CRISES

HYPERTENSION
R RUKMA JUSLIM
SUBDEP JANTUNG RSAL
DR RAMELAN
 DEFINITION
H. Emergency
Acute end organ damaged
(CV;Renal;CNS;Eyes)
H.Urgency
Without acute end organ damaged
Malignant 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
 Factors in the pathomechanism of
hypertensive crisis

CONTRIBUTING TO CRITICAL INCREASE IN BP

LOCAL FACTORS SYSTEMIC FACTORS
FG, Free radicals Renin, A II, catecholamine,

Endothelial damage ET
Platelet-aggregation Vasopressin, pressure
Mitogenic and migration factors natriuresis
proliferation Hypovolemia
Myointimal proliferation

FURTHER INCREASE IN BLOOD PRESSURE

AGGRAVATED ENDOTHELIAL DAMAGE LEAD TO
TISSUE ISCHEMIA
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
Symptoms of Hypertensive Crisis
General symptoms
Cardiac symptoms sweating Cerebral
palpitation flush symptoms
rhythm disturbances pallor
headache
Chest pain dizziness
dizziness
dyspnea fear of death
nausea
tinnitus
Renal symptoms epistaxis
daze

oliguria focal symptoms

Ocular symptoms
hematuria cramp
flashes
proteinuria coma
spotted vision
Electrolyte disturbances
dimmed vision
azotemia
diplopia
uremia Zamplagione B et al : Hypertension 1996
blindness
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
 Severe Hypertension
BP > 180 / 110

Encephalopathy
Progressing target organ damage

Yes No
(HT Emergency)
Admit to ICU New onset Prior similar experience;
Baseline lab (HT Urgency) Negative workup
(Uncontrolled HT)

Parenteral Rx Baseline lab Reinstitute oral Rx

Oral Rx Follow closely

Workup for
identifiable causes:
Renovascular HT

Pathways for management of patients with severe hypertension,

defined as blood pressure (BP) in excess of 180/120 mmHg.
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 g/kg/min
 Nitroglycerin
Coronary ischemia
Onset : 2-5 minutes
Duration: 5-10 minutes
SE : headache, vomiting, tolerance
with prolonged use.
Dose : 5-100g/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 Suppression Suppression Suppression
Vasodilation of Cardiac of SA Node of AV Node
Contractility

Verapamil ++++ ++++ +++++ +++++

(phenylalkylamine)

Diltiazem +++ ++ +++++ ++++

(benzothiazepin)

Nicardipine +++++ 0 + 0
(dihydropyridine)
 Classification Calcium Antagonists
Generation:
First Second Third Latest

Verapamil Felodipine Amlodipine Lercanidipine

Nifedipine Isradipine (hydrophilic) (lipophilic)
Diltiazem Nicardipine
Nimodipine
Nisoldipine
Nitrendipine

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 0 + + +++
Block AV conduction 0 0 + ++
Vasoselectivity ++++ +++ + 0
 NICARDIPINE VS DILTIAZEM

NICARDIPINE DILTIAZEM

Target organ Arteriole (ca Arteriole (ca

Channel) Channel)
Clinical effect Vasodilatation : Vasodilatation :
BP decreased 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 g/kg/menit secara IV infus drip
Untuk penurunan yang cepat : 10 30 g/kg bolus
Hipertensi emergensi : 0,5 6 g/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 (Contd)

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).