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HEART FAILURE

Ali Ghanie
Sub Divisi Kardiologi Bagian Penyakit Dalam
FK UNSRI / RSMH Palembang

HEART FAILURE

Heart Failure (Gagal Jantung) : gagalnya


jantung memompa darah pada kecepatan yang
sesuai dengan kebutuhan jaringan
Circulatory Failure & Overload :
1. Circulatory Failure :
a. Heart failure
b. Non cardiac (peripheral) circul. Failure
Venous return (volume )
Kapasitas vaskular bed
Gangguan vaskular perifer
Oxyhemoglobin

2. Circulatory Congestion :
a. Cardiac gagal jantung
b. Non cardiac :
Volume darah
Venous return (vask. Resistance )
Congestive heart failure (acute chronic) cardiac
origin
Myocardial dysfunction / failure sistolik, diastolik
Forward failure backward failure
Left VS Right Heart Failure
Latent Heart Failure
Compensated heart failure

Stress mekanik (after load / pre load)

Pressure over load


Volume overload
Pressure overload
Kontraksi > kuat : lebih lambat
Hipertrofi konsentris (replikasi sarcomer paralel)
Chamber tetap (<<)
Kontraksi perunit ( ttp total mass )
LV diastolic filling
LV compliance / distensibility

Bukan OK HF

Volume Over Load


Hipertrofi eksentris (replikasi sarcomere seri)
Replikasi paralel (+) (o.k. wall stress)
Pengosongan LV (PD MR) > cepat wall
tension <<
Chamber >> ; tanpa kenaikan tekanan diastole
Bila compliance tekanan diastole

Mekanisme Kompensasi pada Heart Failure

Autonomic nervous system


a. Jantung
: HR, kontraktilitas , kecepatan
relaxasi
b. Circ. Perifer : Vasokonstriksi arterial (after load )
Vasokonstriksi venous (preload )
Ginjal R.A.A
a. Vasokonstriksi arterial (afterload )
b. Retensi Na H20 (PRG & afterload )
c. Kontraktilitas
Frank Starling Law of the Heart
Pemanjangan sarcomerg pada akhir diastole
Kenaikan volume, tekanan

Hipertrofi

- Paralel (konsentris)
- Seri (eksentris)
Oksigen Perifer
a. Redistribusi cardiac output
b. Kurva disosiasi oxygen hemoglobin
c. Ekstraksi O2 jaringan
Metabolisme Anaerob

PENYEBAB OVERALL HEART PUMP


FAILURE
I.

Kelainan Mekanis :
a. Beban tekanan
b. Beban volume regurgitasi,
preload
c. Obstruksi vent. Filling MS. TS
d. Konstriksi pericard
e. Endokard miokard restriksi
f. Ventric. Aneurysm
g. Ventric. Disinergi

II.

III.

Kelainan otot ( miokard )


a. Primer :

Miopati

Miokarditis

Metabolik (DM)

Toxic (alcohol, etc)

Presbycardia
b. Sekunder :

Disdinamik (sekunder o.k. mekanik)

Iskhemia

Kelainan systemik

PPOM

Obat
Gangguan Ritme / Konduksi
a. Standstill
b. Fibrilasi
c. Takhikardi Bradikardi berat
d. Gangguan konduksi

KLASIFIKASI
(Toleransi terhadap Latihan Jasmani)
Menurut NYHA (New York Heart Association )
I. Aktifitas fisik tidak terbatas
II. Aktifitas fisik sedikit terbatas
III. Aktifitas fisik sangat terbatas
IV. Istirahat sesak
Subjektif Anamnese
Objektif uji latih dengan beban

Diagnosis
A. Gagal Jantung Kiri
Dyspnea deffort
Orthopnea
Paroxysmal nocturnal dyspnea
Edema paru
Pernapasan cheyne stokes
Hemoptisis
Berdebar debar

Pembesaran jantung
Takikardi
S3 gallop
P2 mengeras
Ronkhi basah kedua basal paru

CIRCULATORY CIRCUIT

PARU
Kanan

Kiri

B. Gagal Jantung Kanan


Lelah
Mual, anorexia, rasa penuh pada perut
Sesak nafas tidak menyolok
JVP
Hepar >>, nyeri tekan, ikterus (+)
Splenomegali
Ascites
Edema tungkai bawah
Hidrothorak

Penatalaksanaan
1. Pengendalian faktor penyebab

Prosedur operasi
Terapi medis

2. Pengendalian faktor pencetus


3. Memperbaiki faktor yang memperburuk
4. Terapi gagal jantungnya

Gagal Jantung
Perbaikan daya pompa jantung
Pengurangan beban jantung
Mengurangi retensi Na & air

Myocardial Failure

Inotropic

Pump Failure
Tekanan Vena

COP

COP on demand
Vasodilator
Vasokonstriksi simpatis

Renin release

Resistensi Perifer

Edema
Perifer

Edema
Pulm.

Diuretik
Retensi Na / H2O

Angiotensin I
CEI
Angiotensin II

Aldosterone

PUMP (OVERALL H.F.) Mycardial


Failure
Overall HF 1. darah L. min // m2
2. Tekanan atrium
Myocardial failure :
me kecepatan & pemendekan unit otot
jantung melawan afterload (systolic load)

Overall Heart Failure tanpa Myocardial


Failure
1.

2.

3.

4.

