HUMAN FUNCTION MODULE

FINAL REPORT

Major Component

After getting this material and facing any simulation case, students taking second semester
of medical degree in university of Airlangga are able to explain the anatomical,
physiological, pathophysiological of related clinical case, physical examination needed and
its principal.

Scenario

A man, 35 years old-with her wife are going to their doctor, complaining about edema.

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 CHAPTER I

BRAINSTORMING AND COGNITIVE STRATEGY

1.1 Main Problems:

Mr.A got an edema

1.2 Keywords:

A man
35 years old
Edema

1.3 Early Hypothesis:

This man got an edema due to lymph circulation

This man got an edema due to heart circulation problem

This man got an edema due to liver circulation problem

1.4 Additional Questions or Information

Anamnesis

Mr. A got an pitting-edema in lower legs

Mr. A is a street vendor

Mr. A lives in Wonokromo SS. Surabaya

Mr. A got an edema since a month ago, but it get hurts since a week ago

Other symptoms: out of breath when doing daily activities, coughing up phlegm

There is no family history of similar symptom

Mr. A has been going to doctor before, he was diagnosed of heart failure

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Mr. A is active smoker, he smokes 3 packs/day of non-filter cigarettes

Physical Examination

There is hypertrophy in his heart, apex latero-inferior

Weight: 70 kg Height: 160 cm

Hematomegali is positive

mur-mur diastolic apex is positive

Ascites ( abdomen is filled by plasma fluid) is positive

S3 Gallop positive

Anemia is negative

Tremor is negative

Icterus is negative

Vital Sign

Blood pressure: 140/90 mmHg

RR 30X/minutes

Temperature: 37o C

Pulse 110x/minutes

There are pulmonary crackles

Lab Examination

X rays result: Cradiomegali, pulmonary congestion

SGOT: 77 u/L; SGPT: 91 u/L

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EKG: Sinus Takikardi 120 bpm, left ventricle hypertrophy, right ventricle hypertrophy, left
atrium abnormality.

1.5 Learning Issues I

1.5.1 What is Hematomegali?

1.5.2 What is Pulmonary crackles?
1.5.3 What is mur-mur diastolic apex and S3 Gallop?
1.5.4 What is pitting and non-pitting edema and what are the causes of them?
1.5.5 What is the relationship between ascites and an edema?
1.5.6 What is the relationship between smoking, heart, and pulmonary circulation?
1.5.7 What are the causes of heart hypertrophy?
1.5.8 What is the relationship between hypertension and tachycardia due to heart
circulation?
1.5.9 How is the normal of heart function?
1.5.10 How is the normal of liver function?

CHAPTER II

PROBLEM ANALYSIS

2.1 Answer to the learning issues I

2.1.1 What is Hepatomegaly?

Hepatomegaly is the term used to describe an enlarged liver size (liver). Normal liver size
of about 7.5 cm in females and 10.5 cm in males. The liver is located in the upper right
abdominal area, protected by the right rib. If there is hepatomegaly, the liver will be
palpable pass right rib bottom.

Hepatomegaly generally occurs via five mechanisms: inflammation,excessive storage,

infiltration, con-gestion, and obstruction.Infections from viruses, bacteria,fungi, and

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parascites promoteinflammation-induced hepatomegaly.Toxins, radiation, autoimmune
disease, and Kupffer cell hyperplasiaalso may cause hepatomegaly by this mechanism.

In the early stages, hepatomegaly usually no symptoms mean. If the course of the disease
was advancing, there may be symptoms such as:
1. Abdominal pain, especially the upper right;
2. Easily tired;
3. Nausea and vomiting;
4. Yellow skin or the whites of the eyes;
5. Itching all over the body;
6. Swelling of the feet;
7. Vomiting or bloody bowel movements;
8. Shortness of breath, etc.Causes & Risk Factors

Many of the diseases and conditions that can cause an enlarged liver, including:

Liver disease

Cirrhosis

Liver Cirrhosis is a liver condition which has been hardened by their illness. Cirrhosis can
be caused by inflammation of the liver and liver cancer, either as a result of excessive use
of drugs or due to infectious diseases. One function of the liver is to form albumin, a
protein that is needed to keep the blood fluid and the cells remain in place. In cirrhosis,
decreased albumin levels causing edema throughout the body in the amount outstanding,
including in the abdominal cavity.

Liver cancer

Heart failure

Hepatitis caused by viruses - including hepatitis A, B, and C - or be caused by infectious

mononucleosis

Liver disease fatty non-alcoholic.

Disease fatty liver alcoholic

A disorder that causes abnormal proteins accumulate in your heart (amyloidosis)

A disorder that causes copper to accumulate in your liver disease (Wilson)

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 A disorder that causes iron to accumulate in your heart (hemachromatosis)

A disorder causing substances fat to accumulate in your heart (Gaucher's disease)

Liquid-filled bag in your heart (liver cysts)

Tumor cancerous liver, including Hemangioma and Adenoma

Obstruction groove-biliary or gallbladder

Hepatitis toxic cancer

Cancer that begins in other parts of your body and spread to the liver

Leukemia

Lymphoma Problems on the heart and blood vessels

Blockage of blood vessels that serve drain the liver (Budd-Chiari syndrome)

Factors that can increase the risk of liver problems include:

The use of excessive amounts of alcohol. Drinking large amounts of alcohol can damage
your liver.

Drugs, vitamins or supplements in large doses.

Infections. An infectious disease may increase the risk of liver damage include malaria
and

Hepatitis Virus. Hepatitis A, B and C can cause liver damage.

Bad eating habits. Obesity increases the risk of heart disease

2.1.2 What is Pulmonary crackles (Pulmonary Ronki)?

Rhonchi is lowpitched sonorous sound and may have gurgling quality. They originate in
larger airways when there is excessive secretions, abnormal airway collapsibility due to
repetitive rupture of surfactant film covering alveoli. Rhonchi frequently clear after cough
post tussive clearing. Ronchi generated by the flow of air through the respiratory tract that

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contains secretions/exudates or due to narrowed airways or the respiratory tract edema.
There are two types, wet and dry ronchi.

Wet ronchi (crackles damp) is an additional sound like gurgling or bubling, exactly when
inspiration phase. Crackles damp caused by the presence of exudate or fluid in the alveoli
and bronchioles or it could be on the bronchi and trachea.

Dry ronchi could be considered with wheezing is a high-pitched whistling sound during
breathing. It occurs when air moves through narrowed breathing tubes in the lungs. The
sound of wheezing is most obviuous when exhaling or inhaling. Wheezing caused by from
the small breathing tubes (bronchial tubes) deep in the lungs. But it may be due to a
blockage in larger airways or in persons with certain vocal cord problems. (Neil K.
Kaneshiro, 2016)

2.1.3 What is mur-mur diastolic apex and S3 Gallop?

In an abnormal circumstaces, the heart will sound gallop and murmur. Its a sign that the
person will gets heart failure. Heart failure is a pathophysiology when the heart cant
pumpling blood for bodys metabolic. There is four kind of hearts sound, therefore we will
explain the third heart sound because in the vital sign, Mr. A diagnosed with positive third
heart sound (S3) gallop and murmur.

The third heart sound (S3) is a low-frequency, brief vibration occurring in early diastole at
the end of the rapid diastolic filling period of the right or left ventricle. Synonymous terms
include: ventricular gallop, early diastolic gallop, ventricular filling sound, and
protodiastolic gallop. The termgallop was first used in 1847 by Jean-Baptiste Bouillaud to
describe the cadence of the three heart sounds occurring in rapid succession. The best
description of a third heart sound was provided by Pierre Carl Potain, a pupil of Bouillaud.
(Silverman, 1990)

A right ventricular third heart sound is an uncommon finding heard in association with
right ventricular dysfunction from a variety of causes. It is usually heard best while
listening along the right or left lower sternal edge, in the epigastrium, or rarely over the
jugular veins. An inspiratory increase in its intensity identifies a right ventricular gallop.
This diagnostic feature may be absent, however, when right ventricular distention or failure
prevents inspiratory augmentation of venous return.

