CONGESTIVE HEART FAILURE

CASE REPORT SESSION

To fulfill the case report assignment

in the Cardiology Department of Dustira Hospital

Farhan Arsyad
NursyifaDewiAfifah
Marvelo Surya Rahman Djohar
Sarah Maeta
Nur IlmaMailani

FACULTY OF MEDICINE
GENERAL ACHMAD YANI UNIVERSITY
CIMAHI
2019
General Information:
Patient Name : Mr. DH
Ward : Ceremai, Room 3
Medical Record Number : 36268
Gender : Male
Age : 44 Years Old
Religion : Islam
Occupation : No Occupation-Retired
Address : Gaya Kusen no.159 rt 04/04. Cibeber
Date of Entry : 07 February 2019
Date of Examination : 08 February 2019

ANAMNESIS
Chief Complaint:
Breathlessness

Auto-Anamnesis:
Present Illness:
An 44-year-old man presents to the Emergency Room (ER) with breathlessness that
was endured for the past 2 month. He reported that 1 weeks was particularly tough
for him because he couldn't walk 2-3 meters from the place he was sitting without
getting severely short of breath. However, the patient said that when he sat back
down in his chair or whenever he is at rest, the symptoms he felt abated. He stated
that he didn’t come sooner because a few times he felt as though the symptoms
were resolving and thought he would get over it. Each time he tried walking or
moving the shortness of breath became worse again. The patient also complained
of breathlessness that occurred during the night which made it hard to sleep. When
resting, he usually used 3 pillows because it eased his current symptoms to a certain
extent. The patient also had an occasional cough accompanied with leg swelling.

Previous Medical History:

1
About 1 year ago the patient experienced similar breathlessness and was
hospitalized in the same room at Mitra Kasih Hospital for a few days. He stated
that the breathlessness he feels this time around feels worse than before. The patient
rarely went to the hospital to control her previous heart condition, but could not
remember what the name of his heart condition was. Around that same timeframe
the patient stated that he had a high cholesterol level but did not remember the exact
level of his cholesterol results. he also had previous history of hypertension and
took type of medication.

Personal and Social History

The patient has a family member with a history of previous heart conditions or
causes of death that were related with heart disease from his father and his old
brother.

PHYSICAL EXAMINATION
General Condition
Awareness : Compos mentis
Pain impression : Moderate
Sleep : Supine, 3 pillowson a bed
Height : 166 cm
Weight : 85 kilograms
BMI : 30,79 kg/m2
Nutritional level : Obesity I

Vital Signs
Blood pressure : 110/70 mmHg
Pulse : 120 beats/minute
Respiration : 32 breaths/minute
Respiratory Type : Abdominalthoracal
Temperature : 36,6°C

2
Specific Examination
Head
a. Skull : Normocephal
b. Face : Puffy Face (-)
c. Eyes:
- Eyelids : Eyelid edema -/-
- Sclera : Icteric -/-
- Conjunctiva : Anemic -/-
- Pupil : Round, Isochore ± 3 mm
- Eye Lens : Pseudophakia ODS
d. Ears : No abnormalities
e. Nose : No abnormalities
f. Mouth:
- Lips : No abnormalities
- Gums and teeth : No abnormalities
- Tongue : No abnormalities
- Oral cavity : No abnormalities
Neck
a. Inspection
- Trachea : Deviation (-)
- Thyroid gland : No enlargement
- Lymph Nodes : No enlargement
- Widening of vein : Visible
b. Palpation
- Thyroid gland : No enlargement
- Lymph Nodes : Not palpable
- Tumor : None
- Stiff neck : None
- Jugular venous pressure : 5 + 3 cmH2O
- HJR : Negative

