Penatalaksanaan Heart Failure

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

• 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
• 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

• 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
Penatalaksanaan Heart Failure akut/parah

Efek relatif obat-obat adrenergik terhadap reseptor

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

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

Profil obat-obat ACEI

ACEI (kontraindikasi)
• Angioudema (reaksi alergi yang fatal), RF, hamil
• Caution :
– TDS < 80 mmHg
– SrCr > 3 mg/dL
– Serum K > 5,5 mmol/L
ACEI (ESO)
• Pusing, sakit kepala, fatigue, diare
• Angioudema di wajah
• Hipotensi  dosis pertama
• Batuk kering (umum)  5-15% pasien
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
Profil obat-obat diuretik loop

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
Profil obat-obat beta bloker

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)
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
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)
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
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
• 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
• 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
• 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
• 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

• 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