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Review Article

Hypertension emergencies and urgencies

Sudeep Kumar a,*, Tanuj Bhatia b, Aditya Kapoor c

a Additional Professor, Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Road,

Lucknow 226014, UP, Indiab Senior Resident, Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Road, Lucknow 226014, UP, Indiac Professor, Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Road, Lucknow 226014, UP, India

a r t i c l e i n f o

Article history:

Received 20 November 2012

Accepted 25 January 2013

Available online 15 March 2013

Keywords:

Hypertensive crises

Hypertensive emergency

Hypertensive urgency

Malignant hypertension

a b s t r a c t

Where at one hand, the vast majority of hypertensive patients succumb to the complica-

tions of hypertension like atherosclerosis, cerebrovascular diseases and congestive heart

failure, a subset of these have an exacerbation in this gradual course that needs acute

management in the blood pressure control and plays a role in short term outcomes. These

hypertensive crises are now encountered more frequently, in more diverse and aging

population than in earlier times.

Despite the recognized unmet need of timely evaluation and management, fewer than

10% receive the recommended investigations and appropriate treatment often gets

delayed. This review emphasizes the therapeutic implications of correct diagnosis, various

treatment options and targets in different clinical circumstances.

Nicardipine, clevidipine, esmolol and fenoldopam have emerged as potentially superior

drugs in most hypertensive emergencies as compared to other conventional drugs. For

hypertensive urgencies, blood pressure lowering at a gradual pace with oral drugs &

adequate follow up are two important facets of management, making sure that the blood

pressure has been lowered out of a potentially dangerous range.

Impact of optimal management of hypertensive crisis should translate into lesser target

organ damage and eventually fewer complications of stroke, myocardial infarction, or

congestive heart failure.

Copyright ª 2013, Reed Elsevier India Pvt. Ltd. All rights reserved.

1. Introduction

Hypertension no longer affects the middle aged & older adults

predominantly, but with the rapidly expanding epidemic of

obesity & sedentary lifestyles, now equally affects the young

adults & teenagers as well.1 Around 27e30% of population over

the ageof 20 years is affected by this chronicmedicalcondition.2

While chronic hypertension is a major risk factor for car-

diovascular & cerebrovascular outcomes & ESRD, accelerated

elevations in blood pressure can result in acute organ damage& dysfunction. Prompt & precise management of such situa-

tions is essential to prevent permanent organ damage.

Numerous reports in late nineties estimated that around

1% of hypertensive individuals experience hypertensive crisis

at some point of time during their lifetime3,4 although before

the advent of antihypertensive therapy figures were probably

as high as 7%.3,5 Nonetheless, the absolute number of such

individuals has been gradually increasing over the period of

* Corresponding author. Tel.: þ91 522 2495198 (O), þ91 522 2495199 (R); fax: þ91 522 2668573, þ91 522 2668017.E-mail address: [email protected] (S. Kumar).

Available online at www.sciencedirect.com

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c l i n i c a l q u e r i e s : n e p h r o l o g y 2 ( 2 0 1 3 ) 1 e1 4

2211-9477/$ e see front matter Copyright ª 2013, Reed Elsevier India Pvt. Ltd. All rights reserved.

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activation of platelets & coagulation cascade.13,30e33 Various

vasoactive substances that contribute to this vascular injury

are catecholamines, renin, angiotensin,34 endothelin, vaso-

pressin35,36 and more recently added to this list are ouabain,

digoxin,37,38 marinobufagenin & telocinobufagin. These newer

chemicals are grouped under the category of CTS (cardiotonic

steroids) that have short term effects on vascular & cardiac

smooth muscle cells, resulting in BP elevation & cardiac ac-

tivity modulation.37,38 The activation of the RAAS & othervasoactive mediators lead to further vasoconstriction & pro-

