CRISES HYPERTENSION

R RUKMA JUSLIMSUBDEP JANTUNG RSAL

DR RAMELAN

DEFINITION

H. Emergency≈ Acute end organ damaged

(CV;Renal;CNS;Eyes)H.Urgency

≈ Without acute end organ damagedMalignant Hypertension

≈ Elevated BP + Encephalopathy or Acute nephropathy

Target Organ Damage (TOD)

• CNS : encephalopathy, stroke

• Occular : papiledema, blurring of vision

• Cardiac : ADHF, AP, aortic dissection

• Renal : azotemia, hematuria, proteinuria, oliguria

• Hematologic : microangiopathic hemolytic anemia

CLASSIFICATION

Normal : < 120/80

Prehypertension : 120-139 – 80-89

Stage I : 140-159 – 90-99

Stage II : >160/100

Crises : ≥ 180/110

EPIDEMIOLOGY

30% Undiagnosed

Framingham Heart Study:

3,3% 30-39 yrs ; 6,2% 70-79 yrs

♂ > ♀

(1939) Untreated malignant hypertension » 1 year mortality 79%

ETIOLOGY

Essential/primary hypertension

Secondary hypertension

CONTRIBUTING TO CRITICAL INCREASE IN BP

Factors in the pathomechanism of Factors in the pathomechanism of hypertensive crisishypertensive crisis

FURTHER INCREASE IN BLOOD PRESSURE AGGRAVATED ENDOTHELIAL DAMAGE LEAD TO

TISSUE ISCHEMIA

LOCAL FACTORS

• FG, Free radicals

• Endothelial damage

• Platelet-aggregation

• Mitogenic and migration factors

proliferation

• Myointimal proliferation

SYSTEMIC FACTORS

• Renin, A II, catecholamine,

ET

• Vasopressin, pressure

natriuresis

• Hypovolemia

Kaplan, N : Critical Hypertension

Critical degree of hypertension

Local effect Systemic effect (RAA,cathecol,Vasopres)

Endothelian damage ↓

Platelet deposition Pressure natriuresis

Mitogenic & migration factors Hypovolemia

Myointimal proliferation Increase of vasopressors

Vascular damage & Tissue ischemia

SYMTOMP & SIGNS

Headache Focal Neurological sign

Consciousness Retinopathy

Seizures AMI (angina)

Left Ventricle Failure

Acute Renal Failure

Subjective and Laboratory Subjective and Laboratory Symptoms of Hypertensive Crisis Symptoms of Hypertensive Crisis

Cardiac symptoms

palpitation

rhythm disturbances

Chest pain

dyspnea

General symptoms

sweating

flush

pallor

dizziness

fear of death

tinnitus

epistaxis

Ocular symptoms

flashes

spotted vision

dimmed vision

diplopia

blindness

Renal symptoms

oliguria

hematuria

proteinuria

Electrolyte disturbances

azotemia

uremia

Cerebral symptoms

headache

dizziness

nausea

daze

focal symptoms

cramp

coma

Zamplagione B et al : Hypertension 1996

Management of Hypertension

Life style modification

Management of Hypertensive urgency • Goal : prevent to the target organ damage

• Therapeutic consideration :

• Use oral drugs

• Sub lingual drug ?!

• Reach the BP 160/100 mmHg in 24 hours, normal after 24-48 hours

Management of Hypertensive Emergency

JNC 7

• Reduce mean arterial BP by no more than 25% (within minutes to 1 hours)

• If stable , to 160/100 to 110 mmHg (within next 2 to 6 hours)

• If well tolerated and stable, gradual reduction toward a normal BP can be implemented in the next 24 to 48 hours

Management of crises hypertension

Examination :

(Physical; Neurological; Funduscopic)

Laboratory

ECG ; Radiological

↓↓↓↓

URGENCY OR EMERGENCY

↓ ↓

Oral Intravenous

Initial evaluation of patients with a hypertensive emergency

• Laboratory Evaluation– Hematocrit and blood smear– Urine analysis– Automated chemistry : creatinine, glucose,

electrolytes– Electrocardiogram– Chest radiograph

Pathways for management of patients with severe hypertension, defined as blood pressure (BP) in excess of 180/120 mmHg.

