Seorang laki-laki umur 56 tahun datang dengan

keluhan sesak nafas, sesak nafas timbul ketika

melakukan kegitan ringan sehari-hari seperti
berjalan kekamar mandi, sesak nafas hilang jika
pasien istirahat,pasien tidur dengan dua bantal
dan sering terbangun pada malam hari karena
sesak nafas,pada pemeriksaan didapatkan ictus
cordis teraba di ics 6 laa, didapatkan bising
pansistolik diapex grade 5/6 dijalarkan ke axiler
1. Diagnosis fungsional ?
2. Diagnosis anatomi?
3. Diagnosis etiologi?
4. Bagaimana penatalaksanaannya?

GAGAL JANTUNG
[HEART FAILURE]

DEFINISI
DEFINISI GAGAL
GAGAL JANTUNG
JANTUNG
- suatu keadaan patofisiologis di mana jantung tidak
mampu memompa darah sesuai kebutuhan
metabolisme jaringan, atau untuk memenuhi
kebutuhan jaringan harus meningkatkan tekanan
pengisian.
- gagal jantung adalah suatu sindroma klinik yang
kompleks akibat gangguan fungsional/ struktural
jantung yang mengganggu kemampuan pengisian/
memompa ventrikel.

Contractility
Preload

Cardiac Output
Afterload
Frequence & Rhytm

DEFINISI
DEFINISI GAGAL
GAGAL JANTUNG
JANTUNG
Gagal Jantung merupakan akhir dari beberapa
penyakit jantung :
PENYAKIT JANTUNG BAWAAN
PENYAKIT JANTUNG KATUP
PENYAKIT JANTUNG KARDIOMIOPATI
PENYAKIT JANTUNG KORONER
PENYAKIT JANTUNG HIPERTENSI

EPIDEMIOLOGY
Morbidity and Mortality rates remain high.
USA : estimated more than 2 million
patient.
400.000 new patient each year.
900.000 required hospitalization.
200.000 patient die/year.
Annual mortality rate : 40-50% in NYHA
Class IV

Epidemiology
Epidemiology of CHF in the
community
Prevalence

Age
Incidence

(years)
1000 per year)

50
80

(%)

(new cases per

14Epidemiology of CHF: hospital

admissions

Survey
USA hospital admissions
per year
Gillum (1985) 585 000
Yancy and Firth (1988)
UK Hillingdon survey
Parameshwar (1990)
admissions

Admissions

900 000
4.9% of medical hospital

ETIOLOGI GAGAL JANTUNG

1. Peningkatan beban awal
( preload) : MR,AR.TR
2. Penurunan beban awal :
MS,Tamponade,
3. Kelemahan otot jantung :
IMA
4. Penurunan kemampuan
mengembang ventrikel:
LVH
5. Peningkatan beban akhir
( afterload) :
Hipertensi,AS,PS
6. Hilangnya peran sistolik
atrium : Atrial fibrilasi

Paradigma lama : Gagal jantung disebabkan

berkurangnya kontraktilitas dan daya pompa

karena

Paradigma baru : Gagal jantung merupakan remodeling

progresif akibat beban /penyakit pada miokardium

Kompensasi
intrinsik
Kompensasi
neurohumoral
Kompensasi
neurohormonal

Penyakit
primer
Gangguan
Gangguan
sistolik
diastolik
CO
/Kebutuhan jaringan tdk
tercukupi
Kompensasi
Kompensasi
intrinsik
neurohormonal
Kompensasi
neurohumoral
Hipertoni
RAAS
Hipertropi
simpatis
Arginin V
ventrikel
Vasokontriksi
Takikardi
Vasokontriksi
CO meningkat
Retensi air dan
Na
Gagal jantung
Remodeling
Beban

