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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
j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c om / l o c a t e / c q n
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.
http://dx.doi.org/10.1016/j.cqn.2013.01.004
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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.
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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
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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
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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
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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:
20e40 mg P/O every 2e3 h
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:
5e10 mg P/O every 4e6 h
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
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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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