duction of proinflammatory cytokines such as IL-6.39,40

NADPH oxidase activity that generates reactive oxygen spe-

cies are increased, leading to oxidative stress.41

Besides this, endothelial dysfunction is a common de-

nominator of these hypertensive emergencies and may

persist for a long time after the index event. 42,43

The typical lesion of the hypertensive crisis is fibrinoid

necrosis of small arteries and arterioles.29,44 In the cerebral

vasculature, cerebral perfusion seems to affect primarily the

white matter in the parieto-occipital areas of the brain45 &

brainstem,46 possibly because of decreased sympathetic

innervation of vessels in the parieto-occipital region.47

4. Epidemiology

Exact figures regarding this commonly faced medical emer-

gency are largely unknown.32,48 They constitute approximately

one fourth of all medical emergencies.49 Of the hypertensive

crisis, three fourths were urgencies & one fourth were emer-

gencies in an Italian study50

while Brazilian series quotes pro-portionof emergencies to be three fifths of hypertensive crisis.51

Despite recent advances & awareness, both at physician &

patient level, hypertension control is poorly attainable. It is

estimated that only approximately 30% of hypertensive pa-

tients achieve good control of the blood pressure, although

clinical trials say that control rates of 60e70% are attainable.

Despite these discouraging facts, widespread outpatient use

of antihypertensive drugs has reduced the incidence of hy-

pertensive emergencies.6,52 In US, hospitalization for hyper-

tensive emergencies is reported at the rate of 1e2 cases/

million population/year.29 However, poor compliance to

antihypertensive regime53e55 & inability to access health care

sources56

contribute to increased incidence of hypertensivecrisis in the developing nations.

5. Diagnostic evaluation

Hypertensive crisis is thematically a hot topic. From pediatric

to geriatric, from medical to surgical e all subgroups of pa-

tients either have or are on verge of having target organ

damage. The primary goal, hence, is to differentiate between

true hypertensive emergency from hypertensive urgency, as

the therapeutic approaches are different. Our approach, clin-

ical and investigative, should at least help us to overcome this

ambiguity. Another goal is to accurately assess the type andseverity of target organ damage.

This includes a speedy history, current blood pressure &

clinical examination, ECG, chest roentgenogram, basal

biochemistry, funduscopy & urinalysis as essential in-

vestigations & targeted investigations as per clinical hints for

ruling out causes of secondary hypertension or analyzing

target organ damage.

History should essentially include assessment of severity

of hypertension, duration of treatment,9,13 patient’s medica-

tion & compliance to treatment including history of over the

counter medications & recreational drugs. Not to be forgotten

is a thorough and targeted history for any clue to target organ

damage (chest or back pain, dyspnea, throbbing headache,pulsatile abdominal mass). Liquorice, nasal drops, cocaine,

amphetamines, oral contraceptives, steroid, NSAIDs, eryth-

ropoietin and cyclosporine are drugs that may trigger an acute

hypertensive emergency. Dietary and smoking history can be

of additional information. Concomitant medical history &

history of sleep apnea syndrome should be explored.57,58

BP recordings in both sitting & standing position & in the leg

are essential.2,59 Recordings need to be done with an appro-

priate sized cuff as the use of a cuff too small for the arm size,

as in obese individuals, or use of arm cuff over the thigh

may give spuriously high recordings.49,60 Needless to over-

emphasize, that meticulously done clinical examination may

sometimes be extremely helpful in instituting early treatment.

Table 1 e Common hypertensive emergencies orurgencies.

Malignant e accelerated hypertension with papilledemaR

Cardiovascular conditions

Acute MI/unstable anginaR

Acute LVF/pulmonary edemaR

Acute aortic dissectionR, C

Severe hypertension after CABG/vascular surgeryR

Renal conditions

Rapidly progressive glomerulonephritisC

Renovascular hypertensionC

Scleroderma renal crisisC

Post renal transplantation severe hypertensionC

Neurological conditions

Hypertensive encephalopathyR

Intracerebral & Subarachnoid haemorrhageC,R

Acute head injuryC

Atherothrombotic strokeC, R

GuillaineBarre’ syndromeC

Catecholamine excess states

Pheochromocytoma crisisC

MAO Inhibitor e tyramine interactionsC

Alpha-2 agonists drug (Clonidine, alpha methyl dopa)C with-

drawal leading to rebound hypertension

Automatic hyperreflexia after spinal cord injury C

Use of sympathomimetic drugs (Cocaine,

phenylpropanolamine)C

Surgical conditions

Perioperative hypertensionC more commonly with cardiovas-

cular & neurosurgical procedures25

Postoperative bleeding from vascular suture lines26 R

Hypertension after organ transplantationC

Hypertension associated with severe burnsC

Re result of hypertensive emergency.

