OBAT OBAT KARDIO VASKULEROBAT ANTI ARITMIAOBAT HIPERTENSI

ANGIOTENSIN II AVP VASO KONSTRIKSI ALDOSTERON

MESANGIAL E4FFERENTCONTRACTION CONTRACTION

VESSEL MYOCARDIAL NE RELEASEHYPERTROPHY HYPERTROPHY

Na RETENTION CNS DYPSOGENIAACE INHIBITORANGIOTENSIN II RESEPTOR ANTAGONIS

OBAT OBAT ANTI HYPERTENSI APA HYPERTENSIBAGAIMANA PENGATURAN TEKANAN DARAHKENAPA HIPERTENSI HARUS DIOBATIKAPAN HIPERTENSI DIOBATIBAGAIMANA PENGOBATAN HIPERTENSI HIPERTENSI : TEKANAN DARAH SISTOLE / DIASTOLE > 145/90HIPERTENSI 95% ESSENTIAL PENYEBAB TIDAK DIKETAHUI

TAHANAN PERIPERCARDIAC OUTPUTAKTIVITAS SIMPATISPADA OATAK, JANTUNGPEMBULUH DARAHGINJALKELENJAR SUPRARENAL CORTEK DAN MEDULAFAKTOR GINJAL FAKTOR JANTUNGPEMBULIUH DARAH ANTI DIURETIK HORMONBARORESEPTORVOLUME DARAHVISCOSITAS DARAHSODIUM ELEKTROLI

HIPERTENSIGENETIK OBESITAS FOOD HABITRENIN SYMPATHIC DRIVE? ?

HIPERTENSI LANGSUNG

LOAD

JANTUNG PEMBULUH DARAH

HIPERTROPI PROLIFERASI

PAYAH JANTUNG ATHEROSKLEROSISTIDAK LANGSUNG

ATHEROMA

TUJUAN TERAPIMENGHILANGKAN GEJALA

MEMPERPANJANG HIDUP

MENCEGAH KOMPLIKASI

MATA GINJAL

JANTUNG OTAK

TERAPI HIPERTENSI

FAKTOR FAKTOR RESIKOOBESITASMEROKOKENDOKRIN PIL KBGAYA HIDUP STRESSRENO VASCULERKELEBIHAN GARAMNOPRMAL 25-50 MMOL1 GRAM = 17 MMOL200 - 250 MMOL12-15 GRAM NaCl/ HARI

OBAT UNTUK HIPERTENSI

OBAT DI CNSTRANGUILIZERNEURON SIMPATIS SENTRALOBAT DI SARAF SIMPATIS TEPIGANGLIONUJUNG SARAFRESEPTOR ADRENERGIKOBAT LANGSUNG DI PEMB. DARAHOBAT PADA GINJAL DIURETIKOBAT PADA SYSTEM RAAANGIOTENSIN PATHWAYSRESEPTOR ANGIOTENSIN II

OBAT ANTI HIPERTENSI

SITE OF ACTION OBAT MEKANISME KERJA

CEREBRAL CORTEXSEDATIVEGABA TRANGUILIZER

MIBRAINRESERPINPENGOSONGAN NEMETHYLDOPANT PALSUB BLOKER?CLONIDIN ALPHA 2 HAMBAT RELEASE

GANGLION OTONOMHEXAMETHONIUMAMBAT TRANSMISIPEMPIDINESIMPATIS @ PARA S.

SITE OF ACTIONOBATMEKANISME. KERJA

ADRENERGIC AXONRESERPINDEPLESI NABRTYLIUM BLOK RELEASEBETHANIDINEADRE NEURON BLOCKERDEBRISOQUINADRE. NEURON BLOKERGUANETHIDINEDEPLESI NA DAN ADRENEURON BLOKERMETHYL DOPAFALS NERO TRANSMPARGYLINMAO INHIBTOR DAN ADRE. NEURON BLOKER

