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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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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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time, due to absolute increase in number of hypertensive
patients, coupled with better survival from major adverse
cardiovascular & cerebrovascular events.
Unfortunately, there is a lack of randomized trials & little
long term follow up data.6 Additionally, diagnosis overlap
with other cardiac, neurologic, renal or multisystem syn-
dromes makes it difficult to follow & remove confounding
factors while assessing long term follow up. Questionsregarding mortality & morbidity hence remain unanswered.7,8
Moreover, the impact of these clinical situations is often
underappreciated, such that timely evaluation & treatment
are often not instituted, leading to serious adverse outcomes.
2. Terminology
The various terminologies used in context to acute elevations
in blood pressures have often been misused. The consensus
definitions of the various terms are discussed in succession
below.
Hypertensive crises are defined as clinical scenarios associ-ated with severe elevations in systolic & diastolic blood pres-
sure, usually above 180/120 mmHg.2,9,10
Hypertensive crises are further classified as hypertensive
emergencies & urgencies.
Hypertensive emergency is defined as marked elevation in BP
complicated by acute target organ damage such as coronary
ischemia, acute pulmonary edema, dissecting aortic aneu-
rysm, hypertensive encephalopathy, cerebral hemorrhage &
acute renal failure.7,11e14
BP should be reducedpromptly, preferably within minutes,
& with rapidly acting parenteral drugs to limit target organ
damage.
Hypertensive urgency is a less clearly defined conditioncharacterized by severe elevation in blood pressure in an in-
dividual who may have evidence of previous end organ
damage related to hypertension, but in whom there exists no
evidence of on-going or imminent acute target organ dam-
age.11 These patients do not require hospital admission and
the reduction in blood pressure can be gradual, & by oral
medications, as per individual patient characteristics.2,9,11,12,15
2.1. Malignant hypertension
The usage of the term malignant with hypertension by Keith &
Wagener, as early as in 1928,16 was to emphasize that the
downhill course would be similar to most cancers. However,with improvement in inpatient & outpatient management of
hypertension,14 the prognosis of malignant hypertension has
dramatically improved, & it will not be wrong to say that with
appropriate management instituted at the right time, malig-
nant hypertension is no more malignant. Hence, the usage of
terms hypertensive emergencies & urgencies is more in
vogue.2
This clinical entity is characterized by marked elevation of
blood pressure with widespread acute arteriolar injury that
reveals itself as hypertensive neuroretinopathy with striate
haemorrhages, cotton-wool exudates, and often papilledema
in funduscopy.17 All these three funduscopic findings portend
a poor prognosis.18e20
No matter how high theblood pressure, a patientcannot be
labeled to have malignant hypertension in absence of hyper-
tensive neuroretinopathy.17 However, some authors believe
presence of papilledema to be essential for diagnosis of ma-
lignant hypertension, & use the term accelerated hypertension
for patients with haemorrhages, exudates, arteriolar narrow-
ing & spasm but without evidence of papilledema.21,22 Prac-
tically, although, malignant hypertension & acceleratedhypertension are terms used interchangeably for each other.17
Hypertensive encephalopathy is a clinical syndrome with
cerebral malfunction due to severe elevation of blood pres-
sure. Though mostly associated with malignant hyperten-
sion, it may at times occur without neuroretinopathy.19 The
first use of this term was by Oppenheimer & Fishberg in
1928.23 Clinical features include severe headache, blurred
vision or blindness, nausea, vomiting, and mental confusion.
The most dramatic feature is prompt clinical response to
antihypertensive therapy & in case aggressive treatment is
not initiated, stupor, convulsions, and death can ensue
within hours.
At times, even in absence of hypertensive neuro-retinopathy, if acute end-organ dysfunction occurs in the
presence of even moderate hypertension, it may still qualify
as a hypertensive crisis.
3. Pathophysiology of hypertensive crisis
Hypertensive crisis can be the first clinical presentation of hy-
pertension or may punctuate the clinical course of long stand-
ing essential, or more commonly, secondary hypertension.
Volhard & Fahr24 first described the rapidly fatal course of
hypertensive crisis and noticed how its pathophysiology dif-
fers from the changes of chronically elevated blood pressure.Situations that qualify as hypertensive emergencies in
clinical practice are enlisted in Table 1. The theme of pre-
sentation of hypertensive emergencies is quite expressive, but
variable, depending on the target organ involvement, super-
scripted with “R” in the below mentioned table. The triggering
causative factors are superscripted with “C” in the table
below.
Chronic elevations in blood pressure causes compensatory
structural & functional changes in arterial cerebral circula-
tion27 & renal microcirculation28 that maintains autor-
egulation & avoids excessive blood flow at higher BP levels.14
These are the subset of patients of presenting with no recent
evidence of acute target organ damage, & need appropriatemanagement, with slow and gradual reduction in blood
pressure.
In contrast are hypertensive emergencies, in which the
mechanisms leading to severe and rapid elevations in blood
pressure coupled with failure of autoregulatory mechanisms29
lead to target organ damage. The triggering factor could be
delineated in few cases like release of a humoral vasoactive
factors.30,31 However, in many cases; the hypertensive emer-
gency is a non-specific consequence of chronically elevated
blood pressure.13
The endothelial injury occurring as a response to chroni-
cally elevated blood pressure leads to furthervascular damage
and tissue ischemia by increasing vascular permeability &
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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 Drugs used in hypertensive emergencies.
