Lapkas Anak - CHF

8/20/2019 Lapkas Anak - CHF

1/19

Case Report

CONGESTIVE HEART FAILURE

ET CAUSA

RHEUMATIC HEART DISEASE

SUPERVISOR : dr. Sri Sofyani, SpA !"

PRESENTATOR : Sa#$%& Ed'i S$ran(a ))*)**))+

T'%r%a S'in(a$&i ))*)**+-+

PEDIATRIC DEPARTMENT

MEDICAL FACULT OF NORTH SUMATRA UNIVERSIT

H. ADAM MALI! GENERAL HOSPITAL

MEDAN

+*)/


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AC!NO0LEDGMENTS

We are greatly indebted to the Almighty One for giving us blessing to finish this case

report,1 C'roni2 H%ar( Fai&$r% CHF" et causa R'%$#a(i2 H%ar( Di%a% RHD"3.This

case report is a requirement to complete the clinical assistance program in Department of

Child ealth in . Adam !ali" #eneral ospital, !edical $aculty of %orth &umatra

'niversity.

We are also indebted to our supervisor and adviser, dr. &ri &ofyani, &pA ()* for the

time spent to give us guidances, comments, and suggestions. We are grateful because +ithout

her guidance this case report +ouldnt have ta"en its present shape.

This case report has gone through series of developments and corrections. There +ere

critical but constructive comments and relevants suggestions from the revie+ers. opefully

the content +ill be useful for everyone in the future.

!edan, 2- %ovember 2/0

1resentators


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TA4LE OF CONTENTS

AC!NO0LEDMENTS..................................................................................................ii

TA4LE OF CONTENTS............................................................................................... iii

CHAPTER ) INTRODUCTION....................................................................................-

CHAPTER + LITERATURE REVIE0........................................................................5

CHAPTER 6 CASE REPORT..........................................................................................

CHAPTER - DISCUSSION AND SUMMAR..........................................................)7

REFERENCES..................................................................................................................


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CHAPTER )

INTRODUCTION

).) 4a289ro$nd

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 e4ection of

blood throughout the body. eart failure is clinically difficult to recogni5ed, because of the

diversity of the clinical situation, and not specific signs in the early stages of the disease.

6ecent developments allo+ the diagnosis to identify early heart failure, as +ell as the

development of clinical treatments that improve symptoms and quality of life +ill slo+ do+n

the progression of the disease and improve the quality of life. /

&yndrome of heart failure can be caused by various diseases that reduce the heart7s

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 0.8 billion in

'& and 2 billion in the +orld.2 Diagnosing of chronic heart failure is often associated +ith

the mortality and morbidity of the patient that 0 year mortality is as equal as tumour disease. 3

%o+adays in 9ndonesia, chronic heart failure is a cardiovascular disease that the

incidence and prevalence increase continuously. The doctor diagnose results, chronic heart

failure prevalence is ./: or about around 22;.-;-.3

&everity and mortality of acute rheumatic fever and 6heumatic eart Disease (6D*

has occured in developed country since the turn of 2 th century, especially in infant and

children,this disease is an emergency that is very often encountered by health +or"er. 9nfant

and children is not a miniature adults si5e, 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.&ystematic study of heart failure in children in the mid


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infectious diseases. &o 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 +ith in the community and have access to the

public at large.0

).+ O;%2(i


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+.+. Con9%(i syndrome, +ith several definitions, the

commonest being an abnormality of cardiac function +hereby heart in unable to pump at a

rate commensurate +ith the requirement of the metaboli5ing tissues, or does so only at

elevated filling pressures. 9n case of children, this requirement includes gro+th and

development.-

1athophysiological Definition@

Cardiac failure is an inability of the heart to deliver blood (and therefore o>ygen* at a rate

commensurate +ith the requirements of the metaboli5ing tissues at rest or during light

e>ercise. This leads to characteristic systemic pathophysiological responses (neural,

hormonal, renal and others*, symptoms and signs.=

Clinical Definition@

Clinically the term heart failureB is applied to the syndrome of breathlessness and fatigue

associated +ith cardiac disease. 9t is often accompanied by fluid retention (congestionB*, as

indicated by an elevated 4ugular venous pressure and oedema. Conditions leading to a

mismatch bet+een tissue o>ygen 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.=

2.2.2. tiology

tiology of congestive heart failure depending on the age of the child.

