1

HEART FAILURE
PATHOPHYSIOLOGY
AND MANAGEMENT
MOCH. FATHONI
DEPART. OF CARDIOLOGY
MEDICAL FACULTY, SEBELAS MARET UNIV.
 2

GAGAL JANTUNG /
DECOMPENSATIO CORDIS
DEFINISI patofisiologik
KETIDAK MAMPUAN JANTUNG
UNTUK MEMENUHI KEBUTUHAN
METABOLISME JARINGAN PADA
SAAT ISTIRAHAT ATAU KERJA
RINGAN. Hal tersebut akan menyebabkan
response sistemik khusus yang bersifat
patologik (sistem saraf, hormonal, ginjal
dan lainnya) serta adanya tanda dan gejala
yang khas.
 3

GAGAL JANTUNG/
DECOMPENSATIO CORDIS
DEFINISI KLINIK :
MERUPAKAN SINDROMA KLINIK
YANG TERDIRI DARI SESAK NAFAS
DAN RASA CEPAT LELAH YANG
DISEBABKAN OLEH KELAINAN
JANTUNG.
 4

A PREVALENT CONDITION
PREVALENCE OF HEART FAILURE
(PER 1000 POPULATION)

Age (years) Men Women

50-59 8 8

80-89 66 79

All ages 7.4 7.7

Framingham Heart Study: Ho et al. 1993 J Am Coll Cardiol;22:6-13

 5

A GROWING BURDEN
DEATHS FROM HF 1979-1997 (USA)
50000

40000
HF deaths

30000

20000

10000

0
1979 1985 1991 1997

Source: Vital Statistics of the United States, National Center for Health Statistics
 63
HEART FAILURE WAS VIEWED SOLELY AS
HAEMODYNAMIC DISORDER

A major public health

issue
 74

NEURO-HORMONAL ACTIVATION

AS A SIGNIFICANT FACTOR
CONTRIBUTING TO PROGRESSIVE
SYSTOLIC DYSFUNCTION AND
PROGRAMMED MYOCARDIAL CELL
DEATH, ALSO CALLED
APOPTOSIS
 84

NEURO-HORMONAL ACTIVATION

FACT AND PENDING

QUESTION
 NEURO-HORMONE SECRETION IN 9

RESPONSE TO HEART FAILURE

NOREPINEPHRINE CAUSED
VASOCONSTRICTION, INCREASED HEART RATE
AND MYOCYTE TOXICITY

ANGIOTENSIN II CAUSED VASOCONSTRICTION,

STIMULATES RELEASE OF ALDOSTERONE AND
ACTIVATES THE SYMPATHETIC NERVOUS
SYSTEM

ALDOSTERONE CAUSED SODIUM AND WATER

RETENTION
 NEURO-HORMONE SECRETION IN 10

RESPONSE TO HEART FAILURE

ENDOTHELINE CAUSED
VASOCONSTRICTION AND MYOCYTE
TOXICITY

ANTIDIURETIC HORMONE (VASOPRESSINE)

CAUSED VASOCONSTRICTION AND WATER
REABSORPTION

TUMOR NECROSIS FACTOR ALPHA(TNF )

CAUSED DIRECT MYOCITE TOXICITY
NEURO-HORMONE SECRETION IN 11

RESPONSE TO HEART FAILURE

INTERLEUKIN I (IL-1) AND IL-6
CAUSED MYOCYTE TOXICITY
NEURO- HORMONE (ATRIAL
NATRIURETIC PEPTIDE AND
BRAIN NATRIURETIC PEPTIDE)
CAUSED VASODILATATION,
EXCRETION OF SODIUM AND
ANTIPROLIFERATIVE EFFECT ON
MYOCYTES
 12

KLASIFIKASI FUNGSIONAL
GAGAL JANTUNG (NYHA)
1. TIMBUL GEJALA SESAK NAFAS ATAU
CAPAI PADA KEADAAN / AKTIFITAS
FISIK YANG BERAT
2. TIMBUL GEJALA PADA KEGIATAN
FISIK YANG SEDANG
3. TIMBUL GEJALA PADA KEGIATAN
FISIK YANG RINGAN
4. TIMBUL GEJALA PADA KEGIATAN
FISIK YANG SANGAT RINGAN DAN
PADA WAKTU ISTIRAHAT
 13

