1

HEART FAILURE
(GAGAL JANTUNG)
2
I. DEFINISI HEART FAILURE
o Heart failure (HF) is not a diagnosis but a clinical syndrome of
various etiology with a poor prognosis.

o Pada HF, penting pertama kali dibedakan secara klinis antara :

 Left and right HF or global HF (biventricular HF)
 Compensated or decompensated HF
 Acute and chronic HF (chronic HF paling sering ditemukan)

 Systolic HF dan diastolic HF tidak secara langsung bisa

dibedakan secara klinis tanpa pemeriksaan khusus.

o Definisi WHO : Impaired physical exercise as a result of proven

impairment of cardiac function

o Definisi ESC 2008 dan 2013 : HF is abnormality of cardiac

structure or function leading to failure of the heart to deliver
oxygen at a rate commensurate with the requirements of the
metabolising tissue, despite normal filling pressures.
3 DEFINITION OF HEART FAILURE (HF) – ESC 2013
HF is a clinical syndrome in which patients
have the following features:

 Symptoms typical of HF :
(breathlessness at rest or on exercise, fatigue,
tiredness, ankle swelling).

 Signs typical of HF :
(tachycardia, tachypnea, pulmonary rales, pleural effusion,
raised jugular venous pressure, peripheral edema,
hepatomegaly).

 Objective evidence of a structural or functional abnormality

of the heart at rest :
(cardiomegaly, S3, cardiac murmur, abnormality on the
echocardiogram, raised natriuretic peptide concentration).
 FAKTOR FAKTOR YANG MENENTUKAN STROKE VOLUME
4 DAN CARDIAC OUTPUT (FUNGSI VENTRIKEL KIRI)
Fungsi ventrikel kiri didasarkan pada fraksi ejeksi (EF)
5 DEFINITION OF HEART FAILURE WITH reduced EF,
mid-range EF and preserved EF (ESC 2016)
Type of HF HFrEF HFm-rEF HFpEF

1 Symptoms ± Symptoms ± Signs Symptoms ± Signs

Signs

2 LVEF <40% LVEF 40-49% LVEF ≥50%

3 -- 1. Elevated levels 1. Elevated levels

C of natriuretic of natriuretic
R
peptides (BNP) peptides (BNP)
I
T
2. At least one 2. At least one
E additional criterion: additional criterion :
R
I
a. relevant structural a. relevant structural
A
heart disease heart disease
(LVH and/or LAE) (LVH and/or LAE)
b. diastolic dysfunction b. diastolic dysfunction
6
II. KLASSIFIKASI GAGAL JANTUNG
1. According to the affected ventricle : 2. According to time course :
 Left HF  Acute HF ;
 Right HF - AHF e.g. as a result of MCI
 Global HF (biventricular failure) - AHF e.g. as a result of PE
 Chronic HF.

3. According to the degree of compensation : 4. According to the cardiac output (CO):

 Compensated HF;  Low-output HF
- The resting CO is still normal as a result of  High-output HF
physiological compensatory mechanism e.g.
stimulation SNS +cathecolamine release, 5. According to symptoms :
stimulation of RAAS  Forward failure :
 Decompensated HF; - Fall in CO if BP is inadequate,
- Reduced CO with symptoms such as dyspnea with consequent decrease
and reduced performance despite full peripheral perfusion.
implementation of compensatory mechanism  Backward failure :
- LV : increase in LVEDP with left
6. According to the disordered ventricular function : HF, pulmonary congestion/
 Systolic HF pulmonary edema.
 Diastolic HF : -relaxation disorder,
-compliance disorder 7. According to exercise tolerance :
 Exercise-induced HF
8. According to clinical features :  HF at rest
 Symptomatic HF
 Asymptomatic left-ventricular dysfunction 9. According to functional class (NYHA) and
Structural damage (ACC/AHA).
7
NYHA Functional Classification of HF
Severity based on symptoms and physical activity

