HYPERTENSIVE EMERGENCY

Dwi Lestari Partiningrum

Nephrology and Hypertension Division, Internal Medicine Department
Medical Faculty Diponegoro University/ Kariadi Hospital
 Definitions
 Pathophysiology and Clinical Manifestation
 Parenteral Agents for Hypertensive Emergencies
 Management of Spesific Hypertensive
Emergencies

Dwi Lestari
 Definition

 Hypertensive Crisis
 Hypertensive Emergencies

 Hypertensive Urgencies

 (Accelerated) Malignant Hypertension

?
 Hypertensive Crisis

JNC VII 2003

 ≥ 180/110

 Recognition of hypertensive crisis depends on

the clinical state of the patients, not on the

absolute level of blood pressure
 Included Hypertensive Emergency and

Hypertensive Urgency

Dwi Lestari
 DefinitionHypertensive crises

A severe elevation in blood pressure (BP),

such as a diastolic BP above 120 to 130
mmHg, and is classified as either an
emergency or urgency

Dwi Lestari E Grossman & FH Messerli, Comprehensive Hypertension Mosby, 2007

 Definition Hypertensive urgency

A situation with markedly elevated BP but without

severe symptoms or progressive target organ
damage, wherein the BP should be reduced
within hours, often with oral agents
or
When severe elevation in BP is not associated with
end-organ injury

MN.Kaplan; Clin.Hypt 9th ed.2006

Dwi Lestari
E Grossman & FH Messerli, Comprh Hypert Mosby, 2007
 ClinicalHypertensive
implication urgency

Common and no scientific evidence showed that

acute BP lowering is beneficial.
The appropriate approach is to lower BP gradually
over 12 to 24 hours with oral AHAs.
Any drug that lower BP precipitously should be
avoided

Dwi Lestari
MN.Kaplan; Clin.Hypertension 9th ed.2006
 Definition
Hypertensive emergency

A situation that requires immediate reduction in blood pressure

with parenteral agents because of acute or progressing
target organ damage
When BP elevation confers an immediate threat to the integrity
of the cardiovascular system
Relatively rare, and immediate reduction in BP is required to
avoid further end-organ damage, generally by IV therapy in
an IC setting to lower the MAP by 25% over the initial 2 to 4
hours with the most specific AHA

MN.Kaplan; Clin.Hypt 9th ed.2006

Dwi Lestari E Grossman & FH Messerli, Comprehensive Hypertension Mosby, 2007
 (Accelerated) Malignant Hypertension

 Elevated BP associated / manifested clinically

with retinal hemorrhages, exudates and
papilledema (grade 3 Keith-Wagener
retinopathy and grade 4 KW retinopathy)
 Most often occur in patients with long-standing
uncontrolled hypertension
 Maybe difficult to detect, subject to observer
interpretation

Dwi Lestari
 Pathophysiology and
Clinical Manifestation

 Failure of the normal autoregulatory function

 Abrupt increases in systemic vascular resistant

 End organ damage and severity of BP elevation

 Fibrinoid necrosis
 Activation of endothelial vasoactive systems: endothelin,
oxidative stress, RAS
Dwi Lestari
 Endocrine disorders Severe hypertension Essential hypertension
Pregnancy
Renal disorders
Drugs
Critical level
or
rapid rate of rise and
Endothelial damage increased Spontaneous natriuresis
vascular resistance

Endothelial permeability Intravascular volume

depletion

Platelet and fibrin

deposition Decrease in vasodilators, Increase is vasoconstrictors
nitric oxide, prostacyclin (renin-angiotensin,
catecholamines)
Fibrinoid necrosis and
intimal proliferation
Further increase in
blood pressure

Severe blood
pressure elevation

Tissue ischemia

End-organ dysfunction

Dwi Lestari Kitiyakara, JASN 1998

 Critical degree of hypertension

Increase in vasoconstrictors
Endothelial damage (renin-angiotensin,
vasopressin, catecholamines)

Platelet and fibrin Further blood pressure

deposition increase
Intravascular
hemolysis Pressure natriuresis

Fibrinoid necrosis hypovolemia

and intimal
proliferation

Further release of
Increase in blood vasoconstrictors
pressure and
ischemia

Mechanisms of malignant hypertension

Dwi Lestari
 Drugs that can increase BP
 Withdrawl of antihypertensive medications:
clonidine rebound (methyldopa,reserpine),
nifedipine, propanolol
 Phenylpropanolamine (cold preparations)
 Sympathomimetics amines
 Oral contraceptive, erythropoieten
 Corticosteroids, anabolic steroids
 NSAIDS, Cox2 inhibitors
 Cocaine, amphetamine, ethanol
 NaCl

Dwi Lestari
 Prevalence of Hypertensive Crisis

Hypertensive crisis
( % of all pts )
Mainly due to more effective treatment ?

