Case Report

CONGESTIVE HEART FAILURE

ET CAUSA
RHEUMATIC HEART DISEASE

SUPERVISOR

: dr. Sri Sofyani, SpA (K)

PRESENTATOR

: Samuel Edhi Suranta

Theresa Shintauli

110100112
110100242

PEDIATRIC DEPARTMENT
MEDICAL FACULTY OF NORTH SUMATRA UNIVERSITY
H. ADAM MALIK GENERAL HOSPITAL
MEDAN
2015

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ACKNOWLEDGMENTS

We are greatly indebted to the Almighty One for giving us blessing to finish this case
report, Chronic Heart Failure (CHF) et causa Rheumatic Heart Disease (RHD).This
case report is a requirement to complete the clinical assistance program in Department of
Child Health in H. Adam Malik General Hospital, Medical Faculty of North Sumatra
University.
We are also indebted to our supervisor and adviser, dr. Sri Sofyani, SpA (K) for the
time spent to give us guidances, comments, and suggestions. We are grateful because without
her guidance this case report wouldnt have taken its present shape.
This case report has gone through series of developments and corrections. There were
critical but constructive comments and relevants suggestions from the reviewers. Hopefully
the content will be useful for everyone in the future.

Medan, 26 November 2015

Presentators

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TABLE OF CONTENTS

ACKNOWLEDMENTS..................................................................................................ii
TABLE OF CONTENTS...............................................................................................iii
CHAPTER 1 INTRODUCTION....................................................................................4
CHAPTER 2 LITERATURE REVIEW........................................................................6
CHAPTER 3 CASE REPORT..........................................................................................
CHAPTER 4 DISCUSSION AND SUMMARY..........................................................18
REFERENCES..................................................................................................................

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CHAPTER 1
INTRODUCTION
1.1 Background
Congestive heart failure is a collection of clinical symptoms as a result of structural or
functional cardiac disorder that causes impaired ability ventricular filling and ejection of
blood throughout the body. Heart failure is clinically difficult to recognized, because of the
diversity of the clinical situation, and not specific signs in the early stages of the disease.
Recent developments allow the diagnosis to identify early heart failure, as well as the
development of clinical treatments that improve symptoms and quality of life will slow down
the progression of the disease and improve the quality of life.1
Syndrome of heart failure can be caused by various diseases that reduce the heart's
pumping ability. Diseases that often lead to heart failure include coronary artery disease,
hypertension, cardiomyopathy and valvular heart disease.2
Chronic heart failure is a serious health problem that have prevalence 5.8 billion in
US and 23 billion in the world. 2 Diagnosing of chronic heart failure is often associated with
the mortality and morbidity of the patient that 5 year mortality is as equal as tumour disease.3
Nowadays in Indonesia, chronic heart failure is a cardiovascular disease that the
incidence and prevalence increase continuously. The doctor diagnose results, chronic heart
failure prevalence is 0.13% or about around 229.696.4
Severity and mortality of acute rheumatic fever and Rheumatic Heart Disease (RHD)
has occured in developed country since the turn of 20 th century, especially in infant and
children,this disease is an emergency that is very often encountered by health worker. Infant
and children is not a miniature adults size, there are differences in the structure, function,
biochemical, and pharmacological aspects of the heart, so complaints and symptoms are often
variable,and so it is often difficult to distinguish from other disease outside the
heart.Systematic study of heart failure in children in the mid-20 th century said thatthe most
cause of pediatric heart failure remained rheumatic fever. According to WHOs report in
1999 cardiovascular diseases contributes to a third of global deaths of which 78% occured in
low and middle-income countries. Generally rheumatic fever accounts for third of
cardiovascular disease in those countries.
The most plausible explanations for this geographic discrepancy of disease pattern are
poor socio-economic status; assosiated over crowding, sub standard housing condition,
ineffective case finding and inadequate management of initial bacterial pharyngitis.
Therefore, this shows that our country, Indonesia, is still having a very big burden of