ALPHA ADRENOCEPTOR PHENTOLAMINBLOKE ALPHA RESEPTORPENOXY BENZAMINEBLOK ALPHA ADRE RECPLABETOLOL ALPHA DAN BETA BLOKPRAZOSINBLOK ALPHA RECEPTORINDORAMINALPHA ADRE. BLOKER

SITE OF ACTIONOBATMEKANISME KERJA

B ADRENORECEPTORPROPANOLOLCO MENURUN,OXPRENOLOLBARORESPTOR,ALPRENOLOLADAPTASI PANJANG,PINDOLOLPENURUNAN PLASMATIMOLOLRENIN, PLASMA SOTALOLVOLUME MENURUN

ATENOLOLCARDIOSELEKTIFMETOPROLOLBETA BLOKER, EFEKACEBUTOLOLMINIMAL PADA BETA-2

OTOT POLOS VASKULERTHIAZIDEMENURUNKAN Na KDIAZOXIDEUNKNOWNHYDRALAZINEMINOXIDILSOD. NITRO PRUSIDEVERAPRAMILCA ANTAGONISDILTIAZEM

SITE OF ACTIONOBATMEKANISME KERJA

AIR DAN Na EXTRASEL THIAZIDEDEPLESI VOLUMEFUROSEMIDEGARAM NaALSDOTERON ANTAGONISSPIRONOLACTONETRIAMTEREN

RENIN ANGIOTENSIN SYSTEMBETA BLOKERHAMBAT RENIN RELEASECAPTOPRIL BLOK ENZIM YG MERU-BAH ANG I - ANG IISARALARASIN BLOK ANG. RECEPTOR LOSARTANVALSARTAN

DIURETIC THIAZIDE CHLORTHALIDONE INDAPAMIDE LOOP DIURETIC BUMETAMIDE ETHACRINIC ACID UROSEMIDE POTASIUM SPARER AMILORIDE SPIRONOLACTONE TRIAMTERENE

ADRENERGIC INHIBITORPHERIPERAL INH BETA BLOKER GUANADREL ACEBUTOLOL GUANETHIDINE ATENOLOL RESERPINE BETAXOLOLCENTRAL ALPHA AGONIS BISOPROLOL CLONIDINE CARTEOLOL GUANABENZ METOPROLOL GUANFACINE NADOLOL METHYLDOPA PENBUTOLOLALPHA 1 BLOKER PINDOLOL DOXAZOSINPROPANOLOL PRAZOSINTIMOLOL TERAZOSIN ALPHA AND BETA BLOCKERCARVEDILOLLABETOLOL

VASODILATOR DIRECT HIDRALAZINE MINOXIDIL CALCIUM CHANNEL DYHYDROPYRIDINE AMLODIPINE FELODIPINE ISRADIPINE NICARDIPINE NIFEDIPINE NISOLDIPINE DILTIAZEM VRAPRAMIL

VASO DILATORANGIOTENSIN CONVERTING ANGIOTENSIN IIENZYME INHIBITOR RECEP. BLOKERBENAZEPRIL CAPTOPRIL CANDERSARTANENALAPRIL FOSINOPRIL EPROSARTANLISINOPRIL MOEXIPRIL IRBESARTANQUINAPRIL PERINDOPRIL LOSARTANRAMIPRIL TRANDOLAPRIL TELMISARTANVALSARTAN

DISLIPIDEMIAOBESITY + ANDROGEN INCREASE ABD RELEASE OF DOMINAL FAT FREE FATTY ACID PERIPERAL INCREASE DECREASE INSULIN PANCREATIC HEPATIC INSULIN RESISANCE INSULIN SECRE EXTRACTION

HYPERINSULINEMIA

INCREASED SODIUM VASCULARSYMPATHETIC RETENTION HYPERTROPHYACTIVITY

ATENUATEDVASODILATATIONDMIINIDDMHYPERTENSIONXLIPOLYSISOBESITY AND DM, HIPERTENSI

Na K ATPase(co Transport)

Na FluxesK fluxes

Ca Binding Depolarization

Ca ATPase(others)