Severe HypertensionBP > 180 / 110

EncephalopathyProgressing target organ damage

Yes(HT Emergency)

No

New onset(HT Urgency)

Prior similar experience;Negative workup(Uncontrolled HT)

Admit to ICUBaseline lab

Baseline lab

Oral Rx

Reinstitute oral Rx

Follow closely

Parenteral Rx

Workup foridentifiable causes:

Renovascular HT

The Kidney and Hypertension, Bakris, 2004

Ideal Pharmacological Agent

Fast acting

Rapidly reversible

Titratable

Without significant Side Efect

Diuretics

Usually needed to maintain efficacy of other drug

Onset : 5 – 15 minutes

Duration: 2 – 3 hours

SE : Hypovolemic, Hypokalemia

Dose : 20 – 40 mg in 1-2 repeated

Sodium Nitropruside

Most hypertensive emergencies; caution with high intracranial pressure / azotemia

Onset : Immediate

Duration: 1-2 minutes

SE : Nausea, vomiting, muscle

twitching, cyanide intoxication

Dose : 0,25 – 10 µg/kg/min

Nitroglycerin

Coronary ischemia

Onset : 2-5 minutes

Duration: 5-10 minutes

SE : headache, vomiting, tolerance

with prolonged use.

Dose : 5-100µg/min

Nicardipine

Most hypertensive emergencies; caution with acute HF. Strong cerebral & coronary vasodilator. 100 times more water soluble than nifedipin (titratable)

Onset : 5-10 minutes

Duration: 4-6 hours

SE : Headache, tachycardia, local

phlebitis

Dose : 5-15 mg/h

Labetolol

Most hypertensive emergencies, except acute HF.

Onset : 5-10 minutes

Duration: 3-6 hours

SE : Vomiting, burning in throat,

dizziness, nausea, heart block,

orthostatic hypotension

Dose : 20-80 mg bolus every 10 min 2

mg/min

Berbagai Macam Sediaan Parenteral Calcium Channel Bloker

Drug Coronary Vasodilation

Suppressionof Cardiac

Contractility

Suppressionof SA Node

Suppressionof AV Node

Verapamil

(phenylalkylamine)

++++ ++++ +++++ +++++

Diltiazem

(benzothiazepin)

+++ ++ +++++ ++++

Nicardipine

(dihydropyridine)

+++++ 0 + 0

Classification Calcium Antagonists

Generation: First Second Third Latest

VerapamilNifedipineDiltiazem

FelodipineIsradipineNicardipineNimodipineNisoldipineNitrendipine

FelodipineIsradipineNicardipineNimodipineNisoldipineNitrendipine

Amlodipine Lercanidipine(hydrophilic) (lipophilic)

Prototype Tissue selectivity Tissue selectivity Tissue selectivity gradual onset gradual onset Plasma controlled membrane controlled

J Clin Basic Cardiol 1999;2:155

Basic Properties Of The Ccb Nicardipine (Nc), Nifedipine (Nf), Diltiazem (D) and

Verapamil (V)

Nc Nf D V

Systemic vasodilatation

Myocardial depression

Block AV conduction

Vasoselectivity

++

0

0

++++

++

+

0

+++

+

+

+

+

+

+++

++

0

NICARDIPINE VS DILTIAZEM

NICARDIPINE DILTIAZEM

Target organ Arteriole (ca Channel)

Arteriole (ca Channel)

Clinical effect Vasodilatation : BP decreased

Vasodilatation : BP decreased

Heart Rate ↑

Cardiac inotropic

(-) (-)

PERDIPINE Nicardipine injection 2 / 10 mg

MEKANISME KERJA

Menghambat influx ion Ca ke dalam intra sel, dengan memblokade channel calcium ( Ca Channel Blocker / CCB ), sehingga terjadi

penghambatan kontraksi otot .

Sifat vasoselektif tinggi hanya dimiliki oleh PERDIPINE, maka penghambatan ini terutama terjadi pada otot polos pembuluh darah, khususnya pembuluh darah arteri.

DOSIS & PEMAKAIAN• Hipertensi akut selama operasi : 2 – 10 µg/kg/menit secara IV infus drip• Untuk penurunan yang cepat : 10 – 30 µg/kg bolus • Hipertensi emergensi : 0,5 – 6 µg/kg/menit secara IV infus drip

Perdipine mempunyai 2 kemasan :

- 2 mg (isi 2 cc) untuk bolus injeksi

- 10 mg (isi 10 cc) untuk infus drip

Untuk pemakaian dengan infus drip, direkomendasikan menggunakan cairan infus 100cc dan mikro drip (1cc=60 tetes).

Lamanya pemakaian setelah tekanan darah turun dan terkontrol tergantung dari keputusan klinisi untuk pindah ke oral

DOSIS & PEMAKAIAN (Cont’d)

• Penambahan tetesan tergantung dari dosis.Mis. Dimulai dengan dosis 0.5 dengan 15 tetesan monitor, bila dalam 5-15 menit tidak ada perubahan TD naikkan tetesan menjadi 20 tetes (Tidak harus langsung menjadi 30 tetes) tapi dapat bertahap

• Pada pemakaian Perdipine harus disertai dengan monitor tekanan darah & detak jantung

• Apabila ada keputusan untuk pindah ke oral, maka 1 jam sebelum Pd di aff obat oral diberikan dahulu Dosis Pd mulai di turunkan (Tappering Off).