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 
Bukan OK HF
• LV compliance / distensibility 
• 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. 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
III. 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 d’effort
– 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 ˆ
– 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

COP on demand COP ⇊ Tekanan Vena 

Vasodilator

Vasokonstriksi simpatis Resistensi Perifer ⇈ Edema Edema

⇈ Perifer Pulm.

Renin release 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. Acute mechanical overload
• Acute Cor Pulmonale
• Hipertensi
• Acute Volume Overload
2. Chronic severe overload
• High COP (beri-beri, Paget’s disease)
• Value & Congenital Heart Disease
3. Gangguan pengisian (Impaired Cardiac Filling)
• Pericardial Restruction
• Restrictive Myocardial Disease
• Obstruksi mekanik (MS – TS – Tumor)
• Tachycardi
4. 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

Stroke volume

End diastolic Pressure

End diastolic volume End diastolic volume
Left Ventricular Function Curve

Stroke Volume

End diastolic volume

 LV Size
PVR

Preload Stroke
B.P
Volume

Contractility Myocard
fiber short COP

HR

Afterload
 CONTRACTILE STATE
OF MYOCARD

EDV
Blood Volume

Ventrikel Performance
Posisi
Tekanan Intrathoracal
Atrial Contrib
Venous Return
Otot Seklet

STRETCHING EDV
 The Heart Failure Milieu :
From Molecular Biodynamics to a Clinical Syndrome

DNA Molecular Heritable disorders

Genetic

Cellular, Volume overload/

Contractile proteins pressure overload
Organelle
Hormone signal transduction

Contraction CELL Necrosis

Toxins

Pump HEART Remodeling

Integrated
Physiologic milieu Compensatory responses
Organism:
Man
Compensation Prevention Decompensation

Treatment
 Heart Failure Milieu : Disease Process

Mechanical Dysfunction Mechanical Dysfunction

Pressure Overload Myocardial infarction
Hypertension Cardiomyopathy
Aortic/pulmonic Myocarditis
valve stenosis Drug/toxin-induced
Pulmonary hypertension Disease Systemic disease effects
Volume overload
Process
Aortic, mitral, tricuspid
valve insufficiency

Impaired Heart Filling

Pericardial disease
Ventricular hypertrophy
Myocardial restriction
Mitral/tricuspid stenosis
 The Heart Failure Milieu :
Compensatory Mechanisms

Disease
process

Ventricular
dysfunction

Renal Hemodynamic Sympathetic

Renin-angiotensin-aldosterone abnormalities Increased contractility
Salt/water retention Tachycardia
Increased venous tone
Ventricular Compensatory Increased arterial tone
Dilation mechanisms
Hypertrophy
 Renal Considerations in Heart Failure

Angiotensinogen
(liver) The Diuretic
therapy
Renin

Angiotension I
release Kidney Distal tubular
sodium load
Angiotensin-
converting
enzyme
In Renal perfusion
pressure
Angiotension II

Heart Other K+, Ca2+,

prostaglandins
Thirst Sodium
retention
(direct tubular Aldosterone Failure Atrial natriuretic
factor
effect) secretion

Vasoconstriction Vasopressin
 The Heart Failure Milieu :
Clinical Presentation Physical findings
Peripheral edema
Disease
process Ascites
Vascular congestion
Jugular venous distension
Ventricular Rales
dysfunction Tachycardia
Hypotension
Cachexia
Disease-specific findings
Hemodynamic
abnormalities
Physical findings
Azotemia Metabolic
Hyponatremia changes
Hypocalemia Compensatory
Hypomagnesemia mechanisms Symtoms and
Symptoms
Hyperuricemia physical findings Fatique and weakness
Acidosis/alkalosis Dyspnea and fluid retention
Hypoxia/O2 desaturatuion syndromes
Decreased MVO2 Nocturia
Gastrointestinal symptoms
Diminished mentation
 The Heart Failure Milieu :
Disease
End-Organ Failure and Death
process

Systemic organ failure

Ventricular Renal failure
dysfunction Hepatic failure
Respiratory failure
Multi-organ failure
Pulmonary embolism
Hemodynamic
abnormalities Peripheral (cerebral embolism)

Metabolic Death
changes
Compensatory
Sudden
mechanisms End-Organ Death
Failure

Lethal arrhythmia Symtoms and

Electrolyte abnormalities physical findings
Elevated catecholamine levels
Ischemia
Drug-proarrhythmia
 Responses to Hemodynamic Overload
Pressure overload Volume overload

Systolic wall stress Diastolic wall stress

Mechanical transducers

Intracellular signals

Ventricular remodeling

Paralel sarcomeres Series sarcomeres

Concentric hypertrophy Normal Eccentric hypertrophy