3
Armpit : No abnormalities
- Tumors : None
Anterior Thorax
a. Inspection
- Shape : Symmetric
- Movement : Symmetric
- Intercostal space : Not widened or narrowed
- Skin : No abnormalities
- Musculature : No abnormalities
- Ictus cordis : Visible
- Mammae : No abnormalities
b. Palpation
- Skin : No abnormalities
- Musculature : No abnormalities
- Intercostal space : Not widened or narrowed
- Vocal Fremitus : Normal, right = left
- Apical Impulse : Palpable
o Localization: ICS VI, 2 cm lateral from the
left midclavicular line
o Intensity : Strong
o Thrill : No thrill
c. Percussion
- Comparison percussion : Sonor, right = left
- Heart Boundaries :
Upper right = ICS II right parasternal line
Upper left = ICS II left parasternal line
Lower right = ICS IV, right sternal line
Lower left = ICS V, left anterior axillary line
d. Auscultation
- Respiratory Sounds : Rhonchi +/+, wheezing -/-
- Vocal resonance : Normal, right = left

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 - Heart sounds : S1 & S2 regular, murmur (+), gallop (+)
Posterior Thorax
a. Inspection
- Shape : Symmetric
- Movement : Symmetric
- Skin : No abnormalities
- Musculature : No abnormalities
b. Palpation
- Intercostal space : Not widened or narrowed
- Musculature : No abnormalities
- Vocal Fremitus : Normal, right = left
c. Percussion
- Comparison percussion: Sonor, right = left
- Lower boundaries: Left: XI Thoracic Vertebrae
Right: X Thoracic Vertebrae
d. Auscultation
- Respiratory Sounds : Rhonchi +/-, wheezing -/-
- Vocal resonance : Normal, right = left

Abdomen
a. Inspection
- Shape : Flat
- Skin : No abnormalities
- Umbilicus : Indented
b. Auscultation
- Bowel : (+) normal, 10 times/minute
- Additional Sounds : None
c. Palpation
- Wall : Smooth, fluid wave (-)
- Tenderness : None
- Mass / tumor : None

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 - Liver : Not Palpable
- Spleen : Not palpable
- Troube space : Empty
- Kidney : Ballotement -/-
d. Percussion
- Percussion sound: Tympani
- CVA pain: -/-

Extremities:
a. Upper: Warm skin, CRT< 2 seconds, clubbing fingers (-/-)
b. Lower: Warm skin, CRT<2 seconds, Pitting edema (+/+)

DIAGNOSTIC TESTS
Laboratory Results
Blood Test
Hemoglobin :13,9 g/dL
Erythrocyte :5,3 x106/uL
Leukocyte :9,8 x103/uL
Hematocrit :42,1 %
Thrombocyte :207 x103/uL

Diff Count
Basophil : 0,9 %
Eosinophil : 2,8 %
Segment : 57,2 %
Lymphocyte : 30,3 %
Monocyte : 6,8 %

Electrolite
Natrium : 136 mmol/L
Chlorida : 104 mmol/L

6
Calium : 5 mmol/L

Ureum : 37 mg/dl
Creatinin : 1 mg/dl

Electrocardiogram (ECG)

ECG Interpretation:

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Heart Rate : 62 beats/minute
Rhythm : Regular Sinus Rhythm
Axis : Normal
Wave Abnormalities :
T-tall on lead II, aVL, aVF, V4, V5, V6 (Hyperkalemia)

X-Ray Interpretation:
Appearance of the Heart: Cardiomegaly

DIAGNOSIS
Differential Diagnosis:
1. Congestive Heart Failure NYHA Stage III
Clinical Diagnosis : CHF NYHA Stage III
Anatomical Diagnosis :Hyperkalemia
Etiological Diagnosis :Hypertensive Heart Disease

