CHAPTER I

INTRODUCTION

Congestive heart failure is defined as “the state in which the heart is unable to pump blood at

a rate adequate for satisfying the requirements of the tissues with function parameters

remaining within normal limits usually accompanied by effort intolerance, fluid retention,

and reduced longevity” (Denolin, 1983, p. 445). Currently, congestive heart failure or heart

failure, continues to be a major public health problem worldwide. It is the leading cause of

morbidity and mortality in most developed countries. According to the American Heart

Association (2001), approximately 5 million patients have heart failure and nearly 550,000

new patients are diagnosed each year. In addition, nearly 300,000 patients die from heart

failure yearly. In Indonesia, cardiovascular disease is the third most frequent disease

following infectious disease and TBC.

This paper is a case report about Mrs.N, a 65 year old female, currently diagnosed

with Congestive Heart Failure et causa Hypertension Heart Disease. Its purpose is to review

the clinical manifestations, pathophysiology, preanalytical factors, and treatment in a

congestive heart failure patient.

This case report is significant to our future medical care because it helps stress the

importance of identification and treatment of patients with heart. Also, it explores the need

for a thorough case analysis of a client to deliver the best medical care.

1

CHAPTER II

CASE REPORT

2.1 Identification

Name : Mrs. N

Age : 65 years old

Sex : Female

Address : 11 Ulu Palembang

Occupation : Housewife

Religion : Moslem

Hospitalized : Jan, 3rd 2011

2.2 Anamnesis (Auto and Alloanamnesis)

Chief Complaint

Shortness of breath that worsen since about 11 hours before admission.

History Of Illness

A week before admission, the patient complained shortness of breath while walking

about 10 meters far, it was relieves by taken rest. Sudden awakening of the patient after a

couple hours of sleep with a feeling of breathlessness was absent. The shortness of breath

develops in the recumbent position was absent, the patient still sleeping with one pillow,

it was also not influenced by weather and emotional condition, and never produced

“wheez” sounds. Chest pain was absent, palpitation presents with the exertional

dyspnea. There was no complaint of cough, fever, nausea, vomit, epigastric pain,

abdomen bulging, swollen of the eyelids and extremities. Complained about decreasing

of appetite was present. The patient also often awakens of sleeping for urinate, 3-5 times

of frequency, there was no complained of defecation habits. The patient rarely exercise,

there was no history of smoking.

About 11 hours before admission, the patient complained shortness of breath while

she was praying, chest pain was present, it was radiating to the back, palpitation was

present, heavy nape of neck and fatigue were also present. There was no complained of

urinate and defecation habit. She decided to go to Mohammad Hoesin Hospital.

2

History of Past Illness

History of a disease with the same complaints is denied.

History of hypertension is present since 10 years ago, she was go to community

health center, taken captopril, but rarely control.

History of heart disease is absent.

No history of diabetes

History of Family’s Disease

There is no patient’s family who have the same complaints of the disease

2.3 Physical Examination (Jan, 3rd 2011)

General Condition:

General condition : Sick

Sickness condition : Moderate sick

Conciousness : Compos Mentis

Blood Pressure : 160/ 80 mmHg

Pulse Rate : 100 x/m, regular, equal

RR : 32 x/m, thoracoabdominal type

Temperature : 36,7ºC

Dehydration : -

Body Weight : 50 kg

Height : 148 cm

BMI : 22,83 (Normal Weight)

Keadaan Spesifik

Skin

The color of the skin is black-brown, eflorescency and scar (-), normal pigmentation,

enough turgor, icteric (-), cyanosis (-), pale on palm of hands (-), pale on sole of feet (-),

spider naevy (-), subcutaneous nodul (-), normal hair growth.

Lymph nodes

There are no enlargment of the lymph nodes on submandibular, neck, axilaries, and

inguinal.

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Head

Oval, symmetrical, alopecia (-), puffy face (-), deformity (-), malar rash (-).

Eyes

Exopthalmus (-), endopthalmus (-), edematous of superior palpebrae (-), pale of

conjungtiva palpebrae (-), icteric sclera (-), pupils were isokor, Good light response on

both of eyes, symmetrical eyes movements.

Nose

Epistaxis (-), normal nasal septum, normal mucous layer.

Ear

Normal both of meatus accusticus externus, decreasing hearing ability (-).

Neck

Jugular venous pressure (5+2) cmH2O, lymph nodes enlargment (-), thyroid gland

enlargement (-), stiffness (-).