Ce cause of hypertensive emergency.

c l i n i c a l q u e r i e s : n e p h r o l o g y 2 ( 2 0 1 3 ) 1 e1 4 3







Swift cardiac, pulmonary, peripheral vessel & neurological ex-

amination inclusive of fundoscopic inspection essentially

needs to be done. Gallop rhythm (suggestive of heart failure)

and new murmurs of aortic insufficiency (associated with

aortic dissection) and mitral regurgitation (ischemic MR)

deserve special importance in cardiovascular examination.

Some classical signs of secondary hypertension should not be

missed in first examination.10,61 These include abdominal bruit(renovascular hypertension), radiofemoral delay (aortic coarc-

tation), palpable abdominal mass (pheochromocytoma/poly-

cystic kidney disease), central obesity & abdominal striae

(Cushing’s syndrome) & exophthalmos (hyperthyroidism).57,58

Laboratory evaluation of such patients should be expedi-

tious. It should include full blood count with peripheral smear

and a metabolic panel inclusive of renal function indices and

electrolytes9,10,13 Nephritic urinary sediment suggests acute

glomerulonephritis as a potential cause. Endocrinology eval-

uation for plasma renin activity, aldosterone (in patients who

are not on diuretics)62 & catecholamines may guide treatment

in selected cases.

ECG to rule out myocardial ischemia and left ventricularhypertrophy and strain & Chest X-ray to assess cardiac size &

pulmonary edema are indispensable investigations and

should be routinely performed for each patient.9,10,13

As per clinical status & results of preliminary in-

vestigations, Echocardiography (for regional wall motion

analysis, left ventricular hypertrophy, systolic or diastolic

dysfunction & degree of mitral regurgitation), CT scan or MRI

Brain (in neurologic syndromes), Thoracoabdominal CT/MRI

or Abdominal ultrasound (for suspected aortic dissection) may

be needed.63

Notwithstanding, we should remember that prompt ther-

apy should take priority over detailed history, unnecessary

physical evaluation & irrelevant time consuming diagnosticstudies. The pursuit of etiology should never deprive a patient

of hypertensive emergency from receiving the appropriate

antihypertensive drug at the minimum time possible after

contact with the medical care team, especially after knowing

that most of these complications are largely reversible with

appropriate treatment being rendered at the appropriate

time.64,65

6. Treatment of hypertensive emergencies

What is crucial regarding management of hypertensive

emergencies is the need of immediate reduction in bloodpressure levels so as to reverse, or at least, halt the on-going

target organ damage. This usually requires a short acting

intravenous drug that helps in tight control of the blood

pressure, and can be titrated easily by the clinician both for

rate of control of blood pressure and the ultimate target. It is

generally accepted that such a patient should be admitted to

an ICU or a high dependency unit (HDU) for monitoring &

administration of an appropriate parenteral agent.2,9,11,12

The ideal agent to treat hypertensive crisis should be fast

acting, rapidly reversible and titrable without any significant

side effects. There is no single ideal agent & the choice of

pharmacologic agent to treat hypertensive crisis should be

tailored to each individual based on risks, comorbidities and

end organ damage. Table 2 depicts the various agents used for

this purpose.