TREATMENT

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Non-Pharmacological Treatment:
a. Oxygen 2-4L via Nasal Cannula
b. Lifestyle Changes
1. Heart-healthy Diet: Eat an overall healthy dietary pattern that emphasizes a
variety of fruits and vegetables, whole grains, low-fat dairy products, skinless
poultry and fish, nuts and legumes, and non-tropical vegetable oils. Also, limit
saturated fat, trans fat, cholesterol, sodium, red meat, sweets and sugar-sweetened
beverages.
2. Aim for a Healthy Weight: Being obese means that there is more body fat within
the body. With an increase in weight the patient is more likely to develop other
complications like coronary heart disease, high blood pressure, type 2 diabetes,
breathing problems, and certain cancers. Health professionals recommend losing 5
to 10 percent of the patient's initial weight over the course of about 6 months. A
loss of just 3 to 5 percent of the patient's current weight can lower triglycerides and
glucose levels in the blood, as well as lower the risk of developing type 2 diabetes.
Losing more than 3 to 5 percent can improve blood pressure readings, lower bad
LDL cholesterol, and increase good HDL cholesterol.

Pharmacological Treatment:
1. Furosemide: A diuretic which increase urination to help the kidneys eliminate
excess fluid from the body.
2. Candesartan: An Angiotensin II Receptor Blocker that help relax blood vessels,
which lowers blood pressure and makes it easier for the heart to pump blood.
3. Clopidogrel: An antiplatelet drug which works by blocking platelets from
sticking together and prevents them from forming harmful clots which could lead
to a heart attack or stroke. It helps keep blood flowing smoothly in your body.

Prescription
R/ Furosemide 40mg tab No.VII

9
S 1 dd 1
R/ Candesartan 4mg tab No. VII
S 1 dd 1
R/ Clopidogrel 75 mg tab No. VII
S 1 dd 1

RESUME
An 44-years-old man presents to the Emergency Room (ER) with
breathlessness that was endured for the past 2 month. he reported that yesterday
was particularly tough for him because he couldn't walk 2-3 meters from the place
he was sitting without getting severely short of breath. However, the patient said
that when he sat back down in his chair or whenever he is at rest, the symptoms he
felt abated. The patient also complained of breathlessness that occurred during the
night which made it hard to sleep. When resting, he usually used 3 pillows because
it eased him current symptoms to a certain extent.The patient had an occasional
cough accompanied with leg swelling.About 1 year ago the patient experienced
similar breathlessness and was hospitalized in the Intensive Care Unit (ICU) at a
different hospital for a few days before being discharged. He stated that the
breathlessness he feels this time around feels worse than before. Around that same
timeframe the patient stated that he had a high cholesterol level but did not
remember the exact level of her cholesterol results. And he had previous history of
hypertension and took type of medication.
The patient has a family members with a history of previous heart conditions
or causes of death that were related with heart disease from her father.

PHYSICAL EXAMINATION
General Condition
• Awareness : Compos mentis
• Pain impression : Moderate
• Sleep : Supine, 3 pillows on a bed

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• Height : 166 cm
• Weight : 85 kilograms
• BMI : 30,79 kg/m2
• Nutritional level : Obesity I
Vital Signs
• Blood pressure : 120/80 mmHg
• Pulse : 84 beats/minute
• Respiration : 24 breaths/minute
• Respiratory Type : Thoracoabdominal
• Temperature : 36,6°C
Head
Face : Puffy Face (-)
Eyes:
• Eyelids : Eyelid edema -/-
• Sclera : Icteric -/-
• Conjunctiva : Anemic -/-
Ears : No abnormalities
Nose : PCH (-)
Mouth:
No abnormalities
Neck
Jugular venous pressure : 5 + 3 cmH2O
HJR : Negative
Anterior Thorax
a. Inspection
Shape : Symmetric
Movement : Symmetric
Intercostal space : Not widened or narrowed