Dosage & pharmacokinetics Adverse Effects & Caution Comments & Special Uses
Vasodilators
1. Nicardipine hydrochloride: second generation dihydropyridine calcium channel blocker
Dose:
1e3 mg/kg/min IV, alternatively
5e
15 mgIV every hour(bolus dosing independent of body weight)
Onset of action:
5e15 min
Duration of action:
15e30 min; may last for up to 3e4 h
Adverse Effects:
Flushing, hypotension, palpitations,
angina, syncope, peripheral edema,headache, vomiting 66
Caution:
Post operative patients as it potentiates
effects of curare & interacts with inhalant
anesthetics61,67
Avoid in acute heart failure
Comments:
Strong cerebral & coronary vasodilatory property68
Considered as effective as nitroprusside68,69
Associated with decreased norepinephrine levels70
Special Uses:
Particular use in CAD patients as it increases
stroke volume & coronary blood flow with favor-
able effect on myocardial oxygen balance71e74
Postoperative state75
2. Fenoldopam mesylate: dopamine D1 receptor agonist (10 times more potent than dopamine) promoting natriuresis & diuresis76
Dose:
0.8e1.2 mg/kg/min intravenously
Begin with 0.1 mg/kg/min
Increase by 0.1e0.2 at 20 min
intervals
Onset of action:>5 min
Duration of action:
30 min to 1 h without rebound
hypertension when infusion is
discontinued.77
Tachyphylaxis after 48 h78,79
Adverse Effects:
Tachycardia, hypotension, flushing,
headache, hypokalemia, nasal congestion
Caution:
Caution in glaucoma29,67
Comments:
Action mainly in renal & splanchnic arteries & less
in coronary & cerebral arteries36e38
Poorly lipid soluble, does not cross blood brain
barrier (so no CNS activity)80
Special Uses:
Most useful in patient with renal impairment81
Acute heart failure76,82e84
Those undergoing vascular surgery85
3. Clevidipine butyrate: L-type calcium channel blocker
Dose:
0.5e3.5 mg/kg/min Intravenously
Onset of action:
2e4 min e ultra short acting
Duration of action:
5e15 min
Adverse Effects:
Headache, nausea, vomiting, hypotension
Heart failure deterioration
Caution:
Severe aortic stenosis
Acute heart failure
Comments:
Reduces PVR without affecting venous vascular
tone, increases cardiac output with little influence
on left ventricular filling pressure86e89 & without
causing reflex tachycardia90
Rapid metabolism by esterase in blood &
extravascular tissues
Special Uses:
Critically ill patients, minimizing risk of prolonged
hypotension & overshoot hypotension32,86
Post anesthesia hypertension90
4. Sodium nitroprusside: direct arteriolar & venous dilator by releasing nitric oxide, increases cGMP, blocks intracellular calcium release 91
Dose:
0.5e10 mg/kg/min I.V with light
resistant delivery system15,74,92
Onset of action:
Immediate
Intraarterial BP monitoring
recommended because of
tachyphylaxis & rapidity of action
Duration of action:1e2 min
Adverse Effects:
Hypotension, palpitations, headache,
nausea, vomiting.
Obliterates cerebral autoregulation
Thyroid suppression
Coronary steal phenomenon78
Thiocyanate and cyanide toxicity (when
used for > 72 h)10,61
Cyanide removal requires bioavailabilityof thiosulphate & normal liver & renal
functions.79,93
Caution:
High intracranial pressure94
Hepatic or renal failure
Acute coronary syndrome94,95
Comments:
For years considered first choice drug 9,13,29,67
Now relatively abandoned10,32
Special Uses :
Hypertensive encephalopathy96
Aortic dissection
Acute heart failure
5. Nitroglycerin: powerful venodilator & at higher doses is an arteriolar vasodilator. Acts by increasing nitrate receptor.
Dose:
5e100 mg/kg/min I.V
Onset of action:
2e5 min
Duration of action:
5e10 min
Adverse Effects :
Profound headache, vomiting, methemo-
globinemia, tachyphylaxis.
Comments:
Adheres to plastic containers & tubings,61,67
Special Uses:
Coronary ischemia & pulmonary edema
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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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heart failure with an intent to reduce myocardial oxygen
consumption9,61,67 where it may be helpful.
7.2. Hypertensive emergencies associated with aorticdissection
The blood pressure should be rapidly reduced to
systolic < 120 mmHg or < 100 mmHg if tolerated.119,120 A
vasodilator alone is not ideal as this can promote reflex
tachycardia, increase aortic ejection velocity & promote
dissection propagation. Therefore, the standard treatment is a
combination of beta blocker & vasodilator recommended to
effectively reduce BP, heart rate & cardiac contrac-
tility9,29,67,119,120 that lowers the pulsatile load as well as aortic
stress.
Esmolol is the drug of choice although metoprolol is a
reasonable alternative.121,122 Although nitroprusside hastraditionally been used as the vasodilator of choice, fenoldo-
pam or nicardipine are less toxic & equally effective
alternatives.122,123
Even presumptive diagnosis of acute aortic dissection
should prompt us to start parenteral anti hypertensives as
soon as possible. Not invariably, pharmacologic treatment is
only a bridge to surgery, especially in Type A dissection
involving ascending aorta.124,125 Therefore, all patients of
aortic dissection of Type A dissection deserve active surgical
consideration. However, patients with Type B dissections can
be managed with aggressive BP control unless complications
like leak, rupture and impaired flow to vital organs
ensues.125,126
7.3. Hypertensive emergencies presenting with acute
neurologic syndromes
Prompt improvement in patient’s condition with BP reductionis the only definite criterion to diagnose hypertensive
encephalopathy.127
Currently, fenoldopam, nicardipine & labetalol are advo-
cated.29,61,67 Clevidipine has also emerged as an effective
alternative128,129 to be preferred over nitroprusside that was
typically chosen for many years. Since nitroprusside can in-
crease intracranial pressure & reduces cerebral blood flow in
areas with a fixed arterial narrowing 130 & recent evidence of
an increase in mortality in ECLIPSE study when compared to
clevidipine,131 its use for this indication has declined.
