M, Reynolds K, et al. Global burden of hypertension: analysis of worldwide data.Lancet. 2005;365:217-223. Abstract

2. McRae RP Jr, Liebson PR. Hypertensive crisis. Med Clin North Am. 1986;70:749-767. Abstract

3. Martin JF, Higashiama E, Garcia E, et al. Hypertensive crisis profile. Prevalence and clinicalpresentation. Arq Bras Cardiol. 2004;83:131-136. Full text Abstract

4. Hyman DJ, Pavlik VN. Characteristics of patients with uncontrolled hypertension in the United States[published correction appears in N Engl J Med. 2002;346:544]. N Engl J Med. 2001;345:479-486. Fulltext Abstract

5. Bennett NM, Shea S. Hypertensive emergency: case criteria, sociodemographic profile, and previouscare of 100 cases. Am J Public Health. 1988;78:636-640. Full text Abstract

6. Zampaglione B, Pascale C, Marchisio M, et al. Hypertensive urgencies and emergencies: prevalenceand clinical presentation. Hypertension. 1996;27:144-147. Full text Abstract

7. Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment, and control of hypertension in theUnited States, 1988-2000. JAMA. 2003;290:199-200. Full text Abstract

8. Ong KL, Cheung BM, Man YB, et al. Prevalence, awareness, treatment, and control of hypertensionamong United States adults 1999-2004. Hypertension. 2007;49:69-75. Full text Abstract

9. Tisdale JE, Huang MB, Borzak S, et al. Risk factors for hypertensive crisis: importance of out-patientblood pressure control. Fam Pract. 2004;21:420-424. Full text Abstract

10. Shea S, Misra D, Ehrlich MH, et al. Predisposing factors for severe, uncontrolled hypertension in aninner-city minority population. N Engl J Med. 1992;327:776-781. Abstract



http://www.ncbi.nlm.nih.gov/pubmed/10972386?tool=bestpractice.bmj.com

http://stroke.ahajournals.org/content/38/6/2001.full






http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2004001400004&lng=en&nrm=iso&tlng=en


http://content.nejm.org/cgi/content/full/345/7/479



http://www.ajph.org/cgi/reprint/78/6/636


http://hyper.ahajournals.org/cgi/content/full/27/1/144


http://jama.ama-assn.org/cgi/content/full/290/2/199




http://fampra.oxfordjournals.org/cgi/content/full/21/4/420




Hypertensive emergencies References

11. Lip GY, Beevers M, Beevers G. The failure of malignant hypertension to decline: a survey of 24 years'experience in a multiracial population in England. J Hypertens. 1994;12:1297-1305. Abstract

12. Guerin C, Gonthier R, Berthoux FC. Long-term prognosis in malignant or accelerated hypertension.Nephrol Dial Transplant. 1988;3:33-37. Abstract

13. Kaplan NM. Kaplan's clinical hypertension, 9th ed. Philadelphia, PA: Lippincott Williams & Wilkins;2006.

14. Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet. 2000;356:411-417. Abstract

15. Marik PE, Varon J. Hypertensive crises: challenges and management [published correction appears inChest. 2007;132:1721]. Chest. 2007;131:1949-1962. Full text Abstract

16. Fuchs FD. Study of the usefulness of optic fundi examination on patients with hypertension in a clinicalsetting. J Hum Hypertens. 1995;9:547-551. Abstract

17. Van den Born BJH, Honnebier UPF, Koopmans RP, et al. Microangiopathic hemolysis and renal failurein malignant hypertension. Hypertension. 2005;45:246-251. Full text Abstract

18. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection(IRAD): new insights into an old disease. JAMA. 2000;283:897-903. Full text Abstract

19. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection bynoninvasive imaging procedures. N Engl J Med. 1993;328:1-9. Full text Abstract

20. Shiga T, Wajima Z, Apfel CC, et al. Diagnostic accuracy of transesophageal echocardiography, helicalcomputed tomography, and magnetic resonance imaging for suspected thoracic aortic dissection:systematic review and meta-analysis. Arch Intern Med. 2006;166:1350-1356. Full text Abstract

21. Moore AG, Eagle KA, Bruckman D, et al. Choice of computed tomography, transesophagealechocardiography, 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 withischemic stroke. Stroke. 2007;38:1655-1711. Full text Abstract

23. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committeeon Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension.2003;42:1206-1252. Full text Abstract

24. Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneousintracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Qualityof Care and Outcomes in Research Interdisciplinary Working Group. Stroke. 2007;38:2001-2023. Fulltext Abstract

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Hypertensive emergencies ImagesIM

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Images

Figure 1: Fundus photograph of the right eye with multiple dot-blot haemorrhages typical of hypertensiveretinopathy

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 spotsand macular exudates in a radiating star configuration around the fovea


IMAG

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Contributors:

// Authors:

Hector Ventura, MDHeadSection of Cardiomyopathy and Heart Transplantation, Ochsner Clinic Foundation, New Orleans, LADISCLOSURES: HV declares that he has no competing interests.

Madhavi T. Reddy, MDAssistant ProfessorUniversity of Pennsylvania, Philadelphia, PADISCLOSURES: MR is employed by Merck and owns stocks in Merck, and Johnson & Johnson.

// Peer Reviewers:

Aparna Sundaram, DO, MBA, MPHPhysician ConsultantPreventive Medicine, Private Practice, Atlanta, GADISCLOSURES: AS declares that she has no competing interests.

Ethan Cumbler, MDAssistant ProfessorDepartment of Internal Medicine, University of Colorado Health Sciences Center, Denver, CODISCLOSURES: EC declares that he has no competing interests.

Michael Schachter, MB, BSc, FRCPDepartment of Clinical PharmacologySt Mary’s Hospital, Imperial College, London, UKDISCLOSURES: MS declares that he has no competing interests.

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