5
infectious diseases. So appropriate diagnosis treatment and public health interventions are
very important to control the disease. This can be effectively implemented by training the
health center team as they operate mainly with in the community and have access to the
public at large.5
1.2 Objective
This case report is the requirement to complete the clinical assistance program in
Department of Child Health of H. Adam Malik General Hospital, Medical Faculty of Sumatra
Utara University. In addition, this case report can be used as reference to know how to define
rheumatic fever and RHD according to the epidemiology, pathogenesis, clinical
manifestations, diagnostic approaches, and also the principles of management, prevention,
and treatment of patient with rheumatic fever and RHD.

CHAPTER 2
LITERATURE REVIEW

2.2. Congestive Heart Failure

2.2.1. Definition
Congestive Heart failure (CHF) is a complex syndrome, with several definitions, the
commonest being an abnormality of cardiac function whereby heart in unable to pump at a
rate commensurate with the requirement of the metabolizing tissues, or does so only at
elevated filling pressures. In case of children, this requirement includes growth and
development.6
Pathophysiological Definition:
Cardiac failure is an inability of the heart to deliver blood (and therefore oxygen) at a rate
commensurate with the requirements of the metabolizing tissues at rest or during light
exercise. This leads to characteristic systemic pathophysiological responses (neural,
hormonal, renal and others), symptoms and signs.7
Clinical Definition:
Clinically the term heart failure is applied to the syndrome of breathlessness and fatigue
associated with cardiac disease. It is often accompanied by fluid retention (congestion), as
indicated by an elevated jugular venous pressure and oedema. Conditions leading to a
mismatch between tissue oxygen delivery and demand (eg. anemia) may mimic the clinical
signs of heart failure as may conditions causing fluid retention (eg. renal and hepatic failure).
The clinical diagnosis of heart failure, therefore, necessitates both the presence of significant
cardiac disease and typical symptoms and signs.7
2.2.2. Etiology
Etiology of congestive heart failure depending on the age of the child.
Fetus: severe anemia, tachycardia supraventricular, tachycardia ventricular, AV Block total
Neonatus premature: fluid overload, PDA, VSD,Cor pulmonale, hypertension
Neonatus: Cardiomyopathy asphyxia, COA, Myocarditis virus
Baby: VSD, Hemangioma, Cardiomyopathy metabolic, acute hypertension, Tachycardia
supraventricular, Kawasaki disease
Children Teenagers: Rheumatic fever, Endocarditis, glomerulonefritis, myocarditis,
tirotoksikosis,

hemokromtosis-hemosiderosis,

cardiomyopathy.7
2.2.3. Classification

cancer

treatment,

cystic

fibrosis,

7
Part of defining heart failure is defining a spectrum of severity. The well-established
New York Heart Association (NYHA) Heart Failure Classification is not applicable to most
of the pediatric population. The ROSS Heart Failure Classification was developed to provide
a global assessment of heart failure severity in infants, and has subsequently been modified to
apply to all pediatric ages. The modified Ross Classification incorporates feeding difficulties,
growth problems, and symptoms of exercise intolerance into a numeric score comparable
with the NYHA classification for adults more recently.
None of these measures has been validated as surrogate clinical end points in large
numbers of children or patients with congenital heart disease, but neurohormonal activation
and deteriorating clinical status have been shown to correlate with increasing class.8
Ross Heart Failure Classification For Children
Class I
Class II

Asymptomatic
Mild tachypnea or diaphoresis with feeding in infant

Class III

Dyspnea on exertion in older children

Marked tachypnea or diaphoresis with feeding in infant
Marked dispnea on exertion

Class IV

Prolonge feeding times with growth failure

Symptome such as tachypnea, retraction, grunting, or diaphoresis
at rest

New York Heart Association (NYHA) Functional Classification

Class
Class I
Class

Patient Symptoms
No limitation of physical activity. Ordinary physical activity does not cause
undue fatigue, palpitation (feeling heart beats), or dyspnea (shortness of breath).
II Slight limitation of physical activity. Comfortable at rest, but ordinary physical

(Mild)
activity results in fatigue, palpitation, or dyspnea.
Class III Marked limitation of physical activity. Comfortable at rest, but less than ordinary
(Moderate activity causes fatigue, palpitation, or dyspnea.
)
Class
(Severe)

IV Unable to carry out any physical activity without discomfort. Symptoms of

cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is
increased.