Na H antiport(Na Li coutertransportCELL Na CELL Ca CELL pH Na retentionCONTRACTILITYGROWTHHYPOTHESIS ABNORMAL IONIC FLUXES AND CONTRACTILITY

TARGET FUNGSI MEKANISME KERJA CELLULER

LUMEN VASOKONSTRIKSI VASO DILATASIENDOTHELIN NITRIC 0XIDEANGIOTENSIN IIBRADIKININTHROMBOXANE A2HYPERPOLARIZING F.PROSTAGLANDINE H2GROWTH STIMULATION INHIBITIONPLATELET GROWTH DF NITRIC 0XIDEFIBROBLAST GFPROSTAGLANDIN I 2INSULIN LIKE GFENDOTHELINTRANSFORMING GFANGIOTENSIN IIINFLAMATION PROINFLAMATORY ANTI INFLAMATORYADHESION MOLECULE(ELAM, VCAM, ICAM)HOMEOSTASIS PROTROMBOTICANTITHROMBOTICPLASMINOGEN ACTIVATOR PROSTACYCLININHIBITOR TISSUE PLASMINOGENACTIVATOR

FUNGSI SEL ENDOTHEL

NPYNAATP

PEPTIDA ATP

SP ATPCGRP

VIP

P2Y

P2X

VIP

CGRP

SYMPATIS INTRAMURAL SENSORY - MOTOR PARA SIMPATIS

+ + - - -

- - - - -

E

EDRF

H VP AT II

ATP ACH 5HT SP

EDRF PG

SP

SP 5HT M P2Y

SHEAR STRESS

ENDOTHELIUM

MEDIA

ADVENTITIA

BLOOD PRESSURE ENDOTHELIAL CHANGESLEUCOCYTE ADHERNCEPENETRATIONMACROPHAGEACCULMULATIONPERMEABILITY CONSTRICTINGAND RELAXING FACTORSLIPO PROTEINPLASMA COMPN. SMC PROLIFERATIONAND ACCUMULATIONMATRIX NORMO LIPIDEMIA HYPERLIPIDEMIAINTIMAL TICKENINGFIBROUS PALQUEATHEROSCLEROTIC PLAQUEINTIMAL SMCMEDIAL SMCMIGRATION

CENTRAL ANTI HYPERTENSIVE AGENTS METHYL DOPAGUNFACINEGUANBENZCLONIDINEMOXONIDINERILMENIDIN 2 ADRENOCEPTORIMIDAZOLINE RECEPTORSALIVARY NUCLEUS NTS ROSTRAL VENTRO GLAND CEREOLUS LATERAR MEDULLAINHIBITION OF SYMPATETIC ACTIVITY

INHIBITION OF NORADRENALIN RELEASE

DECREASE VASOCONSTRICTION

HYPOTENSIONDRY MOUTYH SEDATIONSELECTIVESELECTIVE NONSELECTIVE

BETA ADRENO RECEPTOR BLOCKING AGENTSNONSELECTIVE SELECTIVE WITH ALPHA BLOCKINGISA - ISA + ISA - ISA +NADOLOL PINDOLOLPROPANOLOL CARTEOLOLTIMOLOL PENBUTOLOL ATENOLOL ACEBUTOLOLESMOLOL PRACTOLOLMETOPROLOLBISOPROLOLBETAXOLOLLABETOLOL

RENIN SUBSTRAT

J-G RENIN

ANGIOTENSIN I

ANGIOTENSIN II VASOKON SYNTHESISSTRICTION ALDOSTERONSODIUM RETENTIONBLOOD PRSSURE ADRENERGIC BLOCKERRENIN INHIBITIONCE INHIBITORANGIOTENSIN BLOCKERFEED BACK