SEBAB GAGAL JANTUNG

PENYAKIT JANTUNG KORONER DAN
PASCA IMA
HIPERTENSI
PENYAKIT KATUB JANTUNG
KARDIOMIOPATI SERTA
MIOKARDITIS
PENYAKIT JANTUNG BAWAAN
PENYAKIT PARU KRONIS CPC
 Common ETIOLOGIES of HF 14
in OLDER Patients

1. CORONARY ARTERY DISEASE : AMI

2. HYPERTENSIVE HEART DISEASE
3. VALVULAR HEART DISEASE ex. AS,MS
4. CARDIOMYOPATHY : Restrictive, Dilated
Hyperthrophic
5. PERICARDIAL DISEASE
6. HIGH OUTPUT SYNDROME ex. ANEMIA,
i HYPERTHYROIDIS
I
7. AGE RELATED DIASTOLIC SYNDROME
 15
Common Comorbidities in OLDER Patients

1. RENAL DYSFUNCTION
2. CHRONIC LUNG DISEASE
3. COGNITIVE DYSFUNCTION:
DIETARY,MEDICATION ec
4. DEPRESSION, SOSIAL ISOLATION
5. URINARY INCONTINENCE
6. NUTRITIONAL DISORDER
7. POLYPHARMACY DRUG INTERACTION
i
I
 16

DIAGNOSA KLINIK
GAGAL JANTUNG
RIWAYAT KLINIK
PEMERIKSAAN FISIK
PEMERIKSAAN EKG
FOTO RONGEN TORAKS
EKOKARDIOGRAM
PEMERIKSAAN
RADIONUKLIR
PEMERIKSAAN INVASIF
 17

RIWAYAT KLINIK
PASCA INFARK MIOKARD
ANGINA PEKTORIS
HIPERTENSI
KELAINAN KATUP/ DEMAM REMATIK
PENYAKIT JANTUNG BAWAAN
PALPITASI
 18
SYMPTOMS OF CHF

THE CLASSIC SYMPTOM OF CHF IS

SHORTNESS OF BREATH
SPECIFIC COMMON SYMPTOM INCLUDE :
1. PAROXYSMAL NOCTURNAL DYSPNEA
(AWAKENING FROM SLEEP WITH SHORTNESS
OF BREATH).
2. ORTHOPNEA.
3. OR NEW ONSET DYSPNEA ON EXERTION.
i
IF HISTORY AND PHYSICAL EXAMINATION CLEARLY
I INDICATE A NON CARDIAC CAUSE FOR THESE SYMPTOMS(
EG. SEVERE PULMONARY DISEASE), THEN HEART
FAILURE EVALUATION IS NOT NECESSARY.
Continued
 19
SYMPTOMS OF CHF

YOUNG ADULT PATIENTS ELDERLY PATIENTS

1. DYSPNEA ON 1. DYSPNEA ON EXERTION

EXERTION 2. CONFUSION
2. DYSPNEA AT REST 3. AGITATION
3. ORTHOPNEA 4. DEPRESSION
4. PAROXISMAL 5. INSOMNIA
NOCTURNAL 6. WEAKNESS
DYSPNEA (PND) 7. ANOREXIA OR NAUSEA
5. FATIGUE 8. COUGH
6. ANKLE SWELLING
 20
PHYSICAL EXAMINATION

SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE

CLASIFIED BY AN CLASSIFIED BY A
EJECTION FRACTION NORMAL EJECTION
LESS THAN 40 % , IS FRACTION ( GREATER
CHARACTERIZED BY THAN OR EQUAL TO 50 %,
A REDUCED CARDIAC IN THE PRESENCE OF
PULMONARY
OUTPUT SECONDARY CONGESTION AND OTHER
TO DEPRESSED HF SYMPTOMS ( FOR EX. .
MYOCARDIAL DYSPNEA D EFFORT,PND ,
CONTRACTILITY. FATIGUE, AND
ORTHOPNEA) AND
FOURTH HEART SOUND.
 21

PEMERIKSAAN PENUNJANG
1. PEMERIKSAAN EKG
2. FOTO RONGEN THORAKS
3. HEMOGLOBIN
4. FUNGSI TIROID
5. FUNGSI GINJAL
6. FUNGSI HATI
7. PEMERIKSAAN EKOKARDIOGRAFI
 22