2.2.4. Pathophysiology

8
When the ventricular end-diastolic volume increase, a healthy heart will increase up to
a maximum cardiac output and cardiac output is achieved can not be enlarged again (FrankStarling principle). Increase in stroke volume achieved in this manner due to the strain of
myocardial fibers, but also raise the wall strain and increase myocardial oxygen consumption.
Heart failure is not a clinical situation involving only one body system but rather a clinical
syndrome due to heart abnormalities so that the heart is unable to pump meet metabolic needs
of the body. Heart failure is characterized with a hemodynamic response, kidneys, nervous
and hormonal real as well as a pathological state of a decrease in heart function. One of
abnormal hemodynamic response is an increase in filling pressure of the heart or
preload.Response to the heart causing some compensation mechanism which aims to improve
blood volume, the volume of the heart chamber,resistance peripheral blood and cardiac
muscle hypertrophy.
This condition also causes activation of the body's compensatory mechanisms that
acute form of hoarding water and salt by the kidneys and nervous system adrenergic
activation. Important to distinguish between the heart's ability to pump with the contractility
of the heart muscle. In some circumstances found excessive load causing failure the heart as a
pump without depression of the heart muscle are intrinsic. On the contrary may also occur
depression intrinsic cardiac muscle but is not clinically visible signs of heart failure due to
cardiac load light. At the beginning of heart failure due to low cardiac output, in the body of
an increase in activity of the sympathetic nervous system and the renin-angiotensinaldosterone system, as well as the release of arginine vasopressin is everything a
compensatory mechanism to maintain blood pressure adequate.
The decline will be followed by a decrease in ventricular contractility cardiac output
which further decrease in blood pressure and a decrease in effective arterial blood
volume.This will stimulate the neurohumoral compensatory mechanisms.
Vasoconstriction and water retention will temporarily increase blood pressure while the
increase preload and increase cardiac contractility through Starling law. If this situation is
not resolved soon, afterload elevation, elevation of preload and cardiac muscle hypertrophy
will further increase the burden of the heart, causing heart failure who are not compensated.
Dilated ventricle systolic dysfunction (decreased ejection fraction) and fluid retention
increases the ventricular volume (dilatation). Dilated cardiac mechanically inefficient will
cause ventricular dysfunction.Congestive heart failure occurs stagnation of blood flow,
systemic embolization of the mural thrombus, and refractory ventricular dysrhythmias.

9
Mechanisms underlying heart failure include impaired ability cardiac contractility,
which causes cardiac output is lower than normal cardiac output. The concept of cardiac
output described by the equation CO = HR x SV where cardiac output is a function of heart
rate multiplied by the stroke volume. Reduced cardiac output resulted in the sympathetic
nervous system will increase heart rate to maintain normal cardiac output. If

the

compensation mechanism to maintain adequate tissue perfusion, the stroke volume must
adjust to maintain cardiac output. But in heart failure all this happened so that the
disturbances in cardiac output that is pumped by the ventricles is inadequate.8

2.2.5. Diagnosis
Thorough history taking and physical examination, including an assessment of the
upper-extremity and lower-extremity blood pressures, are crucial in the evaluation of an
infant or child with congestive heart failure.
Regardless of the etiology, the first manifestation of congestive heart failure is usually
tachycardia. An obvious exception to this finding occurs in congestive heart failure due to a
primary bradyarrhythmia or complete heart block.
As the severity of congestive heart failure increases, signs of venous congestion
usually ensue. Left-sided heart failure is generally associated with signs of pulmonary venous
congestion, whereas right-sided heart failure is associated with signs of systemic venous

