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OBAT OBAT KARDIO VASKULEROBAT ANTI ARITMIAOBAT HIPERTENSI
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ANGIOTENSIN II AVP VASO KONSTRIKSI ALDOSTERON
MESANGIAL E4FFERENTCONTRACTION CONTRACTION
VESSEL MYOCARDIAL NE RELEASEHYPERTROPHY HYPERTROPHY
Na RETENTION CNS DYPSOGENIAACE INHIBITORANGIOTENSIN II RESEPTOR ANTAGONIS
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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
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TAHANAN PERIPERCARDIAC OUTPUTAKTIVITAS SIMPATISPADA OATAK, JANTUNGPEMBULUH DARAHGINJALKELENJAR SUPRARENAL CORTEK DAN MEDULAFAKTOR GINJAL FAKTOR JANTUNGPEMBULIUH DARAH ANTI DIURETIK HORMONBARORESEPTORVOLUME DARAHVISCOSITAS DARAHSODIUM ELEKTROLI
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HIPERTENSIGENETIK OBESITAS FOOD HABITRENIN SYMPATHIC DRIVE? ?
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HIPERTENSI LANGSUNG
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JANTUNG PEMBULUH DARAH
HIPERTROPI PROLIFERASI
PAYAH JANTUNG ATHEROSKLEROSISTIDAK LANGSUNG
ATHEROMA
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TUJUAN TERAPIMENGHILANGKAN GEJALA
MEMPERPANJANG HIDUP
MENCEGAH KOMPLIKASI
MATA GINJAL
JANTUNG OTAK
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TERAPI HIPERTENSI
FAKTOR FAKTOR RESIKOOBESITASMEROKOKENDOKRIN PIL KBGAYA HIDUP STRESSRENO VASCULERKELEBIHAN GARAMNOPRMAL 25-50 MMOL1 GRAM = 17 MMOL200 - 250 MMOL12-15 GRAM NaCl/ HARI
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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
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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.
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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
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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
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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
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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
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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
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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
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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
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NPYNAATP
PEPTIDA ATP
SP ATPCGRP
VIP
P2Y
P2X
VIP
CGRP
SYMPATIS INTRAMURAL SENSORY - MOTOR PARA SIMPATIS
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E
EDRF
H VP AT II
ATP ACH 5HT SP
EDRF PG
SP
SP 5HT M P2Y
SHEAR STRESS
ENDOTHELIUM
MEDIA
ADVENTITIA
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BLOOD PRESSURE ENDOTHELIAL CHANGESLEUCOCYTE ADHERNCEPENETRATIONMACROPHAGEACCULMULATIONPERMEABILITY CONSTRICTINGAND RELAXING FACTORSLIPO PROTEINPLASMA COMPN. SMC PROLIFERATIONAND ACCUMULATIONMATRIX NORMO LIPIDEMIA HYPERLIPIDEMIAINTIMAL TICKENINGFIBROUS PALQUEATHEROSCLEROTIC PLAQUEINTIMAL SMCMEDIAL SMCMIGRATION
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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
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BETA ADRENO RECEPTOR BLOCKING AGENTSNONSELECTIVE SELECTIVE WITH ALPHA BLOCKINGISA - ISA + ISA - ISA +NADOLOL PINDOLOLPROPANOLOL CARTEOLOLTIMOLOL PENBUTOLOL ATENOLOL ACEBUTOLOLESMOLOL PRACTOLOLMETOPROLOLBISOPROLOLBETAXOLOLLABETOLOL
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RENIN SUBSTRAT
J-G RENIN
ANGIOTENSIN I
ANGIOTENSIN II VASOKON SYNTHESISSTRICTION ALDOSTERONSODIUM RETENTIONBLOOD PRSSURE ADRENERGIC BLOCKERRENIN INHIBITIONCE INHIBITORANGIOTENSIN BLOCKERFEED BACK
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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
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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
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NON DIURETICANTI HYPERTENSIVE
BLOOD PRESSURE BLOOD PRESSURE
RENAL SODIUM RETENTION INCREASE FLUID VOLUME
ALDOSTERONE
RENIN SCRETION
VASODILATORMEKANISME GAGALNYA TERAPI DENGAN NON DIURETIC
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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
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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.
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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
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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
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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
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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
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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
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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
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Isolated systolic hypertension
Isolated systolic hypertension (systolic pressure 160 mmHg, diastolic pressure
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Hypertension in diabetes
For patients with diabetes, the aim should be to maintain systolic pressure
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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
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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.
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OBAT ARITMIA JANTUNG
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Na Ca K K NaNa-K ATP ase0+30- 90KONDUKSIADANYA BLOK AUTOMATISITYFREKUENSI AKSI POTENSIAL DAN TERJADINYA ARRITMIA INTRA SEL
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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