Thorax

Normal shape, spider naevy (-)

Lung

Inspection : Symmetrical of static and dynamic right and left were equal

Palpation : Stem fremitus in both lung were equal

Percussion : Sonor

Auscultation : Vesikuler (+) normal, wet soft rales (+) right lung parenchyma,

wheezing (-)

Cor

Inspection : Ictus cordis was not seen

Palpation : Ictus cordis was not palpable

Percussion : Upper heart margin at 2nd intercostal space, right margin at linea

sternalis dextra, left margin at linea axillaris anterior sinistra

Auscultation : HR: 110x/m, Murmur (-), Gallop (-).

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Abdomen

Inspection : Dome shaped, umbilicus flattened

Palpation : Tender, pressure pain(-), liver and spleen was not palpable

Percussion : Shifting dullness (+)

Auscultation : Normal bowel sound

Upper Extremity

Paint on joint (-), pale on finger (-), erythema of palm (-), tremor (-), pitting edema (-/-)

Lower Extremity

Pain on joint (-), varices (-), pale on sole of foot (-), pretibial edema (+/+).

Genital

Vulva edema (-)

2.4 Supportive Examination

Laboratory Finding (January 3rd, 2011)

Complete Blood Count

Haemoglobin : 11,6 g/dl (12-16 g/dl)

Haematocrite : 34% (40-48 vol%)

Leucocyte : 12.200/mm3 (5000-10.000/mm3)

ESR : 30 mm/h (<15 mm/h)

Thrombocytes : 196.000/mm3 (200.000-500.000/mm3)

Diff Count:

Basofil : 0% (0-1%) Eosinofil : 2% (1-3%)

Band : 1% (2-6%) Segment : 77% (50-70%)

Limphocytes : 16% (20-40%) Monocytes : 4% (2-8%)

Clinical Chemistry

BSS : 95 mg/dl

Total cholesterol : 198 mg/dl (<200 mg/dl)

HDL-cholesterol : 55 mg/dl (>55 mg/dl)

LDL-cholesterol : 104 mg/dl (<130 mg dl)

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Triglyceride : 194 mg/dl (<150 mg/dl)

Uric acid : 3,0 mg/dl (F: 2,6-6,0 mg/dl)

Ureum : 30 mg/dl (15-39 mg/dl)

Creatinine : 0,7 mg/dl (0,9-1,3 mg/dl)

Natrium : 139 mmol/L (135-150 mmol/L)

Kalium : 3,3 mmol/L (3,5-5 mmol/L)

SGOT : 15 U/I (<40 U/I)

SGPT : 9 (<41 U/I)

CK-NAK : 31 U/I (80-170 U/I)

CK-MB : 20 U/I (<25 U/I)

Electrocardiography (January 4th, 2011)

Impression: Sinus rhythm

Left Ventricular Hypertrophy

Rontgen Thorax Postero-anterior

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Photo condition is good, symmetric, trachea position in the middle, bones and soft tissues are

in good condition, elongatio aorta, intercostal spaces widening, CTR > 50%, costophrenicus

angle is fine, pulmonary parenchyma is normal.

Impression: Cardiomegaly

Planning Examination

- Echocardiography

- Fluid balance monitoring

2.5. Resume

7

Has been examined a woman, 65 years old, anamnesis found that 1 week before

admission, the patient complained shortness of breath while walking about 10 meters far,

it was relieves by taken rest. Sudden awakening of the patient after a couple hours of

sleep with a feeling of breathlessness was absent. The shortness of breath develops in the

recumbent position was absent, the patient still sleeping with one pillow, it was also not

influenced by weather and emotional condition, and never produced “wheez” sounds.

Chest pain was absent, palpitation presents with the exertional dyspnea. There was no

complaint of cough, fever, nausea, vomit, epigastric pain, abdomen bulging, swollen of

the eyelids and extremities. Complained about decreasing of appetite was present. The

patient also often awakens of sleeping for urinate, 3-5 times of frequency, there was no

complained of defecation habits. The patient rarely exercise, there was no history of

smoking. About 11 hours before admission, the patient complained shortness of breath

while she was praying, chest pain was present, it was radiating to the back, palpitation

was present, heavy nape of neck and fatigue were also present. There was no complained

of urinate and defecation habit. She decided to go to Mohammad Hoesin Hospital.

Physical examination found the blood pressure was 160/80 mmhg, pulse rate 100

bpm, regular, equal, respiratory rate 32 bpm, thoracoabdominal, JVP (5+2) cmH2O, rales

(+), upper heart margin at 2nd intercostal space, right margin at linea sternalis dextra,

left margin at linea axillaris anterior sinistra. The abdomen is bulging, shifting dullness

(+), oedema pretibial minimal.