10
congestion. Marked failure of either ventricle, however, can affect the function of the other,
leading to systemic and pulmonary venous congestion.
Later stages of congestive heart failure are characterized by signs and symptoms of
low cardiac output. Generally, congestive heart failure with normal cardiac output is called
compensated congestive heart failure, and congestive heart failure with inadequate cardiac
output is considered decompensated.
Signs of congestive heart failure vary with the age of the child.Signs of pulmonary
venous congestion in an infant generally include tachypnea, respiratory distress (retractions),
grunting, and difficulty with feeding. Often, children with congestive heart failure have
diaphoresis during feedings, which is possibly related to a catecholamine surge that occurs
when they are challenged with eating while in respiratory distress.
Right-sided venous congestion is characterized by hepatosplenomegaly and, less
frequently, by edema or ascites. Jugular venous distention is not a reliable indicator of
systemic venous congestion in infants, because the jugular veins are difficult to observe. In
addition, the distance from the right atrium to the angle of the jaw may be no more than 8-10
cm, even when the individual is sitting upright.
Uncompensated congestive heart failure in an infant primarily manifests as a failure to
thrive. In severe cases, failure to thrive may be followed by signs of renal and hepatic failure.
In older children, left-sided venous congestion causes tachypnea, respiratory distress,
and wheezing. Right-sided congestion may result in hepatosplenomegaly, jugular venous
distention, edema, ascites, and/or pleural effusions.
Older children with uncompensated congestive heart failure may have fatigue or
lower-than-usual energy levels. Patients may complain of cool extremities, abdominal pain,
nausea/vomiting, exercise intolerance, dizziness, or syncope.
Clinical findings may include hypotension, cool extremities with poor peripheral
perfusion, a thready pulse, and decreased urine output. Chemical evidence of renal and liver
dysfunction may be present, as well as a diminished level of consciousness. Children with
uncompensated congestive heart failure, particularly older children, generally have a lower
cardiac output than that which most experienced clinicians would estimate on the basis of the
clinical signs.9
Signs and symptoms of congestive heart failure include the following:

Tachycardia

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Venous congestion - Right-sided (hepatomegaly, ascites, abdominal pain, pleural

effusion, edema, jugular venous distention); left-sided (tachypnea, retractions, nasal
flaring or grunting, rales, pulmonary edema)

Low cardiac output - Fatigue or low energy, pallor, sweating, cool extremities,
nausea/vomiting, poor growth, dizziness, altered consciousness, and syncope
Appropriate laboratory testing includes assessment of the following: oxygen

saturation, complete blood count (CBC), hemoglobin concentration, electrolyte levels,

