DR - fifi-KUL antiHIPERTENSI 2012

FARMAKOTERAPI
padaHIPERTENSI
Fathiyah Safithri
Laboratorium Farmakologi FK-UMM

2012
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Tujuan Instruksional Khusus
Setelah mengikuti perkuliahan / diskusi diharapkan mahasiwa mampu
 Memahami faktor-faktor yang mempengaruhi tekanan darah
 Memahami mekanisme regulasi tekanan darah.
 Memahami site of action dan mekanisme kerja obat-obat yang dapat
digunakan untuk pengobatan hipertensi.
 Menyebutkan 4 kelompok besar obat antihipertensi
 Menerangkan respon kompensasi dari masing-masing kelompok obat
antihipertensi
 menyebutkan 3 mekanisme kerja obat vasodilator dalam
menurunkan tekanan darah.
 Menjelaskan perbedaan antara 2 tipe obat antagonis angiotensin.
 Menjelaskan keuntungan penggunaan obat antihipertensi kombinasi.
JNC 7:
New Blood Pressure Classification
Blood Pressure Classification

SBP* DBP*
(mm Hg)
Normal
<120 and <80
Prehypertension
120-139 or 80-89
Stage 1 hypertension
140-159 or 90-99
Stage 2 hypertension
160 or 100
Partners in
*Treatment determined byHealthcare
highestBP category (SBP or DBP). 3
Education,LLC 2009
Adapted from ChobanianAV et al. JAMA. 2003;289:2560-2572; NHBPEPCC. 2003. NIH Publication No. 03-5233.
Etiology
 Essential hypertension:
 > 90% of cases
 hereditary component
 Secondary hypertension:
 < 10% of cases
 common causes: chronic kidney disease,
renovascular disease
 other causes: Rx drugs, street drugs, natural
products, food, industrial chemicals
Causes of 2˚ Hypertension
 Diseases  Food
 chronic kidney disease substances:
 Cushing's syndrome sodium
 coarctation of the aorta
ethanol
 obstructive sleep apnea
licorice
 parathyroid disease
 pheochromocytoma
 primary aldosteronism
 renovascular disease
 thyroid disease 5
 Prescription drugs:
 prednisone, fludrocortisone, triamcinolone
 amphetamines/anorexiants: phendimetrazine,
phentermine, sibutramine
 antivascular endothelin growth factor agents
 estrogens: usually oral contraceptives
 calcineurin inhibitors: cyclosporine, tacrolimus
 decongestants: phenylpropanolamine & analogs
 erythropoiesis stimulating agents: erythropoietin,
darbepoietin
6
 Prescription drugs:
 NSAIDs, COX-2 inhibitors
 venlafaxine
 bupropion
 bromocriptine
 buspirone
 carbamazepine
 clozapine
 ketamine
 metoclopramide 7
 Street drugs, other natural products:

 cocaine  anabolic steroids
 cocaine withdrawal  narcotic withdrawal
 ephedra alkaloids  methylphenidate
(e.g., ma-huang)  phencyclidine
 “herbal ecstasy”  ketamine
 phenylpropanolamine  ergot-containing
analogs herbal products
 nicotine withdrawal  St. John's wort
Mengapa Hipertensi harus diatasi ?
 Morbiditas dan mortalitas meningkat secara

progresif seiring dengan makin tingginya TD
(MacMahon et al, 1990)
 Mkn tinggi TD, mkn besar resiko terjadinya
kerusakan target organ:
10
Apa tujuan terapi hipertensi ?
Menurunkan mortalitas TARGET Tx