KRITERIA DIAGNOSIS
GAGAL JANTUNG
KRITERIA UTAMA GAGAL
JANTUNG
1. DISPNEA NOKTURNAL
PAROKSISMAL (PND)
2. KARDIOMEGALI
3. GALLOP (S-3)
4. PENINGKATAN TEKANAN VENA
5. REFLEKS HEPATOJUGULAR
6. RONKI
 23
KRITERIA DIAGNOSIS
GAGAL JANTUNG
KRITERIA TAMBAHAN
1. EDEMA PERGELANGAN KAKI
2. BATUK MALAM HARI
3. DISPNEA WAKTU AKTIFITAS
4. HEPATOMEGALI
5. EFUSI PLEURA
6. TAKIKARDIA
DIAGNOSIS DITETAPKAN ATAS ADANYA
2 KRITERIA UTAMA / 1 KRITERIA UTAMA + 2
KRITERIA TAMBAHAN
 JENIS GAGAL JANTUNG DAN
TERAPINYA
ETIOLOGI DAN PATOFISIOLOGI
DISFUNGSI SISTOLIK
GAGAL JANTUNG YANG SERING
BERHUBUNGAN DENGAN
KELAINAN FUNGSI SISTOLIK
DIMANA MIOKARDIUM GAGAL
BERKONTRAKSI SECARA
NORMAL, MENGAKIBATKAN
DILATASI VENTRIKEL KIRI
PENYEBAB TERSERING ADALAH
INFARK MIOKARD, HIPERTENSI
DAN KARDIOMIOPATI
24
PENATALAKSANAAN
PENTING UNTUK MENGENALI
SECARA DINI PASIEN INI KARENA
PROGNOSANYA DAPAT MEMBAIK.
TERAPI : BETA BLOCKER/
PENGHAMBAT BETA, ACE
INHIBITOR/ PENGHAMBAT ACE,
DIKOMBINASIKAN DENGAN
DIURETIKA, DIGITALIS ATAU
VASODILATOR
 JENIS GAGAL JANTUNG DAN
TERAPINYA
ETIOLOGI DAN PATOFISIOLOGI
DISFUNGSI DIASTOLIK
GAGAL JANTUNG YANG
DISEBABKAN OLEH KELAINAN
FUNGSI DIASTOLIK DIMANA
COMPLIANCE/ KEMAMPUAN
MIOKARDIUM MENURUN
MASALAH INI SERING TERJADI
PADA ORANG TUA
25
PENATALAKSANAAN
PENTING UNTUK MENGENALI
SECARA DINI PASIEN INI KARENA
PROGNOSANYA DAPAT MEMBAIK.
TERAPI : MENGATASI PENYAKIT
YANG MENDASARI/
MENGIKUTINYA SEPERTI
HIPERTENSI HARUS DIBERIKAN
OBAT UTK. MENGURANGI TENSI
DAN MENCEGAH HIPERTROFI
VENTRIKEL KIRI.
TANDA-2 KONGESTI /BENDUNGAN
DIKURANGI DENGAN DIURETIKA.
 JENIS GAGAL JANTUNG DAN
TERAPINYA
ETIOLOGI DAN PATOFISIOLOGI
KELAINAN KATUB
GAGAL JANTUNG YANG
DISEBABKAN OLEH KELAINAN
KATUB SERING DITEMUKAN PADA
GOL. SOSIAL EKONOMI RENDAH /
DIDAERAH DIMANA PENYAKIT
DEMAM REUMATIK BANYAK
DIJUMPAI.
STENOSIS AORTA KARENA
KALSIFIKASI MERUPAKAN
MASALAH YANG SERING TERJADI
PADA ORANG TUA.
26
PENATALAKSANAAN
PENTING UNTUK MENGENALI
SECARA DINI PASIEN INI KARENA
PROGNOSANYA DAPAT MEMBAIK.
TERAPI : MENGATASI PENYAKIT
YANG MENDASARI. PEMBEDAHAN
DAN PROSEDUR INTERVANSI
SEPERTI VALVULOPLASTI
/VALVULOTOMI MEMBERIKAN
HASIL YANG BAIK.
KELAINAN REGURGITASI KATUB
YANG TIDAK DAPAT DIOPERASI,
DAPAT DIBERIKAN DIURETIKA
DAN VASODILATOR
 JENIS GAGAL JANTUNG DAN
TERAPINYA
ETIOLOGI DAN PATOFISIOLOGI
KELAINAN JANTUNG BAWAAN
GAGAL JANTUNG YANG
DISEBABKAN OLEH KELAINAN
JANTUNG BAWAAN DAPAT
DITEMUKAN PADA MASA ANAK-
ANAK ATAU MASA DEWASA.
BEBERAPA TIPE SEPERTI DEFECT
ATRIUM MUNGKIN TIDAK
TERLIHAT SECARA DINI, DAN
BARU DIKETAHUI SETELAH
TERJADI GAGAL JANTUNG.
27
PENATALAKSANAAN
PENTING UNTUK MENGENALI
SECARA DINI PASIEN INI KARENA
PROGNOSANYA DAPAT MEMBAIK.
TERAPI : MENGATASI PENYAKIT
YANG MENDASARI. PEMBEDAHAN
DAN PROSEDUR INTERVENSI
SEPERTI KOREKSI/PENUTUPAN
DEFECT MEMBERIKAN HASIL
YANG BAIK.
KELAINAN BAWAAN YANG TIDAK
DAPAT DIOPERASI MIS. ASD +PH
DENGA MPA 70 mm HG, DAPAT
DIBERIKAN DIURETIKA DAN
VASODILATOR
 JENIS GAGAL JANTUNG DAN
TERAPINYA
ETIOLOGI DAN PATOFISIOLOGI
KELAINAN METABOLIK
KELAINAN TIROID, DEFISIENSI
TIAMIN (BERI-BERI), KADAR BESI
YANG BERLEBIH
(HEMOSIDEROSIS DAN
HEMOKROMATOSIS) SERTA
ANEMIA, MERUPAKAN JENIS
GAGAL JANTUNG YANG
DISEBABKAN OLEH KELAINAN
METABOLIK YANG DAPAT
MERUSAK MIOKARDIUM.
28
PENATALAKSANAAN
PENTING UNTUK MENGENALI
SECARA DINI PASIEN INI KARENA
PROGNOSANYA DAPAT MEMBAIK.
TERAPI : DISINI DIPERLUKAN
PERBAIKAN NUTRISI, FAKTOR
HORMONAL DAN METABOLIK
YANG DAPAT MENYEMBUHKAN
KELAINAN INI.
 29