MEKANISME TERAPI DIURETIK KRONIK DAN EFEK SAMPING DIURETIC THERAPY

RENAL REABSORBTIONOF Na AND Mg

SALURESIS AND DIURESIS

PLASMA VOLUME CARDIAC OUTPUT RENAL BLOOD FLOW PRA

POSTURAL GFR ALDOSTERON HYPOTENSION PRERENAL PROXIMAL DISTAL Ca++ KALIURESIS AZOTEMIA REABSORB REABSORB

CL URIC ACID CL CALCIUM HYPOKALEMIA

HYPERURICEMIA HYPERCALCEMIA GLUCOSE TOLERANCEHYPOMAGNESEMIAHYPONATREMIA

EFEK PRIMER DAN SECUNDER OBAT VASODILATORVASODILATOR

VASODILATION SODIUM FLUID RETENTION VOLUME

PERIPERALRESISTANCE ALDOSTERON

ARTERIAL ANGIOTENSINPRESSURE RENIN RELEASE VASOCONSTRICTION

NOREPINEPRIN

SYMPATHETIC HEART RATE ACTIVITY CONTRACTION

VENOUS COMPLIANCE

PERIPHERALRESISTANCECARDIAC OUTPUTSYMPHATETICBLOCKERDIURETIC

NON DIURETICANTI HYPERTENSIVE

BLOOD PRESSURE BLOOD PRESSURE

RENAL SODIUM RETENTION INCREASE FLUID VOLUME

ALDOSTERONE

RENIN SCRETION

VASODILATORMEKANISME GAGALNYA TERAPI DENGAN NON DIURETIC

MENEGAKKAN DIAGNOSE HIPERTENSI

MENCARI AKTOR RESIKO, OBESITAS, DM FAMILI,

MENCARI PENYEBAB HIPERTENSI

MEMAHAMI HEMODINAMIKA HIPERTENSI SEDANG

MEMULAI DENGAN PENGOATAN NON FARMAKOLOGI

PENGOBATAN DENGAN OBAT ANTI HIPERTENSIPENGGUNAAN OBAT LINI PERTAMADENGAN MEMPERTIMANGKAN COST BENEFIT

EDUKASI PENGUNAAN OBAT, KOMPLIANCE, EFFEK SAMPING

MEMONITOR EFFICACY DAN EFEK SAMPING

PENGOBATAN JANGKA LAMA KONTROL RUTINTERAPI HIPERTENSI

PRINSIP PEMILIHAN OBAT ANTI HPERTENSI

TERAPI 1986-2000DIURETICCALCIUM CHANNEL BLOCKERANGIOTENSIN CONVERTING ENZYME INHIBITOR BETA BLOCKERALPHA BLOCKERANGIOTENSIN RESEPTOR ANTAGONIS (1997-2000)OBAT SEHARUSNYA :MENURUNKAN TEKANAN DARAHMENURUNKAN RESIKO CARDIOVASCULERTANPA MENURUNKAN QUALITAS HIDUPMEMPERBAIKI KUALTAS HIDUPEFEK LON ACTING SEHARI SATU TABLETHARGA TERJANGKAUBELUM ADA OBAT YENG MEMENUHI SEMUAKRITERIA DIATAS SAMPAI SAAT KINI.

HIPERTENSI TANPA KOMPLKASI DIMULAI DENGAN DIURETIC ATAU BETA BLOCKERDM : ACE INHIBITOR, A II RECEPTOR ANTAGONISPAYAH JANTUNG: ACE INH. ALPHA BLOCKER,BETA BLCKER, DIURETICHT USIA TUA: DIURETIC, CALCIUM ANTAGONISHT AND MIOKARD INFARK : BETA BLOCKER NON ISA, ACE INHIBITORSEMUA DIMULAI DENGAN DOSIS RENDAH DILAKUKANTIRASI DOSE RESPON KALAU PERLU KOMBINASI DALAMDOSIS RENDAH. DIMULAI DENGAN MERUBAH GAYA/POLA HIDUPTIDAK BERHASIL MENURUNKAN BP < 140/90(TARGET BP LEBIH RENDAH PADA DMTARGET BP TIDAK TERCAPAIRESPON NEG, ADA SIDE EFFECT RESPON TIDAK CUKUPGANTI OBAT DARI KELAS LAINTAMBAHKAN OBAT DARI KELAS LAINTARGET BP TIDAK TERCAPAIPENAMBAHAN OBAT KELAS LAIN TERUS DILAKUKAN DIRUJUK KE SPESIALIST HIPERTENSI