11
 Skin : No abnormalities
Musculature : No abnormalities
Ictus cordis : Visible
b. Palpation
Musculature : No abnormalities
Intercostal space : Not widened or narrowed
Vocal Fremitus : Normal, right = left
Aapical Impulse : Palpable
Localization : ICS VI, 2 cm lateral from the left midclavicular line
Intensity : Strong
Thrill : No thrill
c. Percussion
Comparison percussion : Sonor, right = left
Heart Boundaries:
Upper right = ICS II right parasternal line
Upper left = ICS II left parasternal line
Lower right = ICS IV right sternal line
Lower left = ICS V left anterior axillary line
d. Auscultation
Respiratory Sounds : Rhonchi +/-, wheezing -/-
Vocal resonance : Normal, right = left
Heart sounds : S1 & S2 regular, murmur (-), gallop (-)
c. Percussion
Comparison percussion : Sonor, right = left
Lower boundaries: Left: XI Thoracic Vertebrae
Right : X Thoracic Vertebrae
d. Auscultation
Respiratory Sounds : Rhonchi +/+, wheezing -/-

12
 Vocal resonance : Normal, right = left
Abdomen
A. Inspection
Umbilicus : Indented

b. Auscultation
Bowel : (+) normal, 10 times/minute
Additional Sounds : None
c. Palpation
Wall : Smooth, fluid wave (-)
Tenderness : None
Mass / tumor : None
Liver : Not Palpable
Spleen : Not palpable
Troube space : Empty
Kidney : Ballotement -/-
d. Percussion
Percussion sound : Tympani
CVA pain : -/-
Extremities:
a. Upper: Warm skin, CRT< 2 seconds, clubbing fingers (-/-)
b. Lower: Warm skin, CRT<2 seconds, Pitting edema (+/+)

DIAGNOSTIC TESTS
Blood Test
No abnormalities
Diff Count
No abnormalities

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Renal Function
No abnormalities
Electrolyte
Potassium : 5,90 mmol/L(hyperkalemia)

Profile Lipid
LDL-Cholesterol : 159 mg/dl

ECG INTERPRETATION
• Heart Rate : 62 beats/minute
• Rhythm : Regular Sinus Rhythm
• Axis : Normal
• Wave Abnormalities :T-tall on lead II, aVL, aVL, V4, V5, V6
(Hyperkalemia)

CHEST X-RAY
Appearance of the Heart: Cardiomegaly

DIAGNOSIS
Clinical Dianosis :
Congestive Heart Failure NYHA stage IV
Anatomical Diagnosis :
Hyperkalemia
Etiologic Diagnosis :
Hypertensive Heart Disease

TREATMENT
Non-Pharmacological Treatment:
a. Oxygen 2-4L via Nasal Cannula
b. Lifestyle Changes
1. Heart-healthy Diet

14
 2. Aim for a Healthy Weight
Pharmacological Treatment:
1. Diuretic :Furosemide
2. ARB :Candesartan
3. Antiplatelet :Clopidogrel
Prescription
R/ Furosemide 40mg tab No.VII
S 1 dd 1
R/ Candesartan 4mg tab No. VII
S 1 dd 1
R/ Clopidogrel 75 mg tab No. VII
S 1 dd 1

PROGNOSIS
• Quo ad vitam : dubia ad bonam
• Quo ad functionam: dubia ad malam

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 THEORY

DEFINITION

Heart failure is a clinical syndrome (a set of signs and symptoms) marked

shortness of nadas and fatik (at rest or when activities) caused by abnormalities in
the structure or function of the heart.1(IPD Page 1134) Congestion heart failure is
divided into two i.e. systolic and diastolic heart failure that can only be
distinguished on the basis of an examination of the institution, namely eco-doppler.
Systolic heart failure in which the inability of the heart to contract so that the cardiac
output decreases and causes complaints. While the diastolic heart failure is due to
the disturbance of the ventricular filling disorders dang relaxation. Congestion heart
failure is divided into two i.e. systolic and diastolic heart failure that can only be
distinguished on the basis of an examination of the institution, namely eco-doppler.
Systolic heart failure in which the inability of the heart to contract so that the cardiac
output decreases and causes complaints. While the diastolic heart failure is due to
the disturbance of the ventricular filling disorders dang relaxation.
Causes of heart failure can be caused by some other disease i.e. underline,
old history repeat myocardial miocard, long-standing-hypertension (HHF),
abnormalities of the valve (RHD) heart diease, anemia, heart disease, typhoid post!,
cardiomyopathy, and coronary artery disease.1,2

Classification Of Degrees Failure Based On New York Heart Association (NYHA)

Functional Classification Of Heart

16
 NYHA I Heart disease, but there are no
symptoms or limitations in daily
physical activity is good, (walking,
climbing stairs, etc.)