TATA LAKSANA GAGAL

JANTUNG

TEGAKKAN DIAGNOSA GAGAL JANTUNG SERTA

SINGKIRKAN KEADAAN YANG MENYERUPAI
GAGAL JANTUNG
CARI PENYEBAB DASAR UNTUK DIATASI
DIMANA MUNGKIN
CARI FAKTOR PENCETUS UNTUK DIATASI
DIMANA MUNGKIN
PAHAMI PATOFISIOLOGI
BERIKAN PENGOBATAN / TINDAKAN YANG
SESUAI
 30

TATA LAKSANA GAGAL

JANTUNG

ATASI PENYEBAB DISFUNGSI VENTRIKEL

KIRI.
DISFUNGSI SISTOLIK
DISFUNGSI DIASTOLIK
KELAINAN KATUB
KELAINAN JANTUNG BAWAAN
KELAINAN METABOLIK
KELAINAN PERIKARDIUM/
ENDOKARDIUM.
 31

TATA LAKSANA GAGAL

JANTUNG
TERAPI NON FARMAKOLOGIK :
DIET RENDAH GARAM
MENGURANGI BERAT BADAN
MENGHINDARI FAT YANG BERLEBIHAN
MENGURANGI STRESS PSIKIS
MENGHINDARI ROKOK
OLAH RAGA TERATUR
OPERATIF
TERAPI FARMAKOLOGIK
DIURETIKA
PENGHAMBAT ACE
PENGHAMBAT BETA
DIGITALIS
VASODILATOR
 3