1950’s 1990’s

Dwi Lestari Zampaglione, et al. AHA ; 27 (1) : 144

Retinal findings in hypertensive encephalopathy

Dwi Lestari
Fundoscopic appearance of grade IV hypertensive retinopathy,
 papilloedema (1),

 arteriovenous nipping (2),

 flame-shaped hemorrhages (3),

 soft (4) and hard (5) exudates

 Clinical Manifestation of
Hypertensive Emergency

 Hypertensive encephalopathy
 Dissecting (acute) aortic aneurysm
 Acute left ventricular failure with pulmonary edema
 Acute myocardial infarction & acute coronary
syndrome
 Eclampsia, HELLP sndrome, Pre-eclampsia
severe
 Acute renal failure
 Symptomatic microangiopathic hemolytic anemia

Dwi Lestari Haas, Seminars in Dialysis 2006

 Evaluation
Initial evaluation for patients with HTN emergency
History
• Prior diagnosis & treatment of HTN
• Intake of pressor agents; street drugs,
sympathomimetics
• Symptoms of cerebral, cardiac, pulmonal, and visual
dysfunction
Physical examination
• Blood pressure
• Funduscopy
• Neurologic status
• Cardiopulmonary status
• Blood fluid volume assessment
• Peripheral pulses
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Laboratory evaluation
 Hematocrit and blood smear

 Urine analysis

 Automated chemistry : creatinin, glucose, electrolytes

 ECG

 Plasma renin activity & aldosterone (if primary

aldosteronism is suspected)
 Plasma renin activity before & 1 h after 25 mg captopril

(if renovascular HTN issuspected)

 Spot urine or plasma for metanephrine (if
pheochromocytoma is suspected)
 Chest radiograph (if heart failure or aortic dissection is
suspected)

Dwi Lestari
 SIMPLE APPROACH
TO HYPERTENSIVE CRISIS
BP > 220/120 mmHg
Neurological sign Headache
(encephalopathy or stroke) No neurological signs
Retinopathy grade 3-4 No target organ damage
Severe chest pain
(Ischemia or dissecting aneurism)
URGENCY
Pulmonary edema
Eclampsia
Cathecolamine excess Identify the cause
Acute renal failure In panic attacks or anxiety use
analgesic, anxiolytics
Otherwise use oral antihypertensive
EMERGENCY agents
recheck in 6-24 hours
Intravenous therapy

Dwi Lestari
 Principles of Therapy for Hypertensive
Emergencies

 Patients must be hospitalized for monitoring

 Direct consequences of lowering BP too quickly
 Treated with parenteral
 Lower MAP {1/3(SBP-DBP)+DBP} by no more than 25%
within minute to 2 hours or diastolic 110 mmHg, then
160/100 mmHg within 2-6 hours (JNC VII). Exception for
ischemic stroke
 IV infusion is prefer than bolus

Hypertension.,Brian C. Poole and Anitha Vijayan

Dwi Lestari in Nephrology and Subspeciality Consult,2004
 Parenteral Agents
for Hypertensive Emergencies

Pheripheral Vasodilatation Parenteral Adrenergic Inhibitor

 Sodium Nitroprusside  Labetalol
 Esmolol
 Nitroglycerin *
 Phentolamine
 Nicardipine *
 Diltiazem *
 Diazoxide
 Fenoldopam mesylate
 Enaprilat Centrally acting : Clonidin

Dwi Lestari
 Tatalaksana Hipertensi Emergensi

 Harus dilakukan di rumah sakit

 Pengobatan secara parenteral baik bolus atau
infus.
 Tekanan darah diturunkan dalam hitungan menit
– jam.

Dwi Lestari Konsensus InaSH

 Tatalaksana Hipertensi emergensi

 Langkah penurunan tekanan darah :

− 5-120 menit pertama tekanan darah arteri rata-rata

(Mean Arterial Pressure, MAP) diturunkan 20-25 %
− 2 s/d 6 jam berikutnya tekanan darah diturunkan
sampai 160 / 100 mm Hg
− 6-24 jam berikutnya lagi sampai ≤140 / 90 mmHg.
(tidak boleh ada tanda-tanda iskemia organ)
− Target penurunan tekanan darah tergantung faktor
risiko krisis hipertensi.