Instead of the absolute value of blood pressure, the gov-

erning factor for immediate institution of management is the

presence of target organ damage, as patients with recent

onset or rapidly rising hypertension develop target organ

damage earlier than chronically hypertensive patients who

tolerate equal or higher blood pressures due to structural &functional autoregulatory changes.14,28,29

Understanding these autoregulatory mechanisms is

equally important from therapeutic point of view, as sudden

lowering of blood pressure may actually lead to inadequate

tissue perfusion, which maylead to renal,cerebral or coronary

ischemia.9 According to current American & European

guidelines, the mean BP should be reduced by no more than

20e25% within minutes to 1e2 h2,9 A diastolic blood pressure

between 100 and 110 mm Hg or 25% of initial baseline,

whichever is higher, should be the target in the next 6 h116

Achieving final target blood pressures gradually in 24e48 h

allows autoregulatory mechanisms to “reset”, and thence-

forth the parenteral medications may be replaced by oralmedications. Abrupt lowering of blood pressure is not favor-

able, and this fact is exemplified by the fact that sublingual

nifedipine, known for its potent, but unpredictable & precip-

itous hypotensive effect, increased mortality & morbidity

when used for this indication.117

Patients presenting with hypertensive emergencies may be

volume depleted owing to pressure natriuresis, and prior to

administering parenteral therapy, volume deficit must be

assessed & corrected as it avoids precipitous fall in blood

pressure and maintains adequate organ perfusion.61

Currently, evidence is insufficient to label one drug or drug

class superior over other in reducing morbidity or mortality

related to hypertensive crisis, however logical & consensusopinion regarding choice of pharmacological agent in specific

clinical scenarios exist.

7. Specific hypertensive emergencies

7.1. Hypertensive emergencies involving acute coronary

syndromes

The target blood pressure for hypertensive emergencies

involving cardiac ischemia is that which improves myocardial

perfusion.29

Intravenous nitroglycerin & nitroprusside were previouslyproposed as first line drugs.9,67 Nicardipine that can selec-

tively dilate cerebral & coronary arteries71,72 and clevidipine

that can protect against ischemia-reperfusion injury118 are

successful alternatives.

In presence of acute LVF, vasodilator agents that reduce

afterload like nitroglycerine, nitroprusside & fenoldopam are

preferred agents. Concomitant loop diuretics & ACE inhibition

are essential.

Diazoxide & hydralazine that cause reflex tachycardia

should be avoided.9,29,61,67 Drugs that reduce myocardial

contractility like beta blockers (labetalol, esmolol) should also

be avoided, especially when associated with heart failure,

except in cases with diastolic dysfunction29 or those without








Table 2 e ( continued )

Dosage & pharmacokinetics Adverse Effects & Caution Comments & Special Uses

6. Enalaprilat: Angiotensin-converting enzyme inhibitor

Dose:

5e10 mg/kg/dose every 8e24 h

Alternatively 1.25e5 mg every 6 h

Onset of action:15e30 min

Duration of action:

6e12 h

Adverse Effects:

Hypotension, hyperkalemia, oliguria, rash,

angioedema, agranulocytosis, neutropenia,

cough, fatal hepatic necrosis (rare)

Caution:

Avoid in acute myocardial infarction

Abrupt BP reduction in patients with renal

artery stenosis & hypovolemia13,44

Contraindicated in pregnancy.97,98

Special Uses:

Acute left ventricular failure (non ischemic)98

7. Hydralazine hydrochloride: direct arteriolar vasodilator e Kþ channel opener

Dose:

0.1e0.6 mg/kg/dose every 4e6 h

intravenously

Onset of action:

10e20 min

Duration of action:

1e

4 h

Adverse Effects:

Palpitations, flushing, tachycardia

Fever, rash, headache, arthralgia, SLE-like

syndrome, positive ANA

Peripheral neuropathy

Fluid retention by activating RAAS34

Comments:

Limited use owing to side effects & unpredictable

action61,67,99,100 with precipitous drop in blood

pressure that may last for 12 h

8. Diazoxide: direct acting vasodilator

Dose:

50e150 mg every 5 min I/V or 15

e30 mg/min I/V infusion

Onset of action:

1e5 min

Duration of action:

4e12 h

Adverse Effects:

Nausea, flushing

Reflex sympathetic stimulation101 &

aggravation of angina

Sodium retention, hyperglycemia

Caution:

Avoid in angina, acute MI, aortic dissection

9. Isradipine: Second generation calcium channel blocker

Dose:

0.15 mg/kg/min I.V., increase by

0.0025 mg/kg/min every 15 min.