In patients with acute ischemic stroke, however, aggressive
reduction in blood pressure is controversial, as elevated BP
likely represents an adaptive mechanism to maintain bloodflow to the affected area132 and aggressive lowering of blood
pressure has even documented to expand the ischemic pen-
umbra61,127,133 that may have deleterious and sometimes
catastrophic consequences. Overall, there is no convincing
evidence that elevated blood pressure affects the outcome
during the acute phase of an ischemic stroke,127,134 not even
when initiated in the first few hours of stroke onset.29,61,135,136
Blood pressure usually declines spontaneously to pre-
stroke levels within 4 days of an acute ischemic stroke
without any antihypertensive treatment.137
The current recommendations are to administer antihy-
pertensive treatment in ischemic stroke only if blood pressure
is more than 220/120with mean BP is more than 130 mmHg, &
Table 2 e ( continued )
Dosage & pharmacokinetics Adverse Effects & Caution Comments & Special Uses
Onset of action:
1e2 min
Duration of action:
10e20 min108,109 Caution:
Heart failure
Heart block COPD
Metabolized by rapid hydrolysis of ester linkages
by RBC esterase
Special Uses:
Considered by some as “ ideal beta adrenergicblocker” to be used in critically ill patients32
Aortic dissection
Perioperative states110,111
Any hypertensive crisis with increased heart
rate/cardiac output
Acute MI112
12. Urapidil: selective post synaptic alpha-1 blocker, 5 HT1A receptor agonist
Dose:
12.5e25 mg I.V. bolus followed by
5e40 mg/h I/V infusion
Onset of action:
3e5 min
Duration of action:
4e6 h
Adverse Effects:
Headache, dizziness
Special Uses:
Perioperative states113
13. Phentolamine: Non selective alpha-adrenergic blocker
Dose:
0.05e0.1 mg/kg/dose intravenously
(maximum of 5 mg per dose)67
Onset of action:
1e2 min
Duration of action:
15e30 min
Adverse Effects:
Tachycardia, palpitations,
flushing, headache
Nasal congestion
Exacerbation of peptic ulcer
Special Uses:
Special use in catecholamine excess states114,115
Once initial control is achieved, oral
phenoxybenzamine a long acting alpha
adrenergic antagonist must be used
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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.
r e f e r e n c e s
1. Baker S, Barlow S, Cochran W, et al. Overweight children andadolescents: a clinical report of the North American Societyfor Pediatric Gastroenterology, Hepatology and Nutrition.
J Pediatr Gastroenterol Nutr. 2005;40:533e543.2. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of
the Joint National Committee on Prevention. Detection,Evaluation and Treatment of High Blood Pressure.Hypertension. 2003;42:1206e1252.
3. Zampaglione B, Pascale P, Marchisio M, Cavallo-Perin P.Hypertensive urgencies and emergencies: prevalence andclinical presentation. Hypertension. 1996;27:144e147.
4. Vidt DG. Current concepts in treatment of hypertensiveemergencies. Am Heart J. 1986;111:220e225.
5. Shayne PH, Pitts SR. Severely increased blood pressure in theemergency department. Ann Emerg Med. Apr2003;41(4):513e529.
6. Karz IN, Gore JM, Amin A, et al. Practice patterns, outcomesand end-organ dysfunction for patients with acute severehypertension: the Studying the Treatment of AcuteHypertension (STAT) registry. Am Heart J. 2009;158:599e606.
7. Cherney D, Straus S. Management of patients withhypertensive urgencies and emergencies: a systematicreview of the literature. J Gen Intern Med. 2002;17:937e945.
8. Ml Perez, Musini VM. Pharmacological interventions forhypertensive emergencies: a Cochrane systematic review.A high-quality meta-analysis of randomized control trials inhypertensive emergencies thatcomparedan antihypertensivedrugversus placebo,no treatment or another antihypertensivedrug. J Hum Hypertens. 2008;22:596e607.
9. Agabiri-Rosei E, Salvetri M, Farsang C. European Society of Hypertension Scientific Newsletter: treatment of hypertensive urgencies and emergencies. J Hypertens.2006;24:2482e2485.
10. Varon J. The diagnosis and treatment of hypertensive crises.Postgrad Med. 2009;121:5e13.
11. Vidt DG. Hypertensive crises: emergencies and urgencies. J Clin Hypertens. 2004;6:520e525.
12. Flanigan JS, Vitberg D. Hypertensive emergency and severehypertension: what to treat, who to treat, and how to treat.Med Clin North Am. 2006;90:439e451.
13. Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet.2000;356:411e417.
14. ElIiott WJ. Clinical features and management of selectedhypertensive emergencies. J Clin Hypertens. 2004;6:587e592.
15. Kaplan NM. Treatment or hypertensive emergencies andurgencies. Heart Dis Stroke. 1992;1:373e378.
16. Keith NM, Wagener HP, Kernohan JW. The syndrome of malignant hypertension. Arch Intern Med. 1928;41:141e153.
17. World Health Organization. Arterial hypertension-report of a WHO expert committee. WHO Tech Rep Ser. 1978;628:7.
18. Ahmed ME, Walker JM, Beevers DG, et al. Lack of difference
between malignant and accelerated hypertension. BMJ.1986;292:235e237.
19. McGregor E, Isles CG, Jay JL, et al. Retinal changes inmalignant hypertension. Br Med J. 1986;292:233e234.
20. Bakker RC, Verburgh CA, van Buchem MA, et al.Hypertension, cerebral edema and fundoscopy. Nephrol DialTransplant. 2003;18:2424e2427.
21. Keith NM, Wagener HP, Barker NW. Some different types of essential hypertension: their course and prognosis. Am J MedSci. 1939;197:332.