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The "murmur" is the sound of blood flowing. It may be passing through a heart valve that
has problems, for instance. Or it may be that a condition is making your heart beat faster,
forcing your heart to handle more blood quicker than normal. Heart murmurs are the result,
because turbulence blood circulation so that the valve is narrowed.

The murmur caused by mitral valve prolapse too: normally, your mitral valve closes
completely when the lower left chamber of your heart contracts. It stops blood from
flowing back into the upper left chamber. If part of that valve balloons out so that it doesn't
close properly, you have mitral valve prolapse. This causes a clicking sound as your heart
beats. It's fairly common and it's often not serious. But it can lead to the blood flowing
backward through the valve, also called regurgitation. (WebMD, 2016)

2.1.4 What is pitting and non-pitting edema and what are the causes of them?

1. Pathology of Edema
1. Increased microvascular permeability

Increased microvascular permeability is usually related to the initial reaction of

microvascular against inflammation (inflammation) or immunologic stimuli. This
stimulation induces the release of local mediatorsinduces the release of local mediators
which causes vasodilation and increased microvascular permeability. Increased
permeability is directly caused by mediators such as histamine, bradykinin,
leukotrienes, and substance P which causes contraction of endothelial cells and
widening of the gap (slit) interendothelial. Furthermore, the release of cytokines such
as interleukin-1 (IL-1), tumor necrosis factor (INF), and y-interferon induces
cytoskeletal rearrangements resulting in endothelial cell retraction (retraction) of
endothelial cells and the widening gap interendothelial more persistent. The movement
of intravascular fluid through these gaps to interstitium causing local edema which can
melt the acute inflammatory agent. This reaction ends with the onset of local edema
and will return to normal when the stimulus is happening began to decrease. However,
largelycontinue to cases can lead to leakage of plasma proteins and leukocyte
emigration as the beginning of the formation of an acute inflammatory exudate.

2. Increased intravascular hydrostatic pressure

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Increased intravascular hydrostatic pressure can be caused by an increase in
microvascular blood volume, resulting in increased blood flow to microvascular active
(hyperemia), as occurs in acute inflammation. Increased intravascular hydrostatic
pressure can also occur as a result of passive accumulation of blood (congestion), it is
often caused by heart failure or compression of local venous or obstruction. Increased
microvascular volume and the pressure causes increased filtration and reduces or even
the absorption of fluid back into the blood vessel. When the increase in hydrostatic
pressure affects the party of local microvascular, this event is called by local edema. In
the case of heart failure, congestion could increase the hydrostatic pressure in the portal
venous system (right heart failure) that may cause the occurrence of ascites, whereas
the venous system pulmonary (left heart failure) causes pulmonary edema and if there
is an increase in hydrostatic on both the venous system (general heart failure) will
cause generalized edema. Generalized edema can lead to decreased volume of
circulating plasma that can activate different volume settings responses of
compensation. Increased plasma volume through sodium retention caused by activation
of the renin-angiotensin-aldosterone and water retention is mediated by the release of
antidiuretic hormone (ADH) followed by activation of intravascular volume and
pressure receptors. Results from excessive intravascular volume further complicate the
movement of fluid distribution, followed by heart failure.

3. Decreased intravascular osmotic pressure

Intravascular osmotic pressure drop usually occurs due to a decrease in concentrations

of plasma proteins, especially albumin (hypoalbuminemia). Hypoalbuminemia can
reduce intravascular colloid osmotic pressure which resulted in an increase in fluid
filtration and decreased absorption (absorption), whose top may lead to edema.
Hypoalbuminemia may occur due to decreased production of albumin by the liver or
plasma excessive loss occurs. The decrease hepatic production most often occur due to
lack of adequate protein for synthesis pathway as a result of malnutrition or intestinal
malabsorption of the protein as well as diseases of the liver weight with the mass loss
of hepatocytes or hepatocyte function disorders that can lead to the production of
albumin deficiency. Loss of plasma albumin can occur in gastrointestinal disease
characterized by severe blood loss as the infection caused by the parasite. In kidney
disease, where glomerular and / or tubular function impaired can result in loss of

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 albumin with urine. Plasma exudation that accompanies the burn is a rare cause cause
loss of albumin.

4. Decrease lymphatic flow

Decrease lymphatic flow can reduce the ability of the lymphatic system to eliminate
the excess fluids that normally accumulate in the interstitium during fluid exchange
between plasma and interstitium. This can occur because of the pressure on the lymph
vessels by tumor or swelling inflammation, fibrosis due to narrowing of the lymph
vessels or lymphatics internal blockage by a thrombus. Edema occurs as a result of
damage to the ability of the lymphatic and localized to the affected areas as a result of
disturbances in the lymph vessels.

2. Types of Edema
Pitting edema

If this causes an indentation that stays for some time after the release of the pressure,
this type of edema is referred to as pitting edema. Pitting edema may also be caused by
systemic diseases that affect the various organ systems of the body, or by local
conditions involving the affected extremities. Pitting edema is mainly caused by
complications of vital organs of the body, such as heart, liver, and kidneys.
Malfunctioning of these organs can cause retention of fluid in the body. Pitting edema
is also observed in edema patients with rheumatoid-like diseases such as
rheumatoidarthritis and systemic lupus erythematous. It is also the kind of edema
present in patients receiving intravenous fluids. The indentation made on the skin when
pressure is applied to a pitting edema is due to the fluid leaking out of the capillaries
into the subcutaneous tissue. The extent and duration of the indentation after applying
pressure are good indications of the severity of the pitting edema.

Non-pitting edema
This is the type of edema in which the indentation made by a pressure on the affected
area does not persist. It is often associated with lymphedema, lipoedema and
myxedema. Since the kinds of edema which causes non-pitting edemas involve more
than fluids simply filling up interstitial spaces, it is quite possible that their turgid
nature is due to some internal pressure pressing on the swollen area. In myxedema, for
example, the tissues are gradually filled with water-loving molecules such as
hyaluronan, a carbohydrate-like molecule. These molecules are responsible for

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 attracting fluid to the tissues. They absorb water and swell up to cause the edema. The
osmotic pressure generated by this action is most likely to be the reason why this type
of edema presents as non-pitting edemas. The osmotic pressure would make the
affected area appear taut and feel turgid. A similar mechanism is involved in
lymphedema where the lymphatic system breaks down and the lymph nodes swell up.
The osmotic pressure generated by the swollen lymph nodes may be responsible for the
constant internal pressure pushing the fluids against the skin even when pressure is
applied on the affected area. Non-pitting edema usually affects the legs or arms. If the
pressure applied to the skin does not result in a persistent indentation, this type of
edema is referred to as non-pitting edema. Non-pitting edema may be caused by certain
disorders of the lymphatic system such as lymphedema, a condition of the lymphatic
circulation which may occur after a congenitally, mastectomy, or lymph node
surgery. Another cause of non-pitting edema of the legs is known pretibial myxedema,
which is a case of swelling over the skin that occurs in patients having
hyperthyroidism. Sometimes pitting edema and non-pitting edema may occur without
any underlying disease and this is known as idiopathic edema. This is common in
women who experience it in legs and feet, during their pre-menstrual or pre-
menopausal period.