Maintenance 0.15 mg/kg/minOnset of action:

1e10 min

Duration of action:

1e2 h

Adverse Effects:

Headache, flushing, peripheral edema,

dizziness, tachycardia

Special Uses:

Perioperative states & pregnancy102,103

Adrenergic inhibitors

10. Labetalol hydrochloride: combined alpha 1 and beta blocker (1:7 ratio)104

Dose:

20e80 mg I/V bolus every 10 min

or 0.25e3 mg/kg/h intravenously

Onset of action:

5e10 min13,61

Duration of action:

3e6 h13,61,105

Adverse Effects:

AV conduction disturbances, headache,

bronchospasm, nasal congestion, scalp

tingling

Caution:

Not to be used in acute heart failure, heart

block & COPD9,13,61

Comments:

Reduces PVR without reflex increase in systolic

volume while cerebral, coronary and renal blood

flow is mantained92,104,106,107

Does not require intraarterial BP monitoring

Metabolized in liver by formation of inactive

glucuronide conjugate105

Maintains cardiac output unlike pure beta adren-ergic blockers107

Special Uses:

Aortic dissection

Acute coronary syndrome

Hypertensive encephalopathy

Adrenergic crises

Preeclampsia related crises61,92

11. Esmolol hydrochloride: cardioselective beta-1 adrenergic blocker

Dose:

125e500 mg/kg/min intravenously

0.5e2 mg/kg over 1 min followed

by 50e100 mg/kg/min61,67

Adverse Effects:

AV Conduction disturbance, bronchocon-

striction, skin necrosis after extravasation,

Raynaud’s phenomenon

Comments:

Metabolism independent of renal or hepatic

function








to reduce blood pressure by no more than 10e15% in the first

24 h127,134,138

However, if concomitant non cerebral target organ damage

is present, other rules may apply & patients who are planned

to receive thrombolytic therapy, BP should be kept below

185/110 mmHg.9,61,67,134,138

ACCESS study assessed candesartan (angiotensin receptor

blocker) & found lower 12 month mortalitywhen used in acutephase of stroke.139 However, in the SCAST trial, there was no

reduction in the composite of vascular death, myocardial

infarction or stroke in 6 month follow up with use of cande-

sartan in first 7 days of stroke.140

Use of labetalol or nicardipine was previously suggested if

SBP is >220 mm Hg, DBP is 121e140 mmHg & nitroprusside if

DBP is >140 mmHg.61,67

In intracerebral bleed, rapid BP reduction, although at the

expense of risk of cerebral hypoperfusion141,142 should be

aimed with intent to prevent further bleeding, & this strategy

of intensive BP lowering significantly attenuated hematoma

growth over 72 h in the INTERACT study. 143

Blood pressure more than 180/105 need to be treated incases of intracranial bleed, except in cases of subarachnoid

hemorrhage with normotensive prehaemorrhage status,

where target is 130e160 mmHg systolic.9,29,144

In the setting of haemorrhagic stroke with intracranial

bleed BP of more than 200/110 mm Hg need to be

controlled127,134 However, rapid decline in BP within 24 h is

independently associated with increased mortality.141

In general, if neurologic function worsens, the therapy

should be suspended, and blood pressure should be allowed to

increase.

7.4. Hypertensive emergencies associated with renal

disease

Either renal arterial disease, acute glomerulonephritis or

autoimmune vascular diseases are commonly followed by

furtherdeterioration of remnant renal function, evenwhen BP

is properly lowered.

