Obat Untuk Aritmia, Obat Gagal Jantung
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ANTI ARITMIA
Bagian Farmakologi & ToksikologiFakultas Kedokteran UGM
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Aritmia jantung:jantung berdenyut tidak teratur• Irama jantung normal
ditentukan oleh sel-sel pacemaker di nodus sinoatrialis
• Irama jantung dipengaruhi oleh asetilkolin & noradrenalin
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Potensial aksi jantung terdiri dari 4 fase:
Fase 0 : depolarisasi cepatFase 1 : repolarisasi cepat awalFase 2 : plateauFase 3 : repolarisasi ke potensial
diastolikFase 4 : potensial diastolik
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AritmiaSupraventrikular:
di miokard atrium ataudi nodus
atrioventrikularisventrikular: di ventrikel
• Aritmia terjadi karena adanya fokus ektopik yang terjadi lebih cepat daripada pacemaker normal (nodus sinoatrialis=NSA=SAN)
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Takiaritmia supraventrikular
• Sinus Takikardi, sering & relatif tidak berbahaya
• Takikardi karena reentry pada NSA & atrium
• Takikardi atrial otomatik, sering menyertai infark miokard, kardiomiopati, penyakit paru kronis
• Takikardi atrial multifokal, pada penyakit paru kronis
• Fibrilasi atrium, paling sering pada demam reumatik yang mengenai katup mitral, kardiomiopati, peny. Jantung hipertensif, PJK
• Takikardi reentry pada NAV PSVT
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• Sindroma preeksitasi• Takiaritmia Ventrikuler
• kompleks ventrikular prematur• takikardi ventrikel• fibrilasi ventrikel
• Bradiaritmia sinus• Aritmia karena digitalis
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Mekanisme aritmia• Kelainan pembentukan impuls, disebabkan:
• otomatisasi abnormal• dominasi NSA sebagai pacemaker diambil alih oleh
sel otomatik di atria, nodus AV, sistem his purkinje atau ventrikel bila terjadi depresi NSA, mis. pada bradiaritmia
• otomatisasi sel lain yang meningkat, misalnya pada ektopik prematur, takiaritmia
• NSA tetap sebagai pacemaker, tetapi kec. Pembentukan impulsnya yang abnormal
• Kelainan konduksi impuls, hantaran terganggu:
• terhambat atau berhenti bradiaritmia• reentrant aritmia (circus movement)
• Kedua-duanya
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Mekanisme reentry
• terjadi depolarisasi ventrikel prematur, bila terus-menerus terjadi takikardi ventrikel
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Pedoman terapi
• Mengurangi otomatisitas fokus ektopik, dan atau
• menghentikan mekanisme reentry dengan mempengaruhi kecepatan konduksi dan lamanya masa refrakter
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Klasifikasi antiaritmia
Obat-obat yang efektif pada aritmia supraventrikular
Obat-obat yang efektif pada aritmia ventrikular
Obat-obat yang efektif pada kedua tipe
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Menurut Vaughan-Williams:• Klas I : mengakibatkan perpanjangan
potensial aksi • IA : kinidin, prokainamid, disopiramid, propafenon• IB: lidokain, meksiletin, difenilhidantoin, tokainid• IC: lorkainid, flekainid, enkainid
• Klas II : memblokir pengaruh katekolamin terhadap pembentukan rangsang dan hantaran impuls, serta menghambat reseptor , termasuk blocker : propanolol
• Klas III: meninggikan fase repolarisasi• amiodaron, sotalol
• Klas IV: kardiodepresan, melalui hambatan pemasukan ion Ca lambat (antagonis Ca)• verapamil, gallopamil, diltiazem
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IA: kinidinuntuk aritmia ventrikular dan supraventrikular
Pada jantung:• menurunkan sifat mudah
terangsang• memperkecil kecepatan
depolarisasi dan kecepatan penghantaran
• periode refrakter diperpanjang• amplitudo kontraksi diperpendek
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Efek samping:
Menurunkan tonus vagal:• takikardi• penjalaran impuls atrioventrikular
dipercepat
merugikan kematian
perlu glikosida jantung untuk menaikkan tonus vagal
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Indikasi:
• Aritmia akut:• fibrilasi atrium• takikardi ventrikuler• takikardi supraventikuler paroksismal
• Dosis: maks. 1,5 g per hari (4-6 dosis)
• Kontraindikasi:• insufisiensi otot jantung• AV-block total dan parsial
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IB: Lidokainuntuk aritmia ventrikular• Kardiodepresan lemah• inotropik negatif• menurunkan kecepatan perjalanan impuls
indikasi:• aritmia ventrikular ekstrasistole (setelah
infark miokard)
efek samping:• keracunan SSP: gelisah, koma, kejang-kejang
Dosis: • 0,5-3,5 mg/menit per infus untuk dewasa
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IC: flekainiduntuk takiaritmia ventrikular, menekan ektopik ventrikular
• Dosis: • per oral 2 x 200-600 mg• dosis harian: 2 x 100-150 mg per oral
sehari• iv: inisial 1 mg/kgBB, tidak boleh lebih
dari 2 mg/kgBB
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Verapamil
• Untuk mengubah takikardi supraventrikular menjadi irama sinus: 5-10 mg iv, minimum dalam 2 menit