 Mencegah kerusakan target
 Secara umumTD <
organ (jantung, otak, ginjal,
140/90 ( tanpa
mata)
komplikasi)
 Memperbaiki kualitas hidup
(menghilangkan gejala)  TD <130/80 pada
hipertensi yang
Average Percent Reduction disertai diabetes
Stoke : 35% - 40% mellitus atau
MI : 20% - 25% penyakit ginjal
kronik (JNC VII)
CHF : 50%
Determinants of Arterial Pressure
Blood
Volume
Mean Arterial
Pressure (MAP)
= X Arteriolar
Diameter
Heart
Stroke Volume
Rate
CO : Cardiac Output
TPR : Total Peripheral Resistance
Contractility Filling Pressure
Blood Volume Venous Tone
Mechanisms Controlling CO and TPR
1. Neural /SSO
Sympatis 2. Hormonal
Parasympatis Renal
Ang II
Adrenal
Catecholamines
Aldosterone
3. Local Factors
Artery Vein
Bagaimana Regulasi Tekanan Darah ?
 Neural Regulation /Short-term regulation
 diperantarai reflek baroreseptor-SSO &
kemoreseptor (O2 & CO2)
 mempengaruhi pembuluh darah (diameter) dan
jantung (HR dan kontraktilitas)
 Humoral Regulation / Long-term regulation

 mempengaruhi ginjal (Angiotensin II) & Adrenal
(Katekolamin dan Aldosteron)
 Local Regulation
AutonomicNeural Regulation
Short-TermMechanisms:RefleksBaroreceptor
Short-Term Mechanisms : Refleks Baroreceptor
Long- -TermMechanisms / Humoral Regulation
LocalRegulation:Autoregulasi
 Substansi kimia
lokal
 Mis : NO,
potassium and
hydrogen ions,
ANP, adenosine,
lactic acid,
histamines, kinins,
and
prostaglandins
Bagaimana Terapi Hipertensi ?
 Terapi Non farmakologis : Life style modification
 stop merokok
 diet : kurangi makanan berlemak & asupan garam,
tambah suplemen ion K, Ca, Mg
 menurunkan BB
 aktivitas fisik / OR
 relaksasi (kurangi stress)
 Terapi Farmakologis : Obat antihipertensi
Apa Perlunya Diet Rendah Garam ?
Life style Modifications
Modification Recommendation Systolic Diastolic Chgs

Weight Reduction BMI 18.5-24.9 5-20mm/10 kg wt loss
Adopt DASH eating Diet rich in fruits 8-14 mm Hg
vegetables and low
fat with reduced
saturated and total fat
Dietary Sodium 2.4g Na 2-8 mm Hg
Physical Inactivity Brisk exercise 30” day 4-9 mm Hg
most days of week
Moderation of
Alcohol intake 2 drinks day max 2-4 mm Hg
24 oz beer; 10 oz wine
2 oz 100 proof whiskey
JAMA. 2003:289:2560-2577.
Partners in Healthcare 22
Education,LLC 2009
Life style Modifications
Approximate
Modificatio Systolic
Recommendation Reduction(mm
n a
Hg)
Weightloss Maintainnormalbodyweight(bodymassindex 5–20per10-kg
2 weightloss
18.5–24.9kg/m)
DASH-type Consumeadietrichinfruits,vegetables,andlow- 8–14
dietary fatdairyproductswithareducedcontentof
patterns saturatedandtotalfat
Reducedsalt Reducedailydietarysodiumintakeasmuchas 2–8
intake possible,ideallyto65mmol/day(1.5g/daysodium,
or3.8g/daysodiumchloride)
Physical Regularaerobicphysicalactivity(atleast30 4–9
activity min/day,mostdaysoftheweek)
DASH, Dietary Approaches to Stop Hypertension.
aModerationof Limitconsumptionto2drinks/dayinmenand1
Effects of implementing 2–4for
these modifications are time and dose dependent and could be greater
alcoholintake
some patients. drink/dayinwomenandlighter-weightpersons
23
DiPiro JT, Talbert RL, Yee GC, Matzke GR, WellsBG, Posey LM: Pharmacotherapy:APathophysiologicApproach, 7th Edition:
http://www.accesspharmacy.com/
Additional Recommendations
 Diets high in potassium, calcium and magnesium are

associated with a lower blood pressure
 JNC VII recommends an adequate dietary intake of these
but does not recommend supplementing from an outside
source to lower blood pressure
 Omega-3 fatty acids may lower blood pressure
 Caffeine may increase it but tolerance often develops
 Most studies do not support a relationship between
hypertension and caffeine
 Smoking: discontinuation is important
 Exercise: 30 minutes daily recommended
Partners in Healthcare 24
Education,LLC 2009
OBATANTIHIPERTENSI
Sites of action of the
major classes of
antihypertensive drugs
Penggolongan antiHT
berdasarkan tempat kerjanya
 Sistem Saraf Simpatis di :
 Sentral (CNS) : clonidin, methyldopa
 Ganglion : heksamethonium, trimethapan
 Ujung saraf : reserpin, guanethidin
 Reseptor adrenergik : Prazosin(α1 blocker), Propanolol