Electrocardiography finding was left ventricular hypertrophy, radiologic finding was

cardiomegaly.

2.6. Working Diagnosis

CHF e.c HHD + Hypertension stage I

2.7. Differential Diagnosis

CHF e.c ASHD + Hypertension stage I

2.8. Management

Non-Pharmacology:

1. Bed rest

2. O2 3 L/m

3. Diet Jantung III

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Pharmacology:

IVFD D5% gtt X/m, micro.

Furosemid injection 1 x 1 amp

Captopril 3 x 12,5 mg

Terapi edukatif:

Minum jangan terlalu banyak, sesuaikan antara yang masuk dan keluar.

Hindari stress dan tenangkan pikiran.

Tidak melakukan aktivitas berat.

2.9. Prognosis

Quo ad vitam : dunia ad bonam

Quo ad functionam : dubia ad malam

Follow Up:

Tanggal 4 Januari 2011

S Sesak napas

O: Keadaan umum

Kesadaran

Tekanan darah

Nadi

Pernapasan

Temperatur

Keadaan spesifik

Kepala

Leher

Thorax:

Jantung

Tampak sakit sedang

Compos mentis

150/90 mmHg

96 x/menit

28 x/ menit

36,5 0C

Conjungtiva palpebra pucat (-)

Sklera ikterik(-)

JVP (5+2) cmH2O

Pembesaran KGB (-)

HR96 x/ menit, murmur (-) gallop (-)

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Paru

Abdomen

Genitalia

Ekstremitas

vesikuler normal, ronkhi di basal paru kanan dan kiri,

wheezing (-)

I : Cembung

P : Lemas, hepar dan lien tidak teraba

P : Shifting dullness (+)

A : Bising usus (+) normal

Tidak diperiksa

Edema pretibia (+) minimal

A CHF ec. HHD

P - Istirahat

- O2 3 liter/mnt

- Diet jantung III

- IVFD D5% gtt X/m, mikro.

- Furosemid injeksi 1 x 1 ampul

- Captopril 3 x 12,5mg

Table of Fluid Balance Monitoring

Days Intake Output Selisih

Food Drink IVFD Total Urinate Defecate CWL Total

4/1/11 150 300 250 700 - 450 300 750 -50

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CHAPTER III

THEORETICAL BACKGROUND

Classification. According to the New York Heart Association (1964), congestive heart

failure may be classified into four functional states. “Class I (Mild) are patients with cardiac

disease but without resulting limitatios of physical activity. Ordinary physical activity does

not cause undue fatigue, palpitation, dyspnea (shortness of breath), or anginal pain. Class II

(Mild) are patients with cardiac disease resulting in slight limitation of physical activity. They

are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or

anginal pain. On the other hand, Class III (Moderate) are patients with cardiac disease

resulting in marked limitation of physical activity. They are comfortable at rest, but less than

ordinary activity causes fatigue, palpitation, dyspnea or anginal pain. The last classification is

Class IV (Severe) are patients with cardiac disease where in there is inability to carry out any

physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal

syndrome may be present even at rest. If any physical activity is undertaken, discomfort is

increased (New York Heart Association, 1964).

Causes. “An array of different problems can cause congestive heart failure. (1)

Among them is coronary (ischemic) heart disease resulting from insufficient blood flow to

the myocardium, or heart muscle. This is usually caused by atherosclerosis, the buildup of

fatty substances or plaque on the walls of the arteries that carry blood to the heart muscle.

The heart’s ability to perform decreases because ischemia results in the delivery of less

oxygen and fewer nutrients to the heart muscle. (2) A heart attack may also cause congestive

failure. During a heart attack, the heart muscle is deprived of oxygen, resulting in tissue death

and scarring. The development of heart failure depends on the extent and location of scarring.

(3) Long-standing high blood pressure is another common cause of heart failure. Because

there is greater resistance against which the heart must pump, the heart muscle works harder.

This results in an enlargement of the heart muscle, especially of the left ventricle, the heart’s

main pumping chamber. Eventually, this enlarged muscle tissue weakens, setting the stage

for heart failure, especially if the pumping ability of the enlarged chamber greatly decreases.

(4) Arrhythmias (irregular heartbeats) can also lead to heart failure, but they usually have to

be severe and prolonged, with a rapid rate of more than 140 beats per minute, and must often

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occur in the presence of an already weakened heart. They change the pattern of filling and

pumping of blood from the heart. This condition may also lower output of blood to the point

of heart failure. (5) Valvular heart diseases are another cause of heart failure, which results

when a narrowed or leaking valve fails to direct blood flow properly through the heart. The

problem may be congenital (inborn) or due to an infection such as endocarditis or rheumatic

fever. This increases the heart’s workload, thereby increasing risk of developing heart failure.

