CHAPTER I

INTRODUCTION

1.1.Background
Heart failure is a chronic, progressive condition in which the heart muscle
is unable to pump enough blood to meet the body’s needs for blood and oxygen.
Basically, the heart can’t keep up with its workload.1
Heart failure (HF) is a leading cause of morbidity and mortality, and
causes high health-care-related costs, posing a great burden on both patient and
society. Heart failure become more common with increasing age. The lifetime risk
of developing heart failure is 20% for Americans 40 years of age. In the United
States, Heart Failure incidence has largely remained stable over the past several
decades, with >650,000 new heart failure cases diagnosed annually. HF incidence
increases with age, rising from approximately 20 per 1,000 individuals 65 to 69
years of age to >80 per 1,000 individuals among those 85 years of age.
Approximately 5.1 million persons in the United States have clinically manifest
heart failure, and the prevalence continues to rise.2 In Indonesia prevalence of
heart failure based on diagnosis and highest edition in East Nusa Tenggara
(0.8%), followed by Central Sulawesi (0.7%), while South Sulawesi and Papua
amounted to (0.5%).3
The clinical syndrome of Heart failure may result from disorders of the
pericardium, myocardium, endocardium, heart valves, or great vessels, or from
certain metabolic abnormalities, but most patients with HF have symptoms due to
impaired left ventricular (LV) myocardial function.4
Heart failure does not mean the heart has stopped working. Rather, it means
that the heart works less efficiently than normal. Due to various possible causes, blood
moves through the heart and body at a slower rate, and pressure in the heart increases.
As a result, the heart cannot pump enough oxygen and nutrients to meet the body's
needs. The chambers of the heart may respond by stretching to hold more blood to
pump through the body or by becoming stiff and thickened. This helps to keep the
blood moving, but the heart muscle walls may eventually weaken and become unable

1
to pump as efficiently. As a result, the kidneys may respond by causing the body to
retain fluid (water) and salt. If fluid builds up in the arms, legs, ankles, feet, lungs, or
other organs, the body becomes congested, and congestive heart failure (CHF) is the
term used to describe the condition.5
Left-sided CHF is the most common type of CHF. It occurs when your left
ventricle doesn’t properly pump blood out to your body. As the condition
progresses, fluid can build up in your lungs, which makes breathing difficult.
There are two kinds of left-sided heart failure,first, Systolic heart failure occurs
when the left ventricle fails to contract normally. This reduces the level of force
available to push blood into circulation. Without this force, the heart can’t pump
properly. Second, Diastolic failure, or diastolic dysfunction, happens when the
muscle in the left ventricle becomes stiff. Because it can no longer relax, the heart
can’t quite fill with blood between beats. Right-sided CHF occurs when the right
ventricle has difficulty pumping blood to your lungs. Blood backs up in your
blood vessels, which causes fluid retention in your lower extremities, abdomen,
and other vital organs. It’s possible to have left-sided and right-sided CHF at the
same time. Usually, the disease starts in the left side and then travels to the right
when left untreated. Therefore, this case needs to be studied more deeply.5

2
 CHAPTER II
CASE REPORT

2.1.Anamnese (June 5, 2019)

2.1.1. Patient Identification
No MR : 57-83-16
Name : Mr. M
Gender : Male
Age : 50
Address : Jl. Gub H Bastari Lr. Bersama No. 812 RT/RW
13/ 03 8 ULU/ Silaberanti Ulu 1
Job : No Job
Status : Married
Religion : Islam
Phone Number : 081255248464
Date : May 31, 2019
Room : Ahmad Dahlan 16 Bed 1
Examining Doctor : dr. Ni Made Elva Maya Sari, Sp. Jp.
Financing : JKN BPJS Non PBI

2.1.2. Main Complaint

Shorteness of breath getting harder since ± 1 weeks before entering
the hospital.
2.1.3. History of Presenting Complaint
The patient complains shortness of breath getting harder since ± 1
weeks before entering the hospital. Shortness of breath be affected by
activity if walk ± 10 m and shortness of breath disappears when resting,
shortness of breath is not affected by position, weather, dust and emotions.
Shortness of breath is not accompanied by wheezing and chest pain. Patient
often wake up at night due to shortness of breath. Patient also complained
that there was a cough with sputum without blood and when coughing made
it more short of breath. Patient also complained of swollen on both legs.