(β blocker), atenolol (β1 blocker)
 Ginjal : Diuretik
 Otot polos vaskuler : CCB, Vasodilator
 RAAS : ACE inhibitor, ARB, Direct Renin Inhibitor
DIURETIK
Mekanisme kerja
Ada 3 kelas diuretik utk HT
 Thiazide
Hidrochlorothiazide (HCT),
Chlorothalidone
 Loop diuretics
Furosemide, Torsemide,
Bumetanide
 Diuretik Hemat K+
Amiloride, Triamterene,
Spironolacton
Diuretik
DIURETIK
 Mekanisme kerja :  ES :
- ekskresi Na & H2O  - dizziness,
 Efek pd CVS : - electrolit imbalance
- akut : COP  - hypokalemia,
- kronik : TPR ,COP N - hyperlipidemia,
 KI : - hyperglycemi(Thiazid)
hypersensitivity,
- gout
compromised kidney
function, Tx cardiac glycosides
(K+ effects),
hypovolemia,hyponatremia
Diuretics (cont)
Therapeutic Considerations
Thiazides (most common diuretics for HTN)
Generally start with lower potency diuretics
Generally used to treat mild to moderate HTN
Use with lower dietary Na+ intake,
and K+ supplement or high K+ food
K+ Sparing (combination with other agent)
Loop diuretics (severe HTN, or with CHF)

Osmotic (HTN emergencies)
Maximum antihypertensive effect reached

before maximum diuresis- 2nd agent indicated
SympatholiticsAgents
BlokAdrenergikdi CNS
(CNSagents)
 Site of action : CNS medullary ,
cardiovasc centers  ES : dry mouth, sedasi,
impotence
 Mekanisme kerja :
 KI : mental depression
- agonis R/ α-2 di CNS : NOT 1st line drug,
Clonidine, Guanabenz, Prolong used  retensi Na
Guanfacine & air sering digunakan
bersama diuretic
Aktivasi R/-2 di medulla 
 stop mendadak 
NE release dr SSP rebound SymNS  TD 
peripheral sympathetic  Methlydopa : DOC in
activity  vasc tone  pregnancy
vasodilation  TPR .
- membentuk neurotransmiter
palsu : Methyldopa
Mekanisme Kerja
Clonidin dan Methyldopa
Blok Adrenergik
di Ganglion Otonom
 Contoh : Hexamethonium
 Mekanisme kerja :
memblok reseptor nikotinik di ganglion
Blok Adrenergik di Ujung Saraf
 Contoh : Reserpin,  inhibit uptake of NE into

Guanethidin storage vesicle (also DA,
 Mekanisme kerja : 5-HT)  leads to
- menghambat transport depletion of transmitter
stores (peripheral & CNS
NE ke vesikel sinap :
action)
reserpin
 ES: sedation, mental
- mengosongkan dan
depression, Parkinsonism,
memblok pelepasan NE
gastric acid secretion
dari tempat
penyimpanannya : ulcer
guanethidin
Katzung 9th ed
Blok Adrenergik di
Reseptor Adrenergik
Blok Adrenergik di Reseptor - α1
 Contoh : Prazosin, Oxazosin, Terazosin

 Site of action : otot polos vaskuler perifer
 Mekanisme kerja :
memblok reseptor α-1 → relaksasi otot polos
vaskulerdilatasi vaskulerresistensi vaskuler ↓.
 Efek pd COP <<</(-)
 ES : nausea, postural  reflex tachycardia (-);
hipotensi s.d synkope  Awali dg dosis kecil
 KI : hipersensitif  Pilihan utk : pt dg DM,
asma dg / tanpa
hiperkolesterol, mild-
moderate HT
 Sering dikombinsi dg
diuretic,  antagonist
Blok Adrenergik di Reseptor-β
 β–blocker non selektif : Propanolol

