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GAGAL JANTUNG

(HEART FAILURE)

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Pendahuluan
Definisi :

sindrom klinik yang disebabkan oleh
ketidakmampuan jantung memompa darah secara
cukup untuk kebutuhan metabolik

Berkurangnya kemampuan pengisian ventrikel (disfungsi
diastolik)
Berkurangnya kemampuan kontraktilitas miokard (disfungsi
sistolik)

HF lebih sering terjadi pada laki-laki dp wanita 
insidensi IHD
Prevalensi





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0,3-2% dalam populasi keseluruhan
3-5% dalam populasi umur diatas 65 tahun
8-16% dalam populasi umur diatas 75 tahun
75% penderita HF  > 60 tahun

ETIOLOGI
Faktor resiko paling sering : CAD,
hipertensi dan kardiomiopati idiopatik
 Kondisi akut : AMI, aritmia, embolisme
pulmo, sepsis, dan jantung iskemik
 Perkembangan HF scr gradual : penyakit
liver dan renal, kelainan katup jantung,
anemia, endocarditis bakteri, miokarditis
viral, thyrotoxicosis, kemoterapi, diet Na
berlebihan dan alkohol

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Patofisiologi  CO (istirahat) = 5 L/menit (HR = 70 denyut/menit. dan symptom terjadi bila fraksi ejeksi < 35% Bila fraksi ejeksi <10%  resiko pembentukan trombus di dalam LV  6 .  fraksi ejeksi normal = > 50% (volume yang tersisa dalam ventrikel = 60 ml)  LSVD  fraksi ejeksi < 45%. SV = 70 ml)  Pengisian ventrikel normal = 130 ml.

Mekanisme Kompensasi  Fraksi ejeksi turun  CO turun  mekanisme kompensasi  7 awalnya bermanfaat. tetapi akhirnya dapat memperburuk disfungsi pemompaan  vicious cycle of HF .

Mekanisme kompensasi pada HF  Cardiac output  LVDEP (preload)  SNS activity angiotensinogen  Renin production Angiotensin I Cardiac dilatation ACE Angiotensin II Vascular resistance Angiotensin III (aldosterone) Ventricular hypertrophy kinins PGE2 & PGI2 Sodium retention ACE inactive kinins 8  Blood volume  Sodium uptake By vessels .

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paroxysmal nocturnal dyspnea.Presentasi Klinik     The patient presentation may range from asymptomatic to cardiogenic shock The primary symptoms are dyspnea (particularly on exertion) and fatigue. and cough. tachypnea (pernafasan cepat). Other pulmonary symptoms include orthopnea (pernafasan sulit kecuali posisi tegak). which lead to exercise intolerance. Fluid overload can result in pulmonary congestion and peripheral edema 10 .

nocturia. ascites. nausea.Presentasi Klinik Nonspecific symptoms may include fatigue. cool extremities. bloating. peripheral edema. frothy (berbusa) sputum). hepatojugular reflux. abdominal pain. sometimes with coughing pink. poor appetite. jugular venous distention. anorexia. and weight gain  Physical examination findings may include pulmonary crackles. 11  . ascites. and hepatomegaly. tachycardia. hemoptysis. symptoms of pulmonary edema (extreme breathlessness. an S3 gallop. anxiety. mental status changes. cardiomegaly.

bradycardia. left ventricular hypertrophy  Serum creatinine may be increased because of hypoperfusion  Complete blood count useful to determine if heart failure is a result of reduced oxygencarrying capacity  Chest radiography is useful for detection of cardiac enlargement. atrial fibrillation. and 12pleural effusions  .Diagnosis (Laboratory Test) Electrocardiogram may be normal or it could show numerous abnormalities including acute ST-T–wave changes from myocardial ischemia. pulmonary edema.

wall motion abnormalities. valve function. pericardial effusion. is associated with reduced survival and may indicate worsening volume overload and/or disease progression 13 . serum sodium <130 mEq/L.Diagnosis (Laboratory Test)   Echocardiogram assesses left ventricle size. and ejection fraction Hyponatremia.

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Sistem stage gagal jantung menurut ACC/AHA 15ACC/AHA = American College of Cardiology/ American Hearth Association .

 Slow disease progression. and  Prolong survival.Outcome yang diharapkan The therapeutic goals for chronic HF are to :  Improve quality of life.  Prevent or minimize hospitalizations.  Relieve or reduce symptoms. 16 .

aritmia. anemia. mengobati kondisi medis spt infeksi endocarditis atau hipertensi) Faktor-faktor yang memperburuk HF diidentifikasi dan diminimalkan (demam. obat) Terapi obat untuk mengontrol HF dan meningkatkan survival .Terapi HF  3 pendekatan :    17 Penyebab HF dihilangkan (pembedahan pada struktur abnormal. ketidakpatuhan pengobatan.