KOMBINASI BAT INTI HIPERTENSI

DIURETIC DAN POTASIUM SPARERSPIRONOLACTONE + HYDROCH;LOROTHIAZIDEBETA BLCKER DAN DIURETIKPROPANOLOL + HYDROCHLOROTHIAZIDEACE INHIBOTOR DAN DIURETIKENALAPRIL + HYDROCHLOROTHIAZIDEANGIOTENSIN II RECEPTOR ANTAGONIS DAN DIURETIKLOSARTAN + HIDROCHLOROTHIAZIDECALCIUM CHANNEL BLOCKER DANACE INHIBITORDILTIAZEM + ENALAPRILKOMBONASI YANG LAINCLONIDINE + CHLORTHALIDONEHYDRALAZINE + HYDROCHLOROTHIAZIDEMETHYLDOPA + HYDROCHLOROTHIAZIDERESERPIN + HIDRALAZINE + HYDROCHLOROTHIAZIDERESERPIN + HYDROCHLOROTHIAZIDE

KRISIS HIPERTENSIHYPERTENSIVE MERGENCY HYPERTENSIVE URGENCY

TD MENINGGI MEMBUTUHKAN TD MENINGGI TETAPI TANPA PENURUNAN SEGERA DENGAN KELUHAN ATAU ANCAMAN PEMBERIAN OBAT PARENTERAL KERUSAKAN ORGAN YANG ANCAMAN KERUSAKAN ORGAN PROGRESSIVE, TD DITURUNKAN PERLAHAN DALAM WAKTU JAM

PENYEBAB: CEREBRO VASCULER PENYEBAB: TEKANAN DARAH GINJAL, ECLAMPSIA, BEAH TIDAK DIOBATI ATAU TIDAK CATHECOLAMINE, RAMA KEPALA TERKONROL LKA BAKAR, GANGUAN JANTUNG

OBAT: FUROSEMIDE, NITROPRUSIDE CAPTOPRIL, CLONIDINE, LASIX, NITROGLYSERIN, NICARDIPINE, LABETOLOL, NIFEDIPINE, HYDRALAZINE,ENALAPRILATE, PROPANOLOL, DIBERIKAN PENTHOLAMINE, LABETOLOL SECARA ORAL / SUB LINGUAL DIBERIKAN SECARA PARENTERAL

CRITICAL DEGREE OF HYPERTENSIONLOCAL EFFECTS SYSTEMIC EFFECTSPROSTAGLANDINE RAA, CATHECOLAMINFREE RADIALS VASOPRESSIN

ENDOTHELIAL DAMAGE PRESSURE NATRIURESIS

PLATELET DEPOSITION HYPOVOLEMIA

MITOGENIC AND MIGRATION FURTHER INCREASE FACTORS VASOPRESSOR

MYOINTIMAL PROLIFERATION

FURTHER RISE IN BLOOD PRESSURE AND VASCULAR DAMAGE

TISSUE ISCHEMIA

OBAT MASA DEPAN :

ENDOTHELIN RESEPTOR ANTGONIS

VASOPRESSIN RESEPTOR ANTAGONIS

ENDOTHELIAL PROTECTOR

TRANSCRIPTION MODULATING DRUGS

ANTISENSE GEN THERAPY

OBAT INI MASIH DALAM PENELITIAN FARAKOLOGI DAN TRIAL KLINIK

Hypertension in the elderly

Benefit from antihypertensive therapy is evident up to at least 80 years of age, but it is probably inappropriate to apply a strict age limit when deciding on drug therapy.

Elderly individuals who have a good outlook for longevity should have their blood pressure lowered if they are hypertensive.

The thresholds for treatment are diastolic pressure averaging 90mmHg or systolic pressure averaging 160mmHg over 3 to 6 months observation (despite appropriate non-drug treatment).