Class I No limitation of physical activity. Ordinary physical

activity does not cause undue fatigue, palpitation or
dyspnea.
Class II Slight limitation of physical activity. Comfortable at rest,
but ordinary physical activity results in fatigue,
palpitation, or dyspnea.
Class III Marked limitation of physical activity. Comfortable at
rest, but less than ordinary activity results in fatigue,
palpitation or dyspnea.
Class IV Unable to carry on any physical activity without
discomfort. Symptoms at rest. If any physical activity is
undertaken, discomfort is increased.
8 ACC/AHA Stages of HF
Based on structure and damage to heart muscle

Stage A At high risk for developing HF. No identified

structural or functional abnormality; No signs or
symptoms.
Stage B Developed structural heart disease that is strongly
associated with the development of HF, but
without signs or symptoms.
Stage C Symptomatic HF associated with underlying
structural heart disease.

Stage D Advanced structural heart disease and marked

symptoms of HF at rest despite maximal medical
therapy.
9 DESKRIPSI GAGAL JANTUNG (CHF)
BERDASARKAN KLASSIFIKASI ACC/AHA
STAGE DESCRIPTION

A
High Risk For Hypertension, Diabetes Mellitus, CAD,
Developing HF Family History of Cardiomyopathy

B Previous MI, LV Dysfunction,

Asymptomatic Valvular Heart Disease
Heart Failure

C Structural Heart Disease, Dyspnea and

Symptomatic Fatigue, Impaired Exercise Tolerance
Heart Failure

D Marked Symptoms at Rest Despite

Maximal Medical Therapy
Refractory End-stage HF
10
11 III. AETIOLOGY / PREDISPOSING CAUSES
OF HEART FAILURE

• Hypertension
• Diabetes Mellitus
• Dyslipidemia
• Valvular heart disease
• Coronary artery disease
• Cardiomyopathy
• Rheumatic fever
• Mediastinal radiation
• Sleep apnea disorders
• Exposure to cardiotoxin
agents
• Alcohol abuse
• Smoking
• Collagen vascular
disease
• Thyroid disorder
• Pheochromocytoma
• Old age
• Metabolic syndrome
 IV. FAKTOR APA SAJA YANG MENENTUKAN
12 FUNGSI VENTRIKEL KIRI?
(Cardiac output (CO) is determined by four factors)
13 V. PATHOPHYSIOLOGY OF HEART FAILURE

Relationship between end-diastolic volume and stroke

volume in normal and failing myocardium
14

Pathophysiology of Heart Failure

15

Systolic HF (HFrEF)

Diastolic HF (HFpEF)
 16
Patterns of ventricular remodeling are
different for HFrEF and HFpEF

Left ventricle
normal
HFrEF HFpEF
Volume Pressure
HFrEF – a condition HFpEF – a condition
overload overload
of volume overload of pressure overload
• characterized by Increased Increased • characterized by
diastolic pressure systolic pressure
eccentric hypertrophy concentric
hypertrophic growth
• results in thinning of Increased Increased
the LV walls, diastolic wall stress systolic wall stress • results in normal
decreased systolic − sized LV cavity with
Series addition of new Parallel addition
function and sarcomeres of new myofibrils − thickened walls and
enlarged LV volume preserved systolic
Chamber Wall function
enlargement thickening

Eccentric Concentric
hypertrophy hypertrophy
Left ventricle Left ventricle
volume pressure
overload overload
17
Different co-morbidities and pathophysiological
processes can lead to different types of heart failure
A range of risk factors and co-morbidities contribute to the development of HF

Age
Smoking Myocardial
Obesity infarction Systolic
Hypertension dysfunction
HFrEF
Coronary HFpEF
artery disease Diastolic
Diabetes LV dysfunction
Dyslipidemia hypertrophy

Normal LV structure Subclinical

and function LV remodeling LV dysfunction Clinical HF
Years Years/months
 18

From myocardial infarction (MI) to HF:

Ventricular Remodeling after MI

Fibrous scar Myocyte hypertrophy

Acute
infarction
Increased
interstitial
collagen

Infarct zone thinning Spherical ventricular

and elongation dilation

Konstam MA, et al. J Am Coll Cardiol Img 2011;4:98–108

19
DIAGNOSTIK GAGAL JANTUNG

SUSPECTED HEART FAILURE

Dyspnoea
Fatigue
Oedema

Evidence of underlying cardiac disease

1. Patient history
2. Clinical examination
3. Special examination
(foremost echocardiography)

Confirmation of heart failure

Aetiology
NYHA severity index
Ejection fraction
Systolic/diastolic dysfunction
Complicating arrhythmias?
Optimal treatment strategy
20 GAMBARAN KLINIS
GAGAL JANTUNG
SYMPTOMS
 Exertional dyspnea.
 Orthopnea.
 PND (Paroxysmal
nocturnal dyspnea.
 Fatigue and weakness.
 Nocturnal dry cough.
 Productive of pink frothy
sputum.
 Epigastric discomfort.
 Anorexia.
SIGNS
 Short of breath and cyanosis.
 Cardiac cachexia.
 Pulse may be rapid, weak.
pulsus alternans.
 BP may be normal, low in forward
failure or high in hypertensive pts.
 JVP is elevated in CHF and pure
Right-sided failure.
 Carotid pulse may be abN.
 Apex beat may be displaced
downward and laterally.
 Heart sounds : S3 or S4.
 Murmurs.
 Peripheral edema.
 Crepitations bilateral.
 Pleural effusions.
 Expiratory wheeze
 Hepatomegaly and ascites.
21 COMMON CLINICAL MANIFESTATIONS OF HF
DOMINANT
CLINICAL SYMPTOMS SIGNS
FEATURES
Peripheral edema/ Breathlessness, tiredness, Peripheral edema, raised JVP,
congestion fatigue, anorexia pulmonary edema,
hepatomegaly, ascites, fluid
overload, cachexia
Pulmonary edema Severe brathlessness at Crackles or rales over lungs,
rest effusion, tachycardia, tachypnea
Cardiogenic shock Confusion, weakness, Poor peripheral perfusion,
(LOS) cold periphery systolic BP <90 mmHg, anuria
or oliguria
High BP Breathlessness Usually raised BP, LVH, and
(Hypertensive HF) preserved EF
Right heart failure Breathlessness, fatigue Evidence of RV dysfunction,
raised JVP, peripheral edema,
hepatomegaly, gut congestion
22 COMMON CHEST X-RAY ABNORMALITIES IN HF

ABNORMALITIES CAUSES
Cardiomegaly Dilated LV, RV, atria. Pericardial effusion
Ventricular hypertrophy Hypertension, aortic stenosis, Hypertrophic
cardiomyopathy
Normal pulmonary findings Pulmonary congestion unlikely
Pulmonary venous Elevated LV filling pressure
congestion
Interstitial edema Elevated LV filling pressure
Pleural effusions Elevated filling pressure, HF likely if bilateral,
Pulmonary infection, surgery or malignant effusion
Kerley B-lines Increased lymphatic pressure
Hyperlucent lung fields Emphysema or pulmonary embolism
Pulmonary infection Pneumonia may be secondary to pulmonary
congestion
Pulmonary infiltration Systemic disease
23
KEADAAN YANG DIHUBUNGKAN DENGAN
PROGNOSIS JELEK PADA GAGAL JANTUNG

1. DEMOGRAPHICS: 2. CLINICAL:
- Advanced aged* - Hypotension*
- Ischemic etiology* - NYHA class III_IV*
- Resuscitated- - Recent HF-
sudden death* hospitalization*
- Poor compliance --Tachycardia
- Renal dysfunction - Pulmonary rales
- Diabetes - Aortic stenosis
- Anemia - Low BMI
- COPD - Sleep related
- Depression breathing disorders

