GAGAL JANTUNG

(HEART FAILURE)
Arief Rahman Hakim

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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
 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

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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; 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

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

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 Mekanisme kompensasi pada HF

 Cardiac output angiotensinogen

LVDEP
 SNS activity Renin
(preload) production

Angiotensin I
Cardiac dilatation ACE
Vascular Angiotensin II
resistance
Ventricular Angiotensin III (aldosterone)
hypertrophy

Sodium retention Sodium uptake

kinins PGE2 & PGI2
By vessels
ACE
inactive kinins  Blood volume
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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

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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.

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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

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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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 Sistem stage gagal jantung menurut ACC/AHA

ACC/AHA = American
15 College of Cardiology/ American Hearth Association
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.

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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

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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

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

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

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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

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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

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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

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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

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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

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 Pengobatan HF akut/parah

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Efek relatif obat-obat adrenergik terhadap reseptor

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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

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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

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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

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 Profil obat-obat ACEI

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

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

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 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 ringan dan TD
tinggi
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 Profil obat-obat diuretik loop

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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

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 Profil obat-obat beta bloker

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 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)
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 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
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 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, 20-40 mg BID (awal), target 160 mg BID
 Untuk menggantikan ACEI bila pasien intoleran
(angioudema atau batuk kering)
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 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

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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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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

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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

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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

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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

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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

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