β1–blocker selektif : Atenolol, Metoprolol
 Blok reseptor β1 di jantung →HR dan kontraktilitas jantung ↓ →
CO ↓ → TD ↓
 Blok reseptor β1 di ginjal → release renin ↓
 Blok reseptor β2 presinap → release NE ↓
 Blok reseptor β di CNS →aliran simpatis ↓ →tonus vaskuler ↓
 Efek samping :
insomnia, unpleasant dreams (bisa nembus BBB), erectile
dysfunction, akral dingin (hambat vasodilatasi β2), TG ↑ dan HDL ↓
(hambat metabolisme lemak di hepar),arritmia, hipoglikemia
 Kontraindikasi :
asthma,bradycardia berat, AV block, severe unstable LV failure,
diabetes
Vasodilator
 Calcium Channel Blocker

 Vasodilator Oral : hidralazin, minoksidil
 Vasodilator parenteral
Calcium Channel Blocker
 Contoh : Nifedipine, Verapamil, Diltiazem

 Mekanisme kerja : memblok kanal Ca type-L → hambat
influk Ca ke intrasel →kadar Ca intrasel ↓ → *
kontraktilitas sel otot polos vaskular ↓→ vasodilatasi
→ resistensi perifer ↓
*pd otot jantung →kontraktilitas, HR ↓
Vasodilator:release NO
nitroprussid (i.v)
hidralazin (p.o),
 melepaskan NO → stimulasi
 EDRF / Nitric oxide (NO) /
guanilil siklase → cGMP di otot
cGMPinvolvement
polos relaxation of vascular
 dilate arterioles but not veins smooth
 TPR, BPreflex tachycardia  dilates arterial ( TPR) and
 ES : venous vessels
-reflectory symp activation  venous return , reflex tachy
-headache, nausea, sweating,  Indikasi : hypertensive
flushing emergency, acute CHF
-palpitations, HR angina  ES : metab acidosis,
-lupus reaction (mainly in slow arrhythmias, severe hypotensio
acetylators)
Vasodilator:open K- -channel
minoksidil (p.o), diazoksid (i.v)

membuka kanal K+→  dilates arteriolar vessels
hiperpolarisasi , stabilisasi  TPR reflex HRCO
membran saat resting  inhibits insulin release (via
potensial relaksasi otot opening K beta cell
polos vask membrane)
dilates arterioles, not veins  similar structure as
ES : reflex sympathetic thiazidediuretics but no
stimulation, fluid retention diuretic effect
(value in combination
therapy), hypertrichosis
Sistem Renin-AldosteronAngiotensin
53
53
Katzung 9ed
ACE Inhibitor
 Contoh : Captopril , Enalapril , Quinapril ,

Ramipril
hambat Angiotensin Converting Enzyme shg :
 hambat pembentukan AII → AII merupakan salah
satu vasokonstriktor kuat.
 kadar bradikinin ↑ →menstimulasi release NO dan
prostasiklin → vasodilatasi.
 Keuntungan : respon kompensasi (-)
mencegah remodelling jantung dan vaskuler
Angiotensin II Receptor Blocker (ARB)
 Contoh : Irbesartan, Losartan , Valsartan

 Mekanisme kerja : menduduki R/ AII (AT1).
AT1 tdpt di otot polos vaskuler, korteks adrenal, ginjal, dan otak.
Obat ini tidak mempunyai efek pada metabolisme bradykinin.
Menghambat AII lebih kuat dp ACE inhibitors karena ada enzim
lain yang juga bisa menghasilkan AII.
ES ACE-Inhibitor&ARB
ACE INHIBITOR ARB
DirectReninInhibition
InhibitstheEntireReninSystem1-4 Aliskiren
Class PRA Ang I Ang II
ACEI
ARB
Direct Renin Inhibitor (DRI)
Increased peptide levels have not been shown to overcome the blood pressure–lowering effect of these agents.
ACEI, angiotensin-convertingenzyme inhibitor;Ang, angiotensin;ARB, angiotensinreceptor blocker;
PRA, plasma renin activity.
1.Johnston CI. Blood Press Suppl. 2000;1:9(suppl 1):9-13.