Because of its renal vasodilator effects & lack of toxic me-

tabolites, fenoldopam is preferred in this setting.76 Nicardi-

pine, labetalol or clevidipine are other alternatives. Loop

diuretics are to be used only if there is associated volume

overload.13,29,61

ACE inhibitors are usually contraindicated due to the risk

of further deterioration of renal function, except in the case

of scleroderma renal crisis where it is the drug of choice.The renin-angiotensin-aldosterone system is critically

responsible for hypertension associated with renovascular

disease & some models62 propose a possible explanation of

involvement of this axis in other forms of hypertensive crisis

as well. Even very old reports of surgical removal of an

ischemic kidney preventing hypertensive surges have been

documented.145

7.5. Hypertensive emergencies due to catecholamine

excess states

These situations are best managed with an intravenous alpha

blocker (phentolamine) with a beta blocker added if

necessary.146,147 Caution needs to be exercised in giving beta

blocker prior to adequate alpha blockade as unopposed alpha-

adrenergic stimulation can be dangerous.9,29

Although labetalol was traditionally considered ideal for

this purpose due to its combined alpha & beta adrenergic

blocking properties, but experimental studies do not support

its use in this clinical setting.148,149

Specifically in cocaine induced hypertensive emergency,use of beta adrenergic antagonists can increase coronary

vasoconstriction, fail to control heart rate, increase BP and

decrease survival.150,151

Nicardipine, fenoldopam and verapamil in combination

with benzodiazepines are agents preferred in this setting.152,153

Diuretics are generally avoided as these patients are generally

volume depleted.

7.6. Perioperative hypertensive emergencies

Severe perioperative hypertension can occur in conjunction

with anesthesia induction, intraoperatively due to sympa-thetic vasoconstriction, early postoperatively or after 24e48 h

due to pain or volume overload.154

Perioperative hypertensive emergencies most commonly

occur with carotid surgery, abdominal aortic surgery, periph-

eral vascular procedures, intraperitoneal & intrathoracic

surgeries155& approximately 50% of patients after cardiac sur-

geries. Amongst these, carotid surgery is notorious for being

associated with hypertensive emergences, and actually repre-

sents a face of baroreflex failure.156 Regardless of cause, post-

operative hypertension may be associated with increased risk

of cardiac & neurologic complications. A conservative target is

to control BP up to 10% above the baseline preoperative mean

BP levels.

48

However, patients with heart failure & those whoare at high riskof bleeding willbenefit fromafterload reduction,

and the target in them should be more aggressive.

Postoperative hypertension also seems to be related to

catecholamine surge & sympathetic nervous system stimu-

lation 172 & usually requires treatment for 6 h or less.25 Careful

monitoring of patient response and temporal adjustments of

treatment are of paramount importance for safe management

of hypertensive emergencies in perioperative period.

7.7. Hypertensive emergencies during pregnancy

Preeclampsia affects nearly 7% of pregnancies157 and should be

managed withutmostcaution,& conservatively,due to presenceof the developing fetus. The objective of treatment is to prevent

intracerebral bleed and cardiac failure without compromising

cerebral perfusion and uteroplacental blood flow.158

Hence a target SBP of 140e160 mmHg and DBP between 90

and 105 mmHg is recommended by most authorities & current

guidelines from American College of Obstetricians and

Gynaecologists.158,159

Hydralazine, though was earlier considered as the drug of

choice,160 has gone out ofuse due to increasedrisk ofmaternal

hypotension & fetal heart rate abnormalities.100,161 Associa-

tion with excess of cesarean sections, placental abruptions &

low APGAR scores were noted.161 Labetalol, Urapidil100 &

Nicardipine162,163 have emerged as superior alternatives to








hydralazine.162,164 Oral treatment with methyldopa, long

acting nifedipine & magnesium sulfate may also be useful.

ACE inhibitors & nitroprusside are contraindicated due to

their teratogenic effects.