$etus@ severe anemia, tachycardia supraventricular, tachycardia ventricular, A Eloc" total

%eonatus premature@ fluid overload, 1DA, &D,Cor pulmonale, hypertension

%eonatus@ Cardiomyopathy asphy>ia, COA, !yocarditis virus

Eaby@ &D, emangioma, Cardiomyopathy metabolic, acute hypertension, Tachycardia

supraventricular, )a+asa"i disease

Children Teenagers@ 6heumatic fever, ndocarditis, glomerulonefritis, myocarditis,

tiroto"si"osis, hemo"romtosis


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1art of defining heart failure is defining a spectrum of severity. The +ell


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When the ventricular endimum cardiac output and cardiac output is achieved can not be enlarged again ($ran"<

&tarling principle*. 9ncrease in stro"e volume achieved in this manner due to the strain of

myocardial fibers, but also raise the +all strain and increase myocardial o>ygen consumption.

eart 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. eart failure is characteri5ed +ith a hemodynamic response, "idneys, nervous

and hormonal real as +ell 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.6esponse to the heart causing some compensation mechanism +hich 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 body7s compensatory mechanisms that

acute form of hoarding +ater and salt by the "idneys and nervous system adrenergic

activation. 9mportant to distinguish bet+een the heart7s ability to pump +ith the contractility

of the heart muscle. 9n some circumstances found e>cessive load causing failure the heart as a

pump +ithout 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 lo+ cardiac output, in the body of

an increase in activity of the sympathetic nervous system and the renin


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!echanisms underlying heart failure include impaired ability cardiac contractility,

+hich causes cardiac output is lo+er than normal cardiac output. The concept of cardiac

output described by the equation CO G 6 > & +here cardiac output is a function of heart

rate multiplied by the stro"e volume. 6educed cardiac output resulted in the sympathetic

nervous system +ill increase heart rate to maintain normal cardiac output. 9f the

compensation mechanism to maintain adequate tissue perfusion, the stro"e volume must

ad4ust to maintain cardiac output. Eut in heart failure all this happened so that the

disturbances in cardiac output that is pumped by the ventricles is inadequate. 8

2.2.0. Diagnosis

Thorough history ta"ing and physical e>amination, including an assessment of the

uppertremity and lo+ertremity blood pressures, are crucial in the evaluation of an

infant or child +ith congestive heart failure.

6egardless of the etiology, the first manifestation of congestive heart failure is usually

tachycardia. An obvious e>ception to this finding occurs in congestive heart failure due to a

primary bradyarrhythmia or complete heart bloc" .

As the severity of congestive heart failure increases, signs of venous congestion

usually ensue. Heft


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congestion. !ar"ed failure of either ventricle, ho+ever, can affect the function of the other,

leading to systemic and pulmonary venous congestion.

Hater stages of congestive heart failure are characteri5ed by signs and symptoms of

lo+ cardiac output. #enerally, congestive heart failure +ith normal cardiac output is called

compensated congestive heart failure, and congestive heart failure +ith inadequate cardiac

output is considered decompensated.

&igns of congestive heart failure vary +ith the age of the child.&igns of pulmonary

venous congestion in an infant generally include tachypnea, respiratory distress (retractions*,

grunting, and difficulty +ith feeding. Often, children +ith congestive heart failure have

diaphoresis during feedings, +hich is possibly related to a catecholamine surge that occurs

+hen they are challenged +ith eating +hile in respiratory distress.