2.Widdop RE et al. Hypertension. 2002;40:516-520.
3.Fabiani ME et al. Angiotensin II Receptor Antagonists. 2001:263-278.
4.Lin C et al. Am Heart J. 1996;131:1024-1034.
JNC 7:
Algorithm for Treatmentof Hypertension
Prehypertension (SBP 120-139 mm Hg or DBP 80-89 mm Hg)
LIFESTYLE MODIFICATIONS
Not at Goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with

Prehypertension
diabetes or chronic kidney disease)
INITIAL DRUG CHOICES
Without Compelling Indications With Compelling Indications
Stage 1 Hypertension Stage 2 Hypertension Drug(s)for compelling indications

(SBP 140-159 or DBP 90-99 mm Hg) (SBP 160 or DBP 100 mm Hg)
Other antihypertensive drugs
Thiazide-typediuretics for most; 2-drugcombinations for most
(diuretic,ACEI, ARB, BB, CCB)
may consider ACEI, ARB, BB, (usually thiazide-type diuretics and
as needed.
CCB,or combination. ACEI, or ARB, or BB, or CCB).
If not at goal BP, optimize dosages or add additional drugs until

goal BP is achieved. Consider consultation with hypertension specialist.
AdaptedPartners
from NHBPEPCC.
in Healthcare2003. NIH Publication No. 03-5233. 60
Education,LLC 2009
 Compelling indications:
Ischemic Heart Disease
Recent ST Segment Elevation-MI or non-
ST Segment Elevation-MI
Left Ventricular Systolic Dysfunction
Cerebrovascular Disease
Left Ventricular Hypertrophy
Non Diabetic Chronic Kidney Disease
Renovascular Disease
Smoking
JNC7:ClassificationandManagementof
BloodPressureforAdults
Initial Drug Therapy
SBP* DBP* Without With
BP (mm (mm Lifestyle Compelling Compelling
Classification Hg) Hg) Modification Indications Indications
Normal <120 and <80 Encourage
Drug(s) for
Prehypertensi No antihypertensive compelling
120–139 or 80–89 Yes
on drug indicated. indications.
Thiazide-type diuretic
for most. May Drug(s) for
Stage 1 compelling
140–159 or 90–99 Yes considerACEI,ARB,
hypertension indications.
BB, CCB,
or combination.
Two-drug
combination Other
Stage 2 for most (usually antihypertensive
160 or 100 Yes thiazide-type diuretic drugs (diuretic,
hypertension
and ACEI or ARB or ACEI,ARB, BB,
BB or CCB). CCB) as needed.
JNC 7. May 2003. NIH publication 03-5233.
63
63
JNC7:CompellingIndicationsforIndividual
AntihypertensiveDrugClasses
Recommended Drugs
Compelling Aldo
Indication* DIURETIC BB ACEI ARB CCB ANT
Heart failure • • • • •
Post-MI • • •
High coronary disease
risk • • • •
Diabetes • • • • •
Chronic kidney disease • •
Recurrent stroke
prevention • •
*Compellingindications for antihypertensivedrugs are based on benefitsfrom outcomestudiesor existingclinicalguidelines; the compelling indication ismanaged parallel with the BP.
64 converting Healthcare
ACEI= angiotensin Partners enzyme inhibitor;
ARB= angiotensin receptor blocker; Aldo ANT = aldosterone antagonist;BB= beta-blocker; CCB = calciumchannel blocker.
Adaptedfrom NHBPEPCC.2003.
Education,LLCNIHPublicationNo.
2009 03-5233.
Perkembangan Terapi Antihypertensi
Effective but As effective and As effective and even

poorly tolerated better tolerated better tolerated
1940’s 1950 1957 1960’s 1970’s 1980’s 1990’s 2007
Direct ACE ARBs