22. Tuncel M, Ram VCS. Hypertensive emergencies: etiology &management. Am J Cardiovasc Drugs. 2003;3(1):21e31.
23. Oppenheimer B, Fishberg AM. Hypertensiveencephalopathy. Arch Intern Med. 1928;41:264e278.
24. VolhardF, Fahr TH.Die Brightsche Neirenkrankheit:KlinikPathlogie
und Atlas. vol. 2. B erlin: Springer Verlag; 1914. 247e265.25. Haas CE, LeBlanc JM. Acute postoperative hypertension: a
review of therapeutic options. Am J Health Syst Pharm.2004;61:1661e1680.
26. Gal TJ, Cooperman LH. Hypertension in the immediatepostoperative period. Br J Anaesth. 1975;47:70e74.
27. Strandgaard S, Olesen J, Skinhoj E, Lassen NA.Autoregulation of brain circulation in severe arterialhypertension. Br Med J. 1973;1:507e510.
28. Bidani AK, Griffin KA. Pathophysiology of hypertensive renaldamage: implications for therapy. Hypertension.2004;44:595e601.
29. Elliott WJ. Clinical features in the management of selectedhypertensive emergencies. Prog Cardiovasc Dis.2006;48:316e325.
30. Ault MJ, Ellrodt AG. Pathophysiological events leading to theend-organ effects of acute hypertension. Am J Emerg Med.1985;3:10e15.
31. Wallach R, Karp RB, Reves JG, et al. Pathogenesis of paroxysmal hypertension developing during and aftercoronary bypass surgery: a study of hemodynamic andhumoral factors. Am J Cardiol. 1980;46:559e565.
32. Marik PE, Rivera R. Hypertensive emergencies: an update.A recent overview of the treatment of hypertensiveemergencies. Curr Opin Crit Care. 2011;17:569e580.
33. Beevers G, Lip GY, O’Brien E. The pathophysiology of hypertension. Br Med J. 2001;322:912e916.
34. Blumenfeld JD, Laragh JH. Management of hypertensivecrises: the scientific basis for treatment decisions. Am Heart
J. 2001;14:1154e1167.
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 410
http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004
-
8/20/2019 Jurnal Bagus Krisis HT
11/14
35. Okada M, Matsumori A, Ono K, et al. Cyclic stretchupregulates production of interleukin-8 and monocytechemotactic and activating factor/monocytechemoattractant protein-1 in human endothelial cells.Arterioscler Thromb Vasc Biol. 1998;18:894e901.
36. Verhaar MC, Beutler JJ, Gaillard CA, et al. Progressive vasculardamage in hypertension is associated with increased levels of circulating P-selectin. J Hypertens. 1998;16:45e50.
37. Bagrov AY, Shapiro JI, Fedorova OV. Endogenous cardiotonicsteroids: physiology, pharmacology, and novel therapeutictargets. Pharmacol Rev. 2009;61:9e38.
38. Schoner W, Scheiner-Bobis G. Endogenous and exogenouscardiac glycoside, and their mechanisms of action.Am J Cardiovasc Drugs. 2007;7:173e189.
39. Funakoshi Y, Ichiki T, Ito K, Takeshita A. Induction of interleukin- 6 expression by angiotensin II in rat vascularsmooth muscle cells. Hypertension. 1999;34:118e125.
40. Han Y, Runge MS, Brasier AR. Angiotensin II inducesinterleukin-6 transcription in vascular smooth muscle cellsthrough pleiotropic activation of nuclear factor-kappaB transcription factors. Circ Res. 1999;84:695e703.
41. Lassegue B, Griendling KK. Reactive oxygen species inhypertension: an update. Am J Hypertens. 2004;17:852e860.
42. Van den Born BJ, Van der Hoeven NV, Groot E, et al.Association between thrombotic microangiopathy andreduced ADAMTS 13 activity in malignant hypertension.
J Hypertens. 2008;51:862e866.43. van den Born BJ, Lowenberg EC, van der Hoeven NV, et al.
Endothelial dysfunction, platelet activation, thrombogenesisand fibrinolysis in patients with hypertensive crisis.
J Hypertens. 2011;29:922e927.44. Kaplan NM. Hypertensive crises. In: Kaplan NM, ed. Clinical
Hvpertension. 9th ed. Philadelphia, PA: Lippincott, Wiliiams &Wilkins; 2006:311e324.
45. Garg RK. Posterior leukoencephalopathy. Postgrad Med.2001;77:24e28.
46. Grond M, Reul J. Brainstem edema during a hypertensivecrisis with vasogenic and cytotoxic concerns. Dtsch Med
Wochenschr. 2003;128:2487e2489.47. Beausang-Linder M, Bill A. Cerebral circulation in acute
arterial hypertension: protective effects of sympatheticnervous activity. Acta Physiol Scand. 1981;111:193e199.
48. Papadopoulos DP, Mourouzis I, Thomopoulos C, et al.Hvpertension Crisis. vol. 19. Blood Press; 2010. 328e336.
49. Linfors EW, Feussner JR, Blessing CL, Starmer CF,Neelon FA, McKee PA. Spurious hypertension in the obesepatient. Effect of sphygmomanometer cuff size onprevalence of hypertension. Arch Intern Med.1984;144:1482e1485.
50. Zampaglione B, Pascale C, Marchisio M, Cavailo-Perin P.Hypertensive urgencies and emergencies. Prevalence andclinical presentation. A large population study on theincidence hypertensive urgencies and emergencies among
14,000 emergency room visits. Hypertension. 1996;27:144e147.51. Martin JF, Higashiama E, Gareia E, et al. Hypertensive crisis
profile. Prevalence and clinical presentation. Arq Bras Cardiol.2004;83:131e136.
52. Lane DA, Lip GY, Beevers DC. Improving survival of malignant hypertension patients over 40 years. Am JHypertens. 2009;22:1199e1204.