6ight


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• enous congestion < 6ightygen

saturation, complete blood count (CEC*, hemoglobin concentration, electrolyte levels,

calcium level, cardiac biomar"ers, blood urea nitrogen (E'%* level, creatinine level, and

renal and hepatic function. The CEC count can reveal signs of anemia or infection.

Erain natriuretic peptide (E%1* or N imetry, as +ell as a hypero>ia test in ne+borns, may be useful. The systemic

saturation on room air is a more reliable measure of o>ygenation than are observations for

cyanosis alone, +hich are often misleading. The partial pressure of arterial o>ygen (1aO 2*

+hen the patient is receiving /: o>ygen (hypero>ia test* may help in distinguishing

intracardiac mi>ing malformations from pulmonary disease in the setting of hypo>ia. Elood


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gas abnormalities may sho+ respiratory al"alosis in mild forms of congestive heart failure or

metabolic acidosis in patients +ith evidence of lo+ cardiac output or ductalceptions may include restrictive cardiomyopathy, venous obstruction (total anomalous

pulmonary venous obstruction*, and diastolic dysfunction due to high ventilator mean air+ay

pressures, displaying a normal cardiac si5e on chest radiographs. 9ncreased pulmonary blood

flo+ may be present, along +ith pulmonary edema or venous congestion. (&ee the image

belo+.*

Chest radiograph sho+s signs of congestive heart failure (C$*.

chocardiography is indicated in any child +ith une>plained 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 ta"ing and physical e>amination and often by means of chest radiography.

When oral sedation is performed for echocardiography, note that children +ith a lo+ cardiac

output can depend on endogenous catecholamine levels to maintain tissue perfusion. &edation

can cause +ithdra+al of the endogenous catecholamine drive, resulting in cardiac

decompensation.


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2.2.-. Treatment

The management of congestive heart failure (C$* is difficult and sometimes

dangerous +ithout "no+ledge 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 follo+ing@

• 6educing the preload

• nhancing cardiac contractility

• 6educing the afterload

• 9mproving o>ygen delivery

• nhancing 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.>

1harmacologic Therapy

1reload reduction can be achieved +ith oral (1O* or intravenous (9* diuretics (eg,

furosemide, thia5ides, metola5one*. enous dilators (eg, nitroglycerin* can be administered,

but their use is less common in pediatric practice. Contractility can be supported +ith 9

agents (eg, dopamine* or mi>ed agents (eg, dobutamine, inamrinone, milrinone*. Digo>in

appears to have some benefit in congestive heart failure, but the e>act mechanism is unclear.

Afterload reduction is obtained orally through administration of angiotensin<

converting en5yme (AC* inhibitors or intravenously through administration of other agents,

such as hydrala5ine, nitroprusside, and alprostadil. 1harmaceutical agents used in the

treatment of congestive heart failure are summari5ed in the Table belo+.

Table. 1harmaceutical Agents 'sed in the Treatment of Congestive eart $ailure

A9%n( P%dia(ri2 Do% Co##%n(

Pr%&oad R%d$2(ion

$urosemide / mgJ"gJdose 1O or 9 !ay increase to qid

ydrochlorothia5ide 2 mgJ"gJd 1O divided bid !ay increase to qid

!etola5one .2 mgJ"gJdose 1O'sed +ith loop diuretic, may

increase to bid

Ino(ropi2

Digo>in 1reterm infants@ .0 mgJ"gJd 1O

divided bid or =0: of this dose 9?

...


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age / y@ .0 mgJ"gJd 1O qd or

=0: of this dose 9

Dopamine

0ceed ./


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!ay cause dose


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CHAPTER IV

DISCUSSION AND SUMMAR


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Case Theory

1atient has a history of sore throat, and

has been e>periencing pain in his 4oints

1atient had e>perienced dyspnea


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CHAPTER V

REFERENCES

/. (Eahrami , )ronmal 6, Eluem"e DA, et al. Differences in the incidence of

congestive heart failure by ethnicity? the !ulti

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Lapkas Anak - CHF