calcium level, cardiac biomarkers, blood urea nitrogen (BUN) level, creatinine level, and
renal and hepatic function. The CBC count can reveal signs of anemia or infection.
Brain natriuretic peptide (BNP) or N -terminal prohormone BNP (NT-proBNP) levels
are elevated as a result of ventricular dilation. Elevation of serum BNP level is particularly
useful in distinguishing patients with congestive heart failure from those with a primary
respiratory process. BNP levels of more than 100 pg/mL are associated with congestive heart
failure in adults and children. Normal levels may be slightly higher in neonates. Serial
measurements of BNP levels in children with primary myocardial dysfunction and acute
decompensated heart failure in which levels are persistently elevated and/or there is a lesser
degree of decline in the first week of presentation are adverse prognostic factors.
Cardiac troponin may be elevated in cases of myocarditis or after ischemic injury due
to coronary anomaly or cardiomyopathy, as well as in noncardiac conditions in which cardiac
perfusion may be compromised (sepsis).
The evaluation of serum electrolyte levels in the patient with congestive heart failure
may demonstrate hyponatremia secondary to water retention. Elevated potassium levels may
represent renal compromise or even tissue destruction due to low cardiac output. Significant
tissue hypoxia increases serum lactate concentration and depletes the serum bicarbonate
level. In more chronic congestive heart failure states, reduced renal blood flow may be
expressed as increased BUN and creatinine levels.
12-lead electrocardiogram (ECG) may reveal evidence of structural or coronary artery
disease or a complete atrioventricular block or arrhythmia.
Pulse oximetry, as well as a hyperoxia test in newborns, may be useful. The systemic
saturation on room air is a more reliable measure of oxygenation than are observations for
cyanosis alone, which are often misleading. The partial pressure of arterial oxygen (PaO 2)
when the patient is receiving 100% oxygen (hyperoxia test) may help in distinguishing
intracardiac mixing malformations from pulmonary disease in the setting of hypoxia. Blood

12
gas abnormalities may show respiratory alkalosis in mild forms of congestive heart failure or
metabolic acidosis in patients with evidence of low cardiac output or ductal-dependent
congenital heart disease.7
Radiography and Echocardiography
In the presence of congestive heart failure, the cardiac silhouette is usually enlarged
on the chest radiograph. As with BNP elevation, cardiac enlargement may help to distinguish
patients with congestive heart failure from those with respiratory disease. However,
exceptions may include restrictive cardiomyopathy, venous obstruction (total anomalous
pulmonary venous obstruction), and diastolic dysfunction due to high ventilator mean airway
pressures, displaying a normal cardiac size on chest radiographs. Increased pulmonary blood
flow may be present, along with pulmonary edema or venous congestion. (See the image
below.)

Chest radiograph shows signs of congestive heart failure (CHF).

Echocardiography is indicated in any child with unexplained congestive heart failure
to assess cardiac function and identify potential cardiovascular causes, particularly anatomic
lesions and cardiomyopathy. On the other hand, congestive heart failure itself is not an
echocardiographic diagnosis; therefore, the underlying etiology is best identified by means of
detailed history taking and physical examination and often by means of chest radiography.
When oral sedation is performed for echocardiography, note that children with a low cardiac
output can depend on endogenous catecholamine levels to maintain tissue perfusion. Sedation
can cause withdrawal of the endogenous catecholamine drive, resulting in cardiac
decompensation.

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2.2.6. Treatment
The management of congestive heart failure (CHF) is difficult and sometimes
dangerous without knowledge of the underlying cause. Consequently, the first priority is
acquiring a good understanding of the etiology. The goals of medical therapy for congestive
heart failure include the following:

Reducing the preload

Enhancing cardiac contractility

Reducing the afterload

Improving oxygen delivery

Enhancing nutrition
As previously discussed, the causes of congestive heart failure vary, and they appear

in different patients to variable degrees. Thus, the medical management of congestive heart
failure in children should be tailored to the specific details of each case.7
Pharmacologic Therapy
Preload reduction can be achieved with oral (PO) or intravenous (IV) diuretics (eg,
furosemide, thiazides, metolazone). Venous dilators (eg, nitroglycerin) can be administered,
but their use is less common in pediatric practice. Contractility can be supported with IV
agents (eg, dopamine) or mixed agents (eg, dobutamine, inamrinone, milrinone). Digoxin
appears to have some benefit in congestive heart failure, but the exact mechanism is unclear.
Afterload reduction is obtained orally through administration of angiotensinconverting enzyme (ACE) inhibitors or intravenously through administration of other agents,
such as hydralazine, nitroprusside, and alprostadil. Pharmaceutical agents used in the
treatment of congestive heart failure are summarized in the Table below.
Table. Pharmaceutical Agents Used in the Treatment of Congestive Heart Failure
Agent
Pediatric Dose
Preload Reduction
Furosemide
1 mg/kg/dose PO or IV
Hydrochlorothiazide 2 mg/kg/d PO divided bid

