Gagal Jantung
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
LVDEP Renin
SNS activity
(preload) production
Angiotensin I
Cardiac dilatation ACE
Vascular Angiotensin II
resistance
Ventricular Angiotensin III (aldosterone)
hypertrophy
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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
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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)
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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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