USUAL TREATMENT TODAY

AIMS OF HEART FAILURE MANAGEMENT
TO IMPROVE SYMPTOMS
DIURETICS
DIGOXIN
ACE INHIBITORS
TO IMPROVE SURVIVAL
ACE INHIBITORS
BLOCKERS
ORAL NITRATES PLUS HYDRALAZINE
SPIRONOLACTONE
vies et al. BMJ 2000;320:428-431
 4
HF: MORTALITY REMAINS
HIGH
ACEI
RISK REDUCTION 35% (MORTALITY AND HOSPITALIZATIONS)1

BLOCKERS
RISK REDUCTION 38% (MORTALITY AND HOSPITALIZATIONS)2

ORAL NITRATES AND HYDRALAZINE

BENEFIT VS. PLACEBO; INFERIOR TO ENALAPRIL (MORTALITY)

1 Davies et al. BMJ 2000;320:428-431 (meta analysis: 32 trials, n=7105) 2 Gibbs et al. BMJ
2000;320:495-498 (meta analysis: 18 trials, n=3023)
9
 10
BLOCKADE OF RAS
LOCAL ANG II SYNTHESIS IS INDEPENDENT OF ACE

ANGIOTENSINOGEN
(LIVER)

RENIN CHYMA
INHIBITOR
ANGIOTENSIN I
BRADYKININ
ACE
PEPTIDES INHIBITOR
ANGIOTENSIN II
VALSARTAN
AT1 RECEPTOR BLOCKER

AT1 AT2
ROLE OF AT1 AND AT2 11

RECEPTORS

ANGIOTENSIN II

AT1 AT2

VASOCONSTRICTION VASODILATION
VASCULAR ANTIPROLIFER
PROLIFERATION ATION
ALDOSTERONE SECRETION APOPTOSIS
CARDIAC MYOCYTE
PROLIFERATION
INCREASED SYMPATHETIC
TONE
22
 25

Treatment Strategies for Heart Failure

ALDO PIETRO MAGGIOTTI

Director of the Reseach Center of the Italian Association
Of Hospital
Cardiologist (ANMCO), Pirenze, ITALY
Which patients with HF are suitable 26

for Blocker treatment ?

Patients with symptomatic HF of any cause, EF 40 %, in
NYHA class II/III, clinically stable, already on treatment
wite ACE inh., diuretic, and digitalis

Which patients with HF are more

likely to benefits ?
1. Patients with history of hypertension
2. Heart rate > 90 beat/ mnt.
 Which patients with HF are less likely to
benefits ? 27

Patients with severe biventricular dysfunction

SBP < 100 mmHg

Which patients with HF are

uncertainties still exist ?
1. NYHA class IV, elderly ptns (> 75 years)
2. Asymptomatic LV dysfunction
3. HF by valvular disease or diastolic dysfunction
4. Comorbidities (DM, COPD, renal disease,
peripheral vasculopathy)
 28

Blocker summary

1. At one time contraindicated in the treatment of heart

failure
2. The increased activation of the adrenergic system
induced by heart failure, provides the rationale for the
use of Blockers in heart failure
3. While the effect of Blockers on exercise capacity,
quality of life, and the neurohormonal profile are still
controversial, the LV shape and function, and the need
for hospitalisation are improve by Blockers in heart
failure

Continued
 29

Blocker summary

4. On the basis of all available evidence, all patients with

chronic, stable, mild to moderate, symptomatic HF
(NYHA CLASS II/III), and with the depressed LV
function should be treated with Blockers
5. The studies showed that Blockers significantly reduce
total and sudden mortality in HF patients
6. Blockers tretment should be started in stable patients with
a very low initial dosage and then uptitrated in the maximal
tolerated

Continued
 30

Blocker summary

7. Despite the impressive results in term of morbidity and

martality reduction, and the increasing availability of
Blockers, these data showing only a minority of patients
being treated At one time contraindicated in the
treatment of heart failure
 31

DIURETICS
DIURETICS SHOULD BE USED FOR ALL PATIENTS
WITH SYMPTOMS WHO HAVE EVIDENCE FOR
FLUID RETENTION
SHOUD NOT BE USED ALONE, EVEN IF THE
SYMPTOMS OF HF ARE WELL CONTROLLED.
ALTHOUGH THEY PRODUCED RAPID
SYMPTOMATIC RELIEF, THEY CANNOT
MAINTAIN CLINICAL STABILITY IN LONG- TERM,
SO THEYFORE GENERALLY BE ADMINISTERED
WITH ACE INH/ BLOCKERS
 32