* = powerful predictors
24

3. ELECTROPHYSIOLOGICAL:
- Tachycardia 4. FUNCTIONAL/
- Q-waves EXERTIONAL:
- Wide QRS* - Reduced work
- LVH - Low peak VO2*
- Complex ventricular- - Poor 6 minutes-
arrhythmias* walk distance
- Low HR variability - High VE/VCO2-
- T-wave alternans slope
- Atrial fibrillation (AF) - Periodic breathing

* = powerful predictors
25

5. LABORATORY: 6. IMAGING:
- Marked elevation of BNP/ - Low LVEF*
NT-pro BNP* - Increased LV vol.
- Hyponatremia* - Low cardiac index
- Elevated troponin* - High LV filling-
- Elevated biomarkers, pressure
neurohumoral activation* - Restrictive mitral-
- Elevated creatinine/ filling pattern
BUN - Pulmonary htn.
- Elevated bilirubin - Impaired RV -
- Anemia function
- Elevated uric acid

* = powerful predictors
 EVOLUSI STADIUM KLINIS GAGAL JANTUNG
26
27

PENANGGULANGAN GAGAL JANTUNG

SECARA UMUM
 28 Stages in the evolution of HF
and recommended therapy by stage

Stage A Stage B Stage C Stage D

Pts with : Pts with : Pts with :
Pts who have
•Hypertension • Previous MI • Struct. HD marked
• CAD Struct. • LV systolic Develop Refract. symptoms at rest
• DM dysfunction • Shortness of
Heart Symp.of despite maximal
breath and Symp.of
•Cardiotoxins • Asymptomatic medical therapy.
Disease HF fatigue, reduce HF at rest
• FHx CM Valvular disease exercise tolerance

THERAPY THERAPY THERAPY THERAPY

• Treat Hypertension • All measures • All measures under • All measures under
 Stop smoking under stage A stage A stage A,B and C
• Treat lipid • ACE inhibitor • Drugs for routine use: • Mechanical assist
disorders • Beta-blockers • diuretic device
• Encourage regular • ACE inhibitor • Heart transplantation
exercise • Beta-blockers • Continuous IV
• Stop alcohol • digitalis inotrphic infusions for
& drug use palliation
• ACE inhibition
29 ALGORITMA TERAPI FARMAKOLOGIS GAGAL JANTUNG
AKIBAT DISFUNGSI SISTOLIK VENTRIKEL KIRI

Diagnosis
Dokter umum

Mulai ACEI, lalu Atau ARB bila

Tambahkan diuretik penderita intoleran
dititrasi
 Diperlukan untuk dengan ACEI
mengontrol gejala
kongesti dan retensi
cairan Tambahkan BB
dan dititrasi
Tambahkan digoxin
 Bila penderita tetap
simptomatik
Tambahkan
meskipun telah diberi
spironolakton bila
diuretik, ACEI/ARB,
penderita tetap
BB atau penderita
simptomatik sedang-
dengan AF ----
berat walaupun telah
digunakan sebagai
diterapi optimal
terapi awal

Minta advis ahli untuk

Dokter ahli tindakan lanjut
30
LEVEL OF EVIDENCE

Level A: Well- conducted, large and reliable RCTs (one or

more) or their overview with clear results.

Level B: RCTs (one or more) or their overview with significant

limitations.

Level C:1) High quality and persuasive cohort studies, case

control studies or case series.
2) Lower quality evidence from non -randomized
studies including opinions of experts.
31
TERAPI DIGOXIN PADA GAGAL JANTUNG (CHF)
Proven indication: always acceptable Level A
CHF dengan irama sinus yang sudah diterapi maksimal:
memperbaiki gejala, memperbaiki kapasitas latihan dan
menurunkan kekerapan hospitalisasi.

