GAGAL JANTUNG (HEART FAILURE)

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1 GAGAL JANTUNG (HEART FAILURE)
Sabtu, 30 September 2017 GAGAL JANTUNG (HEART FAILURE) Arief Rahman Hakim

2 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 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

3 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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6 CO (istirahat) = 5 L/menit (HR = 70 denyut/menit; SV = 70 ml)
Patofisiologi CO (istirahat) = 5 L/menit (HR = 70 denyut/menit; SV = 70 ml) Pengisian ventrikel normal = 130 ml; fraksi ejeksi normal = > 50% (volume yang tersisa dalam ventrikel = 60 ml) LSVD  fraksi ejeksi < 45%, dan symptom terjadi bila fraksi ejeksi < 35% Bila fraksi ejeksi <10%  resiko pembentukan trombus di dalam LV

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

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

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

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

12 Diagnosis (Laboratory Test)
Electrocardiogram may be normal or it could show numerous abnormalities including acute ST-T–wave changes from myocardial ischemia, atrial fibrillation, 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 oxygen-carrying capacity Chest radiography is useful for detection of cardiac enlargement, pulmonary edema, and pleural effusions

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

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

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

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

18 Terapi HF Konsep terapi non-obat : Sekarang :
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

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

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

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22 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, terapi inotropik positif secara kontinu, transplantasi kardiak

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

24 Pendekatan umum Stage B:
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, 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

25 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), ACE inhibitor, and β-blocker If diuresis is initiated and symptoms improve, long-term monitoring can begin. If symptoms do not improve, an aldosterone receptor antagonist, ARB (in ACE intolerant patients), digoxin, and/or hydralazine/isosorbide dinitrate (ISDN) may be useful in carefully selected patients. Other general measures include moderate sodium restriction, daily weight measurement, immunization against influenza and pneumococcus, modest physical activity, and avoidance of medications that can exacerbate HF

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

27 Pengobatan HF akut/parah

28 Efek relatif obat-obat adrenergik terhadap reseptor

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

30 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 : vasodilatasi, menghambat akumulasi cairan dan meningkatkan aliran darah ke organ vital (otak, ginjal dan jantung) tanpa ada refleks takikardi

31 ACEI (Dosis) Diawali dosis sangat rendah, 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

32 Profil obat-obat ACEI

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

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

35 Diuretik Pasien HF dg overload volume Mekanisme aksi :
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 ringan dan TD tinggi

36 Profil obat-obat diuretik loop

37 Sabtu, 30 September 2017 Beta Bloker Dulu : KI untuk HF (NIE, bradikardi dan konstriksi perifer) Clinical trial evidence  BB dpt memperlambat progresi, menurunkan hospitalisasi, 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

38 Profil obat-obat beta bloker

39 Digoksin HF disfungsi sistolik LV, sbg terapi tambahan untuk diuretik, ACEI dan BB HF dan fibrilasi atrial Mekanisme aksi  efek PIE dengan menghambat aktivitas Na-K adenosin trifosfatase membran sel  Ca dalam sel  Dosis : 0,25 mg QD, 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); GI (anoreksia, nausea dan vomit); CNS (sakit kepala, fatigue, bingung, disorientasi, gangguan penglihatan)

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

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

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 12,5 mg/hari, target 25 mg/hari Eplerenon 25 mg/hari, target 50 mg/hari ESO : resiko hiperkalemia dan disfungsi renal

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, such as emergency department visits and hospitalizations

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46 Treatment Of Acute Decompensated Heart Failure
Diuretics IV loop diuretics used for acute decompensated HF, 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, thereby improving pulmonary congestion

47 Treatment Of Acute Decompensated Heart Failure
Positive Inotropic Agents Dobutamine β1- 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 2.5 to 5 mcg/kg/min can be increased progressively to 20 mcg/kg/min Dobutamine increases cardiac index because of inotropic stimulation, arterial vasodilation, and a variable increase in heart rate

48 Treatment Of Acute Decompensated Heart Failure
Positive Inotropic Agents Dopamine should generally be avoided in decompensated HF, 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. At doses between 5 to 10 mcg/kg/min, chronotropic and α1- mediated vasoconstricting effects more prominent

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

50 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 IV nitroglycerin decrease preload (venodilation) and mild arterial vasodilation used primarily as a preload reducer for patients with pulmonary congestion