3. Causes of Edema

Edema can also when the balance of substances in your blood is abnormally. Low
albumin or called by hypoalbuminemia. Albumin and other proteins in the blood act
like sponges to keep fluid in the blood vessels. Low albumin may contribute to edema,
but its not usually the only cause. It causes the colloid osmotic pressure low and
hydrostatic pressure increase. The fluid in the blood vessels flows into interstitial
space.

Edema is a part of most allergic reactions. In response to the allergen, nearby blood
vessels leak fluid into the affected area. Obstruction of flow, If drainage of fluid from a
part of your body is blocked, fluid can back up. A blood clot in the deep veins of your
leg can cause leg edema. A tumor blocking the flow of blood or fluid called lymph can
cause edema. Critical illness, Burns, life-threatening infections, or other critical
illnesses can cause a reaction that allows fluid to leak into tissues almost everywhere.
This can cause edema all over your body. Heart disease ( congestive heart failure ),
when the heart weakens and pumps blood less effectively, fluid can slowly build up,

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 creating leg edema. If fluid buildup occurs quickly, fluid in the lungs, known as
pulmonary edema, can develop. If your heart failure is on the right side of your heart,
edema can develop in the abdomen, as well. Liver disease, Severe liver disease (such
as cirrhosis) causes you to retain fluid. Cirrhosis also leads to low levels of albumin
and other proteins in your blood. Fluid leaks into the abdomen and can also cause leg
edema. A kidney condition called nephrotic syndrome can result in severe leg edema
and sometimes whole-body edema. Pregnancy, Mild leg edema is common during
pregnancy. But serious complications of pregnancy like deep vein thrombosis and
preeclampsia can also cause edema. Cerebral edema ( brain edema ), Head trauma,
low blood sodium(called hyponatremia), high altitudes, brain tumors, and a block in
fluid drainage (known as hydrocephalus) can cause edema. Headaches, confusion,
unconsciousness, and coma can be symptoms of cerebral edema.

2.1.5 What is the relationship between ascites and an edema?

Ascites is the accumulation of fluid in the abdominal cavity. Ascites is a common sign in
people due to cirrhosis, a severe liver disease, and usually develops when the heart begins
to fail. Its presence can also cause significant sign of other medical problems, such as
Budd-Chiari syndrome. In general, the development of ascites showed advanced liver
disease and patients should be referred for consideration of liver transplantation.

A common cause of ascites are cirrhosis. Other conditions such as heart failure, kidney
failure, infection or cancer can also cause ascites. Ascites due to a combination of high
pressure in the blood vessels running through the liver (portal hypertension) and decreased
function of the liver caused by scarring of the liver, cirrhosis.

Most patients who develop ascites see abdominal distension and rapid weight loss. Some
people also complain of leg swelling, shortness of breath due to mechanical impingement
on the diaphragm and the accumulation of fluid around the lungs. Additional symptoms or
other complications are bruising, gynecomastia, hematemesis, or mental changes due to
encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may

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complain of chronic fatigue or weight loss. While those with ascites due to heart failure
may also complain of shortness of breath as well as wheezing and exercise intolerance.

To determine the diagnosis of ascites to do a complete blood count (CBC), basic metabolic
profile, liver enzymes, and coagulation. However, many experts recommend a diagnostic
paracentesis performed if the ascites is new or if patients with ascites is being treated in
hospital. The liquid then reviewed for gross appearance, protein level, albumin, and cell
counts (red and white). Additional tests are also conducted if there are indications such as
microbiological culture, Gram stain and cytopathology. The serum-ascites albumin
gradient (SAAG) is probably a better discriminant of measures older (transudate compared
exudate) for the causes of ascites. A high gradient (> 1.1 g / dL) indicates the ascites is due
to portal hypertension. A gradient is low (<1.1 g / dL) indicates the ascites non-portal
hypertension etiology. Causes of high SAAG ( "transudate") is cirrhosis - 81% (alcohol at
65%, the virus in 10%, cryptogenic at 6%), heart failure - 3%, liver vein occlusion: Budd-
Chiari syndrome or disease veno-occlusive, constrictive pericarditis, kwashiorkor (a small
protein-energy malnutrition). While the causes of low SAAG ( "exudate") are: cancer
(metastases and primary peritoneal carcinomatosis) - 10%, infection: Tuberculosis - 2% or
spontaneous bacterial peritonitis, pancreatitis - 1%, serositis, nephrotic syndrome,
hereditary angioedema. Other rare-disease ie Meigs syndrome, vasculitis, hypothyroidism,
kidney dialysis, peritoneal mesothelioma, and stomach tuberculosis.

Ultrasound investigation is often performed prior attempts to remove fluid from the
abdomen. It can reveal the size and shape of the abdominal organs, and Doppler studies
may show the direction of flow in the portal vein, as well as detecting Budd-Chiari
syndrome (hepatic vein thrombosis) and portal vein thrombosis. Additionally, the
sonographer can make an estimation of the amount of ascites, and ascites hard-to-drain can
be drained under ultrasound guidance. An abdominal CT scan is more accurate alternate to
reveal abdominal organ structure and morphology.

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So ascites can be classified into three classes: Class 1: mild, only visible on ultrasound and
CT, Grade 2: detectable with flank bulging and shifting dullness, and Grade 3: directly
visible, confirmed with wave / vibration test fluid.

2.1.6 What is the relationship between smoking, heart, and pulmonary circulation?

Cigarette is smoking media which is made of tobacco as raw material for all variation
tobacco, like cigar, white cigarette, linting cigarette, and crackle cigarette- rokok kretek.
Crackle cigarette is made of real tobacco (not synthesis like the order), and clove, which
make this cigarette is peculiar from Indonesia. Because of tobacco contained, it certainly
contains nicotine.

Pusat Jantung Nasional (2014) explains that nicotine leads to stimulate adrenalin hormone
which results in heart rate increased and HDL decreased, and cause atherosclerosis so that
it come out hypertension. Furthermore, it has effect that bring about thrombus, clog artery,
then the artery will narrowed. If it sudden in coronary artery, it will brings to ischemia or
more dangerous is myocardial infarction, core tissue death, and so it will make irregular
heart rhythm and heart failure that cause edema in leg and lung.

2.1.7 What are the causes of heart hypertrophy?

The Swollen heart layman's terms that are often used for medical term Cardiomegaly.
Cardiomegaly is a condition of an enlarged heart size due to certain disorders that cause the
heart to work harder than normal . Enlargement of the heart can lead to the ability to pump
blood becomes ineffective in the long term will lead to heart failure . Enlargement of the
heart require lifelong treatment to control symptoms and prevent complications . Swelling
of the heart often does not give you any symptoms and is often discovered when the
disease or complications have occurred accidentally in a routine medical examination.
Patients with high blood pressure, chronic swelling asymptomatic heart, this is due to the
compensation of heart against the swelling that occurs to a certain extent such
compensation can no longer afford to allow effective blood flow. New symptoms will arise
when the heart has begun can not compensate anymore, this state is called decompensated
heart or heart failure. Presenting symptoms may include shortness of breath becomes short

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even especially when the move or in the supine sleeping position, swelling in the legs,
fatigue with activity, and palpitations. In patients with symptoms of heart rhythm disorders
palpitations will be more prominent, it can also be perceived irregular pulse, and
claustrophobic. In patients with high blood pressure may be a stroke which is characterized
by weak next to the body, loss of speech, and loss of consciousness. In patients with
impaired coronary blood vessels can occur tightness accompanied by chest pain left as
pressed or squeezed radiating to the left arm or translucent to the rear. The most frequent
cause swelling of the heart are coronary heart disease and high blood pressure . Other
causes that can cause swelling of the heart is a viral infection of the heart that causes
inflammation of the heart , obsesitas , old age , heart valve disease , pregnancy ,
hyperthyroidism , kidney disease , and congenital heart disease .