3
Chest pain (-), chest palpitations (-), night cough (+), fever (-), nausea (-),
vomiting (-), defecate and urination no complaints.
Patient said that 1 year ago the patient felt both of his legs swollen
accompanied by shortness of breath and healed after being hospitalized.
Os admitted that he had shortness of breath which had been felt for 2
years and was getting worse. Shortness of breath is not affected by activity,
position, weather, dust and emotions. Shortness of breath is not
accompanied by wheezing and chest pain. Swollen leg (-), chest palpitations
(-), night cough (-), fever (-), nausea (-), vomiting (-), defecate and urination
no complaints.

Past Medical History

 History of kidney disease is denied
 History of liver disease is denied
 History of thyroid disease is denied
 History of diabetes mellitus is denied
 History of hypertension is existed since ± 11 years ago, uncontrolled
 History of asthma is denied
 History of heart disease is denied
 History of gastritis denied

Family History
 History of kidney disease is denied
 History of diabetes mellitus is denied
 History of hypertension is unknown
 History of asthma is denied
 History of heart disease is denied

Lifestyle
 History of smoking : Yes, one day one pack of cigarettes but
stop since 2 years ago.
 Drinking coffee : No

4
  Drinking alkohol : No
 Drinking herbs : No
 Doing Sports : Seldom
 Eating history : 3 times a day, 1 plate per meal.
Socio-Economic History
The patient doesn’t have a job, economically disadvantaged.
Nutritional Status
Diet before illness: 3 times / day, 1 plate of rice, regularly.
Diet variations
 Carbohydrates: 2-3x rice, 1/2 medium portion of rice dishes a day.
 Protein: 1 piece of fish or 1 piece of chicken size medium, a bowl of
peanuts.
 Fat: Meat (1-2x / week)
 Vegetables: 2x / day
 Fruit: Rarely
 Milk: Rarely
Impression:
Qualitatively sufficient nutrition, quantitatively meet balanced nutritional
intake that is the staple food of 2-3 servings of carbohydrates, 2-3 servings
of animal protein, 2-3 servings of vegetable protein and 2-3 servings of
vegetables.

2.2.Physical Examination
Done on June 5, 2019
General Conditions:
1. Illness : Medium
2. Awareness : Compos mentis
3. Dispneu : Yes
4. Weight before illness : 60 kg
5. Weight after illness : 55 kg
6. Height : 163 cm
7. Nutritional state : BMI: 20,7 (Normal)

5
8. Blood pressure : 180/110 mmHg
9. Pulse
- Frequency : 93 times per minute
- Rhythm : Regular
- Contents : Enough
- Voltage : Enough
- Quality : Good
10. Breathing
- Frequency : 29 times per minute
- Rhythm : Regular
- Type : Thorakoabdominal
11. Temperature : 36.7 ° C
Specific Conditions:
1. Head Examination:
- Form : Normocephali
- Hair : Black, thick, not easily revoked
- Symmetrical Face : Symmetrical
- Face : Brown
2. Eye Examination:
- Eksophtalmus : None
- Enophtalmus : None
- Palpebra : Edema (-/-)
- Conjunctiva : Anemic (-/-)
- Sklera : Not jaundice
- Pupil : Isokor, light reflexes are on the left and right
- Eye movements : All directions
3. Ear Examination:
- Ear canal : Roomy
- Serumen : None
- Secret : None
- Tragus Press Pain : None
- Hearing Loss : None

