Tata Laksana HF

ANISA DEVIANDA F
Algoritma terapi untuk pasien gagal jantung stage A & B menurut ACC/AHAa

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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 17
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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