vasodilators inhibitors
Peripheral Thiazides -blockers
sympatholytics diuretics
Ganglion Central 2
agonists Calcium
blockers
antagonists-
Calcium DHPs
Veratrum
antagonists-
alkaloids
non DHPs
-blockers
Penggunaan Dual Combinations
Kolom 1 Kolom 2
• Thiazide diuretic • Beta adrenergic blocker
• Long-acting calcium channel • ACE Inhibitor
blocker *
• ARB
Tujuan : meningkatkan efek hipotensif

kombinasikan obat pada kolom 1 dengan obat pd kolom 2
Terapi Antihipertensi Kombinasi
1990’
1950’ 1960’ 1970’ 1980’ s-
s s s s
2000s
Ser-Ap-Es
(reserpine/hydralazine/ ACE inhibitor/thiazide
hydrochlorothiazide)
Methyldopa/thiazide
Butiserpine (reserpine/butalbital) ACE inhibitor/CCB

Hyphex ARB/thiazide
(hexamethonium/hydralazine) Thiazide/K+-sparing Low-dose
Hypotensin A, B, & C diuretic blocker/thiazide
(pentolinium/hydralazine/resperi blocker/thiazide
ne) Clonidine/thiazide
Renir (reserpine/ephedrine)
Verapene (rauwolfia/veratrum)
Penyebab Kurangnya Respon terhadap
Terapi Hipertensi
 Pseudoresisten : salah diagnosa, pseudohipertensi
pada lansia, salah pemeriksaan
 Penderita tidak patuh dalam menjalani terapi (biaya,
instruksi tdk jelas, ESO, pemakaian tdk praktis)
 Volume overload (asupan garam berlebih, kerusakan
ginjal yg berat, retensi cairan akibat penurunan TD,
terapi diuretik tidak adekuat.
 Kondisi tertentu : perokok, obesitas, resistensi
insulin, peminum alkohol, serangan cemas/panik
 Obat : dosis terlalu rendah, kombinasi tdk cocok
 Interaksi obat : simpatomimetik, nasal decongestan,
apetite suppressan, kokain, kafein, kontrasepsi oral,
steroid adrenal,antidepressan, NSAID
Mekanisme Gagal Terapi Hipertensi
akibat Respon Kompensasi
Krisis Hipertensi
• Hipertensi Gawat (Emmergency)

• Hipertensi Darurat (Urgency)
Hipertensi Emergensi
Penatalaksanaan HT Emergensi
 TD harus turun dalam hitungan menit, ok

ada ancaman kerusakan target organ
 Obat parenteral (i.v):
- sodium nitroprussid
- nitrogliserin
- diltiazem HCl
- hidralazin
HypertensiveEmergency
Drug Dose Onset Duratio AdverseEffects SpecialIndications
(min) n
(min)
Sodium 0.25– Immedia 1–2 Nausea,vomiting,muscl Mosthypertensive
nitroprussid 10mcg/kg/min te e emergencies;caution
e intravenousinfusio twitching,sweating, withhighintracranial
n thiocyanateandcyanide pressure,azotemia,ori
(requiresspecial intoxication n
deliverysystem) chronickidneydisease
Nicardipine 5–15mg/h 5–10 15– Tachycardia,headache, Mosthypertensive
hydrochlorid intravenous 30;may flushing,localphlebitis emergenciesexcept
e exceed24 acuteheartfailure;
0 cautionwithcoronary
ischemia
Clevidipine 1- 2-4 5-15 Headache,syncope, Mosthypertensive
butyrate 2mg/hintravenous dyspnea,nausea,vomitin emergenciesexcept
infusion;maydoubl g severeaorticstenosis;
e cautionwithheart
doseevery90sec failure
initially;maximum:
32mg/h;typical
73
maintenancedose:4
to6mg/h
Fenoldopam 0.1– <5 30 Tachycardia,headache,