6
4. Nose Examination:
- Deforestation : None
- Secret : None
- Epithaxis : None
- Mucosa Hyperiperemia : None
- Septum Deviation : None
5. Mouth and Sores Examination
- Lips : Dry lips, Cyanosis does not exist
- Teeth : Complete
- Gum : Normal
- Tongue : Sprue is absent, papillary atrophy is absent, white or
yellow spots are absent
- Tonsils : T1 / T1, calm
- Faring : Not hyperemic
6. Neck Examination
- Inspection : Symmetrical, no lumps appear
- Palpation : No thyroid enlargement, no KGB enlargement
- JVP : 5+2 cmH2O
7. Skin
- Hyperpigmentation : Not found
- Ikteric : None
- Ptekhie : None
- Cyanosis : None
- Pale on palms : None
- Pale on the soles of the feet : None
- Turgor : Come back fast
8. Thoracic Examination
Front Lungs
Symmetrical, the movement of the right and left hemithorax is the
Inspection :
same. There is no retraction, there are no widening ribs.
There is no tenderness, the right hemithoracic fremitus is the not
Palpation :
same as the left hemithorax.
Percussion : Redup from ICS V in the left lung fields.

7
 The right hemithoracic breathing sound is not same as the left,
Auscultation : vesicular type of breathing sounds weakened in the left lung than
right, ronkhi (+) and no wheezing.

Rear Lungs
Inspection : Right and left symmetrical.
There is no tenderness, the right hemithoracic fremitus is the not
Palpation :
same as the left hemithorax.
Percussion : Redup from ICS V in the left lung fields.
The right hemithoracic breathing sound is not same as the left,
Auscultation : vesicular type of breathing sounds weakened in the left lung than
right, ronkhi (+) and no wheezing.

Heart
Ictus cordis and pulsation seen in ICS VI linea axilaris anterior
Inspection :
sinistra.
Ictus cordis palpable in ICS VI linea axilaris anterior sinistra, thrill is
Palpation :
not palpable, tenderness is absent.
Above: ICS II linea parasternalis sinistra.
Percussion : Bottom Right: ICS VI linea midclavicularis dextra
Lower Left: ICS VI linea axilaris anterior sinistra
Auscultation : M1> M2, T1> T2, A2> A1, P2> P1, no murmur, no gallop.

9. Abdomen Examination
Flat, no inflammation, no medusa caput, no spider naevi, no lump,
Inspection :
prominent umbilicus (-), umbilical hernia (-)
Palpation : Limp, no tenderness, liver not palpable, spleen not palpable.
Percussion : Timpani, shift dullness (-), undulation (-)
Auscultation : bowel sounds(+)

10. Extremities
Warm acral in both superior extremities, no edema, muscle strength:
Superior :
5, no joint pain, no erythema, CRT<2 second
Warm akral on both inferior extremities, edema (+), muscle strength:
Inferior :
5, no joint pain, no erythema, CRT<2 second

8
 11. Genitalia Examination
No inspection.

2.3.Neurological Examination
No inspection.

2.4.Supporting Investigation
Laboratory Examination
Laboratorium Examination
Hematology (May 31, 2019)

Parameter Result Normal Result

Hematology
Haemoglobin 13,9 g/dl 14-18 g/dl
Leukocyte 8.500/ ul 4.200-11.000/ul
Hematocrit 40,3 % 42,0-52,0 %
Platelets 185.000/ ul 150.000 – 440.000/ ul
Calculate type
- Eosinophil 3,4 % 1 -3 %
- Basophil 0,9 % 0–1%
- Neutrophil 57,9 % 40 – 60 %
- Limfocyte 20,1 % 20 – 50 %
- Monocyte 17,7 % 2–8%
LED
LED 1 hour 19 mm/hour <10
Clinical Chemistry
BSS Stic 142 mg/dl 70 – 140 mg/dl
Ureum 27 mg/dL 10-50 mg/dL
Kreatinin 1,3 mg/dL 0,60- 1,50 mg/dL
Natrium 137 mEq/L 135,0 – 148,0 mEq/L
Potassium 3,3 mEq/L 3,5 – 5,5 mEq/L

9
Interpretation:
- Hemoglobin, hematocrit, potassium decreases
- Eosinofil, monocyte, LED 1 hour, and BSS Stic increase

EKG Examination

Interpretation:
- Sinus rhythm
- HR: 91 x/menit, Regular
- Normal axis
- P wave normal
- Interval PR normal
- Q wave patologis in V2 and V3
- Segmen ST normal
- T wave: T inverted V5, V6, I, and II

