GAGAL

JANTUNG
KRONIK
 DEFINISI

Sindroma klinis ditandai gejala dan tanda

abnormalitas struktur dan fungsi jantung,
yang menyebabkan kegagalan jantung untuk
memenuhi kebutuhan oksigen metabolisme
tubuh
Gagal jantung merupakan bentuk akhir dan manifestasi
terberat dari hampir semua bentuk penyakit jantung
seperti atherosclerosis coroner, infark miokard, kelainan
katup, hipertensi, penyakit jantung bawaan dan
kardiomiopati.

Pathophysiology of heart disease, Leonard S Lily, page 216

 Cardiac Physiology

Preload Contractility Afterload

CO = SV x HR

Stroke Volume Heart Rate

HR: parasympathetic and sympathetic
tone

SV: preload, afterload, contractility

Cardiac Output

4 02/05/17
 Stroke Volume

PRELOAD : Passive stretch of muscle prior to contraction function of LVEDP

AFTERLOAD : Force opposing/stretching muscle after contraction begins measured by
SVR (Systemic Vascular Resistance)
CONTRACTILITY : ability of the muscle to contract at a given force for a given stretch,
independent of preload or afterload forces

5 02/05/17
 Frank Starling Mechanism

6 02/05/17
 Pathophysiology
Systolic dyfunctions :
The contractile state of the
myocardium
The preload of the ventricle
The afterload applied to the
ventricle
The heart rate
Dysfunction of myocardium :
Myocardial damage :
myocardial infarction;
Cardiomyopathy;
Myocarditis
Metabolic disturbance :
ischemia and hypoxia;
diabetes

Overload for myocardium :

Pressure overload (afterload) : Hypertension, aortic stenosis;
Pulmonary hypertension
Volume overload (preload) : Mitral regurgitation
Restriction of cardiac dilation : Pericardial effusion
8 02/05/17
 Ventricular Remodeling

Ventricular remodeling is the process by which

mechanical, neurohormonal, and possibly genetic
factors alter ventricular size, shape, and function.
Its hallmarks include hypertrophy, loss of myocytes, and
increased interstitial fibrosis.

Ventricular remodeling in diastolic and systolic heart failure

Normal heart Hypertrophied heart Dilated heart

(diastolic heart failure) (systolic heart failure)
 EPIDEMIOLOGI

Sekitar 1-2 % orang dewasa di negara maju menderita gagal jantung. Dengan prevalensi
meningkat 10 % pada usia lebih dari 70 tahun

Setengah pasien gagal jantung merupakan heart failure-reduced EF

Heart failure-preserved EF sering terjadi pada usia yang lebih tua dan wanita, riwayat
HT, dan AF

Penyebab kematian lebih tinggi pada HFrEF daripada HFpEF.

ESC guidelines 2016 for the diagnosis and treatment of acute and chronic heart failure
 PATOFISIOLOGI

Penyebab gagal jantung bisa dibagi menjadi :

1.Relaksasi dan pengisian ventrikel yang terganggu
(preload)
2.Afterload yang meningkat
3.Kontraktilitas jantung yang menurun

Pathophysiology of heart disease, Leonard S Lily, page 224

Pathophysiology of heart disease, Leonard S Lily, page 224
 Clinical classification
According to the course of disease
Acute HF
Chronic HF
According to the cardiac output (CO)
Low-output HF
High-output HF
According to the location of heart failure
Left -side heart failure (LHF)
Right-side heart failure (RHF)
Biventricular failure (whole heart failure)
According to the function impaired
Systolic failure
Diastolic failure
 Heart failure with reduced EF

Ventrikel yang terkena memiliki kapasitas yang terbatas

untuk memompa darah karena kontraktilitas yang menurun
atau afterload yang meningkat SV menurun ESV
meningkat EDV meningkat tekanan LV meningkat
tekanan LA meningkat tekanan hidrostatik kapiler
pulmonal meningkat kongesti pulmonal

Pathophysiology of heart disease, Leonard S Lily, page 225

 Heart failure with preserved EF
Fungsi diastolic yang tidak normal EDP
meningkat ditansmisikan retrograde ke vena
pulmonal dan sistemik kongesti vascular
sistemik dan paru

Pathophysiology of heart disease, Leonard S Lily, page 226

 Gagal jantung kanan dan gagal jantung kiri
Gagal jantung kiri adanya tanda dan gejala peningkatan tekanan dan
kongesti di vena pulmonal dan kapiler.
Gagal jantung kanan adanya gejala dan tanda peningkatan tekanan
dan kongesti di vena sistemik dan kapiler. Ditandai dengan peningkatan
JVP dan kongesti hepar.
Gagal jantung kanan biasanya terjadi setelah gagal jantung kiri

Hursts the heart volume one page 720

 MEKANISME KOMPENSASI
1. Frank starling mechanism

SV menurun ESV meningkat EDV meningkat

meningkatkan peregangan dari miofibers
meningkatkan kontraksi dan SV di kontraksi selanjutnya.