NYHA II Symptoms are mild (mild shortness of

breath and/or angina) and there is the
limitation of physical activity in the
light of ordinary everyday

NYHA III There is daily physical activity

limitations due to the symptoms of
heart failure on a lighter level. (20-100
m). Patients only feel comfortable with
rest

NYHA IV There was heavy activity limitations,

such as the symptoms appear at rest

Based on the criteria of Framingham

1. Mayor Criteria
 Dyspneu nocturnal paroxysmal / orthopneu
 JVP increased
 Wet ronkhi
 Cardiomegali
 Acute Pulmonary Edema
 Gallop S3
 Vena pressure >16 cm H2O

2. Minor Criteria
 Edema of the extremities

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  Night Cough
 Dsypneu on effort
 Hepatomegaly
 Pleural effusion
 vital Capacity decreased from nomal 1/3
 Flutter (>120x/menit)

Diagnostic criteria at least 1 major and 2 minor

 Shortness of breath is not accompanied by

 Hypertension History since 16 years ago accompanied by high cholesterol
history
 Takipeneu dan Flutter

RISK FACTORS OF CHF

- Dietary indiscretion
- Myocardial ischemia/infarction
- Arrhythmias (tachycardia or bradycardia)
- Discontinuation of HF therapy
- Infection
- Anemia
- Alcohol consumption
- Pregnancy
- Worsening hypertension
- Acute valvular insufficiency
- Initiation of medication that worsen HF
Calcium antagonist
Beta blocker
NSAID
Antiarrhythmic agents (all class I agents, sotalol Class III)
Anti TNF antibodies

18
PATHOPHYSIOLOGY
The common pathophysiologic state that perpetuates the progression of heart failure
is extremely complex, regardless of the precipitating event. Compensatory
mechanisms exist on every level of organization, from the subcellular all the way
through to organ-to-organ interactions. Only when this network of adaptations
becomes overwhelmed does heart failure ensue
1. Adaptations
Most important among the adaptations are the following:
 The Frank-Starling mechanism, in which an increased preload helps to
sustain cardiac performance
 Alterations in myocyte regeneration and death
 Myocardial hypertrophy with or without cardiac chamber dilatation, in
which the mass of contractile tissue is augmented
 Activation of neurohumoral systems
The release of norepinephrine by adrenergic cardiac nerves augments
myocardial contractility and includes activation of the renin-angiotensin-
aldosterone system [RAAS], the sympathetic nervous system [SNS], and other
neurohumoral adjustments that act to maintain arterial pressure and perfusion of
vital organs.
In acute heart failure, the finite adaptive mechanisms that may be adequate
to maintain the overall contractile performance of the heart at relatively normal
levels become maladaptive when trying to sustain adequate cardiac performance.
The primary myocardial response to chronic increased wall stress is
myocyte hypertrophy, death/apoptosis, and regeneration. This process eventually
leads to remodeling, usually the eccentric type. Eccentric remodeling further
worsens the loading conditions on the remaining myocytes and perpetuates the
deleterious cycle. The idea of lowering wall stress to slow the process of remodeling
has long been exploited in treating heart failure patients.
The reduction of cardiac output following myocardial injury sets into
motion a cascade of hemodynamic and neurohormonal derangements that provoke