2.1.8 What is the relationship between hypertension and tachycardia due to heart
circulation?

Based on Smeltzer (2001) Systemic Hypertension is an increasing of blood pressure above

140/90 mmHg, so called pulmonal hypertension which is the increasing of blood pressure
due to pulmonal congestion. It can be one of the causes of Heart Failure, complex
syndrome which happens because ventricular dysfunction or failure of harassment charge
heart pump that cant meet the needs of the body's metabolism. Heart failure is major
manifestation of all hearth diseases.

There are several symptom of heart failure such as fatigue, out of breath, pulmo
congestion, and edema in ankle. Besides, there are several signs, such as tachycardia,
tachypnea, crackles , pleural effusion , JVP increase , peripheral edema, hepatomegaly.
The classic sign ronkhi heart failure includes jugular venous pressure, refluks
abdominojugular, S3 gallop and pitting edema lower extremities. Edema peripheral can be
caused by insufficiency veins, kidney disease or medications such as calcium channel
blockers. Older patients can have a normal physical examination. Breathing Cheyne -
Stokes can be the only signs of heart failure is suspected.

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Heart failure can be divided in systolic and diastolic disfunctions. In systolic dysfunction ,
ventricular capacity to pump blood disrupted because of interference cardiac muscle
contractility which may be caused by destruction of myocytes , myocyte function
abnormalities or fibrosis , as well as due to pressure overload which causes resistance or
flow resistance so that the stroke volume be reduced. Meanwhile, diastolic dysfunction
occurs due to interference

Myocardial relaxation , the ventricular wall stiffness and reduced left ventricular
compliance causes disturbances in ventricular filling time diastolic . The commonest
causes of diastolic dysfunction is coronary heart disease, hypertension with left ventricular
hypertrophy and hypertrophic cardiomyopathy.

Besides, heart failure can be divided into low put and high put heart failure.
Low HF output caused by hypertension, dilated cardiomyopathy, valve disease and
pericardial. High Output HF decreases systemic vascular resistance such as
hyperthyroidism, anemia, pregnancy, fistula A-V, beriberi and Paget's disease.

The other types of heart failure are Acute and Chronic Heart Failure. The classic example
is the acute heart failure rips valve leaflets abruptly due endocarditis, trauma or myocardial
infarction large. Cardiac output drops unexpectedly causes a decrease in blood pressure
without peripheral edema. Example of chronic heart failure is dilated cardiomyopathy.
Peripheral congestion is very striking, but blood pressure are well preserved

Last but not least, heart failure can be divided into Right Heart Failure and Left Heart
Failure. Left Heart failure due to left ventricular weakness, improve pulmonary venous
pressure and the lungs causing shortness of breath and patients orthopnea. Right heart
failure occurs when Right ventricular debilitating disorder such as primary pulmonary
hypertension / Secondary, chronic pulmonary thromboembolism resulting in systemic
venous congestion cause peripheral edema, hepatomegaly and jugular venous distention.

Tabel 1

Klasifikasi Tekanan Darah TDS*mmHg TDD*mmHg

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Normal <120 <80

Pre-Hipertensi 120-139 80-89

Hipertensi Stage 1` 140-159 90-99

Hipertensi Stage 2 >160 >100

Source: JNC 7

2.1.9 How is the normal of heart function?

From just days following conception until death, the beat goes on. Throughout an average
human life span, the heart contracts about 3 billion times, never stoping except for a
fraction of a second to fill between beats. Within about 3 weeks after conception, the heart
of developing embryo starts to function. It is the first organ to become functional. At this
time, the human embryo is only a few millimeters long.

The heart develops so early and is so crucial throughtout life because circulatory system is
the bodys transport system. A human embryo, having little yolk available as food, depends
on promptly estabilishing a circulatory system that can interact with the mothers
circulation to pick up and distribute to the developing tissues the supplies needed for
survival and growth. Thus begins the story of the circulatory system, which serves
throughout life as a vital pipeline for transporting materials on which the cells of the body
absolutely depend.

The circulatory system has three components :

The heart is the pump that imparts pressure to the blood to establish the pressure gradient
needed for blood to flow to the tissues. Like all liquids, blood flows down a pressure
gradient from an area of higher pressure to an are of lower pressure.

The blood vessels are the passageways through wich blood is directed and distributed from
the heart to all parts of the body and subsequently returned to the heart. The smallest of the
blood vessels are designed for rapid exchange of materials between the surrounding tissues
and the blood within the vessels.

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Blood is the transport medium within wich materials being transported long distances in
the body, such as O2, CO2, nutrients, wastes, electrolytes and hormones, are dissolved or
suspended. (Sherwood, n.d.). Human physiology.

At the time of pulsing, any slack heart chamber and fill with blood (called diastole), then
the heart to contract and pump blood out of the third chamber of the heart (called systole).
Both atrium loosen and contract simultaneously, and both ventricles also loosens and
contracts simultaneously. The blood ran out of oxygen and contain a lot of carbon dioxide
from the body flows through two veins encouraged (vena cava) leading into the right
atrium. After the right atrium filled with blood, he'll push blood into the right ventricle.
Blood from the right ventricle to be pumped through the pulmonary valve into the
pulmonary artery, leading to the lungs. Blood will flow through very small vessels
(capillaries) that surrounds the air pockets in the lungs, absorb oxygen and release carbon
dioxide that is subsequently exhaled. Oxygen-rich blood to flow in the pulmonary veins to
the left atrium. Circulation of blood between the right heart, lungs and the left atrium
called the pulmonary circulation. The blood in the left atrium will be driven into the left
ventricle, which then pumps oxygen-rich blood is passed through the aortic valve into the
aorta (the largest artery in the body). Blood rich in oxygen is supplied to the entire body,
except the lungs.

2.1.10 How is the normal of pulmonary function?

The main function of the lungs that is for gas exchange between the blood and the
atmosphere. The gas exchange aims to provide oxygen to the tissues and remove carbon
dioxide. Oxygen and carbon dioxide needs continue to change 14 in accordance with the
level of activity and a person's metabolism, but breathing should still be able to maintain
oxygen and carbon dioxide. Air enters the lungs through a pipe system that narrows
(bronchi and bronchioles) that branches in both the main pulmonary (trachea). The pipeline
ends in the bubbles of the lungs (alveoli) which is the last air pockets where oxygen and
carbon dioxide removed from the place where the blood flow. There are over 300 million
alveoli in human lungs are elastic. The air space is maintained in an open state by a
chemical surfactant that can counteract the tendency of alveoli to deflate.

To carry out these functions, respiration can be divided into four basic mechanisms:

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1. Pulmonary ventilation, which means the entrance and exit of air between the alveoli and
the atmosphere

2. Diffusion of oxygen and carbon dioxide between the alveoli and blood

3. Transport of oxygen and carbon dioxide in the blood and body fluids into and out of
cells

4. Setting ventilation (Guyton and Hall, 2006)

2.2 Concept Mapping I

2.3 Description of Concept Mapping I

It begins from the scenario that Mr. A (35) is a smoker. His cigarette is crackle
type, so it means he is completely exposed by nicotine, which has a HDL
boosting effect and adrenaline hormone stimulation, every day that leads to
hypertension. Hypertension results in RR 30x/min, bilateral rhonchi breath
sound, and dyspnea with cough and serous sputum. Furthermore, hypertension
make his cardiac pulse 110x/min, and then tachycardia. Tachycardia brings

19
about s3 gallop, murmur diastolic apex, and hypertrophy of latero-inferior
cardiac apex which will increase SGOT and SGPT level and decreasing of left
ventricle volume. Because left ventricle volume decreased, the impact is the
cardiac output will decreased as left ventricle volume. After that, much blood
still in atrium until back to pulmonary vein, then to pulmonary artery, right
atrium until the pressure increase so that blood in right atrium back to body
vein, portal vein and internal jugular vein. Portal vein is obstructed, so that
hepatomegaly appearing, then decreasing of albumin in blood vessel.
Decreasing of albumin impacts to edema in the lower extremity and ascites. In
addition, obstruction in internal jugular vein will distension.