Patofisiologi Klasik
Gagal Jantung
Penyakit
primer

tekana
n aorta

cardiac
output

Stimulasi
sistem
neurohumo
ral/neuroh
ormonal
Vasokonstrik
si

Dilatasi
ventrike
l

Gagal
Jantung

Keluarnya
Renin /
angiotensin
catecholami
ns

volume
vaskular

afterload

Preload

Aktivasi jalur neurohumoral pada gagal

jantung
Coronary Disease

Cardiomyopathy

Cardiac Overload

Left Ventricular Dysfunction

Vasoconstriction

Neurohormonal Activation
Cathecholamines
RAAS
AVP
Endothelin

peripheral organ
blood flow
skeletal
muscle flow
Exercise intolerance

RBF
Na+ retention

Cardiac remodelling
LV dilatation

LV
hypertrophy

Arrhythmias
Edema, congestion

Ruffolo, J.Cardiovasc, Pharmacol, 1998

Sudden death

Pump failure

Peran Angiotensin II dalam gagal jantung

Coronary artery disease
Pressure overload
Cardiomyopathy
Left ventricular dysfunction
Arterial blood pressure
Renin release

Angiotensin II

Vasoconstriction
Peripheral organ blood flow
Skeletal muscle
Blood flow

Vascular and cardiac

hypertrophy

Aldosterone release
Cardiac remodelling

Na+ and water retention

Renal
blood flow

Exercise intolerance

Left ventricular
dilation & hypertrophy
Pump failure

Edema

Rantai Kejadian Menuju Endstage Heart Disease

Infark
myokard
Trombosis
koroner
Iskemik
myokar
d

Silent
Angina

Strok CAD PAD

e
Atherosklerosi
s
LVH
Faktor risiko

(Kolesterol, Hipertensi,
Diabetes mellitus,
Merokok)

Arritmia

Kematian
mendad
ak

Remodeling
Dilatasi
ventrikel

Gagal
jantung
Endstage
Heart
Disease

Hipertensi menuju
congestive heart failure
LVH

Diastolic
dysfunction
CHF

Hipertensi
MI

Death

Systolic
dysfunction

LV
Subclinical
Overt
Normal LV
remodeling LV dysfunction Heart Failure
Structure & Function

EVOLVING MODELS OF HEART

FAILURE

Cardiorenal

Hemodynamic

Neurohormonal

Vasodilators or

ACE-I, -blockers

Digitalis and

positive inotropes

and other agents

Diuretic to

to relieve

to block

Perfuse kidneys

ventricular wall

neurohormonal

stress

activation

1940s

1960s

1970s

1990s - 2000

Gambaran klinik
1. Mekanisme kompensasi : Berdebar,
keringat dingin, takikardi
2. Sindrom low out put : Lesu, lelah,
lemah, tak bergairah, bingung,
konsentrasi menurun, gelisah
3. Sindrom kongesti : Sesak nafas,
edema paru, JVP meninggi, Asites,
Hepatomegali, Edema tungkai,
Edema tungkai, batuk darah
4. Sindrom remodeling : Hipertrofi dan
dilatasi ventrikel, bising jantung, irama
gallop S3

Gagal Jantung
Gejala utama :
Dispnea
Mudah lelah
Edema perifer
BB bertambah
Batuk kronik

Kriteria Gagal Jantung

menurut Framingham Heart
Study
KRITERIA MAYOR
PAROXYSMAL NOCTURNAL DYSPNEU
DYSPNOE ON EFFORT
PENINGKATAN TEKANAN VENA JUGULARIS
RONKHI PARU
KARDIOMEGALI
UDEMA PARU AKUT
GALLOP S3
PEMANJANGAN WAKTU SIRKULASI (>25 DETIK)
REFLUKS HEPATO JUGULAR

Kriteria Gagal Jantung

menurut Framingham Heart
Study
KRITERIA MINOR
UDEMA PERGELANGAN KAKI
BATUK MALAM
HEPATOMEGALI
EFUSI PLEURA
TAKIKARDIA (>120 X/MENIT)
PENURUNAN KAPASITAS VITAL PARU
(1/3 DARI MAKSIMAL)

Kriteria Gagal Jantung

menurut Framingham Heart
Study
KRITERIA MAYOR ATAU MINOR
DISEBUT GAGAL JANTUNG KONGESTIF
BILA MEMENUHI 2 KRITERIA MAYOR
ATAU 1 MAYOR DENGAN 2 MINOR.