10
Chest X-Ray

Interpretation:
 Cardiomegaly
 Congestive pulmonum

11
2.5.Resume
 The patient complains shortness of breath getting harder since ± 1 weeks
before entering the hospital.
 Shortness of breath be affected by activity if walk ± 10 m and shortness of
breath disappears when resting, shortness of breath is not affected by
position, weather, dust and emotions.
 Shortness of breath is not accompanied by wheezing and chest pain.
Patient often wake up at night due to shortness of breath.
 Patient also complained that there was a cough with sputum without blood
and when coughing made it more short of breath.
 Patient also complained of swollen on both legs
 Patient said that 1 year ago the patient felt both of his legs swollen
accompanied by shortness of breath and healed after being hospitalized.
 Os admitted that he had shortness of breath which had been felt for 2 years
and was getting worse.
Physical examination results found that the general condition appeared to
be moderate, blood pressure 180/110 mmHg, HR 93 x/minutes, respiratory
rate 29 x/minutes, temperature 36.7 ºC. JVP 5 + 2 cmH2O indicates an
increase jugular vein. thoracic percussion redup from ICS V in the left lung
fields, the right hemithoracic breathing sound is not same as the left, vesicular
type of breathing sounds weakened in the left lung than right and ronkhi
(+/+). Ictus cordis and pulsations seen in ICS VI linea axilaris anterior
sinistra, ictus cordis is palpable, the right hemithoracic fremitus is the not
same as the left hemithorax. Line of right heart: ICS VI linea midclavicularis
dextra, left heart border: ICS VI linea axilaris anterior sinistra. Upper heart
border: ICS II linea parasternalis sinistra. Legs swollen.
The laboratory results of hemoglobin, hematocrit, potassium decreases.
Eosinophil, monosyte, LED 1 hour, and BSS Stic increase. ECG examination
results show sinus rhythm, HR: 93 x/menit, regular, axis normal, P wave
normal, interval PR normal, Q wave patologis in V2 and V3, segmen ST
normal, T wave: T inverted V5, V6, I, and II. Chest X-Ray result
cardiomegaly and congestive pulmonum.

12
2.6.Working Diagnose
Congestive Heart Failure ec Hypertensive Heart Disease

2.7.Different Diagnose
1. Congestive heart failure ec hypertensive heart disease
2. Chronic Obstructive Pulmonary Disease (COPD)

2.8.Treatment
Non pharmacology
1. Bed rest
Pharmacology
1. Oksigen nasal canul 3 L/minute
2. IVFD RL gtt xx/m
3. Inj. Furosemid 3x1 ampl
4. Ramipril 1x2,5 mg tab
5. Aspilet 1x80 mg tab
6. Digoxin 1x1/2 tab
7. KSR 2x1 tab
8. Spironolactone 1x50 mg

2.9.Additional examination
- Echocardiography
- Brain Natriuretic Peptide (BNP)

2.10. Prognose
- Quo Ad Vitam : Dubia ad bonam
- Quo Ad Fungsionam : Dubia ad malam

2.11. Follow Up
On June 5, 2019, patient complained shortness of breath. Blood
pressure 180/110 mmHg, pulse 93 x / minute and breathing 29 x / minute,
temperature 37.2 ºC. JVP 5 + 2 cmH2O indicates an increase jugular vein.

13
thoracic percussion redup from ICS V in the left lung fields, the right
hemithoracic breathing sound is not same as the left, vesicular type of
breathing sounds weakened in the left lung than right and ronkhi (+/+).
Ictus cordis and pulsations seen in ICS VI linea axilaris anterior sinistra,
ictus cordis is palpable, the right hemithoracic fremitus is the not same as
the left hemithorax, line of right heart: ICS VI linea midclavicularis dextra,
left heart border: ICS VI linea axilaris anterior sinistra. Upper heart border:
ICS II linea parasternalis sinistra. Legs swollen. Therapy continues.
On June 6, 2019, patient complained shortness of breath. Blood
pressure 160/100 mmHg, pulse 84 x / minute and breathing 28 x / minute,
temperature 36.5 ºC. JVP 5 + 2 cmH2O indicates an increase jugular vein.
thoracic percussion redup from ICS V in the left lung fields, the right
hemithoracic breathing sound is not same as the left, vesicular type of
breathing sounds weakened in the left lung than right and ronkhi (+/+).
Ictus cordis and pulsations seen in ICS VI linea axilaris anterior sinistra,
ictus cordis is palpable, the right hemithoracic fremitus is the not same as
the left hemithorax, line of right heart: ICS VI linea midclavicularis dextra,
left heart border: ICS VI linea axilaris anterior sinistra. Upper heart border:
ICS II linea parasternalis sinistra. Legs swollen. Therapy continues.