Mekanisme kompensasi ini memiliki batas pada akhirnya

SV menurun, kontraktilitas menurun, EDV meningkat
kongesti paru dan edema
Pathophysiology of heart disease, Leonard S Lily, page 227
2. Neurohormonal compensatory mechanism
Adrenergic nervous system

Renin-angiotensin aldosterone system

Antidiuretic hormone

Pathophysiology of heart disease, Leonard S Lily, page 228

Pathophysiology of heart disease, Leonard S
Lily, page 228
 Natriuretic peptides

- Atrial natriuretic peptide : disimpan di sel atrial

dan dilepaskan sebagai respon dari distensi atrial

- B-Type natriuretic peptide : diproduksi ketika

miokardium ventrikel mengalami stress

hemodinamik

Pathophysiology of heart disease, Leonard S Lily, page 230

 Etiology of HF
Hypertensive heart disease
Coronary artery disease
Valvular disease
Heart inflammation : pericarditis, myocarditis.
Cardiomyopathy
Venous disease (deep vein thrombosis) right
heart failure

ghennersdorf DGK ESC SES March 2013

 The precipitating causes

Infection : especially lung infection

Arrhythmia : Tachycardia atrial fibrillation
Bradycardia
Excessive physical activity
Pregnancy and delivery
Anemia
Administration of inappropriate drug
Medication noncompliance
Excess fluid intake
Thyrotoxicosis
ESC guidelines 2012 for the diagnosis and treatment of
heart failure
Pathophysiology of heart disease, Leonard S Lily, page 233
 Acute versus Chronic
Acute heart failure
develops rapidly
can be immediately life
threatening due to lack of time to
undergo compensatory adaptations.
may result from CABG, acute
infection (sepsis), acute myocardial
infarction, valve dysfunction,
severe arrhythmias, etc.
can often be managed successfully
by pharmacological or surgical
26
interventions.
Chronic heart failure
a long-term condition
(months/years) that is
associated with the heart
undergoing adaptive
responses (e.g., dilation,
hypertrophy) to a precipitating
cause.
These adaptive responses,
however, can be deleterious in
the long-term and lead to a
worsening condition. 02/05/17
 Systolic versus
SYSTOLIC HEART Diastolic
DIASTOLIC HEART
FAILURE FAILURE
Systolic cant pump

Aortic Stenosis
Diastolic- cant fill
HTN
Mitral Stenosis
Aortic Insufficiency
Tamponade
Mitral Regurgitation
Hypertrophy
Muscle Loss
Infiltration
Ischemia
Fibrosis
Fibrosis
27 02/05/17

02/05/17
Infiltration 27
Diastolic HF vs Systolic HF
 Manifestasi Klinis
Symptoms
Left-sided heart failure :
- dyspnea
- orthopnea
- Paroxysmal nocturnal dyspnea
- Fatigue
Right-sided heart failure :
- Peripheral edema
- Right upper quadrant discomfort

Pathophysiology of heart disease, Leonard S Lily, page 232

What Are The Symptoms
of Heart Failure?

Think FACES...
Fatigue
Activities limited
Chest congestion
Edema or ankle swelling
Shortness of breath
 Clinical Data

HEART SOUNDS!!!
Systolic Murmurs
Mitral Regurgitation
Aortic Stenosis
Diastolic Murmurs
Mitral Stenosis Mitral Stenosis
Aortic Insufficiency
S3: Rapid filling of a diseased ventricle

32 02/05/17
 Clinical Data

CXR(Chest X-Ray)
Kerleys lines : A and B
Pulmonary Edema
Cephalization
Pleural Effusions (bilateral)
EKG(Electrocardiogram)
Left atrial enlargement
Arrhythmias
Hypertrophy (left or right)

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 Clinical Data

Laboratory Data

Chemistry
Renal Function: Be Wary

BNP(Brain Natriuretic Peptide) Test

Used in ER departments the world over
Pulmonary versus cardiac dyspnea

34 02/05/17
Physical signs
Left-sided heart failure :
- Diaphoresis (sweating)
- Tachycardia, tachypnea
- Pulmonary rales
- Loud P2
- S3 gallop (in systolic dysfunction)
- S4 gallop (in diastolic dysfunction)
Right-sided heart failure :
- Jugular venous distention
- Hepatomegaly
- Peripheral edema

Pathophysiology of heart disease, Leonard S Lily, page 232

 Anamnesis

Cepat lelah bila beraktivitas

Sesak nafas, PND, DOE, OE
Bengkak pada tungkai
Riwayat menderita penyakit jantung
Pemeriksaan Fisik

Sesak nafas, frekuensi nafas

Nadi
Iktus cordis bergeser
Peningkatan vena jugularis
Hepatomegali/ hepatojugular reflux (+)
Edema tungkai
Ascites
Kriteria
diagnosis
 Diagnostic Test