19
activation of neuroendocrine systems, most notably the above-mentioned
adrenergic systems and RAAS.
The release of epinephrine and norepinephrine, along with the vasoactive
substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which
increases calcium afterload and, via an increase in cyclic adenosine monophosphate
(cAMP), causes an increase in cytosolic calcium entry. The increased calcium entry
into the myocytes augments myocardial contractility and impairs myocardial
relaxation (lusitropy).
The calcium overload may induce arrhythmias and lead to sudden death.
The increase in afterload and myocardial contractility (known as inotropy) and the
impairment in myocardial lusitropy lead to an increase in myocardial energy
expenditure and a further decrease in cardiac output. The increase in myocardial
energy expenditure leads to myocardial cell death/apoptosis, which results in heart
failure and further reduction in cardiac output, perpetuating a cycle of further
increased neurohumoral stimulation and further adverse hemodynamic and
myocardial responses.
In addition, the activation of the RAAS leads to salt and water retention,
resulting in increased preload and further increases in myocardial energy
expenditure. Increases in renin, mediated by a decreased stretch of the glomerular
afferent arteriole, reduce delivery of chloride to the macula densa and increase
beta1-adrenergic activity as a response to decreased cardiac output. This results in
an increase in angiotensin II (Ang II) levels and, in turn, aldosterone levels, causing
stimulation of the release of aldosterone. Ang II, along with ET-1, is crucial in
maintaining effective intravascular homeostasis as mediated by vasoconstriction
and aldosterone-induced salt and water retention.
The concept of the heart as a self-renewing organ is a relatively recent
development. This paradigm for myocyte biology created an entire field of research
aimed directly at augmenting myocardial regeneration. The rate of myocyte
turnover has been shown to increase during times of pathologic stress. In heart
failure, this mechanism for replacement becomes overwhelmed by an even faster
increase in the rate of myocyte loss. This imbalance of hypertrophy and death over

20
regeneration is the final common pathway at the cellular level for the progression
of remodeling and heart failure.

2. Angiotensin II
Research indicates that local cardiac Ang II production (which decreases
lusitropy, increases inotropy, and increases afterload) leads to increased myocardial
energy expenditure. Ang II has also been shown in vitro and in vivo to increase the
rate of myocyte apoptosis. [18] In this fashion, Ang II has similar actions to
norepinephrine in heart failure.
Ang II also mediates myocardial cellular hypertrophy and may promote progressive
loss of myocardial function. The neurohumoral factors above lead to myocyte
hypertrophy and interstitial fibrosis, resulting in increased myocardial volume and
increased myocardial mass, as well as myocyte loss. As a result, the cardiac
architecture changes which, in turn, leads to further increase in myocardial volume
and mass.

3. Myocytes and myocardial remodeling

In the failing heart, increased myocardial volume is characterized by larger
myocytes approaching the end of their life cycle. [19] As more myocytes drop out,
an increased load is placed on the remaining myocardium, and this unfavorable
environment is transmitted to the progenitor cells responsible for replacing lost
myocytes.
Progenitor cells become progressively less effective as the underlying
pathologic process worsens and myocardial failure accelerates. These features—
namely, the increased myocardial volume and mass, along with a net loss of
myocytes—are the hallmark of myocardial remodeling. This remodeling process
leads to early adaptive mechanisms, such as augmentation of stroke volume (Frank-
Starling mechanism) and decreased wall stress (Laplace law) and, later, to
maladaptive mechanisms such as increased myocardial oxygen demand,
myocardial ischemia, impaired contractility, and arrhythmogenesis.
As heart failure advances, there is a relative decline in the counterregulatory
effects of endogenous vasodilators, including nitric oxide (NO), prostaglandins

21
(PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic
peptide (BNP). This decline occurs simultaneously with the increase in
vasoconstrictor substances from the RAAS and the adrenergic system, which
fosters further increases in vasoconstriction and thus preload and afterload. This
results in cellular proliferation, adverse myocardial remodeling, and antinatriuresis,
with total body fluid excess and worsening of heart failure symptoms.