ANTIARRHYTMIC DRUG
In addition to progressive pump dysfunction, 25
70 % of all deaths patients with HF, caused by
ventricel arrhytmia
Of the available antiarrhytmia, amiodarone is
the only one which seem to be potentially
beneficial in patients with HF, suppressing atrial
and ventricular arrhytmia
 NITRATES 33

The use of nitrates in HF is most commonly

,in patients who cannot tolerate ACE
inhibitors due to hypotension or renal
insufficiency .

Ca. antagonists
Ca. Antagonists are not recommended for use
in HFdue to their association with an increased
risk of cardiovascular event
 34

THE OTHERS MANAGEMENT

For the patients who have survived cardiac

arrest the preferred treatment may be
implantable- defibrillator (ICD)
Sceletal myoblast transfer
Education for managing lifestyle modification
and optimizing of medical therapy
 5 35
535

CYTOKINES
CYTOKINES ARE BEING IMPLICATED
FOR PATHOGENIC ROLE IN HF
PROGRESSION
Cytokines antagonist : IL-6 antagonist and
TNF antagonist currently under
investigation for HF treatment
 36

CONCLUSIONS
THE PHARMACOLOGICAL TREATMENT OF
HF HAS BECOME COMBINED SYMPTOMATIC
- PREVENTIVE MANAGEMENT STATEGY
EARLY RECOGNATION AND PREVENTION
THERAPIES COMBINED WITH LIFESTYLE
MODIFICATION, ARE ESSENTIAL
 38

CONCLUSIONS
APPLY THE GUIDELINES TO EVERY
PATIENTS AS INDIVIDUAL, ADJUSTING THE
TREATMENT REGIMEN AS INDICATED BY A
PATIENTS S CONDITION AND WHAT THE
GROWING MEDICAL EVIDENCE BASE DEEMS
APPROPRIATE
THERE ARE MANY APPROACHS WERE
DESCRIBED AS THE RECENT MANAGEMENT
THANK YOU
 A PREVALENT CONDITION
PREVALENCE OF HF (PER 1000 POPULATION)

Age (years) Men Women

50-59 8 8

80-89 66 79

All ages 7.4 7.7

Framingham Heart Study: Ho et al. 1993 J Am Coll Cardiol;22:6-13

 A GROWING BURDEN
DEATHS FROM HF 1979-1997 (USA)
50000

40000
HF deaths

30000

20000

10000

0
1979 1985 1991 1997

ital Statistics of the United States, National Center for Health Statistics
 HF: MORTALITY REMAINS
HIGH
ACEI
RISK REDUCTION 35% (MORTALITY AND
HOSPITALIZATIONS)1

BLOCKERS
RISK REDUCTION 38% (MORTALITY AND
HOSPITALIZATIONS)2

ORAL NITRATES AND HYDRALAZINE

BENEFIT VS. PLACEBO; INFERIOR TO
ENALAPRIL (MORTALITY)
HOWEVER: 4-YEAR MORTALITY REMAINS ~40%

MJ 2000;320:428-431 (metanalysis: 32 trials, n=7105) 2 Gibbs et al. BMJ 2000;320:495-498 (metanalysis: 18 tria
USUAL TREATMENT TODAY
AIMS OF HEART FAILURE MANAGEMENT

TO IMPROVE SYMPTOMS
DIURETICS
DIGOXIN
ACE INHIBITORS
TO IMPROVE SURVIVAL
ACE INHIBITORS
BLOCKERS
ORAL NITRATES PLUS HYDRALAZINE
SPIRONOLACTONE
Davies et al. BMJ 2000;320:428-431
 AN ECONOMIC BURDEN
ANNUAL COST OF HF ESTIMATED TO BE
$22.5 BILLION (USA)

Healthcare
Drugs
Indirect Costs providers Home health/Other
medical durables
2.2 1.5 1.1 2.2

15.5

Hospital/Nursing home
Costs in billions of dollars

American Heart Association, 2000 Heart and Stroke Statistical Update

 SEKIAN
TERIMA KASIH