GAGAL JANTUNG

(HEART FAILURE)

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

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

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

Mekanisme Kompensasi

Fraksi ejeksi turun CO turun

mekanisme kompensasi

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

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

10

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-Twave 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 oxygencarrying capacity
Chest radiography is useful for detection of
cardiac enlargement, pulmonary edema, and
12pleural effusions

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

15ACC/AHA =

American 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 :

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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

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:

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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

Pendekatan umum

Stage B:

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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 -blockers regardless of the
ejection fraction.
Patients with reduced ejection fractions (less than
40%) should also receive both agents

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 -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 :

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vasodilatasi, menghambat akumulasi cairan dan

meningkatkan aliran darah ke organ vital (otak, ginjal dan
jantung) tanpa ada refleks takikardi

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 :

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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

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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
35 ringan dan TD tinggi

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,
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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
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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

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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

Treatment Of Acute Decompensated

Heart Failure

Positive Inotropic Agents

Dobutamine

1- and 2-receptor agonist with 1-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

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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
1-receptors more prominent with doses of 2 to 5
mcg/kg/min.
At doses between 5 to 10 mcg/kg/min,
chronotropic and 1-mediated vasoconstricting
effects more prominent

Treatment Of Acute Decompensated

Heart Failure

Vasodilators

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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

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

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IV nitroglycerin decrease preload (venodilation) and

mild arterial vasodilation
used primarily as a preload reducer for patients with
pulmonary congestion