A low dose of a thiazide is the clear drug of first choice, with addition of another antihypertensive drug when necessary.Clinical pharmacology of hypertension

Isolated systolic hypertension

Isolated systolic hypertension (systolic pressure 160 mmHg, diastolic pressure

Hypertension in diabetes

For patients with diabetes, the aim should be to maintain systolic pressure

Hypertension in renal disease

The threshold for antihypertensive treatment in patients with renal impairment or persistent proteinuria is a systolic blood pressure 140mmHg or a diastolic blood pressure 90 mmHg.

Optimal blood pressure is a systolic blood pressure

Accelerated or very severe hypertension

Accelerated (or malignant) hypertension or very severe hypertension (e.g. diastolic blood pressure >140mmHg) requires urgent treatment in hospital, but it is not an indication for parenteral antihypertensive therapy.

Normally treatment should be by mouth with a beta-blocker (atenolol or labetalol) or a long-acting calcium-channel blocker (e.g. amlodipine or modified-release nifedipine).

Within the first 24 hours the diastolic blood pressure should be reduced to 100110mmHg. Over the next 2 or 3 days blood pressure should be normalised by using beta-blockers, calcium-channel blockers, diuretics, vasodilators, or ACE inhibitors.

Very rapid reduction in blood pressure can reduce organ perfusion leading to cerebral infarction and blindness, deterioration in renal function, and myocardial ischaemia.

Parenteral antihypertensive drugs are rarely necessary; sodium nitroprusside by infusion is the drug of choice on the rare occasions when parenteral treatment is necessary.

OBAT ARITMIA JANTUNG

Na Ca K K NaNa-K ATP ase0+30- 90KONDUKSIADANYA BLOK AUTOMATISITYFREKUENSI AKSI POTENSIAL DAN TERJADINYA ARRITMIA INTRA SEL

PENGOBATAN ARITMIA :JENIS ARITMIAS DIIDENTIFIKASI

PENYEBAB YANG REVERSIBLE DIHILANGKAN

DINILAI KEPENTINGAN RISK DAN BENEFIT DARI TERAPI

ATRIAL ARITMIA DAN AV NODAL REENTRAN TAKIKARDIVERNTIKULAR ARITMIA ----- ANCAMAN SUDEN DEATH PEMILHAN OBAT HARUS DIPAHAMI

FARMAKODINAMI OBAT OBAT ARITMIA

FARMAKOKINETIK OBAT ARITMIA

PENYAKIT YANG MENYERTAI ARITMIA

ARRITMIA JANTUNG SUPRAVENTRIKULER VENTRIKULER

FOKUS ECTOPIK DI ATAS A-V NODE DI VENTRIKEL

HEMODINAMIK RINGAN BERAT COLLAPS

SUDDEN DEATH TIDAK ANCAMAN

CONTOH ATRIAL TAKIKARDI VES ATRIAL FLUTER VENT. TAKIKARDI VEBNT FIBRILASI

PENYEBAB ARITMIA YANG REVERSIBELOBAT OBATANDIGITALISANTI ARRITMIATHEOPHILINCATHECOLAMINETRISIKLIK ANTI DEPRESAN PHENOTHIAZINEANOREKSIAN OBAT ANAESTHESI

FAKTOR JANTUNGISKEMIA JANTUNGCHF

PENYAKIT LAINTHYROTOKSIKOSIS LUNG DISEASE

GANGGUAN METABOLIKASIDOSISALKALOSISHYPOKSIAHYPERKALEMIAHYPOMAGNESEMIAHYPOKALEMIA ARRITMIA JANTUNG HILANG APABILA FAKTOR TERSEBUTDIPERBAIKI

DIAGNOSEPEMERIKSAAN ECG

DILAKUKAN MONITOR 24 72 JAMDILAKUKAN TEST EXERCISE PEMERIKSAAN ELEKTRO FISIOLOGIS PEMERIKSAAN 12 LEAD ECG ATAU OESOPHAGUS ECG

DIHILANGKAN PENYEBAB

DILAKUKAN TERAPI OBAT

DILAKUKAN TERAPI DEFIBRILASI

PEMASANGAN PACU JANTUNG

OBAT ARRITMIA JANTUNG :