Comment
May increase to qid
May increase to qid
Used with loop diuretic, may

Metolazone

0.2 mg/kg/dose PO

Inotropic
Digoxin

Preterm infants: 0.005 mg/kg/d PO ...

divided bid or 75% of this dose IV;

increase to bid

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age 10 y: 0.005 mg/kg/d PO qd or
75% of this dose IV
5-10 mcg/kg/min IV (usual dosage;
Dopamine

maximal dosage may be up to 28

mcg/kg/min)

Gradually

5-10 mcg/kg/min IV

Epinephrine

0.01-0.03 mcg/kg/min IV

upward

to

upward

to

desired effect
Gradually

Dobutamine

titrate

titrate

desired effect
Not
to
exceed

0.1-0.3

mcg/kg/min
Typically used without loading
dose,

especially

in

unstable

patients
Milrinone

0.3-1 mcg/kg/min IV

Load: 50 mcg/kg IV over 15 min

Afterload Reduction
Captopril
0.1-0.5 mg/kg/d PO divided q8h

Enalapril

Lisinopril

0.1 mg/kg/d PO divided qd/bid, not

to exceed 0.5 mg/kg/d

...
Adults: 2.5-5 mg/day PO qd/bid
initially; titrate slowly at 1- to 2wk intervals; target dose is 10-20
mg PO bid; not to exceed 40
mg/day
Adults: Usual dosage is 10mg

Not established

PO qd (range, 2.5-10 mg)

Initial dose for hypertension is 0.1

Losartan

mg/kg/day
treatment

PO;
of

dosage
CHF

is

for

Adults: 25-100 mg/d PO qd or

not

divided bid

established in children
Nitroprusside

0.5-10 mcg/kg/min IV

Nitroglycerin
Nesiritide

0.1-0.5 mcg/kg/min IV
0.01-0.03 mcg/kg/min IV

May need to monitor cyanide

level
Vasodilator
Initiate with 0.01 mcg/kg/min

15
May
Alprostadil*
Beta-Blockade

0.03-0.1 mcg/kg/min IV

cause

dose-related

hypotension
...
Adults: 12.5-25 mg PO bid

Limited data suggest a therapeutic

dosage range of 0.2-0.4 mg/kg/dose
Carvedilol

PO bid; initiate with lower dose and

gradually increase dose q2-3wk to Initiate with 3.125 mg PO bid
therapeutic range

Metoprolol
Not established
Selective Aldosterone Antagonists
Spironolactone

1-3.3 mg/kg/day PO in single or

divided doses

Eplerenone
Not established
*Prostaglandin E1 (PGE1).

Adults: 25-100 mg PO qd
Adults: 12.5-50 mg PO qd;
reduce dose to 25 mg qod if
hyperkalemia occurs
25-50 mg PO qd

Managing Acute Congestive Heart Failure in Child

Long-standing but unrecognized congestive heart failure may present acutely;
similarly, an acute presentation may represent an acute onset of acquired cardiac disease
(myocarditis or arrhythmia). Management of acute decompensation involves treatment of
presenting symptoms and adjustment or initiation of long-term therapy.
In older children with acute congestive heart failure, admit to the ICU for diuresis
with IV furosemide. For patients with significant hypotension, IV dopamine (5-10
mcg/kg/min) or milrinone (0.3-1 mcg/kg/min) infusion is appropriate until stabilization is
achieved. Older children may require the placement of a central venous or pulmonary artery
catheter to monitor venous pressure and cardiac output during stabilization.
Nitrates (nitroprusside, nitroglycerin) or nesiritide may be useful in patients with
elevated pulmonary capillary wedge pressure and pulmonary congestion due to their venous
dilating effects. Nesiritide carries the additional theoretical benefits of reversing deleterious
neurohumoral responses and increasing natriuresis. Small studies have been conducted to
measure hemodynamic effects of nesiritide in children with dilated cardiomyopathy.
However, nesiritide has demonstrated no mortality advantage compared with nitroglycerin for
acute decompensated heart failure in a large adult trial.10