Acute mechanical overload


Acute Cor Pulmonale
Hipertensi
Acute Volume Overload
Chronic severe overload
High COP (beri-beri, Pagets disease)
Value & Congenital Heart Disease
Gangguan pengisian (Impaired Cardiac Filling)
Pericardial Restruction
Restrictive Myocardial Disease
Obstruksi mekanik (MS TS Tumor)
Tachycardi
Low Cardiac output Heart block / bradicardy

Myocardial Failure tanpa overall H.F.


1. Systolic unloading of ventricle
Mitral Regurgitation
Vasodilator drugs
2. Compensated myocardial failure
3. Segmental contraction disorder
Iskhemik miokard transient
Infark miokard

Cardiac Performance (Kemampuan ?)


PREDIKTOR :
Preload : - a change in initial length
- tegangan FFG ventrikel akhir diastole
diperngaruhi - Venous Return
- Total volume
- Distribusi volume
Posisi tubuh
tekanan intrathorak
tekanan intrapericard
tonus vena
kontraksi atrium

After load : Force / Stress pada ventrikel segera


sesudah pemendekan otot ventrikel.
Dipengaruhi

- PVR

- Fisik arteri
- Volume pada ejeksi
Kontraktilitas : performance
Saraf simpatis
Catecholamin
Inotropik agent
Depressant
Mass lost
Intrinsic myocardial depression

Left Ventricular Function Curve

End diastolic Pressure

Stroke volume

End diastolic volume

End diastolic volume

Stroke Volume

Left Ventricular Function Curve

End diastolic volume

LV Size
PVR
Preload

Contractility

Stroke
Volume
Myocard
fiber short

COP
HR

Afterload

B.P

Performance

CONTRACTILE STATE
OF MYOCARD

EDV

Posisi
Tekanan Intrathoracal
Atrial Contrib
Venous Return

Ventrikel Performance

Blood Volume

Otot Seklet
STRETCHING

EDV

The Heart Failure Milieu :


From Molecular Biodynamics to a Clinical Syndrome
DNA

Contractile proteins

Molecular
Genetic

Heritable disorders

Cellular,
Organelle

Volume overload/
pressure overload
Hormone signal transduction

Contraction

CELL

Pump

HEART

Physiologic milieu
Compensation

Integrated
Organism:
Man
Prevention
Treatment

Necrosis
Toxins
Remodeling
Compensatory responses
Decompensation

Heart Failure Milieu : Disease Process


Mechanical Dysfunction
Pressure Overload
Hypertension
Aortic/pulmonic
valve stenosis
Pulmonary hypertension
Volume overload
Aortic, mitral, tricuspid
valve insufficiency
Impaired Heart Filling
Pericardial disease
Ventricular hypertrophy
Myocardial restriction
Mitral/tricuspid stenosis

Disease
Process

Mechanical Dysfunction
Myocardial infarction
Cardiomyopathy
Myocarditis
Drug/toxin-induced
Systemic disease effects

The Heart Failure Milieu :


Compensatory Mechanisms

Disease
process
Ventricular
dysfunction

Renal
Renin-angiotensin-aldosterone
Salt/water retention

Ventricular
Dilation
Hypertrophy

Hemodynamic
abnormalities

Compensatory
mechanisms

Sympathetic
Increased contractility
Tachycardia
Increased venous tone
Increased arterial tone

Renal Considerations in Heart Failure

The

Angiotensinogen
(liver)
Renin
release
Angiotension I

Angiotension II

Thirst

Sodium
retention
(direct tubular
effect)

Vasoconstriction

Angiotensinconverting
enzyme

Aldosterone
secretion

Kidney

Diuretic
therapy
Distal tubular
sodium load

In

Renal perfusion
pressure

Heart

Other K+, Ca2+,


prostaglandins

Failure

Atrial natriuretic
factor

Vasopressin

The Heart Failure Milieu :


Physical findings

Clinical Presentation
Disease
process

Ventricular
dysfunction

Physical findings
Azotemia
Hyponatremia
Hypocalemia
Hypomagnesemia
Hyperuricemia
Acidosis/alkalosis
Hypoxia/O2 desaturatuion
Decreased MVO2

Hemodynamic
abnormalities

Peripheral edema
Ascites
Vascular congestion
Jugular venous distension
Rales
Tachycardia
Hypotension
Cachexia
Disease-specific findings

Metabolic
changes
Compensatory
mechanisms Symtoms and
physical findings

Symptoms
Fatique and weakness
Dyspnea and fluid retention
syndromes
Nocturia
Gastrointestinal symptoms
Diminished mentation

The Heart Failure Milieu :


Disease
process

End-Organ Failure and Death


Systemic organ failure
Renal failure
Hepatic failure
Respiratory failure
Multi-organ failure
Pulmonary embolism
Peripheral (cerebral embolism)

Ventricular
dysfunction

Hemodynamic
abnormalities
Metabolic
changes
Compensatory
mechanisms
End-Organ
Failure

Lethal arrhythmia
Electrolyte abnormalities
Elevated catecholamine levels
Ischemia
Drug-proarrhythmia

Symtoms and
physical findings

Death
Sudden
Death

Responses to Hemodynamic Overload


Pressure overload

Volume overload

Systolic wall stress

Diastolic wall stress


Mechanical transducers
Intracellular signals
Ventricular remodeling

Paralel sarcomeres
Concentric hypertrophy

Series sarcomeres
Normal

Eccentric hypertrophy