Terapi HF  Konsep terapi non-obat :  Dulu  mengurangi aktivitas dan bedrest total adalah standar perawatan pasien  Sekarang :  Regular exercise (walking or cycling) direkomendasikan untuk pasien HF stabil kelas I-III  Dietary sodium (approximately 2 to 3 g of sodium per day)  restriction of fluid intake (maximum 2 L/day from all sources)  Berhenti merokok dan minum alkohol  Revaskularisasi atau transplantasi 18 .

glikosida).Terapi HF  Konsep terapi obat Dulu  fokus pada lemahnya jantung (digitalis. dan diuretik)  Sekarang  status patofisiologi sistemik keseluruhan  19 .

Algoritma terapi untuk pasien gagal jantung stage A & B menurut ACC/AHA 20 .

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terapi inotropik positif secara kontinu.Terapi untuk HF tingkat D • penderita HF advanced (gagal jantung dekompensasi) : • pasien yang mengalami simptom saat istirahat • pasien yang bolak-balik hopitalisasi • pasien yang harus di rs dengan intervensi khusus • terapi khusus : support sirkulasi mekanik. transplantasi kardiak 22 .

Angiotensin-converting enzyme (ACE) inhibitors (or angiotensin receptor blockers [ARBs]) should be strongly considered for antihypertensive therapy in patients with multiple vascular risk factors . and dyslipidemia according to current treatment guidelines. Strategies include smoking cessation and control of hypertension. diabetes mellitus.Pendekatan umum  Stage A:    23 The emphasis is on identifying and modifying risk factors to prevent development of structural heart disease and subsequent HF.

patients with a previous MI should receive both ACE inhibitors (or ARBs in patients intolerant of ACE inhibitors) and β-blockers regardless of the ejection fraction. Patients with reduced ejection fractions (less than 40%) should also receive both agents .Pendekatan umum  Stage B:     24 In these patients with structural heart disease but no symptoms. treatment is targeted at minimizing additional injury and preventing or slowing the remodeling process. In addition to treatment measures outlined for stage A.

an aldosterone receptor antagonist. immunization against influenza and pneumococcus. daily weight measurement. and/or hydralazine/isosorbide dinitrate (ISDN) may be useful in carefully selected patients.  If symptoms do not improve. digoxin. modest physical activity. long-term monitoring can begin.Pendekatan umum  Stage C: Most patients with structural heart disease and previous or current HF symptoms should receive the treatments for Stages A and B as well as initiation and titration of a diuretic (if clinical evidence of fluid retention).  Other general measures include moderate sodium restriction. and β-blocker  If diuresis is initiated and symptoms improve. and avoidance of medications that can exacerbate HF  25 . ARB (in ACE intolerant patients). ACE inhibitor.

Pendekatan umum  Stage  D: Patients with symptoms at rest despite maximal medical therapy should be considered for specialized therapies. including mechanical circulatory support. or hospice care 26 . continuous intravenous positive inotropic therapy. cardiac transplantation.

Pengobatan HF akut/parah 27 .

Efek relatif obat-obat adrenergik terhadap reseptor 28 .

dan kuinapril 29 . lisinopril.  kardiak indeks dan fraksi ijeksi    Contoh : kaptopril. enalapril. fosinopril.ACE Inhibitor  Untuk pasien disfungsi sistolik LV dan fraksi ejeksi LV < 40%  Efek : menurunkan preload dan afterload.

ginjal dan jantung) tanpa ada refleks takikardi .ACE Inhibitor (mekanisme aksi)   Aktivasi sindrom RAA  peran ACE  mekanisme kompensasi utama dalam HF ACEI  menghambat ACE  Angiotensin II  :     vasodilatasi dan menurunkan resistensi vaskular sistemik (afterload ) secara tidak langsung Aldosteron   retensi air dan Na   K serum   preload  Bradikinin   vasodilatasi Manfaat ACEI :  30 vasodilatasi. menghambat akumulasi cairan dan meningkatkan aliran darah ke organ vital (otak.

ditingkatkan secara gradual jika telah ditoleransi  Dosis dititrasi sampai dosis target  morbiditas & mortalitas   Pengamatan  fungsi renal dan serum kalium 1-2 mgg setelah terapi dimulai dan scr periodik  31 .ACEI (Dosis) Diawali dosis sangat rendah.

Profil obat-obat ACEI 32 .

RF.5 mmol/L . hamil  Caution :    33 TDS < 80 mmHg SrCr > 3 mg/dL Serum K > 5.ACEI (kontraindikasi)  Angioudema (reaksi alergi yang fatal).

ACEI (ESO)     Pusing. diare Angioudema di wajah Hipotensi  dosis pertama Batuk kering (umum)  5-15% pasien 34 . fatigue. sakit kepala.

Diuretik  Pasien HF dg overload volume   kombinasi + ACEI dan/ BB Mekanisme aksi :  ekskresi air dan Na   preaload  Diuretik loop  lebih poten  Diuretik tiazid (HCT)  diuretik lemah jarang digunakan pada HF sbg terapi tunggal  Digunakan sebagai kombinasi dengan diuretik loop untuk meningkatkan efektifitas diuresis  Lebih disukai jika untuk pasien retensi cairan 35 ringan dan TD tinggi  .