Create PDF files without this message by purchasing novaPDF printer (http://www.novapdf.com) Mosthypertensive
mesylate 0.3mcg/kg/min nausea,flushing
HypertensiveEmergency
Drug Dose Onset Durati AdverseEffects Special
(min) on Indications
(min)
Nitroglycerin 5–100mcg/min 2–5 5–10 Headache,vomiting, Coronary
intravenousinfusion methemoglobinemia, ischemia
tolerancewithprolongedus
e
Hydralazine 12–20mgintravenous 10–20 60–240 Tachycardia,flushing, Eclampsia
hydrochloride 10– 20–30 240– headachevomiting,
50mgintramuscular 360 aggravationofangina
Labetalol 5–10 180– Vomiting,scalptingling, Mosthypertensi
20–80mgintravenous
hydrochloride 360 bronchoconstriction,dizzine ve
bolusevery10min;0.5–
ss, emergencies
2.0mg/minintravenous
nausea,heartblock, exceptacute
infusion
orthostatichypotension heartfailure
Esmolol 250–500mcg/kg/min 1–2 10–20 Hypotension,nausea, Aorticdissection;
hydrochloride intravenousbolus,then asthma,first-degreeheart perioperative
50–100mcg/kg/min block,heartfailure
intravenousinfusion;
mayrepeatbolusafter5
minorincreaseinfusion 74
to300mcg/min
Hipertensi Urgensi
 Penanganan
- dalam hitungan jam
- Obat HT diberikan secara per oral, sublingual
MonitoringAntihypertensives
Class Parameters
Diuretics bloodpressure
BUN/serumcreatinine
serumelectrolytes(K+,Mg2+,Na+)
uricacid(forthiazides)
β-Blockers bloodpressure
heartrate
Aldosteroneantagonists bloodpressure
ACEinhibitors BUN/serumcreatinine
AngiotensinIIreceptorblockers serumpotassium
DirectRenininhibitors
Calciumchannelblockers bloodpressure
heartrate
76
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DR - fifi-KUL antiHIPERTENSI 2012

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FARMAKOTERAPI

Laboratorium Farmakologi FK-UMM

Blood Pressure Classification

 Street drugs, other natural products:

 Morbiditas dan mortalitas meningkat secara

Menurunkan mortalitas TARGET Tx

Blood Volume Venous Tone

 Humoral Regulation / Long-term regulation

 Terapi Non farmakologis : Life style modification

 Terapi Farmakologis : Obat antihipertensi

Modification Recommendation Systolic Diastolic Chgs

 Diets high in potassium, calcium and magnesium are

 Ganglion : heksamethonium, trimethapan

 Ujung saraf : reserpin, guanethidin

 Reseptor adrenergik : Prazosin(α1 blocker), Propanolol

 Otot polos vaskuler : CCB, Vasodilator

 RAAS : ACE inhibitor, ARB, Direct Renin Inhibitor

Loop diuretics (severe HTN, or with CHF)

Maximum antihypertensive effect reached

 Contoh : Reserpin,  inhibit uptake of NE into

 Contoh : Prazosin, Oxazosin, Terazosin

 β–blocker non selektif : Propanolol

 Calcium Channel Blocker

 Contoh : Nifedipine, Verapamil, Diltiazem

minoksidil (p.o), diazoksid (i.v)

 Contoh : Captopril , Enalapril , Quinapril ,

 Contoh : Irbesartan, Losartan , Valsartan

Class PRA Ang I Ang II

Direct Renin Inhibitor (DRI)

1.Johnston CI. Blood Press Suppl. 2000;1:9(suppl 1):9-13.

Prehypertension (SBP 120-139 mm Hg or DBP 80-89 mm Hg)

Not at Goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with

INITIAL DRUG CHOICES

Without Compelling Indications With Compelling Indications

Stage 1 Hypertension Stage 2 Hypertension Drug(s)for compelling indications

If not at goal BP, optimize dosages or add additional drugs until

JNC 7. May 2003. NIH publication 03-5233.

Effective but As effective and As effective and even

Direct ACE ARBs

Tujuan : meningkatkan efek hipotensif

Butiserpine (reserpine/butalbital) ACE inhibitor/CCB

• Hipertensi Gawat (Emmergency)

 TD harus turun dalam hitungan menit, ok

Fenoldopam 0.1– <5 30 Tachycardia,headache,

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