53. Shea S, Misra D, Ehrlich MH, et al. Predisposing factors forsevere uncontrolled hypertension in an inter-city minoritypopulation. N Engl J Med. 1992;327:776e781.
54. Moser M, Hebert PR. Prevention of disease progression, leftventricular hypertrophy and congestive heart failure inhypertension treatment trials. J Am Coll Cardiol.1996;27:1214e1218.
55. Saguner AM, Dur S, Perrig M, et al. Risk factors promoting hypertensive crises: evidence from a longitudinal study. Am
J Hypertens. 2010;23:775e780.56. Bennett NM, Shea S. Hypertensive emergency: case criteria,
sociodemographic profile, and previous care of 100 cases.Am J Public Health. 1988;78:636e640.
57. Mansoor M, Frishman W. Comprehensive management of hypertensive emergencies and urgencies. Heart Dis.
2002;4:358e371.58. Schulenburg M. Management of hypertensive emergencies:
implications for the critical care nurse. Crit Care Nurs Q .2007;30:86e93.
59. Maneia G, De Backer G, Dominiczak A, et al. 2007 guidelinesfor the management of arterial hypertension: the task forcefor the management of arterial hypertension of theEuropean Society of Hvpertension (ESH) and of the EuropeanSociety of Cardiology (ESC). J Hypertens. 2007;25:1105e1187.
60. Graves JW. Prevalence of blood pressure cuff sizes in areferral practice of 430 consecutive adult hypertensives.Blood Press Monit. 2001;6:17e20.
61. Marik PE, Varon J. Hypertensive crises: challenges andmanagement. Chest. 2007;131:1949e1962.
62. Mullins JJ, Peters J, Ganten D. Fulminant hypertension in
transgenic rats harbouring the mouse Ren-2 gene. Nature.1990;344:541e544.
63. Gandhi SK, Powers JC, Nomeir AM, et al. The pathogenesis of acute pulmonary edema associated with hypertension.N Engl J Med. 2001;344:17e22.
64. Ram CV. Management of hypertensive emergencies:changing therapeutic options. Am Heart J.1991;122:356e363.
65. Ram CVS. Hypertensive encephalopathy: recognition andmanagement. Arch Intern Med. 1978;138(12):1851e1853.
66. Squara P, Denjean D, Godard P, et al. Enoximone vsnicardipine during the early postoperative course of patientsundergoing cardiac surgery: a prospective study of twotherapeutic strategies. Chest. 1994;106:52e58.
67. Feldstein C. Management of hypertensive crises. Am J Ther.
2007;14:135e139.68. Halpern NA, Sladen RN, Goldberg JS, et al. Nicardipine
infusion for postoperative hypertension after surgery of thehead and neck. Crit Care Med. 1990;18:950e955.
69. Neutel JM, Smith DH, Walllin D, et al. A comparison orintravenous nicardipine and sodium nitroprusside in theimmediate treatment of severe hypertension. Am JHypertens. 1994;7:623e628.
70. Yang HJ, Kim JG, Lim VS, Ryoo E, Hyun SY, Lee G. Nicardipineversus nitroprusside infusion as antihypertensive therapy inhypertensive emergencies. J Int Med Res. 2004;32:118e123.
71. Lambert CR, Hill JA, Nichols WW, et al. Coronary andsystemic hemodynamic effects of nicardipine. Am J Cardiol.1985;55:652e656.
72. Vincent JL, Berlor G, Preiser JC, et al. Intravenous nicardipine
in the treatment of postoperative arterial hypertension. J Cardiothorac Vasc Anesth. 1997;11:160e164.
73. Lambert CR, Hill JA, Feldman RL, Pepine CJ. Effects ornicardipine on exercise- and pacing-induced myocardialischemia in angina pectoris. Am J Cardiol. 1987;60:471e476.
74. Lambert CR, Hill JA, Feldman RL, Pepine Cl. Effects ornicardipine on left ventricular function and energetics inman. Int J Cardiol. 1986;10:237e250.
75. Goldberg ME, Clark S, Joseph J, et al. Nicardipine versusplacebo for the treatment of postoperative hypertension. AmHeart J. 1990;119:446e450.
76. Murphy MB, Murray C, Shorten GD. Fenoldopam: a selectiveperipheral dopamine-receptor agonist for the treatment of severe hypertension. N Engl J Med. 2001;345:1548e1557.
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 11
http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004
-
8/20/2019 Jurnal Bagus Krisis HT
12/14
77. Haas AR, Marik PE. Current diagnosis and management of hypertensive emergency. Semin Dial. 2006;19(6):502e512.
78. Mann T, Cohn PF, Holman LB, Green LH, Markis lE,Phillips DA. Effect of nitroprusside on regional myocardialblood flow in coronary artery disease. Results in 25 patientsand comparison with nitroglycerin. Circulation.1978;57:732e738.
79. Pasch T, Schulz V, Hoppenshauser G. Nitroprusside-induced
formation of cyanide and its detoxication with thiosulphateduring deliberate hypotension. J Cardiovasc Pharmacol.1983;5:77e85.
80. Panacek EA, Bednarczyk EM, Dunbar LM, et al. Randomized,prospective trial of fenoldopam vs sodium nitroprusside inthe treatment of acute severe hypertension. Acad Emerg Med.1995;2:959e965.
81. Reisin E, Huth MM, Nguyen BP, Weed SG, Gonzalez FM.Intravenous fenoldopam versus sodium nitroprusside inpatients with severe hypertension. Hypertension.1990;15:159e162.
82. Tumlin JA, Dunbar LM, Oparil S, et al. Fenoldopam, adopamine agonist, for hypertensive emergency: a multicenterrandomized trial. Acad Emerg Med. 2000;7:653e662.
83. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive
emergencies and urgencies. Cardiol Clin. 2006;24:135e146.84. ElliottWJ, Weber RR, NelsonKS, et al. Renal and hemodynamic
effects of intravenous fenoldopam versus nitroprusside insevere hypertension. Circulation. 1990;81:970e977.
85. Goldberg ME, Cantillo J, Nemiroff MS, et al. Fenoldopaminfusion for the treatment of postoperative hypertension.
J Clin Anesth. 1993;5:386e391.86. Prlesi L, Cheng-Lai A. Clevidipine: a novel ultra-shaft-acting
calcium antagonist. Cardiol Rev. 2009;17:147e152.87. Ericsson H, Fakr C, Jolin-Mellgard A, et al. Clinical and
pharmacokinetic results with a new ultrashort-acting calcium antagonist, clevidipine, following graduallyincreasing intravenous doses to healthy volunteers. Br J ClinPharmacol. 1999;47:531e538.
88. Powroznyk AV, Vuylsteke A, Naughton C, et al. Comparison
of clevidipine with sodium nitroprusside in the control of blood pressure after coronary artery surgery. Eur JAnaesthesiol. 2003;20:697e703.
89. Kieler-Jensen N, Jolin-Mellgard A, Nordlander M,Ricksten SE. Coronary and systemic hemodynamic effects of clevidipine, an ultrashort-acting calcium antagonist. fortreatment of hypertension after coronary artery surgery.Acta Anaesthesiol Scand. 2000;144:186e193.
90. Nordlander M, Bjorkman JA, RegardH CG, Thalen P.Pharmacokinetics and hemodynamic effects of an ultrashort-acting calcium antagonist. Br J Anaesth. 1996;76(suppl):A24.
91. Shepherd AM, Irvine NA. Differential hemodynamic andsympathoadrenal affects of sodium nitroprusside andhydralazine in hypertensive subjects. J Cardiovasc Pharmacol.1986;8:527e533.
92. Pearce CJ, Wallin JD. Labetalol and other agents that blockboth alpha and beta-adrenergic receptors. Cleve Clin J Med.1994;61:59e69.
93. Hall VA, Guest JM. Sodium nitroprusside-induced cyanideintoxication and prevention with sodium thiosulphateprophylaxis. Am J Crit Care. 1992;2:19e27.
94. Griswold WR, Reznik V, Mendoza SA. Nitroprusside-inducedintracranial hypertension [letter]. JAMA.1981;246:2679e2680.
95. Kondo T, Brock M, Bach H. Effect of intra-arterial sodiumnitroprusside on intracranial pressure and cerebralautoregulation. Jpn Heart J. 1984;25:231e237.
96. Kaplan N. Management of hypertensive emergencies. Lancet.1994;344:1335e1338.
97. DiPette DJ, Ferraro JC, Evans RR, Martin M. Enalaprilat, anintravenous angiotensin-converting enzyme inhibitor, inhypertensive crises. Clin Pharmacol Ther. 1985;38:199e204.
98. Hirschl MM, Binder M, Bur A, et al. Impact of the renin-angiotensin-aldosterone system on blood pressure responseto intravenous enalaprilat in patients with hypertensivecrises. J Hum Hypertens. 1997;11:177e183.
99. Ludden TM, Shepherd AM, McNay JL, Lin MS. Hydralazinekinetics in hypertensive patients after intravenousadministration. Clin Pharmacol Ther. 1980;28:736e742.
100. Magee LA, Abalos E, von Dadelszen P, et al. How to managehypertension in pregnancy effectively. Br J Clin Pharmacol.2011;72:394e401.
101. Huysmans FT, Thien T, Koene RA. Acute treatment of hypertension with slow infusion of diazoxide. Arch InternMed. 1983;143:882e884.
102. Brogden RN, Sorkin EM. Isradipine e an update of itspharmacodynamic and pharmacokinetic properties andtherapeutic efficacy in the treatment of mild to moderatehypertension. Drugs. 1995;49:618e649.
103. Maharaj B, Khedun SM, Moodley J, et al. Intravenousisradipine in the management of severe hypertension in
pregnant and nonpregnant patients. A pilot study. Am JHypertens. 1994;7:615e635.
104. Lund-Johansen P. Pharmacology of combined a-b-blockade:II. Haemodynamic effects of labetalol. Drugs. 1984;28(suppl2):35e50.
105. Kanot J, Allonen H, Kleimola T, Mantyla R. Pharmacokineticsof labetalol in healthy volunteers. Int J Clin Pharmacol TherToxicol. 1981;19:41e44.
106. Olsen KS, Svendsen LB, Larsen FS, Paulson OB. Effect of labetalol on cerebral blood flow, oxygen metabolism andautoregulation in healthy humans. Br J Anaesth.1995;75:51e54.
107. Marx PG, Reid DS. Labetalol infusion in acute myocardialinfarction with systemic hypertension. Br J Clin Pharmacol.1979;8:233Se238S.
108. Gray RJ. Managing critically ill patients with esmolol. Anultrashort-acting beta-adrenergic blocker. Chest.1988;93:398e403.
109. Lowenthal DT, Porter RS, Saris SD, et al. Clinicalpharmacology, pharmacodynamics and interactions withesmolol. Am J Cardiol. 1985;56:14Fe18F.
110. Smerling A, Gersony WM. Esmolol for severe hypertensionfollowing repair of aortic coarctation. Crit Care Med.1990;18:1288e1290.
111. Gray RJ, Bateman TM, Czer LS, Conklin C, Matloff JM. Use of esmolol in hypertension after cardiac surgery. Am J Cardiol.1985;56:49Fe56F.
112. Mooss AN, Hilleman DE, Mohiuddin SM, Hunter CB. Safety of esmolol in patients with acute myocardial infarction treatedwith thrombolytic therapy who had relative
contraindications to beta-blocker therapy. Ann Pharmacother.1994;28:701e703.