Profil obat-obat diuretik loop 36 .

menurunkan mortalitas untuk pasien HF Mekanisme kompensasi  aktivasi SNS  BB (efek antiaritmia) ACC/AHA merekomendasikan penggunaannya untuk seluruh pasien HF yang stabil dan yg mengalami penurunan LVEF jika tidak ada KI 37 . menurunkan hospitalisasi.Beta Bloker     Dulu :  KI untuk HF (NIE. bradikardi dan konstriksi perifer) Clinical trial evidence  BB dpt memperlambat progresi.

Profil obat-obat beta bloker 38 .

Digoksin HF disfungsi sistolik LV. gangguan penglihatan)  . GI (anoreksia.25 mg QD. ACEI dan BB  HF dan fibrilasi atrial  Mekanisme aksi  efek PIE dengan menghambat aktivitas Na-K adenosin trifosfatase membran sel  Ca dalam sel   Dosis : 0. nausea dan vomit). bingung. CNS (sakit kepala. 39 disorientasi. sbg terapi tambahan untuk diuretik. lansia 0.125 mg QD  ESO : toksisitas digoksin tjd pada 20% pasien dan 18% meninggal akibat aritmia (ritme kardiak ektopik dan re-entrant dan heart block). fatigue.

muka 40  . stroke volume dan CO meningkat)  Fixed dose kombinasi :   ISDN 20 mg dan hidralazin 37.Kombinasi hidralazin/ISDN Mekanisme aksi : nitrat sebagai vasodilator vena (menurunkan preload). hipotensi  ESO : refleks takikardi.5 mg (tid) Tambahan untuk mengoptimalkan terapi standar yg persisten symptoms  Firstline therapy untuk pasien intoleran ACEI/ARB karena insufisiensi ginjal. hidralazine vasodilator langsung pada arteri (menurunkan resistensi sistemik. sakit kepala. hiperkalemia.

4-8 mg OD (awal). target 32 mg OD Valsartan. enkefalin dan senyawa P)  tidak ada ES batuk spt ACEI yang dipacu akumulasi bradikinin  FDA approve :     Candesartan. target 160 mg BID Untuk menggantikan ACEI bila pasien intoleran (angioudema atau batuk kering) 41 . 20-40 mg BID (awal).Antagonis reseptor angiotensin II tipe 1 (AT1)  mengeblok efek angiotensi II dg menghambat stimulasi reseptor AT1 Tidak mengeblok degradasi vasoaktif (bradikinin.

5 mg/hari. target 50 mg/hari ESO : resiko hiperkalemia dan disfungsi renal 42 .Antagonis Aldosteron (ARA)    Spironolakton dan eplerenon mengeblok reseptor mineralocortikoid (target aldosteron)  menghambat reabsorpsi Na dan ekskresi K Efek pada jantung  mengurangi fibrosis kardiak dan remodelling ventrikel Dosis awal :    spironolakton 12. target 25 mg/hari Eplerenon 25 mg/hari.

such as emergency department visits and hospitalizations 43 .Treatment Of Acute Decompensated Heart Failure  decompensated HF  patients with new or worsening signs or symptoms  caused by volume overload and/or hypoperfusion  need for additional medical care.

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Treatment Of Acute Decompensated Heart Failure  Diuretics   46 IV loop diuretics used for acute decompensated HF. thereby improving pulmonary congestion . with furosemide being the most widely studied and used agent Bolus diuretic administration decreases preload by functional venodilation within 5 to 15 minutes and later (>20 min) via sodium and water excretion.

and β2-receptor agonist with α1-agonist effects The net vascular effect  vasodilation Potent inotropic effect without producing a significant change in heart rate  Initial doses of 2. and a variable increase in heart rate 47 .5 to 5 mcg/kg/min can be increased progressively to 20 mcg/kg/min  Dobutamine increases cardiac index because of inotropic stimulation. arterial vasodilation.Treatment Of Acute Decompensated Heart Failure   Positive Inotropic Agents Dobutamine    β1.

but its pharmacologic actions preferable to dobutamine in patients with marked systemic hypotension or cardiogenic shock Positive inotropic effects mediated primarily by β1-receptors more prominent with doses of 2 to 5 mcg/kg/min.Treatment Of Acute Decompensated Heart Failure   Positive Inotropic Agents Dopamine    48 should generally be avoided in decompensated HF. chronotropic and α1-mediated vasoconstricting effects more prominent . At doses between 5 to 10 mcg/kg/min.

reducing symptoms of pulmonary congestion in patients with high cardiac filling pressures .Treatment Of Acute Decompensated Heart Failure  Vasodilators   49 Arterial vasodilators act reducing afterload and causing a reflex increase in cardiac output Venodilators act as preload reducers by increasing venous capacitance.

Treatment Of Acute Decompensated Heart Failure   Vasodilators Nitroprusside    Sodium nitroprusside  mixed arterial-venous vasodilator  acts directly on vascular smooth muscle to increase cardiac index and decrease venous pressure Effective in the short-term management of severe HF Nitroglycerin   50 IV nitroglycerin decrease preload (venodilation) and mild arterial vasodilation used primarily as a preload reducer for patients with pulmonary congestion .