Dwi Lestari
 Obat parenteral
pd Hipertensi emergensi
 Clonidine

 Centrally acting -2 Agonist

 Good oral bioavailability, a relatively rapid onset of oral
action.
 Disadvantage : acute use parogressive sedation, dry
mouth, somnolence, “rebound hypertension’
 Use oral, transdermal (FDA)
 0.1 – 0.2 po repeat hourly as required
 Dose 0.15–0.3 mg over a period of 5 minutes . Reduced
MAP in 25% within minutes to 1 hour

Dwi Lestari
 Clonidin (Catapres) IV (150 mcg/ampul)
 Clonidin 900 mcg (6ampul) dalam glucosa 5 %
dengan tetesan mikro disesuaikan dengan kebutuhan.
Dosis awal 12 tetes / menit dan setiap 15 menit dapat
dinaikkan 4 tetes.
 Bila sasaran tekanan darah tercapai dilakukan
observasi 4 jam dan diteruskan dengan tablet oral
sesuai kebutuhan.
 Clonidin tidak boleh dihentikan mendadak. Dosis
diturunkan - perlahan-lahan oleh karena bahaya
“rebound phenomen “ dimana tekanan darah naik
kembali secara cepat bila obat dihentikan.

Dwi Lestari
 Nitroglycerin

 A venous dilator and slight arteriolar dilatation

 Most useful in patients with symptomatic
coronary disease and in those with hypertension
following coronary bypass.
 Initial dose 5 µg/min, max dose 100 µg/min.
 Onset 2 to 5 minutes, duration action 5 to 10
minutes
 Side effect : headache and tachycardia

Dwi Lestari
 Diltiazem

 Inhibit the influx Ca during membran

depolarization of cardiac and smooth muscle
cell
 Contra indication : sick sinus syndrome,
second and third degree AV block

Dwi Lestari
 Diltiazem IV (10 dan 50mg/ ampul).
 Diltiazem 10 mg IV bolus diberikan dalam 1-3 menit
diteruskan dengan infus 50 mg /jam selama 20 menit
 Bila penurunan tekanan darah mencapai 20-25 %
dosis diberikan 30 mg/jam sampai sasaran tekanan
darah tercapai.
 Berikutnya diberikan dosis pemeliharaan 5-10 mg/
jam, selama 4 jam, kemudian diganti tablet sesuai
kebutuhan.
 Perlu perhatian khusus pada gangguan konduksi dan
gagal jantung.

Dwi Lestari
 Nicardipine

 Dihydropyridine CCB
 Initial dose :5 mg/h to a maximum 15 mg/h
 Increased by 2.5 mg/h
 Limitation : longer half life time (precludes rapid
titration)
 Side effect : reduced both cerebral and coronary
ischemia, tachycardia, increase myocardial
oxigen demand, headache, nausea and vomiting
 Cannot use in severe coronary ischemia

Dwi Lestari
 Nicardipin (Perdipin) IV (2 dan 10 mg / ampul)

 Nicardipin
bolus diberikan 10-50mcg/Kg BB
 Diteruskan dengan 0.5-6mcg/kg BB/menit
sampai mencapai sasaran tekanan darah.
 Kemudian diganti dengan antihipertensi oral.

Dwi Lestari
 DOSIS PERDIPINE
DIV Bolus
(g/kg/min) (g/kg)
Acute hypertensive crises during surgery 2 - 10 10 – 30

Hypertensive emergencies 0.5 – 6

Acute hypertensive crises during surgery

Hypertensive emergencies

0.5 1 2 6 (g/kg/min) 10

Dwi Lestari
Dwi Lestari
 Recommended Antihypertensive Agents for Hypertensive Crises
Conditions
Acute pulmonary
edema/systolic dysfunction
Acute pulmonary
edema/diastolic dysfunction
Acute myocardial ischemia
Hypertensive encephalopathy
Acute aortic dissection
Pre-eclampsia, eclampsia
Acute renal
failure/microangiopathic
anemia
Sympathetic crisis/cocaine
overdose
APH
Acute ischemic
stroke/intracerebral bleed
Dwi Lestari
Preferred Antihypertensive Agents
Nicardipine, fedoldopam, or nitroprusside in combination with
nitroglycerin and a loop diuretic
Esmolol, metoprolol, labetalol, diltiazem, verapamil in
combintaion with low-dose nitroglycerin and a loop diuretic
Labetalol or esmolol in combination with nitroglycerin
Nicardipine, Diltiazem, labelatol, or fenoldopam
Labetalol or combination of nicardipine and esmolol or
combination of nitroprusside with either esmolol or IV metoprolol
Labetalol or nicardipine
Nicardipine or fenoldopam
Verapamil, diltiazem, or nicardipine in combination with a
benzodiazepine
Esmolol, nicardipine, or labetalol
Nicardipine, Diltiazem, labetalol, or fenoldopam
 Summary
 Hypertension Crisis included
Hypertensive Emergency and Hypertensive
Urgency
 HE  required immediate reduction in BP
to avoid further end-organ damage, by IV
therapy to lower the MAP by 25
 Parenteral agents for hypertensive
emergency : Clonidin, Nitroglycerin,
Diltiazem, Nicardipine
Dwi Lestari
Dwi Lestari