113. Dooley M, Goa KL. Urapidil. A reappraisal of its use in themanagement of hypertension. Drugs. 1998;56:929e955.
114. Ziegler MG. Advances in the acute therapy of hypertension.Crit Care Med. 1992;20:1630e1631.
115. Cohn LH. Aortic dissection: new aspects of diagnosis andtreatment. Hosp Pract (Off Ed). 1994;29:47e56.
116. Strandgaard S, Paulson OB. Cerebral autoregulation. Stroke.1984;15:413e416.
117. Meggs WJ. Nifedipine for hypertensive emergencies. JAMA.1997;277:787e791.
118. Segawa D, Sjoquist PO, Wang QD, et al. Time-dependentcardioprotection with calcium antagonism and experimental
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 412
http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004
-
8/20/2019 Jurnal Bagus Krisis HT
13/14
studies with clevidipine in ischemic-reperfused pig hearts:part II. J Cardiovasc Pharmacol. 2002;40:339e345.
119. Khan lA, Nair CK. Clinical, diagnostic and managementperspectives of aortic d issection. Chest. 2002;122:311e328.
120. Estrera AL, Miller III CC, Safi HJ, et al. Outcomes of medicalmanagement of acute type B aortic dissection. Circulation.2006;114:1384e1389.
121. O’Connor B, Luntley JB. Acute dissection of the thoracic
aorta. Esmolol is safer than and as effective as labetalol[letter.comment]. BMJ. 1995;310:875.
122. Hoshino T, Ohmae M, Sakai A. Spontaneous resolution of adissection of the descending aorta after medical treatmentwith a beta blocker and a calcium antagonist. Br Heart J.1987;58:82e84.
123. Iguchi A, Tabayashi K. Outcome of medically treated Stanfordtype B aortic dissection. Jpn Circ J. 1998;62:102e105.
124. Pitt MP, Bonser RS. The natural history of thoracic aorticaneurysm disease: an overview. J Cardiovasc Surg.1997;12:270e278.
125. Borst HG, Laas J. Surgical treatment or thoracic aorticaneurysms. Adv Card Surg. 1993;4:47e87.
126. Chen K, Varon J, Wenker OC, Judge DK, Fromm RE,Sternbach GL. Acute thoracic aortic dissection: the basics.
J Emerg Med. 1997;15:859e867.127. Lavin P. Management of hypertension in patients with acute
stroke. Arch Intern Med. 1986;146:66e68.128. Bergese SD, Puente EG. Clevidipine butyrate: a promising
new drug for the management of acute hypertension. ExpertOpin Pharmacother. 2010;11:281e295.
129. Noviawary I, Uzun G, Qureshi Al. Drug evaluation of clevidipine for acute hypertension. - a nice overview of thepotential benefits of clevidipine for hypertensive emergencies.Expert Opin Pharmacother. 2008;9:2519e2529.
130. Hiremarh IS, Patki SA, Kinikar SJ, Tulpule MR. Sodiumnitroprusside in hypertensive emergencies. J Assoc PhysiciansIndia. 1986;34:716e717.
131. Aronson S, Dyke CM, Stierer KA, et al. The ECLIPSE trials:comparative studies of clevidipine to nitroglycerin, sodium
nitroprusside, and nicardipine for acute hypertensiontreatment in cardiac surgery patients. Report of the ECLIPSEprogram analyzing data from three randomized, open-labelstudies, with more than 1500 patients with perioperativeacute hypertension that compared the safety and efficacy of clevidipine versus nitroglycerin, sodium nitroprusside andnicardipine and showed that patients receiving clevidipinehad lower mortality than those on nitroprusside. AnesthAnalg. 2008;107:1110e1121.
132. Papadopoulos DP, Papademetriou V. Aggressive bloodpressure control and stroke prevention: role of calciumchannel blockers. J Hypertens. 2008;26:844e852.
133. Semplicini A, Maresca A, Boscolo G, et al. Hvpertension inacute ischemic stroke: a compensatory mechanism or anadditional damaging factor? Arch Intern Med.
2003;163:211e216.134. Adams Jr HP, del Zoppo G, Alberts MJ, et al. Guidelines for
the early management of adults with ischemic stroke: aguideline from the American Heart Association/AmericanStroke Association Stroke Council, Clinical CardiologyCouncil, Cardiovascular Radiology and Intervention Council,and the Atherosclerotic Peripheral Vascular Disease andQuality of Care Outcomes in Research InterdisciplinaryWorking Groups: the American Academy of Neurologyaffirms the value of this guideline as an educational tool forneurologists. Stroke. 2007;38:1655e1711.
135. Ahmed N, Nasman P, Wahlgren NG. Effect of intravenousnimodipine on blood pressure and outcome after acutestroke. Stroke. 2000;31:1250e1255.
136. Hillis AE, Ulatowski JA, Barker PB, et al. A pilot randomizedtrial of induced blood pressure elevation: effects on functionand focal perfusion in acute and subacute stroke. CerebrovascDis. 2003;16:236e246.
137. Wallace J, Levy LL. Blood pressure after stroke. JAMA.1981;246:2177e2180.
138. Adams H, Adams R, Del ZG, Goldstein LB. Guidelines for theearly management of patients with ischemic stroke: 2005
guidelines update a scientific statement from the StrokeCouncil of the American Heart Association/American StrokeAssociation. Stroke. 2005;36:916e923.
139. Schrader J, Luders S, Kulschewski A, et al. The access study:evaluation of acute candesartan cilexetil therapy strokesurvivors. Stroke. 2003;34:1699e1703.
140. Sandser EC, Bath PM, Boyscn G, et al. The angiotensin-receptor blocker candesartan for treatment of acute stroke(SCAST): a randomised placebo-controlled, double-blindtrial. Lancet. 2011;377:741e750.
