Heart Failure

Heart Failure
Results from any
structural or functional
abnormality that
impairs the ability of
the ventricle to eject
blood (Systolic Heart
Failure) or to fill with
blood (Diastolic
Heart Failure)
 Epidemiology of Heart Failure
Approximately 4 to 5 million Americans with
symptomatic HF and an equal number with
asymptomatic
Most common cause of hospitalization
Increasing for past several decades
Improved survival after MI
Better diagnosis
Aging population
Proven therapies are underutilized
Types of Heart Failure
Low-Output Heart Failure
Systolic Heart Failure:
decreased cardiac output
Decreased Left ventricular ejection fraction
Diastolic Heart Failure:
Elevated Left and Right ventricular end-diastolic
pressures
May have normal LVEF
High-Output Heart Failure
Seen with peripheral shunting, low-systemic vascular
resistance, hyperthryoidism, beri-beri, carcinoid, anemia
Often have normal cardiac output
Right-Ventricular Failure
Seen with pulmonary hypertension, large RV infarctions.
Causes of Low-Output Heart Failure

Systolic Dysfunction
Coronary Artery Disease
Idiopathic dilated cardiomyopathy (DCM)
50% idiopathic (at least 25% familial)
9 % mycoarditis (viral)
Ischemic heart disease, perpartum, hypertension,
HIV, connective tissue disease, substance abuse,
doxorubicin
Hypertension
Valvular Heart Disease
Diastolic Dysfunction
Hypertension
Coronary artery disease
Hypertrophic obstructive cardiomyopathy (HCM)
Restrictive cardiomyopathy
Comparison of Systolic & Diastolic Heart Failure

NEJM 2003;348:20
Clinical Presentation of Heart Failure

Due to excess fluid accumulation:

Dyspnea (most sensitive symptom)
Edema
Hepatic congestion
Ascites
Orthopnea, Paroxysmal Nocturnal Dyspnea
(PND)
Due to reduction in cardiac ouput:
Fatigue (especially with exertion)
Weakness
Physical Examination in Heart Failure
S3 gallop
Low sensitivity, but highly specific
Cool, pale, cyanotic extremities
Have sinus tachycardia, diaphoresis and peripheral
vasoconstriction
Crackles or decreased breath sounds at bases
(effusions) on lung exam
Elevated jugular venous pressure
Lower extremity edema
Ascites
Hepatomegaly
Splenomegaly
Displaced PMI
Apical impulse that is laterally displaced past the
midclavicular line is usually indicative of left ventricular
enlargement>
Chest X-ray in Heart Failure

Cardiomegaly
Cephalization of the pulmonary
vessels
Kerley B-lines
Pleural effusions
Cardiomegaly
Pulmonary vessel congestion
Pulmonary Edema due to Heart Failure
 Heart failure criteria (NYHA)

Major Minor

1) acute pulmonary oedema 1) nocturnal cough

2) paroxysmal nocturnal dyspnoea 2) effort dyspnoea
(orthopnoea) 3) VC by 1/3
3) pulmonary subcrepitant rales 4) pleural transudate
4) jugular venous pressure (JVD) 5) tachycardia > 120 / min.
5) hepato-jugular reflex 6) peripheral oedema
6) heart silhouette 7) hepatomegaly
7) gallop rhythm (3-rd and 4-th sound)
Classification of Heart Failure

New York Heart Association (NYHA)

Class I symptoms of HF only at
levels that would limit normal
individuals.
Class II symptoms of HF with
ordinary exertion
Class III symptoms of HF on less
than ordinary exertion
Class IV symptoms of HF at rest
Classification of Heart Failure (cont.)