2.4 Learning Issues II

2.4.1 What is the relation between SGOT and SGPT due to heart function?

2.4.2 How is the pathological of cardiac-pulmonary edema?

2.4.3 What is Cardiac Output?

2.4.4 How is the presence of normal EKG?

2.4.5 What is Right Heart Failure?

2.4.6 What is Left Heart Failure?

CHAPTER III

PROBLEM SOLVING

20
3.1 Answering of Learning Issues II

3.1.1 What is the relation between SGOT and SGPT due to heart function?

A. SGOT (AST)
SGOT (Serum Glutamic Oxaloacetic Transaminase) or as known as AST (Aspartate
Aminotransferase) is an enzyme that found in cardiac muscle and liver. In a middle
concentration, it might be found in kidneys and pancreas, and in a low
concentration it might be found in a blood
SGOT/AST is mostly detected with photometry with photometer,
spectrophotometer,or with chemistry analyser. AST levels are often compared with
results of other tests, such as alkaline phosphates (ALP), total protein,
and bilirubin to help determine which form of liver disease is present.AST is often
measured to monitor treatment of persons with liver disease and may be ordered
either by itself or along with other tests for this purpose. Sometimes AST may be
used to monitor people who are taking medications that are potentially toxic to the
liver. If AST levels increase, then the person may be switched to another
medication.
Normally, level of AST in a blood are low. The normal range is 10 to 34 U/L. to be
more specific, the normal range for man is: 0-50 U/L and the normal range for
woman is 0-35 U/L.
An increased of AST level is usually a sign of disease. There are some kind of
disease based on the amount of increasing of AST such as:
a. A high increase (>5 times normal): an acute damage of hepatoseluler, myocard
infarction, collaps circulation, acute pancreatitis, infectiosa of mononucleosis
b. A middle increase (3-5 times normal): obstruction of the a duct of empedu,
aritmia jantung, gagal jantung kongestif, tumor hati (metastasis atau primer),
distrophia muscularis
c. A low increase (until 3 times normal): perycarditis, cirrhosis, lung infarction,
delirium tremeus, cerebrovascular accident (CVA)

AST may also increase after a heart attacks and with muscle injury. With heart and
muscle injury, AST is often much higher than ALT. AST is als (often 3-5 times as
high) and levels tend to stay higher than ALT for longer than with liver injury. AST
is also increase in alcoholic.

B. SGPT (ALT)

21
 SGPT (Serum Glutamic Pyruvic Transaminase) or as known as ALT (Alanine
Aminotransferase) is found mostly in the cells of the liver and kidney.The alanine
aminotransferase (ALT) test is typically used to detect liver injury. It is often
ordered in conjunction withaspartate aminotransferase (AST) as part of a liver
panel or comprehensive metabolic panel (CMP) to screen for and/or help
diagnose liver disease.When the liver is damaged, ALT is released into the blood.
This makes ALT a useful test for early detection of liver damage.
AST and ALT are considered to be two of the most important tests to detect liver
injury, although ALT is more specific to the liver than is AST. Sometimes AST is
compared directly to ALT and an AST/ALT ratio is calculated. This ratio may be
used to distinguish between different causes of liver damage and to help recognize
heart or muscle injury.
ALT is often used to monitor the treatment of persons who have liver disease, to see
if the treatment is working, and may be ordered either by itself or along with other
tests for this purpose.
A low level of ALT in the blood is expected and is normal. a normal range of ALT
in men is: 0-50 U/L and in woman is: 0-35 U/L.
An increased of ALT level is usually a sign of disease. Liver disease is the most
common reason for higher than normal levels of ALT. There are some kind of
disease based on the amount of increasing of AST such as:
a. If >20 times normal: acute hepatitis, and necrosis of a liver
b. Increasing in 3-10 times normal: mononuclear infection, chronic hepatitis,
clogged up of bile, Reye syndrome and infarct of myocardium (SGOT > SGPT)
c. Increasing in 1-3 times normal: pancreatitis, Laennec cirrhosis, bile cirrhosis.

ALT levels often vary between normal and slightly increased, so the test may be
ordered frequently to see if there is a pattern.ALT is often performed together with
a test for AST or as part of a liver panel.

In most types of liver diseases, the ALT level is higher than AST and the AST/ALT
ratio will be low (less than 1). There are a few exceptions; the AST/ALT ratio is usually
greater than 1 in alcoholic hepatitis, cirrhosis, and with heart or muscle injury and may
be greater than 1 for a day or two after onset of acute hepatitis.

3.1.2 How is the pathological of cardiac-pulmonary edema?

22
This case is related with left and right heart failure. Such, first phase at left ventricle
which does not pump maximum that reside volume from cardiac output still in left
atrium then disturb vena pulmonary pressure. Sovari (2015) explainsvena pulmonary
pressure increase and interstitial fluid back to pulmonary capillary until it become
wider and hydrostatic pressure increased. After that, interstitial fluid will be directed by
lymph. If continuous, lymph capacity overload and accumulate in alveoli and it will
diffuse to lung interstitial space. Further accumulated, the fluid will cross to alveolar
epithelium so that it leads to alveolar flooding. Thus, this patient suffers dyspnea,
rhonchi, serous sputum and in thorax roentgen show pleura effusion because the
accumulated fluid is abundant.

3.1.3 What is Cardiac Output?

Cardiac output is the volume of blood pumped by the heart per minute (mL blood/min).
Cardiac output is a function of heart rate and stroke volume. The heart rate is simply
the number of heart beats per minute. The stroke volume is the volume of blood, in
milliliters (mL), pumped out of the heart with each beat. Increasing either heart rate or
stroke volume increases cardiac output.

Cardiac Output in mL/min = heart rate (beats/min) X stroke volume (mL/beat)

An average person has a resting heart rate of 70 beats/minute and a resting stroke
volume of 70 mL/beat. The cardiac output for this person at rest is:

Cardiac Output = 70 (beats/min) X 70 (mL/beat) = 4900 mL/minute.

The total volume of blood in the circulatory system of an average person is about 5
liters (5000 mL). According to our calculations, the entire volume of blood within the
circulatory sytem is pumped by the heart each minute (at rest). During vigorous
exercise, the cardiac output can increase up to 7 fold (35 liters/minute)

23
Control of Heart Rate
The SA node of the heart is enervated by both sympathetic and parasympathetic nerve
fibers. Under conditions of rest the parasympathetic fibers release acetylcholine, which
acts to slow the pacemaker potential of the SA node and thus reduce heart rate. Under
conditions of physical or emotional activity sympathetic nerve fibers release nor
epinephrine, which acts to speed up the pacemaker potential of the SA node thus
increasing heart rate. Sympathetic nervous system activity also causes the release of
epinephrine from the adrenal medulla. Epinephrine enters the blood stream, and is
delivered to the heart where it binds with SA node receptors. Binding of epinephrine
leads to further increase in heart rate.
Control of Stroke Volume
Under conditions of rest, the heart does not fill to its maximum capacity. If the heart
were to fill more per beat then it could pump out more blood per beat, thus increasing
stroke volume. Also, the ventricles of the heart empty only about 50% of their volume
during systole. If the heart were to contract more strongly then the heart could pump
out more blood per beat. In other words, a stronger contraction would lead to a larger
stroke volume. During periods of exercise, the stroke volume increases because of both
these mechanisms; the heart fills up with more blood and the heart contracts more
strongly.
Stroke volume is increased by 2 mechanisms:
1. increase in end-diastolic volume
2. increase in sympathetic system activity
End-diastolic Volume

