heart failure

1. HEART FAILURE
ALI GHANIE
Divisi Kardiologi Bagian Ilmu Penyakit Dalam FK UNSRI/RSMH
Palembang

2. PENDAHULUAN
• Di Indonesia kejadian HF sekitar 0.13% ( ? )
• Meningkatnya kejadian hipertensi, meningkatnya
survival infark, bertambahnya usia harapan hidup
merupakan salah satu sebab kenaikan angka HF.
• Di Amerika gagal jantung merupakan problem
kesehatan masyarakat dimana 5.1 juta penduduk
mengalami gagal jantung dan diyakini akan meningkat
sampai 25 % ditahun 2030. Gagal jantung merupakan
penyebab utama dari 56.000 kematian setiap tahun
dari 275.000 kematian.

3. DEFINISI
Paul Wood pada tahun 1950
menyebutnya sebagai kegagalan
jantung mempertahankan sirkulasi
yang adekwat untuk memenuhi
kebutuhan jaringan meskipun
tekanan pengisian normal.
Thomas Lewis pada tahun
1933 menyebutkan HF secara
sederhana sebagai suatu
keadaan dimana jantung
tidak mampu mengeluarkan
darah secara adekwat.

4. Lanjutan
• Beberapa definisi lain berupaya untuk merangkum kelainan
struktur, fungsi, gejala dan tanda gagal jantung secara
menyeluruh, akibat gangguan pengisian dan ejeksi
(pengosongan) ventrikel.
Braunwald E pada tahun 1980
mendefinisikan gagal jantung
sebagai suatu keadaan dimana
jantung tidak mampu memenuhi
kebutuhan metabolisme jaringan
dari waktu kewaktu

5. Lanjutan
• Braunwald E, merevisi definisi Gagal jantung
sebagai suatu keadaan dimana terjadi gangguan
struktur dan fungsi jantung yang berakibat
gagalnya distribusi oksigen yang sesuai dengan
kebutuhan metabolisme jaringan meskipun
tekanan pengisian normal.
• ACC/AHA (2008) menyatakan gagal jantung
sebagai suatu sindroma klinik akibat abnormalitas
struktur dan fungsi jantung sehingga terjadi
gangguan pengisian dan pengosongan jantung.

6. CIRCULATORY CIRCUIT
Kanan Kiri
LUNG LA
RA LV
RV
VC
AO
Ali Ghanie, hopecardis 2015,Jakarta

7. Cardiac
Performance
CONTRACTILITY
PRELOAD
AFTER LOAD

8. TERMINOLOGI
• Gagal jantung kongestif, bila tekanan atrium kiri
dan kanan lebih dari normal
• Heart failure v Congestive Heart Failure
• Myocardial Failure without overall heart failure
• Myocardial Failure with overall H Failure
• Overall H F without myocardial failure
Ali Ghanie, hopecardis 2015

9. Lanjutan
• Left sided HF, melibatkan ventrikel kiri dengan kongesti
paru
• Right sided HF, melibatkan ventrikel kanan dengan
kongesti sistemik
• Backward –v – Forward failure
• Bisided HF, Left –Right as circuit, jarang isolated, kecuali
RV HF karena paru
• Kalau kita lihat terminologi diatas pada prinsipnya
klasifikasi gagal jantung dapat berupa waktu akut v
khronis, lokasi jantung yang terlibat kanan v kiri,
gangguan ejeksi berupa systolic dan gangguan pengisian
ventrikel berupa diastolic failure.

10. HEART
FAILURE
McMurray et al. Eur Heart J 2012;33:1787–847
Aetiology of HF
VALVULAR HEART DISEASE
• Mitral
• Aortic
• Trisuspid
• Pulmonary
MYOCARDIAL DISEASE
• Coronary artery disease
• Hypertension
• Cardiomyopathy
ENDOCARDIAL DISEASE
• With/without hypereosinophilia
• Endocardial fibroelastosis
PERICARDIAL DISEASE
• Constrictive pericarditis
• Pericardial effusion
HIGH OUTPUT STATES
• Anaemia
• Sepsis
• Thyrotoxicosis
• Paget‘s disease
• Arteriovenous fistula
ARRHYTHMIA
• Tachyarrhythmia
• Atrial
• Ventricular
• Bradyarrhythmia
• Sinus node dysfunction
CONDUCTION DISORDERS
• Atrioventricular block
VOLUME OVERLOAD
• Renal failure
• Iatrogenic (e.g. post-
operative fluid infusion
CONGENITAL
HEART DISEASE

11. Addressing Heart Failure in 2013
Katz AM
Heart Failure

12. 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

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

14. 14
NP system counter balance the unfavourable prolonged effect of SNS
and RAS, but quickly degraded by Neprilysin
ANG=angiotensin; AT1R=angiotensin type 1 receptor; NP=natriuretic peptide; NPRs=natriuretic peptide receptors;
RAAS=renin-angiotensin-aldosterone system; SNS=sympathetic nervous system
Levin et al. N Engl J Med 1998;339:321–8;Nathisuwan & Talbert. Pharmacotherapy 2002;22:27–42; Kemp & Conte.
Cardiovascular Pathology 2012;365–371; Schrier et al. Kidney Int 2000;57:141825;Schrier & Abraham N Engl J Med 2009;341:577–85;
Boerrigter, Burnett. Expert Opin Invest Drugs 2004;13:643–52; Ferro et al. Circulation 1998;97:2323–30;
Brewster et al. Am J Med Sci 2003;326:15–24
RAAS
Ang II AT1R
HFSYMPTOMS
&PROGRESSION
NP system
Vasodilation
 Blood pressure
 Sympathetic tone
 Natriuresis/diuresis
 Vasopressin
 Aldosterone
 Fibrosis
 Hypertrophy
NPRs NPs
Epinephrine
Norepinephrine
α1, β1, β2
receptors
SNS
Vasoconstriction
Blood pressure 
Sympathetic tone 
Aldosterone 
Hypertrophy 
Fibrosis 
Sodium and water retention 
Vasoconstriction
RAAS activity 
Vasopressin 
Heart rate 
Contractility 
Inactive
fragments