I. SODIUM CHANNEL BLOKER : KELAS I a KELAS I bKELAS I c

II. BETA ADRENERGIK AGONIS

III PROLONGATION OF THE ACTION POTENTIAL

IV. A-V NODAL CALCIUM CHANNEL BLOCKER

LAIN LAIN

DATA FARMAKOKINETIK OBAT ARITMIA YANG DIBERIKANSECARA INTRA VENAOBAT LOADING MAINTENANCE THER. PLASMA CONC

LIDOCAIN 3-4 MG/KG 1-4 MG/MIN 1.5-5 UG/ML

BRETYLIUM 5-30 MG/KG 1-4MG/MIN -

PROCAINAMIDE 10-20 MG/KG 1-4 MG/MIN 4-10 UG/ML 20 MG/MIN

VERAPRAMIL 1-20 MG/KG

ADENOSIN 2-20 MG/KG

ESMOLOL 500 UG/KG(50UG/KG/MIN) 100-200 UG/KG

PROPANOLOL 1-5 MG

PENYAKIT DAN OAT OBAT YANG MENYEBABKAN PERUBAHAN FARMAKOKINETIK

CONGESTIVE HEART FAILURE ---- DISTRIBUSI OBAT

KELAINAN HEPAR ------- METABOLISME OBATBINDING PROTEIN

GAGAL GINJAL ------------------- EKSKRESI OBAT MENURUN

PENGOBATAN LAIN MISALNYA PHENO BARBITAL MENINGKATKAN METABOLISME OBAT

OBAT PILIHAN PENAALAKSANAN ARITMIA

ARITMIA ACUT KRONIS

ATRIAL FIBRILASI/ FLUTER DIGITALIS , VERAPRAMIL SAMA BETA BLOKERAV NODAL ENTRY ADENOSINE , VERAPRAMIL QUINIDINE, PROCAINAMIDE AMIODARONE, FLECAINIDE

WOLF PARKINSON WHITE ADENOSINE, VERAPRAMIL KELAS Ic DAN Kelas 1aSYNDEROME BETA BLOKER

ATRIAL FIBRILASI DENGAN PROCAIN AMIDE PROCAINAMIDE , QUINIDINEPREEXCITEN VENRICULAER KELAS IcCOMPLEXES

AUTOMATIC ATRIAL A-V NODAL BLOKER VERAPRAMIL, KELAS IaTAKHIKARDI KELAS Ic

AKUTKRONISPREMATURE VENTRICULAR BEAT AND NO SUSTAINED VENTRIKULAR ARRITMIA ASYMPTOMATIC - - SYMPTOMATIC - BETA BLOKERKELAS Ia/ Ic SUSTAINED VENTRK. TAKIKARDI LIDOCAIN KELAS Ia PROCAINAMIDE KELAS Ic BRETYLIUM BETA BLOKER

VNTRIKULAR FIBRILASI LIDOCAIN - PROCAINAMIDE BRETYLIUM

WIDE COMPLEX TAKHIKARDI PROCAINAMIDE LIDOCAINE ADENOSINE HINDARI VERAPRAMIL

NAROW COMPLEX TAKHIKARDI ADENOSINE VERAPRAMIL

KONTRA INDIKASI RELATIF OBAT ANTI ARRITMIA

NON CARDIACPENYAKIT GI QUINIDINEPROSTATISM, RETENSI URINEGLAUCOMA DYSOPYRAMIDEARTRITIS INFLAMASIMEXILETIN , TOCAINIDETREMORLIDOCAINBRONCHO SPASMBETA BLOKER, PROPAFENONEPENY. PARUAMIODARONEPSIEN MUDA AMIODARONE, PRODCAINAMIDE

CARDIACCHFDYSOPYRAMIDE, FLECAINIDE,STENOSIS AORTABETA ANTAGONIS, VERAPRAMIL,CARDIOMYOPATHIBRETYLIUM, KELAS 1 a dan IIIHYPERTENSI PU;LMONAL