24
An increase in venous return of blood to the heart will result in greater filling of the
ventricles during diastole. Consequently the volume of blood in the ventricles at the
end of diastole, called end-diastolic volume, will be increased. A larger end-diastolic
volume will stretch the heart. Stretching the muscles of the heart optimizes the length-
strength relationship of the cardiac muscle fibers, resulting in stronger contractility and
greater stroke volume.
Starling's Law
Starling's Law describes the relationship between end-diastolic volume and stroke
volume. It states that the heart will pump out whatever volume is delivered to it. If the
end-diastolic volume doubles then stroke volume will double.
An Increase in Sympathetic Activity Increases Stroke Volume
The cardiac muscle cells of the ventricular myocardium are richly enervated by
sympathetic nerve fibers. Release of norepinephrine by these fibers causes an increase
in the strength of myocardiall contraction, thus increasing stroke volume.
Norepinephrine is thought to increase the intracellular concentration of calcium in
myocardial cells, thus facilitating faster actin/myosin cross bridging. Also, a general
sympathetic response by the body will induce the release of epinephrine from the
adrenal medulla. Epinephrine, like norepinephrine will stimulate an increase in the
strength of myocardial contraction and thus increase stroke volume.

3.1.4 How is the presence of normal EKG?

The EKG is a tool of remarkable clinical power, remarkable both for the ease with
which it can be mastered and for the extraordinary range of situations in which it can
provide helpful and even critical information. One glance at an EKG can diagnose an
evolving myocardial infarction, identify a potentially life-threatening arrhythmia,
pinpoint the chronic effects of sustained hypertension or the acute effects of a massive
pulmonary embolus, or simply provide a measure of reassurance to someone who
wants to begin an exercise program.

Remember, however, that the EKG is only a tool and, like any tool, is only as capable
as its user. Put a chisel in my hand and you are unlikely to get Michelangelo's David.
(Thaler, 2012)

Orientation of the Waves of the normal EKG

25
1. The P wave is small and usually positive in the left lateral and inferior leads. It is
often biphasic in leads III and VI. It is usually most positive in lead II and most
negative in lead Avr.
2. The QRS complex is large, and tall R waves (positive deflection) are usually seen
in mmost left lateral and inferior leads. R wave progression refers to the sequential
enlargement of R waves as one proceeds across the precordial leads from V1 to V5.
A small initial Q wave, representing septal depolarization, can often be seen in one
or several of the left lateral leads, and sometimes in the inferior leads.
3. The T wave is variable, but it is usually positive in leads with tall R waves.

Left ventricular hypertrophy looking at the

limb leads

26
 Right ventricular hypertrophy
looking at the limb leads

Right ventricular hypertrophy

27looking at the precordial leads
Left Atrial Enlargement

Sinus tachycardia

28
 Sinus Tachycardia

Normal sinus rhythm is the normal rhythm of the heart. Depolarization originates
spontaneously within the sinus node. The rate is regular and between 60 and 100 beats
per minute. If the rhythm speeds up beyond 100, it is called sinus tachycardia.

Sinus tachycardia can be normal or pathologic. Strenuous exercise, for example, can
accelerate the heart rate well over 100 beats per minute, whereas resting heart rates
below 60 beats per minute are typical in well-conditioned athletes. On the other hand,
alterations in the rate at which the sinus node fires can accompany significant heart
disease. Sinus tachycardia can occur in patients with congestive heart failure or severe
lung disease, or it can be the only presenting sign of hyperthyroidism in the elderly.

Hyperthrophy

The terms hypertrophy and enlargement are often used interchangeably, but here, we
want to make a not terribly subtle distinction. Hypertrophy refers to an increase in
muscle mass. The wall of a hypertrophied ventricle is thick and powerful. Most
hypertrophy is caused by pressure overload, in which the heart is forced to pump blood
against an increased resistance, as in patients with systemic hypertension or aortic
stenosis. Just as weight lifters develop powerful pectoral muscles as they bench-press
progressively heavier and heavier weights, so the heart muscle grows thicker and
stronger (at least for a while) as it is called on to eject blood against increasing
resistance.
Enlargement refers to dilatation of a particular chamber. An enlarged ventricle can hold
more blood than a normal ventricle. Enlargement is typically caused by volume
overload; the chamber dilates to accommodate an increased amount of blood.
Enlargement is most often seen with certain valvular diseases. Aortic insufficiency, for
example, may cause left ventricular enlargement, and mitral insufficiency may result in
left atrial enlargement. Enlargement and hypertrophy frequently coexist. This is not
surprising, because both represent ways in which the heart tries to increase its cardiac
output.

Right Ventricular Hypertrophy

29
Looking at the Limb Leads

In the limb leads, the most common feature associated with right ventricular
hypertrophy is right axis deviation; that is, the electrical axis of the QRS complex,
normally between 0 and +90, veers off between +90 and +180. This reflects the
new electrical dominance of the usually electrically submissive right ventricle. Many
cardiologists feel that the QRS axis must exceed +100 in order to make the diagnosis
of right ventricular hypertrophy. Therefore, the QRS complex in lead I (oriented at 0)
must be more negative than positive.

Looking at the Precordial Leads

The precordial leads can also be helpful in diagnosing right ventricular hypertrophy. As
you might expect, the normal pattern of R-wave progression, whereby the R-wave
amplitude enlarges as you proceed leftward from lead V1 to V5, is disrupted. Instead of
the R-wave amplitude increasing as the leads move closer to the left ventricle, the
reverse may occur. There may be a large R wave in lead V1, which lies over the
hypertrophied right ventricle, and a small R wave in leads V5 and V6, which lies over
the normal, but now electrically humble, left ventricle. Similarly, the S wave in lead V1
is small, whereas the S wave in lead V6 is large. These criteria have been expressed in
the simplest possible mathematics: In lead V1, the R wave is larger than the S wave. In
lead V6, the S wave is larger than the R wave.

Left Ventricular Hypertrophy

The diagnosis of left ventricular hypertrophy is somewhat more complicated. Left axis
deviation beyond 15 is often seen, but by and large, this is not a very useful
diagnostic feature. Instead, increased R-wave amplitude in those leads overlying the
left ventricle forms the basis for the EKG diagnosis of left ventricular hypertrophy.
Unfortunately, there are almost as many criteria for diagnosing left ventricular
hypertrophy on the EKG as there are books about EKGs. Nevertheless, all the criteria
reflect a common theme: There should be increased R-wave amplitude in leads
overlying the left ventricle and increased S-wave amplitude in leads overlying the right
ventricle. The various criteria vary in their sensitivity and specificity. Those listed here
are not the only ones, but they will serve you well.

Looking at the Precordial Leads

30
In general, the precordial leads are more sensitive than the limb leads for the diagnosis
of left ventricular hypertrophy. The most useful criteria in the precordial leads are as
follows: 1. The R-wave amplitude in lead V5 or V6 plus the S wave amplitude in lead
V1 or V2 exceeds 35 mm. 2. The R-wave amplitude in lead V5 exceeds 26 mm. 3.
The R-wave amplitude in lead V6 exceeds 20 mm. 4. The R-wave amplitude in lead
V6 exceeds the R-wave amplitude in lead V5. The more criteria that are positive, the
greater the likelihood that the patient has left ventricular hypertrophy. It is, sadly, worth
your while to memorize all of these criteria, but if you want to be selective,choose the
first because it probably has the best predictive value.