Acceptable indication but of uncertain efficacy and may be

controversial Level B
CHF dengan fibrilasi atrium dan denyut jantung terkontrol.

Acceptable indication but of uncertain efficacy and may be

controversial Level A
Gagal jantung simptomatik akibat disfungsi diastolik.

Not proven: potentially harmful (contraindicated) Level A

Bradikardia dan blok atrioventrikular.
Aritmia ventrikel yang signifikan.
Disfungsi ginjal.
Gangguan elektrolit terutama hipokalemia
32

TERAPI DIURETIK PADA GAGAL JANTUNG

Proven indication: always acceptable Level A

Memperbaiki gejala pada kasus bendungan(kongesti).
Memperbaiki kapasitas latihan.

Acceptable indication but of uncertain efficacy and may be controversial

Level B
Terapi jangka panjang bersama sama dengan obat gagal
jantung lainnya, seperti ACE inhibitors, vasodilators dan beta-
blockers.

Not proven: potentially harmful (contraindicated) Level C

Gagal jantung tanpa kongesti atau edema tungkai dengan
hipokalemia serta hiperurisemia yang tidak dikoreksi.
33
TERAPI ANTAGONIS ALDOSTERONE PADA CHF
(SPIRONOLAKTON)

Proven indication: always acceptable Level A

Memperbaiki kelangsungan hidup pada CHF berat.
Menurunkan morbiditas pada CHF berat.
Memperbaiki kelangsungan hidup dengan disfungsi ventrikel
kiri atau gagal jantung segera pasca infark miokard.

Acceptable indication but of uncertain efficacy and may be

controversial Level B
Menurunkan morbiditas pada gagal jantung ringan-sedang.
Menurunkan mortalitas pada gagal jantung ringan-sedang.
Monitor yang ketat pada penderita dengan risiko tinggi
terjadi hiperkalemia termasuk DM, ACE0inhibitor dosis
tinggi, dan gagal ginjal.
34 TERAPI VASODILATOR PADA GAGAL JANTUNG

Proven indication: always acceptable Level A

Menurunkan afterload dengan cepat pada kasus gagal jantung
akut.
Kombinasi hydralazine+ISDN dapat digunakan sebagai terapi
jangka panjang pada penderita yang tidak toleran terhadap
ACE-inhibitors or ARB.

Acceptable indication but of uncertain efficacy and may be

controversial Level B
Calcium channel blockers generasi ketiga bisa digunakan
untuk terapi simptomatik yang disertai gejala angina pektoris
atau hipertensi.

Not proven: potentially harmful (contraindicated) Level C

Vasodilators lain selain hydralazine-ISDN dan CCB generasi
ke-3 bisa meningkatkan mortalitas selama terapi jangka
panjang.
Terapi penderita yang disertai stenois aorta dan stenosis
mitral yang signifikan.
35 TERAPI ACE-INHIBITOR PADA GAGAL JANTUNG

Proven indication: always acceptable Level A

Gagal jantung kronis simptomatik dan adanya disfungsi sistolik
miokard.
memperbaiki kelangsungan hidup dan menurunkan morbiditas.
Gejala berkurang dan kapasitas latihan diperbaiki.
Pasca IMA yang disertai gejala klinis gagal jantung (EF <40%).
Mencegah kejadian kardiovaskular termasuk gagal jantung pada
penderita aterosklerosis, penderita DM dan adanya faktor risiko
lainnya.

Acceptable indication but of uncertain efficacy and may be controversial

Level A
Gagal jantung akibat disfungsi diastolik.