(6) Cardiomyopathy, a disease of the heart muscle itself, can also lead to heart failure. Causes

of cardiomyopathy include infection, alcohol abuse, and cocaine abuse. When heart failure

seems to have no known causes, it is known as idiopathic heart failure” (Soufer, 1992).

Manifestations. Soufer (1992) further elaborates the manifestations often seen in

patients with heart failure. The particular symptoms that an individual experiences are

determined by which side of the heart is involved in the heart failure. For example, the “left

atrium receives oxygenated blood from the lungs and passes it onto the left ventricle, which

pumps it to the rest of the body” (Porth, 2007). When the left side isn’t pumping efficiently,

blood backs up in the vessels of the lungs, and sometimes fluid is forced out of the lung

vessels and into the breathing spaces themselves. This pulmonary congestion causes

shortness of breath. The other major symptoms of left-sided heart failure are fatigue, dyspnea,

orthopnea, paroxysmal nocturnal dyspnea , and the sputum production that comes from

pulmonary congestion (Soufer, 1992).

Porth (2007) adds that right-sided failure occurs when there is resistance to the flow

of blood from the right heart structures (right atrium, right ventricle, pulmonary or lung

artery) into the lungs or when the tricuspid valve, which separates the right atrium from the

right ventricle, fails to work properly. This results in a backup of fluid and pressure in the

veins that empty into the right side of the heart. Pressure then builds up in the liver and the

veins in the legs. The liver enlarges and may become painful and swelling of the ankles or

legs occurs (Soufer, 1992). The major symptoms of right-sided heart failure are edema and

nocturia (Woods, et. al, 2010). The different types of edema possible are dependent edema,

edema that results in enlargement or swelling of the liver, ascites, and edema of the skin or

soft tissues.

Because congestive heart failure causes the body to fill with excess fluids, the kidneys

may not be able to dispose of the extra sodium and water, a condition known as kidney

failure. Sodium that would normally be eliminated through the urine remains in the body,

12

causing it to retain even more water, thereby aggravating the problem of excess fluid

associated with congestive heart failure (Soufer, 1992).

Complications. Watson (2000) discovered that the common complications of heart

failure include irregular heart rhythms or arrythmias, stroke, thromboembolism and

organdysfunctions. (1) One of these are malignant ventricular arrhythmias which are

commonin end stage heart failure. For example, sustained ventricular tachycardia occurs in

up to10% of patients with advanced heart failure who are referred for cardiac

transplantation(Watson, 2000). In patients with ischemic heart disease, these arrhythmias

often havemechanisms in scarred myocardial tissue. An episode of sustained ventricular

tachycardia indicates a high risk for recurrent ventricular arrhythmias and sudden cardiac

death. Congestive heart failure predisposes to (2) stroke and (3) thromboembolism, with an

overall estimated annual incidence of approximately 2% (Watson, 2000). Factors contributing

to the increased thromboembolic risk in patients with heart failure include low cardiac output

(with relative stasis of blood in dilated cardiac chambers), regional wall motion abnormalities

(including formation of a left ventricular aneurysm), and associated atrial fibrillation.

Patients with heart failure and chronic venous insufficiency may also be immobile,

and this contributes to their increased risk of thrombosis, including deep venous thrombosis

and pulmonary embolism. Mild to moderate heart failure is associated with an annual risk of

stroke of about 1.5% (compared with a risk ofless than 0.5% in those without heart failure),

rising to 4% in patients with severe heartfailure (Watson, 2000). (4) Organ dysfunction

occurs when there is a decrease in theoxygen supply to the different organ tissues in the body.

Because of the lack of oxygen,compensatory mechanisms act but eventually decompensate

leading to dysfunction of organs (Porth, 2007).

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CHAPTER IV

CASE ANALYSIS

Heart failure is clinical syndrome (a group of signs and symptoms), caused by impairment of

heart structure and function, which is heart incapable to pump the blood to fulfill the need

metabolic tissue. Heart failure is marked by shortness of breath (dyspnea d'effort, orthopnea,

paroxysmal nocturnal dypsnea, cheyne-stokes respiration) and fatigue (at rest or activity).

The dyspnea be espoused oedema can come from pulmo, heart, kidney, and also from

liver. Based on anamneses and physical examination with supporting investigation the

dyspnea that come from the lung, kidney, and liver can be ruled out.