8. Treatment of hypertensive urgencies

Hypertensive crisis without evidence of target organ damage

can usually be treated with orally acting antihypertensive

agents with close ambulatory care.29 The lowering of blood

pressure, if done precipitously, can do more harm than good9

by causing a shift in the pressure/flow auto-regulatory curve

to the right.27

In essence, if BP lowering at a gradual pace is impor-

tant,11,12 equally important is assuring adequate follow up to

an appropriate site of care of chronic hypertension2,29 making

sure that the blood pressure has been lowered out of a

potentially dangerous range.11,12

Moreover, placebo-controlled trials have shown that BP

decreases spontaneously in a substantial proportion of

patients. This raises concern whether BP lowering, even

gradual, does, at all confer any benefit to a patient presenting

with hypertensive urgency.29,165

Notwithstanding, the potential of every hypertensive ur-

gency to transform into a hypertensive emergency should be

kept in mind & appropriate management of hypertension

with slow and controlled reduction of the blood pressure

should be the cornerstone in management of any form of witnessed severe hypertension.

The drug of choice for a hypertensive urgency should be

effective, quick acting and unlikely to cause alterations in

mental status or produce hypotension. This widens the

armamentarium of drugs available for this purpose. These

drugs are summarized in Table 3 below.

Although evidence regarding the preferred time to reach

goal BP and type of BP lowering medication is limited, there is

evidence that a steep decrease in BP, such as reported with

sublingual nifedipine tablets, can lead to cerebral, cardiac and

renal ischemia166 & use of nifedipine immediate-release for-

mulations must be abandoned as a treatment option of any

form of hypertensive crises.58,167,168

Table 3 e Drugs used in hypertensive urgencies.

Dosage & Pharmacokinetics Adverse Effects & Caution Comments & Special Uses

1. Captopril: ACE inhibitor

Dose:

12.5e25 mg P/O every 1e2 h

Onset of action:

15e

30 minDuration of action:

4e6 h

Adverse Effects:

Angioedema, cough,

acute renal failure9,44

Caution:

Contraindicated in pregnancy97,98

Special Uses:

Preferable for patients with evidence

of left ventricular dysfunction

2. Clonidine: central alpha 2 agonist

Dose:

0.1e0.2 mg P/O every 1e2 h

Onset of action:

30e60 min

Duration of action:

6e8 h

Adverse Effects:

Sedation, dry mouth, bradycardia,

rebound hypertension

Comments:

Poorly lipid soluble, does not cross

blood brain barrier, No CNS activity

3. Labetalol: combined alpha 1 and beta blocker (1:7 ratio)104

Dose:

200e400 mg P/O every 2e3 h

Onset of action:

30e120 minDuration of action:

6e8 h

Adverse Effects:

Bronchoconstriction, Heart block, CHF

Special Uses:

Preeclampsia related crises61,92

4. Furosemide: loop diuretic

Dose:


Onset of action:

30e60 min

Duration of action:

8e12 h

Adverse Effects:

Volume depletion, hyponatremia,

hypokalemia9,11,12

Comments:

Not a primary drug but to be

considered as an add on therapy

5. Isradipine: second generation calcium channel blocker

Dose:


Onset of action:

30e90 minDuration of action:

8e16 h

Adverse Effects:

Headache, tachycardia, flushing,

peripheral edema

Special Uses:

May be considered in preeclampsia

related crisis & perioperative states102,103








9. Conclusion

To summarize, hypertensive crisis as a clinical presentation of

hypertension is far less common than routinely detected

chronic hypertension. Hypertensive emergencies are a po-

tential threat for permanent organ damage, significant

morbidity & mortality. Triage of these emergencies from ur-gencies is crucial to ensure delivery of appropriate therapy to

the appropriate candidate in timely fashion.

Still, the potential threat of permanent target organ damage

associated with this clinical diagnosis, if not detected & treated

in time, should make the optimal implementation of recom-

mended therapy a commitment on part of the treating physi-

cian. The appropriate therapeutic approach needs to be

individualized for every patient. However, admission to ICU,

use of titratable IV hypotensive agents, and expeditious eval-

uation are cornerstone in management of hypertensive emer-

gencies. The pharmacological evolution in the last decade has

witnessed the transition of usage from nifedipine, hydralazine

& nitroprusside to esmolol, nicardipine & fenoldopam that areequally potent, if not more, and have fewer adverse effects. It

should be stressed that the use of oral or sublingual nifedipine

should be avoided to prevent increased mortality.

Conflicts of interest

All authors have none to declare.

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