Patients surviving %

100

Progression Further damage

Excessive wall stress
Neurohormonal
Mechanism of death
activation
Sudden death
Myocardial ischemia
40%
Worsening CHF
40%
Other 20%

<5%
to 80%

Asymptomatic
Severe

Annual
mortality

10%

20 to 30%

Mild

Moderate

Left ventricular dysfunction and

symptoms

30

Progression of Cardiovascular Disease

Coronary
artery Hypertension
disease

Left ventricular
remodeling

Arrhythmia

Remodeling

Low ejection
fraction

Pump
failure

Cardiomyopathy Valvular
disease

Death

Neurohormonal stimulation
Endothelial dysfunction
Vasoconstriction
Renal sodium retention

Noncardiac
factors

Symptoms:
Dyspnea
Fatigue
Edema

Chronic
heart
failure

Stages of Heart Failure

Stages

Examples

Stage A: At high risk for HF but

without structural heart disease
or symptoms of HF

HTN, CAD, DM, cardiotoxins,

FHx of CM

Stage B: Structural heart disease

but without symptoms of HF

Previous MI, LV systolic dysfunction,

asymptomatic
valvular disease

Stage C: Structural heart disease

with prior or current symptoms
of HF

Known structural heart disease,

SOB and fatigue, reduced exercise
tolerance

Stage D: Refractory HF requiring

specialized interventions

Marked symptoms at rest

despite maximal medical therapy
ACC/AHA Heart Failure Practice Guidelines 2001

DIAGNOSIS
1. Anamnesis
2. Pemeriksaan fisik
3. Pemeriksaan tambahan :
laboratorium, X foto thorax, EKG,
Echokardiografi,Kateterisasi jantung

1.
2.
3.
4.
5.

Darah tepi : lekositosis

Urinalisis : jumlah urin berkurang
Foto dada : Kardiomegali, tanda kongesti paru
EKG : Kardiomegali, ggn irama, iskemia
Echokardiografi : Kardiomegali, penurunan
kontraktilitas, kelainan katup, penurunan fraksi
terpompa
6. Kateterisasi : tanda kongesti paru
( peningkatan LVEDP,atrium kiri,a. pulmonalis)

MANAGEMENT
Change in Activity & Diet :
Bed Rest/Restriction of physical
activity
Sodium & Fluid `restriction
Reducing Emotional stress
Calory restriction in overweight
patient

Correction of precipitating
factors :
Dysrhytmia
Infection : most frequent
Pregnancy
Anemia
Volume Excess
Psychosocial stress
Cardiotoxic drug

Treatment Options
in Heart Failure
Digoxin
Diuretics
Afterload reduction
ACE inhibitors: ACEI
Angiotensin II receptor blockers: ARBs
Nonspecific vasodilators

Beta blockers
Aldosterone antagonists

Primary Targets of Treatment in Heart Failure.

The Donkey Analogy

Ventricular dysfunction limits a patient's
ability to perform the routine activities of
daily living

Digitalis Compounds
Like the carrot placed in front of the
donkey

Diuretics, ACE Inhibitors

Reduce the number of sacks on the
wagon

-Blockers
Limit the donkeys speed, thus saving
energy

Cardiac Resynchronization
Therapy
Increase the donkeys (heart)
efficiency

Stages in the evolution of HF and recommended therapy

by stage
Stage A

Stage B

Pts with:
Pts with:
Previous MI
Hypertension
Struct. LV systolic
CAD
Heart
DM
dysfunction
Disease
Asymptomatic
Cardiotoxins
Valvular disease

Stage C
Pts with:
Struct. HD
Develop. Shortness of
Symp. of
breath and fatigue,
HF
reduce exercise
tolerance

Stage D
Pts who have
Refract. marked symptoms
Symp. of at rest despite
HF at rest maximal medical
therapy

THERAPY

THERAPY

THERAPY

THERAPY

Treat Hypertension
Stop smoking
cessation
Treat lipid disorders
Encourage regular
exercise
Stop alcohol &
drug use
ACE inhibition

All measures under

stage A
ACE inhibitor
Beta-blockers

All measures under

stage A
Drugs for routine use:
diuretic
ACE inhibitor
Beta-blockers
digitalis

All measures under

stage A, B and C
Mechanical assist
device
Heart transplantation
Continuous IV
inotrophic infusions
for palliation

ACC/AHA Guidelines for the

Evaluation and Management of Chronic Heart Failure in the Adult 2001

Be a Good Student with Active Learning and Share

Knowledge Each Other
Think Globally but Act Locally
(WHO Statement)

GOOD LUCK!!!