15. Modalitas Diagnostik
• Diagnosis fisik
• Laboratorium
• Elektrokardiogram
• Chest x Ray
• Echocardiography
• Magnetic resonance imaging
• Kateterisasi

16. Cardiothoracic ratio > 50% is specific, not sensitive
Useful to exclude other causes of SOB

17. Basal edema, CTR > 50%, Shoe
shaped, ECHO : HVK,HFpEF

18. Edema paru akut ec HHD
Echo : reduced EF

19. ECHOCARDIOGRAPHY

24. ≥I present
PATIENT WITH SUSPECTED
HF
(non-acute onset)
ASSESSMENT OF HF PROBABILITY
1. Clinical history
2. Physical examination
3. ECG
ECHOCARDIOGRAPHY
If HF confirmed (based on all available data):
Determine aetiology and start appropriate treatment
NATRIURETIC PEPTIDES
• NT-proBNP ≥ 125 pg/mL
• BNP ≥35 pg/mL
HF unlikely:
Consider other
diagnosis
Yes
All absent
No
Normal
Assessment of
natriuretic peptides not
routinely done in
clinical practice
DIAGNOSTIC
ALGORITHM FOR
HEART FAILURE
OF NON-ACUTE
ONSET
EHJ,doi:10.1093/eurheart/ehw128, 2016

25. Responses to Hemodynamic Overload
Pressure overload
Systolic wall stress
Mechanical
transducers
Volume overload
Diastolic wall stress
Intracellular signals
Ventricular remodeling
Paralel sarcomeres Series sarcomeres
Concentric hypertrophy Normal Eccentric hypertrophy

26. THERAPY
• Digitalis
• Inotropic
• Angiotensin Converting Enzym Inhinbitor
• Angiotensin Receptor blocade
• Beta Blocker
• ivabradin
• Sacubitril/valsartan
• Diuretic, furosemid, spironolactone

27. bisoprolol, carvedilol,
nebifolol
Pharmacological treatment was developed to counter 2 core
pathophysiology pathway
Cardiac structure/function abnormality
Activation of compensatory mechanisms to maintain
cardiac output and organ perfusion1
NP=natriuretic peptide; RAAS=renin angiotensin aldosterone system;SNS=sympathetic nervous system
1. Francis et al. Ann Intern Med 1984;101:370–7; 2. Clerico et al. Am J Physiol Heart Circ Physiol 2011;301:H12–H20;
3. Von Lueder et al. Circ Heart Fail 2013;6:594–605 4. Luchner & Schunkert. Cardiovasc Res 2004;63:443–9;
5. Thysgesen et al. Eur Heart J 2012;33:2001–6
SNS RAAS NP system
β blocker RAAS blocker
ACEi : captopril, Lisinopril
ARB : valsartan,
candesartan
MRA : spironolactone
?

28. The Heart Failure Milieu :
Compensatory Mechanisms
Disease
process
Ventricular
dysfunction
Hemodynamic
abnormalities
Compensatory
mechanisms
Sympathetic
Increased contractility
Tachycardia
Increased venous tone
Increased arterial tone
Renal
Renin-angiotensin-
aldosterone
Salt/water retention
Ventricular
Dilation
Hypertrophy

29. The Heart Failure Milieu :
From Molecular Biodynamics to a Clinical Syndrome
Molecular
Genetic
Cellular,
Organelle
CELL
HEART
Integrated
Organism:
Man
Prevention
Treatment
DNA
Contractile proteins
Contraction
Pump
Physiologic milieu
Compensation
Heritable disorders
Volume overload/
pressure overload
Hormone signal transduction
Necrosis
Toxins
Remodeling
Compensatory responses
Decompensation

30. 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
Mechanical Dysfunction
Myocardial infarction
Cardiomyopathy
Myocarditis
Drug/toxin-induced
Systemic disease effects
Disease
Process

31. Renal Considerations in Heart Failure
Angiotensinogen
(liver)
Angiotension I
Angiotension II
Thirst Sodium
retention
(direct tubular
effect)
Vasoconstriction
Renin
release
Angiotensin-
converting
enzyme
The
Kidney
In
Heart
Failure
Aldosterone
secretion
Diuretic
therapy
Distal tubular
sodium load
Renal perfusion
pressure
Other K+, Ca2+,
prostaglandins
Atrial natriuretic
factor
Vasopressin

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

33. Symtoms and
physical findings
Death
The Heart Failure Milieu :
End-Organ Failure and Death
Disease
process
Ventricular
dysfunction
Hemodynamic
abnormalities
Metabolic
changes
Compensatory
mechanisms End-Organ
Failure
Sudden
Death
Systemic organ failure
Renal failure
Hepatic failure
Respiratory failure
Multi-organ failure
Pulmonary embolism
Peripheral (cerebral embolism)
Lethal arrhythmia
Electrolyte abnormalities
Elevated catecholamine levels
Ischemia
Drug-proarrhythmia