141. Qureshi AI, Bliwise DL, Bliwise NG, et al. Rate of 24-hourblood pressure decline and mortality after spontaneousintracerebral hemorrhage: a retrospective analysis with arandom effects regression model. Crit Care Med.1999;27:480e485.
142. Qureshi AI, Hams-Lane P, Kirmani JF, et al. Treatment of acute hypertension in patients with intracerebralhemorrhage using American Heart Association guidelines.Crit Care Med. 2006;34:1975e1980.
143. Anderson CS, Huang Y, Arima H, et al. Effects of earlyintensive blood pressure-lowering treatment on the growthof hematoma and perihematomal edema in acuteintracerebral hemorrhage: the Intensive Blood PressureReduction in Acute Cerebral Haemorrhage Trial (INTERACT).Stroke. 2010;41:307e312.
144. Morgensrern LB, Hemphill III JC, Anderson C, et al.Guidelines for the management of spontaneousintracerebral hemorrhage: a guideline for healthcareprofessionals from the American Heart Association/American Stroke Association. Stroke. 2010;41:2108e2129.
145. Laragh JH. Vasoconstriction-volume analysis forunderstanding and treating hypertension: the use of reninand aldosterone profiles. Am J Med. 1973;55:261e274.
146. Hollander JE, Carter WA, Hoffman RS. Use of phentolaminefor cocaine-induced myocardial ischemia. N Engl J Med.1992;327:361.
147. Roberts AJ, Niarchos AP, Subramanian VA, et al. Systemichypertension associated with coronary artery bypasssurgery. J Thorac Cardiovasc Surg. 1977;74:856e859.
148. Gay GR, Loper KA. The use of labetalol in the management of cocaine crisis. Ann Emerg Med. 1982;17:282e283.
149. Boehrer JD, Moliterno DJ, Willard JE, Hillis LD, Lange RA.Influence of labetalol on cocaine-induced coronaryvasoconstriction in humans. Am J Med. 1993;94:608e610.
150. Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of
cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990;112:897e903.
151. Pitts WR, Lange RA, Cigarroa JE, Hillis LD. Cocaine-inducedmyocardial ischemia and infarction: pathophysiology,recognition and management. Prog Cardiovasc Dis.1997;40:65e76.
152. Negus BH, Willard JE, Hillis LD, et al. Alleviation off cocaine-induced coronary vasoconstriction with intravenousverapamil. Am J Cardiol. 1994;73:510e513.
153. Moore NA, Rees G, Sanger G, Awere S. Effect of I-typecalcium channel modulators on stimulant-inducedhyperactivity. Neuropharmacology. 1993;32:719e720.
154. Varon J, Marik P. Perioperative hypertension management.Vasc Health Risk Manag. 2008;4:615e627.
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 13
http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004
-
8/20/2019 Jurnal Bagus Krisis HT
14/14
155. Goldman L, Caldera DL. Risks of general anesthesia andelective operation in the hypertensive patient.Anesthesiology. 1979;50:285e289.
156. Ketch T, Biaggioni I, Robertson R, Robertsoon D. Four faces of baroreflex failure: hypertensive crisis, volatile hypertension,orthostatic tachycardia and malignant vagotonia. Circulation.2002;105:2518e2523.
157. Smith CB, Flower LW, Reinhardt CE. Control of hypertensive
emergencies. Postgrad Med. 1991;89:111e116.158. Sibai BM. Diagnosis, prevention and management of
eclampsia. Obstet Gvnecol. 2005;105:402e410.159. American College of Obstetricians and Gynecologists.
Diagnosis and management of preeclampsia and eclampsia.ACOGPracticeBulletinNo. 33. Obstet Gynecol. 2002;99:159e167.
160. Martin Jr IN, Thigpen BD, Moore RC, Rose CH, Cushman J,May W. Stroke and severe preeclampsia and eclampsia: aparadigm shift focusing on systolic blood pressure. ObstetGynecol. 2005;105:246e254.
161. Magee LA, Cham C, Waterman EJ, Ohlsson A, von DP.Hydralazine for treatment of severe hypertensionin pregnancy: meta-analysis. BMJ. 2003;327:955e960.
162. Pickles CJ, Broughton PF, Symonds EM. A randomisedplacebo controlled trial of labetalol in the treatment of mild
to moderate pregnancy induced hypertension. Br J ObstetGynaecol. 1992;99:964e968.
163. Jannet D, Carbonne B, Sebban E, Milliez J. Nicardipine versusmetoprolol in the treatment of hypertension during pregnancy: a randomized comparative trial. Obstet Gynecol.1994;84:354e359.
164. Mabie WC, Gonzalez AR, Sibai BM, Amon E. A comparativetrial of labetalol and hydralazine in the acute management
of severe hypertension complicating pregnancy. ObstetGynecol. 1987;70:328e333.
165. Zeller KR, Von KL, Matthews C. Rapid reduction of severeasymptomatic hypertension. A prospective controlled trial.Arch Intern Med. 1989;149:2186e2189.
166. Grossman E, Messerli FH, Grodzicki T, Kowey P. Should amoratorium be placed on sublingual nifedipine capsulesgiven for hypertensive emergencies andpseudoemergencies? JAMA. 1996;276:1328e1331.
167. van Harten J, Burggraaf K, Danhof M, van Brummelen P,Breimer DD. Negligible sublingual absorption or nifedipine.Lancet. 1987;2:1363e1365.
168. Huysmans FT, Sluiter HE, Thien TA, Koene RA. Acutetreatment of hypertensive crisis with nifedipine. Br J ClinPharmacol; 1983.
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 414
http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004http://dx.doi.org/10.1016/j.cqn.2013.01.004