ACC/AHA Guidelines
Stage A High risk of HF, without
structural heart disease or symptoms
Stage B Heart disease with
asymptomatic left ventricular
dysfunction
Stage C Prior or current symptoms
of HF
Stage D Advanced heart disease and
severely symptomatic or refractory HF
 GAGAL JANTUNG
* Gagal jantung :
jantung tidak dapat memenuhi
kebutuhan metabolisme tubuh

* Gagal jantung kongestif :

gagal jantung yang mengakibatkan
tertimbunnya cairan di sistem vena
paru dan atau sistem vena sistemik
 GAGAL JANTUNG

Sindroma klinik akibat dari :

* Penurunan kekuatan kontraksi jantung

* Aliran darah keliru (beban volume)
* Hambatan aliran darah (beban tekanan)
* Kombinasi
PATOFISIOLOGI GAGAL JANTUNG

Jantung memompa darah dengan kekuatan

kurang dari normal

* Miokarditis
* Kardiomiopati
* Kawasaki
PATOFISIOLOGI GAGAL JANTUNG

Jantung memompa dengan kekuatan

normal, tetapi route aliran darah yang
dipompa keliru (beban volume)
PATOFISIOLOGI GAGAL JANTUNG

Jantung memompa dengan kekuatan yang

normal tapi mendapat hambatan pada
jalan keluar jantung (beban tekanan)
 DIAGNOSIS GAGAL JANTUNG

1. Riwayat dan Gejala klinis

2. Elektrokardiogram (pembesaran rongga
jantung, disritmia)
3. Foto polos dada (pelebaran rongga
jantung, edema paru)
4. Exercise test
5. Kateterisasi dan Angiokardiografi (struktur
dan fungsi)
6. Ekhokardiografi
7. MRI (struktur dan fungsi)
 DETERMINAN FUNGSI JANTUNG

1. Frekuensi denyut jantung

2. Kontraktilitas otot jantung
3. Preload
4. Afterload
Factors Involved in Regulation of Cardiac Output
 Hemodynamics
Myocardial
Contractility

Stroke Volume Preload

Cardiac Output Afterload

Blood
Pressure Heart Rate
Systemic Vascular
Resist ance
 Frekuensi denyut jantung

Frekuensi denyut jantung X isi sekuncup = curah jantung

Ada nilai optimal frekuensi denyut jantung

Melebihi nilai optimal frekuensi denyut jantung berakibat ;

* waktu untuk relaksasi memendek

* pengisian ventrikel menurun
* volume akhir diastolik ventrikel menurun
* isi sekuncup menurun
* kebutuhan oksigen miokard meningkat
* perfusi koroner menurun
 Kontraktilitas otot jantung
Aktivitas memendek serabut otot jantung
intrinsik (kemampuan inotropik) dan
ditentukan oleh perubahan kadar kalsium
intrasel

Tidak dipengaruhi oleh besarnya preload

maupun afterload
 Preload
Derajat regangan otot jantung pada
saat akan kontraksi (sistole) atau
selama relaksasi (diastole).

Secara histologis merupakan ukuran

panjang sarkomer (unit kontraktil otot
jantung).
 Preload

Secara klinis, preload diestimasikan dengan

pengukuran tekanan vena sentral (pengganti
tekanan atrium kanan) dan tekanan
pulmonary wedge (pengganti tekanan atrium
kiri).

Hukum Starling, bertambahnya volume akhir

diastole sampai titik optimal akan
meningkatkan curah jantung semata-mata
oleh faktor mekanik dan bukan oleh
perubahan kontraktilitas otot jantung
 Afterload

* Adalah beban yang dihadapi otot jantung

saat sistole (kontraksi/ejeksi)

* Diestimasikan sebagai tekanan aorta.

* Peningkatan afterload akan meningkatkan

beban yang dihadapi otot jantung sehingga
menurunkan volume sekuncup dan curah
jantung.
 MEKANISME KOMPENSASI
GAGAL JANTUNG KONGESTIF
1. Keseimbangan cairan dan dilatasi miokard.

2. Perubahan Kontraktilitas Otot Jantung

3. Redistribusi Curah Jantung dan Peningkatan

Ekstraksi Oksigen

4. Hipertrofi Otot Jantung

5. Bertambah panjangnya otot jantung.

 MEKANISME KOMPENSASI
GAGAL JANTUNG KONGESTIF

6. Disosiasi Oksigen-Hemoglobin

7. Peningkatan Prostaglandin dan

Prostasiklin.