COMPLICATIONS
Abnormal Heart Rhythm
In a normal heart, the upper chambers (called the atria) and lower chambers (the
ventricles) squeeze and relax in turn to move blood through body. If ticker is weak,
these chambers might not squeeze at the right time. heart might beat too slowly,
too quickly, or in an irregular pattern. When the rhythm is off, heart can't pump
enough blood out to body.
Atrial fibrillation (AFib) is one type of abnormal heart rhythm that heart failure can
cause. It causes heart to quiver and skip instead of beating.
An irregular heartbeat can cause blood to pool, which might lead to clots. A clot
that forms in a vein is called venous thromboembolism. The clot can break free and
travel to lungs. Then it's called pulmonary embolism. Or a clot can travel to brain.
If it blocks a blood vessel there, could have a stroke.

Heart Valve Problems

Heart has four valves that open and close to keep blood flowing in and out of
heart. As the damage gets worse and heart has to work harder to pump out blood, it
gets bigger. The change in size can damage the valves.

Kidney Damage or Failure

Kidneys filter wastes and extra fluid out of blood. Just like other organs, they
need a steady supply of blood to work like they should.

22
Without the amount of blood they need, they won’t be able to remove enough
wastes from blood. This is called kidney failure. It's treated with dialysis or a
kidney transplant.
Kidney disease can also make heart failure worse. Damaged kidneys they can't
remove as much water from blood as healthy ones. 'll start to hold onto fluid, which
boosts blood pressure. High blood pressure makes heart work even harder.

Anemia
This is a lack of the red blood cells that move oxygen to ody's tissues. If patient
have anemia, the body may not get enough oxygen. Kidneys make a protein called
erythropoietin (EPO), which helps body make new red blood cells. Kidney damage
from heart failure prevents the body from making enough EPO.

Liver Damage
Liver breaks down toxins so the body can remove them. It also stores bile, a
fluid used to digest food.Heart failure can rob the liver of the blood it needs to work.
The fluid buildup that comes with it puts extra pressure on the portal vein, which
brings blood to liver. This can scar the organ to the point where it doesn't work as
well as it should.

Lung Problems
A damaged heart can't pump blood as effectively from lungs out to body. Blood
backs up, raising pressure in the veins inside the lungs. This pushes fluid into the
air sacs. As liquid builds up, it gets harder to breathe. This is called pulmonary
edema.

Extreme Weight Loss and Muscle Loss

Heart failure can affect muscle and fat metabolism. In the late stages, might lose a
lot of weight and muscle mass. The muscles can get smaller and weaker

23
TREATMENT
Non Pharmacology
-Education about heart failure, causes and how to recognize and efforts when
complaints arise, and the basis of treatment
- Diet and control of salt intake can only be given 1g, and 1 liter / day fluid intake.
- Weight monitoring, in cases with sudden weight gain can be considered for an
increase in diuretic doses.
- Patients must be hospitalized because they tend to not be able to maintain the need
for fast-acting drugs, namely bypassing intravenously.

Pharmacology
Get patients requested to be hospitalized for parenteral therapy. Angiotensin
Converting Enzym Inhibitors or Angiotensin Receptor Blockers (ARBs) are first-
line drugs. Must be given as soon as possible. The mechanism of action of the
angiotensin receptor works by reducing blood pressure through the renin-
angiotensin-aldosterone system. Angiotensin receptor blockers inhibit angiotension
II binding with its receptors in blood vessels resulting in vasodilation, decreased
vasopressin production, and reduced aldosterone secretion. These three decreases.
Hydralazine and isosorbidedinitrate (h-isdn) can be used as alternatives.
Candesartan is given an initial dose of 4 mg or 8 mg given x / day and with a target
dose of 32 mg given as much as 1 x / day.
Combinations with essential drugs for treatment are found to contain excessive fluid
in the lungs where there are full complaints of pulmonary edema. The
administration of diuretics can be given from a minimum dose of furosemide 20-40
mg but must be careful with side effects which can occur hypokalemia,
hypomagnosis, and hyponatraemia.

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