Not proven: potentially harmful (contraindicated) Level C

Terapi pada penderita dengan stenosis aorta atau stenosis
mitral yang signifikan.
Terapi pada penderita hipotensi (TDS <80 mmHg)
Terapi pada penderita dengan disfungsi ginjal
36
TERAPI INOTROPIK PADA GAGAL JANTUNG

Proven indication: always acceptable

Terapi jangka pendek memperbaiki gejala pada penderita
gagal jantung berat. Level A
Sebagai jembatan persiapan tindakan bedah yang definitif,
seperti transplantasi jantung. Level C

Acceptable indication but of uncertain efficacy and may be

controversial Level B
Terapi jangka panjang pada penderita dengan gagal jantung
kronis yang sudah refrakter dengan terapi medis yang
maksimal.

Not proven: potentially harmful (contraindicated) Level B

Terapi jangka pendek intermitten pada gagal jantung kronis.
37
TERAPI BETA-BLOCKER PADA CHF
Proven indication: always acceptable Level A
Memperbaiki kelangsungan hidup jangka panjang pada
penderita gagal jantung ringan-berat.
Memperbaiki fungsi jantung dan mengurangi gejala pada
penderita gagal jantung kronis simptomatik, yang telah
memperoleh terapi konvensional dengan ACE-inhibitor (atau ARB),
diuretika, atau digitalis.
Memperbaiki outcomes penderita dengan IMA dan disfungsi
ventrikel kiri dengan atau tanpa gagal jantung simptomatik.
Terapi simptomatik penderita dengan gagal jantung yang tidak
toleran dengan obat ACE-inhibitor.

Acceptable indication but of uncertain efficacy and may be

controversial Level B
Gagal jantung simptomatik akibat disfungsi diastolik.

Not proven: potentially harmful (contraindicated) Level C

Acute decompensated heart failure (ADHF) dengan hipotensi
dan/atau bradikardia.
38

TERAPI ANTI-ARITMIK PADA GAGAL JANTUNG

Proven indication: always acceptable Level A

Terapi dengan Beta-adrenergic blockade (BB) pada penderita
euvolemik dengan gagal jantung kronis.

Not proven: potentially harmful (contraindicated) Level A

Terapi anti-aritmik klas I pada penderita gagal jantung
dengan aritmia ventrikel asimptomatik.
Terapi anti-aritmik klas III pada penderita gagal jantung
dengan aritmia ventrikel asimptomatik atau bila digunakan
sebagai prevensi primer terhadap mati mendadak (sudden
cardiac death).
 REKOMENDASI TERAPI GAGAL JANTUNG
39
Tujuan terapi Jenis obat Level of evidence
 Mengurangi gejala kongesti, Diuretika Level A
meningkatkan kapasitas latihan

 Menurunkan mortalitas pada gagal ACE-inhibitor Level A

jantung ringan-sedang Beta-blocker Level A

 Menurunkan mortalitas pada gagal ACE-inhibitor Level A

jantung berat Beta-blocker Level A
Spironolakton Level A
 Menurunkan mortalitas pada penderita
yang tidak toleran dengan ACE-inhibitor ARB (AIIRA) Level A

 Menurunkan morbiditas dan gejala pada ACEinhibitor/ARB Level A

gagal jantung ringan-berat Beta-blocker Level A
Spironolakton Level A
Digoxin Level A
 Perbaikan gejala jangka pendek pada Inotropik non- Level B
penderita gagal jantung berat digitalis
 Tindakan bedah pada gagal jantung tahap Transplantasi Level B
akhir jantung
 Tindakan antara persiapan transplantasi LV assist device Level B
40

ACUTE HEART FAILURE (AHF)

DEFINITION :

• AHF is defined as a rapid onset or change in the signs

and symptoms of HF, resulting in the need of urgent
therapy.

• It may present as new HF or worsening HF in the presence

of chronic HF.

• It may be associated with worsening symptoms or signs or

as a medical emergency such as
Acute Pulmonary Edema.
41
42

BNP = 600
BNP = 100-400

BNP = 400-1000 BNP = >1000

43

The patients with AHF will usually present

in one of 6 clinical categories

1. Worsening or decompensated Chronic HF :

2. Pulmonary edema.
3. Hypertensive HF.
4. Cardiogenic shock.
5. Isolated right HF.
6. Acute Coronary Syndrome and HF
44
CAUSES AND PRECIPITATING FACTORS OF AHF

• ACS, Mechanical complications of AMI, RV Infarction.