Looking at the Limb Leads

The most useful criteria in the limb leads are as follows: 1. The R-wave amplitude in
lead aVL exceeds 11 mm. 2. The R-wave amplitude in lead aVF exceeds 20 mm. 3.
The R-wave amplitude in lead I exceeds 13 mm. 4. The R-wave amplitude in lead I
plus the S-wave amplitude in lead III exceeds 25 mm. Again, if you aspire to
electrocardiographic nirvana, learn them all. If you must pick one, pick the first; it is
the most specific for left ventricular hypertrophy. In other words, if this criterion is
present, there is a good chance the patient has left ventricular hypertrophy, but relying
on this criterion alone will sometimes lead you to miss the diagnosis (i.e., it is not very
sensitive).

When Both Ventricles Are Hypertrophied

What happens when both the right ventricle and left ventricle are hypertrophied? As
you might expect, there may be a combination of features (e.g., criteria for left
ventricular hypertrophy in the precordial leads with right axis deviation in the limb
leads), but in most cases, the effects of the usually dominant left ventricle obscure
those of the right ventricle.

3.1.5 What is Right Heart Failure?

Heart failure is the inability of the heart to maintain output heart (Caridiac Output =
CO) in meeting the needs of the body's metabolism. If the filling pressure is increased
resulting in pulmonary edema and dams in the venous system, then the condition is
called congestive heart failure
(Kabo & Karim, 2002)

31
 Disruption cardiac function in terms of their effects on changes in three main
determinants of Myocardial function is freeload is the degree of stretch fibers
myocardium at the end of ventricular filling or diastolic. Afterload (end load) namely
the amount of voltage that must be achieved ventricular wall during systole to pump
blood. myocardial contractility strength changes contraction

Heart Failure Clinical Manifestations

1. Heart Failure Left and Right
2. Heart Failure High Output and Low Output
3. Acute and Chronic Heart Failure
4. Forward and backward heart failure

When the right venterikel fails to pump blood, then that stands out is
congestive viscera and peripheral tissues. This happens because the right side of the
heart not able to clear the blood with adequate volume so it can not accommodate all
the blood that normally return of the venous circulation. Clinical manifestations
seemed include lower extremity edema (edema dependent), which usually is pitting
edema, weight gain, hepatomegaly (enlarged liver), jugular venous distention (venous
neck), ascites (Accumulation of fluid in the peritoneal cavity), anorexia and nausea,
nocturia and weak. Right heart failure is usually the result of left heart failure. This is
because if the cardiac left ventricle fails to pump blood throughout the body, the blood
in it going back to the lungs and increased pressure in the pulmonary veins. This
increased pressure can cause damage to the right side of the heart and leads to right
heart failure.

3.1.5 What is Left Heart Failure?

Congestive lungs occurs in ventricle left, because the left can not afford ventricle pump
blood coming from the lungs. Increased pressure in the pulmonary circulation cause
fluid pushed into lung tissue. Clinical manifestations can occur include dyspnea, cough,
fatigue, rapid heart rate (tachycardia) with sound S3, anxiety, restlessness, and right
heart failure. If left ventricular heart failure, the left side must work harder to pump the
blood to the same amount of blood.

There are two type of left ventricular heart failure: systolic failure and diastolic failure.
Systolic failure occurs when the left ventricle loses its ability to contract normally. The

32
 heart cant pump for circulation to all body. Diastolic failure occurs when the left
ventricle loses ability to relax normally. The heart cant properly fill with blood during
resting period between each beat. (Heart.org, 2016). In the additional information, Mr.
A gets left atrial disorder, because there is constriction in the mitral valve. So, his left
atrium work harder to distribute the blood to left ventricle, then the muscle become
stiff.

3.2 Concept Mapping II

3.3 Final Hypothesis
Mr, A is having left heart failure which spreading becomes right heart failure(Congestion
Heart Failure) that causes hypertension, hepatomegaly, and periphery edema.

3.4 Conclusion

The weakness of ventricles muscle cause Mr. As both ventricle hypertrophies. This

condition is becoming worse by his smoking habit. It results HDL decreases and becomes
atherosclerosis. This condition makes the decreasing of stroke rate. Because the cardiac
output is stay still, so the heart beat is increasing. Mr.As heart works harder than before.

33
The weak of left ventricle affect the work of left atrium and pulmonary vein- called left
heart failure. The pressure in pulmonary vein is stronger which affects pulmonary system.
This pressure is spreading back into right ventricle and may affect right atrium. This
condition can cause right heart failure. Because of that, right ventricle is going
hypertrophy. The weakness of right side of heart affects veins, including porta vein which
bring back the blood from the liver. The high pressure of porta vein cause Hepatomegaly.
If so, the albumin rate inside the liver is decreasing and cause abdomen ascites. Besides,
the high pressure of porta vein causes the decreasing of colloid osmotic pressure becomes
periphery edema.

CHAPTER IV

CRITICAL APPRAISAL

4.1 Journal Appraisal

4.1. Journal Appraisal

JOURNAL APPRAISAL

Group : 8A

Title : Studies on the Cardiomegaly of the Spontaneously Hypertensive

Rat

1. FORMAT PAPER

Item Available / Not Available

Title A (Page102)
Abstract and or Summary A (Page 102)
Introduction, background A (Page 102)
Method A (Page 102)

34
 Result A (Page 104)
Discussion A (Page 107)
Conclusions A (Page 107)
Acknowledgement A (Page 109)
Reference A (Page 109)

A: Available

NA: Not Available

Conclusion : Complete/Not Complete

2. VALIDTY OF RESEARCH

The purpose of the present study was to investigate the mitochondria of the heart of the
spontaneously hypertensive rat at various stages of developing hypertrophy and approaching
cardiac failure.

Methodology

Item Result
Design Cohort
Hierarchy of Evidence 3
Sample Normotensive Wistar rats were obtained from a
local supplier. Only male rats were used.
Systolic blood pres- sure was determined using
a tail cuff and a mercury ma- nometer.
Sample Size using 43 normotensive rats showed that the
relationship of heart weight and body weight
could be expressed by the equation:
Inclusion Criteria Only male rats were used
Sampling Frame Spontaneously hypertensive rats of the
Okamoto- Wistar strain were obtained from the

35
 colony of rats maintained by the Specialized
Center for Research in Hypertension at Indiana
University School of Medicine. Normotensive
Wistar rats were obtained from a local supplier.
Only male rats were used. Systolic blood pres-
sure was determined using a tail cuff and a
mercury manometer.
Methodology Heart mitochondria were prepared, by a
modification of the method of Chao and Davis
(16). Rats were either lightly anesthetized with
ether or killed by decapitation after cervical
dislocation. Their hearts were quickly re-
moved and placed in an ice-cold solution of
0.25M sucrose containing 10 mM
ethylenediaminetetraacetate (EDTA), pH 7.5.
The ventricles were trimmed of atria and great
vessels, weighed, and measured for length. The
heart was sectioned transversely midway
between the aortic root and the apex of the left
ventricle. The thickness of the left ventricular
wall, the diameter of the left ventric- ular
cavity, and the width of the heart was
measured. The hearts were then finely minced
and suspended in ice-cold sucrose-EDTA
medium. Each heart was homog- enized
separately on ice using a Brinkman Instruments
Polytron for 10 seconds at low speed and then
for 4 sec- onds at full speed. A sample of the
homogenate was re- moved and used for
determinations of protein content by the Biuret
method (17) and cytochrome oxidase and
adenosine triphosphatase (ATPase) activities.
The remainder of the homogenate was
centrifuged at 1,000 g for 10 minutes. The
supernatant fluid obtained was centrifuged at
12,000 g for 10 minutes. For 2- and 4-month-
old rats, supernatant fluid from four hearts had