• fibrilasi atrium: 10 mg iv (2-5 menit)• mencegah takikardi
supraventrikular paroksismal: 4 x 80-120 mg/hari (oral)
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Atrial fibrillation (AF)
• rapid and irregular atrial fibrillatory waves• rate of 350 to 600 impulses/minute • normal atrioventricular (AV) nodal conduction• ventricular response of 90 up to 140 to 170
beats/min
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PRESENTATION OF RECENT ONSET ATRIAL FIBRILLATION
•mild symptoms
palpitations
fatigue
lightheadednes
increased urination
mild shortness of
breath
• severe symptomsdyspnea
angina
hypotension
presyncope
infrequently syncope
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Treatment of AF
•Reversion to sinus rhythm•Maintenance of sinus rhythm•Control of the ventricular rate in patients with chronic AF•Prevention of systemic embolization
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Reversion to sinus rhythm
• DC cardioversion• Pharmacologic cardioversion with class IA ( quinidine, rocainamide, disopyramide) class IC ( flecainide, propafenone) class III (amiodarone, sotalol)•Surgical or percutaneous catheter ablation
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PHARMACOLOGICAL CARDIOVERSION
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DC cardioversion indicated in patients who are hemodynamically unstable
rapid heart rate produces complications requiring urgent cardioversion:
Active ischemia Significant hypotension
Preexcitation syndrome
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ALGORHYTM OF ATRIAL FIBRILATION
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ALGORHYTHM OF ATRIAL FIBRILATION
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Maintenance of sinus rhythm
• Only 20 to 30 percent of patients who are successfully cardioverted maintain sinus rhythm for more than one year without chronic antiarrhythmic therapy
• Class IA, IC, and III drugs are useful for maintenance of sinus rhythm
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Slowing the ventricular rate in chronic atrial fibrillation
•Calcium channel blockers: verapamil, diltiazem
•Decreased sympathetic tone: beta blockade
•Enhancement of parasympathetic tone with vagotonic drugs: digoxin
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Prevention of systemic embolization
• Anticoagulation during restoration of sinus rhythm : warfarin, heparin
• Anticoagulation in chronic AF:
warfarin Warfarin is associated with a 45 to 82 percent
reduction in the risk of stroke in patients with chronic AF
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OBAT PADA GAGAL JANTUNG
BAGIAN FARMAKOLOGIFAKULTAS KEDOKTERAN
UNIVERSITAS GADJAH MADA YOGYAKARTA
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Heart failure (HF)
• is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood
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Classification of severity quantify the degree of functional limitation imposed by heart failure, developed by the New York Heart Association (NYHA)• Class I - symptoms of heart failure
only at levels that would limit
normal individuals • Class II - symptoms of heart failure with ordinary exertion• Class III -symptoms of heart failure on less than ordinary exertion• Class IV -symptoms of heart failure at rest
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Physical
Decreased cardiac
tachycardia diaphoresis peripheral vasoconstriction cool
pale
cyanotic extremities
Volume overload Pulmonary
congestion Peripheral
edema Elevated jugular
venous pressure
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Pharmacotherapeutic approach to congestive heart failure
• Problem• Fatigue• Edema• Poor cardiac
contractility• Dyspnea• Congestion• Increased cardiac
preload and afterload
• Irreversible heart failure
Approach• Rest, positive inotropes • salt restriction, diuretics
• Positive inotropes
• Diuretics (thiazides/loop)
• Nitrovasodilators• ACEinhibitors
venodilators, vasodilators
• Heart transplatation
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Positive inotropes that improve cardiac contractility • Cardiac glycosides (e.g. digoxin)• Phosphodiesterase inhibitors (e.g. amrinone)
• ß1Agonists (e.g dobutamide)
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Additional drugs used in CHF to reduce edema and cardiac preload ant afterload
• Diuretics (e.g thiazides, furosemide)
• Angiotensin-converting enzyme (ACE) ingibitors (e.g captopril)
• Nitrovasodilators (e.g intravenous nitroprusside, oral hydralazine, topical nitroglycerin)
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Adverse effects of drugs used in the treatment of congestive heart failure
• Cardiac glycosides
• Phosphodiesterase
inhibitiors 1 agonists• Diuretics• ACE inhibitors • Nitrovasodilator
• narrow therapeutic index may precipitate arrythmias
• thrombocytopenia,arrhytmias
• tachyarrytmias
• Electrolyte imbalance
• Hyperkalemia, cough
• Hypotension