• Valve stenosis, Valvular regurgitation, Endocarditis, Aortic dissection.

• Postpartum cardiomyopathy, Acute myocarditis.

• Hypertension, Acute arrhythmias.

• Septicemia, Thyrotoxicosis, Anemia, Shunts, Tamponade, Pulmonary

embolism.

• Decompensation of preexisting Chronic HF: Lack of adherence,

volume overload, Infections (pneumonia), Cerebrovascular insult,
Surgery, Renal dysfunction, Asthma, Drug abuse, Alcohol abuse.
45
GOALS OF TREATMENT IN AHF
 Immediate (ED/ICU/CCU):
 Improve symptoms
 Restore oxygenation
 Improve organ perfusion and hemodynamic
 Limit cardiac/renal damage
 Minimize ICU length of stay

 Intermediate (In hospital):

 Stabilize patients and optimize treatment strategy
 Initiate appropriate (life-saving) pharmacological therapy
 Consider device therapy in appropriate patients
 Minimize hospital length of stay

 Long-term and predischarge management:

 Plan follow-up strategy
 Educate and initiate appropriate lifestyle adjustments
 Provide adequate secondary prophylaxis
 Prevent early readmission
 Improve quality of life and survival
46 The following management options are considered
appropriate in patients with AHF

 Oxygen : it is recommended to administer O2 as early as possible

in hypoxemic patients to achieve an arterial O2 saturation ≥95%.

 Non-invasive ventilation (NIV) : (with a sealed face-mask)

NIV with positive end-expiratory pressure (PEEP) should be considered
as early as possible in every patients with Acute cardiogenic pulmonary
edema and hypertensive acute HF.

 Morphine and its analogues in AHF : Morphine relieves dyspnea and

other symptoms in patients with AHF and may be improve cooperation
for the application of NIV (dose: 2,5-5 mg IV line).

 Loop diuretics : Excessive treatment may lead to hypovolemia and

hyponatremia.
47
The following management options…………
 Vasodilators : Are recommended at an early stage for HF patients
without symptomatic hypotension .
 Vasodilators relieve pulmonary congestion usually without compromising
stroke volume or increasing oxygen demand in AHF, particularly in
patients with ACS.
 Hypotension (SBP <90 mmHg) should be avoided, especially in patients
with renal dysfunction

 Inotropic agents : should be considered in patients with low output state,

in the presence of signs of hypoperfusion or congestion despite the use of
vaso dilators and/or diuretics.
 Dopamine, Dobutamine, Milrinone, Enoximone, Levosimendan.

 Vasopressors : Norepinephrine are not recommended as first-line agent

and are only indicated in cardiogenic shock when the combination of an
inotropic agent and fluid challenge fails to restore adequate BP.

 Cardiac glycoside: In AHF, cardiac glycoside produce a small increase

in cardiac output and reduction of filling pressure . It may be useful to
slow ventricular rate in rapid AF
 PROGNOSIS
Heart failure mortality statistics
All heart failure patients, even those who are considered asymptomatic (NYHA class I)
or mildly symptomatic (NYHA class II), are at high risk of dying

IN A CLINICAL TRIAL WITH MEDIAN FOLLOW-UP OF ~3YEARS

34 %
OF NYHA CLASS I AND II
42 %
OF NYHA CLASS III AND IV
PATIENTS DIED PATIENTS DIED

Prognosis : The 5-year mortality (all 4 NYHA classes together) is

50%. This the same as the prognosis of a malignancy.
 NYHA II : 1-year mortality 10-20%
 NYHA III : 1-year mortality 30-40%
 NYHA IV : 1-year mortality 40-50%
TERIMA
KASIH