14
 CHAPTER III
CASE ANALYSIS

The patient complained of shorteness of breath getting harder since ± 1

weeks before entering the hospital. Shortness of breath be affected by activity if
walk ± 10 m and shortness of breath disappears when resting, shortness of breath
is not affected by position, weather, dust and emotions. Shortness of breath is not
accompanied by wheezing and chest pain. Patient often wake up at night due to
shortness of breath. Patient also complained that there was a cough with sputum
without blood and when coughing made it more short of breath. Patient also
complained of swollen on both legs.
Physical examination results found that the general condition appeared to be
moderate, blood pressure 180/110 mmHg, HR 93 x/minutes, respiratory rate 29
x/minutes, temperature 36.7 ºC. JVP 5 + 2 cmH2O indicates an increase jugular
vein. thoracic percussion redup from ICS V in the left lung fields, the right
hemithoracic breathing sound is not same as the left, vesicular type of breathing
sounds weakened in the left lung than right and ronkhi (+/+). Ictus cordis and
pulsations seen in ICS VI linea axilaris anterior sinistra, ictus cordis is palpable,
the right hemithoracic fremitus is the not same as the left hemithorax, line of right
heart: ICS VI linea midclavicularis dextra, left heart border: ICS VI linea axilaris
anterior sinistra. Upper heart border: ICS II linea parasternalis sinistra. Legs
swollen. The laboratory results of hemoglobin, hematocrit, potassium decreases.
Eosinofil, monosit, LED 1 hour, and BSS Stic increase. ECG examination results
show sinus rhythm, HR: 93 x/menit, regular , axis normal, P wave normal, PR
interval normal , Q wave patologis in V2 and V3,ST segmen normal, T wave: T
inverted V5, V6, I, and II. Chest X-Ray result cardiomegaly and congestive
pulmonum.
Shortness of breath is not affected by position, weather, dust and emotions.
Shortness of breath is not accompanied by wheezing and chest pain it means
shortness of breath that occurs not because of asthma. The symptoms of asthma
are cough, rhonchus, wheezing, chest tightness.7

15
 The results of physical examination this patient had no barrel chest,
widening between the ribs, hipersonor, long expiratory. Chest X-Ray result
cardiomegaly and congestive pulmonum, so that diagnostic chronic obstuctive
pulmonary disease (COPD) can be removed for this case.6
Congestive Heart failure is a common clinical syndrome characterized by
dyspnea, fatigue, and signs of volume overload, which may include peripheral
edema and pulmonary rales. Shortness of breath experienced by this patient is
more directed at heart failure because there is a several criteria of Framigham
based on the anamnesis, physical examination and investigation.8
Major criteria found in the patients, such as paroxysmal nocturnal dyspnea,
cardiomegaly, increases jugular vein and ronchi and minor criteria ankle edema,
nocturnal cough, dyspnea d’effort. The Framingham criteria found were 4 major
criteria, and 3 minor criteria so that the diagnosis of Congestive Heart Failure
(CHF) could be established.8
Table 1. Framingham Diagnostic Criteria for Heart Failure

Major Criteria Minor Criteria

Acute pulmonary edema Ankle edema
Cardiomegaly Dyspnea d’effort
Hapatojugular reflex Hapatomegaly
Neck vein distension Nocturnal cough
Paroxysmal nocturnal dyspnea or Pleural effusion
orthopnea
Ronchi Tachycardia (>120 beats per minute)
Third heart sound gallop
Heart failure is diagnosed when two major criteria or one major and two
minor criteria are met

Table 1 Framingham Diagnostic Criteria for Heart Failure

Source (King, M. et al. (2012).