Chest X-Ray
Transthoracic Echocardiography (TTE)
Transoesophageal Echocardiography (TOE) : untuk keadaan
tertentu seperti pasien dengan gangguan katup, curiga
diseksi aorta, curiga endokarditis atau penyakit jantung
bawaan.
Stress echocardiography : menilai viabilitas miokardium,
disfungsi diastolik pada preserved LVEF
Cardiac magnetic resonance : gold standar untuk mengukur
volume, massa dan EF dari ventrikel kanan dan kiri.
 Single proton emission CT (SPECT) : menilai iskemia dan
viabilitas miokardium
Positron emission tomography : menilai iskemia dan
viabilitas
Coronary angiography
Cardiac computed tomography

ESC guidelines 2016 for the diagnosis and treatment of acute and chronic heart failure
ESC guidelines 2016 for the diagnosis and treatment of acute and chronic heart
failure
Algoritma
pasien HF
 Treatment Strategies of
HF
Etiology therapy
Treatment of etiology causes
Treatment of precipitating causes
Improve life-style
Lessen cardiac load
Rest
Limitation of salt intake
Water intake
Diuretics
Drug treatment for CHF
Diuretics, ACE
inhibitors
Reduce the number of sacks
on the wagon
 Diuretics
Indicated in patients with symptoms of fluid
retention

Initiated with low doses followed by increments in

dosage until urine output increases and weight
decreases by 0.5-1kg daily

Benefits :
Improves symptoms of congestion
Can improve cardiac output

Limitations :
Excessive volume depletion
Electrolyte disturbance
 ACE Inhibitor
All patients with symptomatic heart failure and
functional class I with reduced LV function, unless
contraindicated or not tolerated
Should be continued indefinitely and titrate to optimal
dosage in the absence of symptoms or adverse effects
on end-organ perfusion
Increases exercise capacity and improves functional
class
Attenuation of LV remodeling post MI
 Beta-blockers
Limit donkeys speed, thus
saving energy

Initiate with low dosage

Titration to target dosage
 Digitalis

Like the carrot placed in front of the

donkey
 Digitalis
Enhances LV function, normalizes baroreceptor-mediated
reflexes and increases cardiac output at rest and during
exercise
Should be used in conjunction with diuretics, ACE
inhibitors and beta-blockers
Also recommended in patients with heart failure who
have atrial fibrillation
Adverse effects include cardiac arrhythmias, GI
symptoms and neurological complaints (eg. visual
disturbances, confusion)
 CRT/CRT-D
Increase the donkeys (heart)
efficiency CRT device:
Pts with NYHA Class /

Symptomatic despite
optimal medical therapy
QRS 130 msec

LVEF 35%
 Treatment Strategies of
HF
Aldosterone antagonist:
RALES, serious HF
Angiotensin receptor blocker:
substitute, not replace
TripleTherapy
TripleThe rapyfor
for
most patients ACE,
B-Blocker and MRA
Heart failure:
More than just drugs.

Dietary counseling
Patient education
Physical activity
Medication compliance
Aggressive follow-up
Sudden death assessment
 Questions to determine
therapeutic strategy in CHF
patients
Is heart failure present?

What caused the problem?

What precipitated deterioration?

How severe is the heart failure?

What is the best chronic therapeutic strategy?

Can the initiating/precipitating problem be cured, and

can the state of HF be attenuated?
What is the prognosis?
 ventricular filling occurs during this phase.

Intra atrial pressure recordings reveal two peaks and two descents. The a waveis the
atrial pressure generated during atrial systole immediately preceding ventricular systole.
The peak atrial pressure recorded during ventricular systole before the tricuspid and
mitral valves open is the v wave.

120 mmHg

Aortic Valve Opens Aortic Valve Closes

80 mmHg
Aortic Pressure

Mitral Valve Opens

Mitral Valve Closes

v
LA Pressure
a wave
wave
10 mmHg
62 LV Pressure 02/05/17
Diastole Systole Diastole
 Terapi

Tujuan terapi gagal jantung :

Memperbaiki tanda dan gejala yang muncul
Mencegah perawatan inap di rumah sakit
Menurunkan angka kematian

ESC guidelines 2016 for the diagnosis and treatment of acute and chronic heart failure
 Terapi pada heart failure-reduced EF
(systolic heart failure)
ACE-Inhibitor
Beta-blocker
Mineralocorticoid/aldosterone receptor antagonist
Diuretics
ARNI (angiotensin receptor nephrilysin inhibitor)
ARB
Ivabradine
Digoxin dan digitalis glikosid lain
Kombinasi hydralazine dan isosorbide dinitrat
Omega-3 polyunsaturated fatty acid

ESC guidelines 2016 for the diagnosis and treatment of acute and chronic heart failure
 Terapi pada HFpEF

ESC guidelines 2016 for the diagnosis and treatment of acute and chronic heart failure
TERIMA KASIH