16

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CHAPTER IV
DISCUSSION AND SUMMARY

Case
Theory
Patient has a history of sore throat, and -Rheumatic fever develops in some
has been experiencing pain in his joints

children and adolescents following

pahryngitis.
-Based on Jones Criteria which was
revised

in

1992,to

diagnose

Rheumatic fever patient has to have

either 2 major or 1 major 2 minor
symptoms.
Symptoms may include:
-Fever
-Swollen, tender, red and extremely
painful jointsparticularly the knees,
ankles, elbows, or wrists
-Nodules over swollen joints
-Red, raised, lattice-like rash, usually
on the chest, back, and abdomen
Patient had experienced dyspnea

-Shortness of breath, chest discomfort

-Uncontrolled movements of arms,
legs, or facial muscles
-Weakness and shortness of breath

Accumulation of extra fluid in body

and in heart and lungs makes it difficult
for the heart to pump out all the blood
leading to constant accumulation of
blood in lungs leading to dyspnea
Based on Chest X-Ray The Patient has - Depending on the cause of heart
Cardiomegaly

failure, the chest radiograph may show

cardiomegaly,

defined

as

cardiothoracic ratio of greater than 0.5

on the posterior film.
The patient treated with furosemide,
- Benzatine Penicilline G is given
Spironolactone, ceftriaxone, Benzatine

to

prevent

recurrence

of

18

19
CHAPTER V
REFERENCES
1.

(Bahrami H, Kronmal R, Bluemke DA, et al. Differences in the incidence of

congestive heart failure by ethnicity; the Multi-Ethnic Study of Atherosclerosis.

Arch Intern Med. 2008; 168: 2138-45.) (Chatterjee NA, Fifer MA. Heart failure.
Dalam: Lilly LS. Pathophysiology of heart disease. Edisi Kelima. Lippincott
2.

Williams & Wilkins, 2011; 226-230.)

Chris T, Frans L, Hanifati S, et al. Kapita selekta Kedokteran, jilid IV, edisi II.

3.

Jakarta : Media Aesculapius, 2014.

Curtis LH, Whellan DJ, Hammill BG, et al. Incidence and prevalence of heart

4.

failure in elderly persons, 1994-2003. Arch intern Med. 2008; 168: 418-24.
Departemen Kesehatan Republik Indonesia, 2015. Info datin Situasi Kesehatan

5.

Jantung. Available from : www.depkes.go.id/infodatinjantung.pdf.

Yadeta D, Tesfaye G, et al. Rheumatic Fever and Rheumatic Heart Disease for the

7.

Ethiopian Health Center Team. Debub University. 2005 June.

McMurray, J. 2013. Concise Guide tothe Management of Heart Failure. World
Health Organization: Departement Cardiology Western General Hospital,
Scotland.
Bernstein, Daniel. 2000. Gagal Jantung Kongestif. Dalam: Wahab, A Samik. Ilmu

8.

Kesehatan Anak Nelson Ed. 15. Vol:2. EGC, Jakarta: 1658-1662

Hsu, Daphne., Pearson, Gail D. 2009. Heart Failure in Children. American Heart

9.

Assosiation . 63-70, 490-8.

Cotran RS, Kumar V, Collins T, Robbins SL. Robbins Pathologic Basis of

10.

Disease. 6th ed. Philadelphia, Pa: WB Saunders Co; 1999.

Bernstein, Daniel. 2000. Gagal Jantung Kongestif. Dalam: Wahab, A Samik. Ilmu

6.

Kesehatan Anak Nelson Ed. 15. Vol:2. EGC, Jakarta: 1658-1662