From anamnesis patient complain shortness of breath be affected by activity

if walk ± 10 m and shortness of breath disappears when resting based on New

16
 York Heart Association Functional Classification of Heart Failure patient is at
NYHA III. The New York Heart Association classification system is the simplest
and most widely used method to gauge symptom severity. The classification
system is a well-established predictor of mortality and can be used at diagnosis
and to monitor treatment response.8

Table 2. New York Heart Association Functional Classification of Heart Failure

Class Description
I No limitations of physical activity, no heart failure symptoms
II Mild limitations of physical activity, heart failure symptoms with
significant exertion; comfortable at rest or with mild activity
III Marked limitation of physical activity, heart failure symptoms with
mild exertion; only comfortable at rest
IV Discomfort with any activity, heart failure symptoms occur at rest

Table 2 NYHA Classification of Heart Failure

Source (King, M. et al. (2012).

Based on anamnesis, patient have history of hypertension is existed since

± 11 years ago, uncontrolled. Hypertension remains a significant risk factor for
development of congestive heart failure (CHF), with various mechanisms
contributing to both systolic and diastolic dysfunction. The pathogenesis of
myocardial changes includes structural remodeling, left ventricular hypertrophy,
and fibrosis.9
Table 3. Causes of Heart Failure
Common
 Coronary artery disease
 Hypertension
 Idiopathic cardiomyopathy
 Valvular heart disease
Less common
 Arrhytmia (e.g., tachycardia, bradicardia, heart block)
 Collagen vascular disease (e.g., systemic lupus erythematosus,

17
 scleroderma)
 Endocrine/metabolic disorders (e.g., thyroid disease, diabetes melitus,
pheochromocytoma, other genetic disorders)
 Hypertrophic cardiomyopathy
 Myocarditis
 Pericarditis
 Postpartum cardiomyopathy
 Restrictive cardiomyopathies (e.g., amyloidosis, hemochromatosis,
sarcoidosis, other genetic disorders)

Table 3 Causes of Heart Failure

Source (King, M. et al. (2012).

There is a history of smoking habits since 20 years ago, smoking can

stimulate the process of atherosclerosis because of the direct effect on the artery
wall. Therefore, smoking can increase the risk of heart failure.6
ECG examination results show sinus rhythm, HR: 93 x/menit, regular, axis
normal, P wave normal, PR interval normal , Q wave patologist in V2 and V3,ST
segmen normal, T wave: T inverted V5, V6, I, and II. Q wave patologist indicate
patient have infark miokard transmural. T inverted indicate patient have infark
miokard transmural or aneurisma.10
Chest X-Ray result cardiomegaly and congestive pulmonum. Chest
radiography should be performed initially to evaluate for heart failure because it
can identify pulmonary causes of dyspnea (e.g., pneumonia, pneumothorax,
mass). Pulmonary venous congestion and interstitial edema on chest radiography
in a patient with dyspnea make the diagnosis of heart failure more likely. Other
findings, such as pleural effusion or cardiomegaly, may slightly increase the
likelihood of heart failure, but their absence is only slightly useful in decreasing
the probability of heart failure.8
Pathophysiology of congestive heart failure make cardiomegaly at first the
heart tries to make up for this by:

18
  Enlarging. The heart stretches to contract more strongly and keep up with
the demand to pump more blood. Over time this causes the heart to
become enlarged.
 Developing more muscle mass. The increase in muscle mass occurs
because the contracting cells of the heart get bigger. This lets the heart
pump more strongly, at least initially.
 Pumping faster. This helps increase the heart’s output.6
The body also tries to compensate in other ways:
 The blood vessels narrow to keep blood pressure up, trying to make up for
the heart’s loss of power.
 The body diverts blood away from less important tissues and organs (like
the kidneys), the heart and brain.
These temporary measures mask the problem of heart failure, but they don’t solve
it. Heart failure continues and worsens until these compensating processes no
longer work.6
Picture 1 is an algorithm for the evaluation and diagnosis of heart failure.
When a patient presents with symptoms of heart failure, the initial evaluation is
performed to identify alternative or reversible causes of heart failure and to
confirm its presence. If the Framingham criteria are not met, or if the BNP level is
normal, systolic heart failure is essentially ruled out. Echocardiography should be
performed to assess LVEF when heart failure is suspected or if diastolic heart
failure is still suspected when systolic heart failure is ruled out. Treatment options
are guided by the final diagnosis and echocardiography results, with a
consideration to evaluate for CAD.