8. Peningkatan Bradikin dan Kalikrenin

9. Perubahan aktifitas mitokondria otot jantung

10. Pelepasan Endotelin

11. Pelepasan Vasopresin

 PENGOBATAN GAGAL JANTUNG
KONGESTIF

1. MENCARI PENYEBAB GAGAL JANTUNG KONGESTIF

SEKALIGUS MENGHILANGKAN DENGAN CARA
MEDIKAMENTOSA.

2. MENCARI PENYEBAB GAGAL JANTUNG KONGESTIF

SEKALIGUS MEMPERSIAPKAN TINDAKAN TANPA
ATAU DENGAN PEMBEDAHAN JANTUNG.

3. MENCARI SEKALIGUS MENGHILANGKAN FAKTOR

PENCETUS TIMBULNYA GAGAL JANTUNG
KONGESTIF.
 PENGOBATAN GAGAL JANTUNG
KONGESTIF

4. MENGENDALIKAN KONDISI AKIBAT DARI GAGAL

JANTUNG
KONGESTIF
a. Retensi air dan garam serta
keseimbangan elektrolit
b. Mengendalikan takidisritmia
C. Menurunkan kebutuhan oksigen di
dalam sel
 PENGOBATAN GAGAL JANTUNG
KONGESTIF
5. MENINGKATKAN KINERJA/KONTRAKTILITAS OTOT
JANTUNG
6. Terapi oksigen secara adekuat,
7. pemberian sedativa,
8. pemberian kalori yang cukup, preparat besi, terapi
infeksi berulang,
9. pendekatan yang informatif terhadap keluarga
penderita
Stepped Approach to Treating Heart Failure

NEJM 2003;348:2013
 Heart failure (1)

Definition:

Heart disability to maintain proper circulation.

[Osler - 1892]

Impairment of heart function leading to

decrease of tissue perfusion which becomes not
sufficient for maintenance of cellular metabolism.

A state in which the heart cannot provide

sufficient cardiac output to satisfy the metabolic
needs of the body.
 Heart failure (2)

Systolic heart failure:

Impairment of heart function leading to decrease of
cardiac output and tissue perfusion with normal end-
diastolic left ventricle (LV) pressure.

Diastolic heart failure:

Impairment of heart function where sufficient cardiac
output and tissue perfusion is related to the excess of the
LV end-diastolic pressure.
 Heart failure (3)

heart failure

systolic congestive

contractility relaxation

pressure overload muscular tone

volume overload pericardial restriction

Pathophysiology of heart failure.

 Etiology of systolic heart failure
1) cardiomyocyte contractility
a) coronary heart disease (CHD)
b) myocardial infarction
c) myocarditis (i.e. rheumatic disease)
d) dilated cardiomyopathy
2) preload (volume overload) - LV dilatation
a) mitral or aortic regurgitation
b) atrial or ventricular septal defect
3) afterload (pressure overload) - LV concentric hypertrophy
a) aortic or pulmonary stenosis
b) arterial or pulmonary hypertension
 Etiology of diastolic (congestive) heart failure
1) cardiomyocyte relaxation
a) coronary heart disease (CHD)
b) myocardial infarction
c) ventricular hypertrophy
d) restrictive cardiomyopathy
2) muscular tone
a) ventricular hypertrophy
b) hypertrophic cardiomyopathy
3) pericardial restriction
a) pericardial exudate (pericarditis)
b) pericardial tamponade
 Acute heart failure
(simultaneously systolic and diastolic)
1) unstable angina pectoris, heart infarct
2) ventricular fibrillation (ischaemic)
3) acute valvular rupture (heart infarct of trauma)
4) acute pericardial tamponade (heart infarct or trauma)
5) pulmonary embolism

Heart failure with high stroke volume

1) tissue metabolism (fever, hyperthyroidism, thyreotoxicosis)
2) vascular dilation (hepatic cirrhosis, Pagets disease)
3) blood oxygen capacity (anaemia)
 Clinical manifestation (1)