Reviewed from the aspect of clinical manifestation according to the

symptomatologist, has been described the clinical feature of left heart failure are weakness,

fatigue, palpitation, dyspnea and cough, also the objective sign is tachycardia, dyspnea

(dyspnea d'effort, orthopnea, paroxysmal nocturnal dypsnea, cheyne-stokes respiration), soft

wet rales at basal pulmo, additional heart sound (heart sound III) and heart expansion. The

right heart failure with heel oedema phenomenon and leg oedema, hepatomegaly, acites, dam

vena jugularis Congestive heart failure is the combination from both of heart failure clinical

types.

From result anamneses and physical examination in this patient were found dyspnea

d'effort, palpitation, fatigue, vena jugularis dam, wet soft rales at basal pulmo, takhikardia,

heart expansion, ascites, and oedema pretibial minimal so that fulfil criteria clinical

description congestive heart failure.

Based on classification New York Heart Association as 4 class (NYHA1-4) where

dyspnea and fatigue as evaluation. In class 1 there is no complaint, class 2 symptom appear in

moderate activity, class 3 symptom is appearing in light activity and class 4 symptom is

appear at the (time) of rest in this patient dyspnea is appear at the (time) of activity (class 2).

Based on criteria framingham minimal one major criteria and two minor criterias that

is: major criteria shaped paroksisimal nocturnal menypneu, menytensi vena neck, ronki paru,

cardiomegaly, acute pulmo oedema, gallop s3, increasing of jugular venous pressure, refluks

hepatojugular. minor criteria shaped oedema extremity, nighttime cough, dyspnea d'effort,

hepatomegaly, pleural effusion, vital capacity depreciation, tachycardi (> 120 x/minute)s.

14

Farmingham’s Score for this patient:

Major Criteria

" paroxysmal nocturnal dyspneu (-)

" vena neck distention (-)

" rales (+)

" cardiomegaly (-)

" acute pulmonary eodema (-)

" gallop s3 (-)

" increasing of jugular venous pressure (+)

" refluks hepatojugular (-)

Minor Criteria

" extremity oedema (+)

" nighttime cough (-)

" dyspneu d'effort (+)

" Hepatomegaly (-)

" pleural effusion (-)

" vital capacity depreciation 1/3 from normal (-)

" takikardi (>120 x/minute) (-)

This patient got two major criterias and two minor criterias. Therefore we conclude that the

functional diagnoses is congestive heart failure. The anatomical diagnoses is based on

physical examination found of expansion of the heart which is confirmed by the rontgen

thorax with impression is cardiomegaly

Hypertension is considering as the etiology of the disease in this patient. Long-

standing high blood pressure is another common cause of heart failure. Because there is

greater resistance against which the heart must pump, the heart muscle works harder. This

results in an enlargement of the heart muscle, especially of the left ventricle, the heart’s main

pumping chamber. Eventually, this enlarged muscle tissue weakens, setting the stage for

heart failure, especially if the pumping ability of the enlarged chamber greatly decreases.

The management of heart failure is depend on etiology, haemodynamic, clinical

manifestation and the severity of heart failure. Therapy consists of 5 components shaped

15

handling in general, base cure disease, prevent furthermore damage in heart, and restrain

degree CHF.

In general heart failure class 3 and 4 necessary to limit activity restly in place sleep

but necessary to avoid to sleep long, stop the bad habit that increase heart sickness

appearance, salt degree restriction (Na) but this is not yet need because the medicine that

chosen to treat the patient is to increase expenditure of Na. Diet food in heart disease in

hospital is diets heart. Diet heart consists of to diet heart I is liquid food, diet heart II is

porridge filters, diet heart III is porridge, diet heart IV is rice food. Diet that given in this

patient is diets heart III because patient stills aware and may not do too much activity.

Therapy based on symptoms is the restriction of liquid intake because many liquid

will be absorbed and total liquid will increase so that make the heart work heavier. Therapy

that given is furosemid, the aim is to deacrease ascites with reducing heart load without

reducing cardiac output. While captopril given is to demote the blood pressure, because this

patient is also suffered from hypertension stage 1.

Prognosis maintained based on from heart pump ability for compensation with

clinical symptoms repair after the therapy. To determine heart pump ability is need to see the

ejection fraction of the heart that can be maintained from echocardiology with clinical

symptoms of congestive heart failure and OMI anteroseptal so that the result of 3 days of

therapy doesn’t show repairment but inclined to be worse.

16

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Denolin H, Kuhn H, Krayenbuehl HP, et al. (1983). The definition of heart failure. Eur

Heart J (1983)4:445–8. Retrieved from http://aje.oxfordjournals.org/lookup/ijlink?

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