19
 Picture 1 Evaluation and Diagnosis of Heart Failure
Source (King, M. et al. (2012).

This patient was given treatment in the form of a loop diuretic, furosemid.
Diuretics are an important and usually necessary first step in the pharmacologic
treatment of CHF. Diurectics function to reduce edema by reduction of blood
volume and venous pressures and salt restriction (to reduce fluid retention) in
patients with current or previous heart failure symptoms and reduced left
ventricular (LV) ejection fraction (EF) for symptomatic relief.11
Ramipril 1x2,5 mg tab, Angiotensin-converting enzyme (ACE) inhibitors
are very important medicines for managing heart failure. ACE inhibitors block the
action of a protein (enzyme) that causes blood vessels to narrow. As a result,
blood vessels relax and widen. This lowers blood pressure and makes it easier for
your heart to pump blood. These medicines also help your body release water and
salt (sodium), which also helps lower blood pressure.11
Aspilet 1x80 mg tab, Aspilet prevents blood clots from forming in the
arteries. Antiplatelet works by reducing platelet aggregation, which can inhibit

20
thrombus formation in arterial circulation It can help certain people lower their
risk of a heart failure or stroke.11
Digoxin 1x1/2 tab, digoxin therapy has no effect on mortality in heart
failure. Digoxin may be useful for maintaining clinical stability and exercise
capacity in patients with symptomatic heart failure. Digoxin appears to be of most
benefit in patients with severe heart failure, cardiomegaly and a third heart sound.
Digoxin should be used as a second-line drug after diuretics, angiotensin-
converting enzyme inhibitors and beta-blockers in patients with congestive heart
failure who are in sinus rhythm. Digoxin should be used as a first-line drug in
patients with congestive heart failure who are in atrial fibrillation.11
KSR 2x1 tab, mineral supplements with a function to treat or prevent low
amounts of potassium in the blood. The normal level of potassium in the blood is
very important. Potassium helps cells, kidneys, heart, muscles, and nerves
function properly.11
Spironolactone 1x50 mg, spironolactone is an aldosterone antagonist.
spironolactone is a weak diuretic and its use is combined with other diuretics
(HCT and furosemide) to prevent hypokalemia.11

21
 CHAPTER IV
CONCLUSION

A case has been reported regarding a 50-years-old man came with a

complaint of Shorteness of breath since ± 1 weeks before entering the hospital.
Patient also complained that there was a cough with sputum without blood and
when coughing made it more short of breath. Patient also complained of swollen
on both legs.
Physical examination results found that the general condition appeared to
be moderate, blood pressure 180/110 mmHg, HR 93 x/minutes, respiratory rate 29
x/minutes, temperature 36.7 ºC. JVP 5 + 2 cmH2O indicates an increase jugular
vein. Thoracic percussion redup from ICS V in the left lung fields, the right
hemithoracic breathing sound is not same as the left, vesicular type of breathing
sounds weakened in the left lung than right and ronkhi (+/+). Ictus cordis and
pulsations seen in ICS VI linea axilaris anterior sinistra, ictus cordis is palpable,
the right hemithoracic fremitus is the not same as the left hemithorax, line of right
heart: ICS VI linea midclavicularis dextra, left heart border: ICS VI linea axilaris
anterior sinistra. Upper heart border: ICS II linea parasternalis sinistra. Legs
swollen.
The laboratory results of hemoglobin, hematocrit, potassium decreases.
Eosinophil, monosyte, LED 1 hour, and BSS Stic increase. ECG examination
results show sinus rhythm, HR: 93 x/menit, regular , normal axis, normal P wave,
interval PR normal, Q wave patologis in V2 and V3, segmen ST normal, T wave:
T inverted V5, V6, I, and II. Chest X-Ray result cardiomegaly and congestive
pulmonum.
Based on the history, physical examination and investigation, diagnosis in
the case of possible congestive heart failure.

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