Think about heart failure FACES

Fatigability
Activities limited
Chest (pulmonary) congestion
Edema (swelling) of ankles
Shortness of breath
(Heart Failure Society of America, 2000)
 Clinical manifestation (2)
left ventricular failure right ventricular failure

1) pulmonary haemostasis 1) symptoms of pulmonary

pulmonary oedema haemostasis (reason of failure)

a) effort resting dyspnoea 2) elevated jugular venous

b) paroxysmal nocturnal dyspnoea pressure
(orthopnoea)
c) wheezing
d) coughing up of foamy fluid with 3) symptoms of peripheral
blood haemostasis
a) ascites
2) symptoms of cardiac output b) peripheral oedema
a) tachycardia c) hepatojugular reflux
b) pale and cold skin d) liver and spleen
c) excessive sweating

3) symptoms of coronary artery

disease
 Heart failure (16)
Physical signs:
1) Blood pressure
a) diastolic BP
b) systolic BP - sustained or occasional
c) central venous pressure (CVP)
2) Apical impulses - displaced and sustained
3) Heart sounds
a) S3 - increased and rapid filling of ventricle
b) S4 - hypertrophy and stiffness of ventricle wall
4) Inspiratory rales over the lungs
5) Sympathetic nervous system activity
- pale, cold and sweaty skin
 Heart failure (17)

ECG:
1) arrhythmia
2) LV or RV hypertrophy
3) Left-branch bundle block (LBBB)
4) recent MI or old scare

Chest X-ray:
1) heart size
ECHO:
2) dilated upper lobe veins
1) wall motion
3) pleural exudate
2) valvular abnormality
3) intra-cardiac shunts
4) EF (N > 60 , HF < 40%)
BNP
 Heart failure (7)
Pathophysiology of systemic changes
1) hemodynamic changes
2) neurohormonal changes
3) intracellular changes

Hemodynamic changes (1)

From hemodynamic point heart

failure is related to systolic and / or
diastolic dysfunction.
 Heart failure (8)

Hemodynamic changes (2)

systolic dysfunction diastolic dysfunction

 Heart failure (9)
Hemodynamic changes (3)

Volume-pressure loop in
acute and chronic heart
failure.
 Heart failure (10)
Hemodynamic changes (4)

Volume-pressure loop in
heart failure with high
stroke volume.
 Heart failure (11)
Neurohormonal changes

N/H changes Favorable effect Unfavor. effect

HR , contractility, Arteriolar constriction

Sympathetic activity vasoconst. V return, After load workload
filling O2 consumption
Renin-Angiotensin Salt & water retention VR Vasoconstriction
Aldosterone after load

Vasopressin Same effect Same effect

interleukins &TNF May have roles in myocyte Apoptosis

hypertrophy

Vasoconstriction VR After load

Endothelin
 Heart failure (12)

Cellular changes

1) changes in adrenergic receptors

a) slight of 1 activity
b) 1 desensitisation due to long-time stimulation
2) changes in Ca2+ handling
3) changes in contractile proteins
4) stimulation of apoptosis
5) amount of fibrous tissue
 Heart failure (13)
1) heterometric autoregulation
preload end-diastolic volume contractility
end-diastolic volume contractility

2) concentric or eccentric hypertrophy

concentric hypertrophy contractility end-diastolic volume
eccentric hypertrophy end-diastolic volume contractility

3) sympathetic activation
arterial baroreceptor activation contractility, peripheral resistance,
RAA activity
long-time sympathetic stimulation 1 receptor activity
1 receptor activity
4) hormonal compensation
RAA system angiotensin blood volume peripheral resistance
ADH blood volume peripheral resistance

ANP, BNP, CNP volume overload

 Dysfunction of cardiac mechanoreceptors in HF
mechanoreceptors ADH
SNS
chemoreceptors ADH efferent
activity
SNS
mechanoreceptors
tachycardia efferent
natriuretic peptides activity

P RBF
HF
P GFR
Vascular
contraction
RBF
GFR
blood volume

bradycardia

water and Na+

oedemas blood volume
retention

tachycardia,
adrenergic
vascular stimulation
contraction