36

Measurement and or Assessment
37
to be combined to obtain adequate quantities of
mitochondria. For 6- and 12-month-old rats,
two hearts had to be combined for each
mitochondrial preparation. The resulting
mitochondrial pellets were suspended in 20 ml
of 0.6M KC1 and 5 mM imidazole, pH 7.4, and
al- lowed to stand on ice for 1 hour to remove
contaminating actomyosin. The suspensions
were then centrifuged at 10,000 g for 10
minutes. The supernatant fluid was dis- carded
and each pellet was suspended in a small
volume of sucrose-EDTA medium. The pellets
were "cut" at each step with a glass rod in
favor of the mitochondria.
The mitochondrial content of the
heart was deter- mined by measuring
the activity of the mitochondrial
enzyme, cytochrome oxidase, in both
the total heart homogenate and each
mitochondrial preparation. The
proportion of the heart protein that
was mitochondrial could then be
calculated by the following equations:
Mitochondrial protein (mg) =
Cytochrome oxidase of heart (units)/
Cytochrome oxidase of mitochondria,
(units/mg protein)
% Mitochondrial protein = 100 x total
mg of rnitochondrial protein / total mg
of heart protein
Cytochrome oxidase activity was measured by
the method of Griffiths and Wharton (18)
except that oxygen consumption was measured
polarographically rather than manometrically.
Prior to assay, both the mito- chondrial
preparations and the homogenates were treated
for 15 minutes on ice with sodium
deoxycholate (1 mg/mg protein), pH 8.0; this
procedure fostered maximum activation. The
incubation medium for de- termining
 cytochrome oxidase had a total volume of 5 ml
and contained 20 mM potassium phosphate, pH
7.2, 0.1 mM EDTA, 0.05 mM cytochrome C,
20 mM sodium as- corbate, 6 //g of rotenone,
and either 2 mg of homogenate protein or 0.4
mg of mitochondrial protein. Linearity with
time and protein concentration was established.
Oxy- gen uptake was measured at 30C using a
Beckman oxy- gen analyzer with a Clark type
of oxygen electrode. This method of
determining cytochrome oxidase activity gave
reproducible results and consistently low
standard errors of the mean. All determinations
were conducted in duplicate. In addition, at the
end of each series of assays, those done first
were rechecked; the results had not changed
because of storage on ice. Hearts from both
control and hypertensive rats were always
homogenized, activated, and assayed on the
same day. The reaction mixture for determining
the rate of state- 3 respiration with intact
mitochondria contained 0.25M sucrose, 5 mM
Tris-Cl, pH 7.4, 10 mM potassium phos- phate,
pH 7.4, 5 mM pyruvate, 5 mM malate, 0.4 mM
adenosine diphosphate (ADP), and 1 mg
mitochondrial protein/ml. Oxygen uptake was
measured at 30C using a Beck- man oxygen
analyzer with a Clark oxygen electrode.
Instrument Systolic blood pres- sure was determined using
a tail cuff and a mercury manometer.
Randomization -
Intervention -
Analysis Method STATISTICAL ANALYSIS OF THE DATA
Regression lines for the ratios of heart weight
to body weight and heart mitochondrial protein
to body weight in normotensive rats were

38
 determined by the least- squares method using
a linear regression program. Con- fidence
limits (95%) for this regression line at any
value of x are given by YR + 2SEYRI.
Deviation of the data for the hypertensive rats
above these lines was analyzed for statistical
significance by a one-tailed Student's t-test.
Other results were analyzed for statistical
significance by a two-tailed Student's t-test.

a) Compatibility of The Design and The Objective of The Study : Compatible

b) Compatibility of The Measurement & The instruments : Compatible

Conclusion : Valid / not valid

3. The Importance of the research

The findings relationship about mitochondria of the heart of the spontaneously

hypertensive rat at various stages of developing hypertrophy and approaching cardiac failure

39
4.3. Appraisal
Source For Searching Method Information Validity Importance Applicability
Founda Result Founda Result Founda Result
Answering type
tion tion tion
Learning
Issues
Hepatomegaly in 1.5.1. Internet : Online journal Idea Valid Content Valid Is it Yes
Neonates and http://google.co.id
What is (pdf) of applica
Children : Keywords :
https://pedclerk.bsd Hepatomega Informa ble?
hepatomegaly
.uchicago.edu/sites/
ly? tion
pedclerk.uchicago.e
du/files/uploads/Ped
iatrics%20in
%20Review-2000-
Wolf-303-10.pdf
1.5.2. Internet : Article and Idea Valid Content Valid Is it Yes
http://google.co.id
Wheezing : What is web of applica
Keywords : Suara
https://www. Pulmonaly Informa ble?
nlm.nih.gov/ pada nafas
medlineplus/ Crackles? tion
ency/article/0
03070.htm
and
ISTILAH
PADA
SUARA
NAFAS :
http://dokud
ok.com/ilmu-
dasar/istilah-
pada-suara-
nafas/
1.5.3. Internet : Online book Idea Valid Content Valid Is it Yes
Clinical Methods: http://google.co.id
What is (HTML) and of applica
The http://www.ncbi.nlm.
mur- nih.gov/ Article Informa ble?
History,
Keywords : heart
Physical, murdiastoli tion
and sound
c apex and
Laborator
s3 Gallop?
y
Examinati
ons. 3rd
edition.
Chapter
24The
Third
Heart
Sound :
http://www
.ncbi.nlm.n
ih.gov/boo
ks/NBK342
/ and
What Are
Heart
Murmurs?
:
http://www
.webmd.co
m/heart-
disease/gui
de/heart-
murmur-
causes-
treatments
Ascites : 1.5.4. Internet : Article and Idea Valid Content Valid Is it Yes
https://www.nlm.nih http://google.co.id
What is web of applica
.gov/medlineplus/en Keywords : edema,
cy/article/000286.ht pitting and Informa ble?
pitting
m and Ascites: A
non pitting tion
Common Problem
in People with edema and
Cirrhosis :
what are the
http://patients.gi.or
g/topics/ascites/ and causes of

40
Ascites : them?
https://en.wikipedia.
org/wiki/Ascites
Ascites : 1.5.5. Internet : Article and Idea Valid Content Valid Is it Yes
https://www.nlm.nih http://google.co.id
What is web of applica
.gov/medlineplus/en Keywords : Acites
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between tion
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in People with asites and an
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edema?
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g/topics/ascites/ and
Ascites :
https://en.wikipedia.
org/wiki/Ascites
1.5.6. Internet : Article and Idea Valid Content Valid Is it Yes
http://google.co.id
ROKOK DAN What is the web of applica
http://emedicine.meds
KESEHATA relationship cape.com Informa ble?
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: between tion
http://www.p relationship, smoking,
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artikel and
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.com/article/1
57452-
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(Cardiomegaly) : http://google.co.id
What are the (pdf) and of applica
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com/heart- causes of nih.gov/ article Informa ble?
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Cardiomegaly of the
Spontaneously
Hypertensive Rat :
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rnals.org/content/35
/1/102.full.pdf and
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sitywarriors.org/enl
arged-heart-atau-
kardiomegali.html
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pdf and Keywords :
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41
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Keywords : Cardiac
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apter%20II.pdf

42
4.3 References

"ALT: The Test | Alanine Aminotransferase; ALT Test: Alanine Aminotransferase; SGPT; GPT;
Serum Glutamic-Pyruvic Transaminase; Alanine Transaminase | Lab Tests Online".
https://labtestsonline.org/understanding/analytes/alt/tab/test. N.p., 2016. Web. 5 June 2016.

Anand, I., Ferrari, R., Kalra, G., Wahi, P., Poole-Wilson, P. and Harris, P. (1989).Edema of cardiac
origin. Studies of body water and sodium, renal function, hemodynamic indexes, and plasma
hormones in untreated congestive cardiac failure. Circulation, 80(2), pp.299-305.

"AST: The Test | Aspartate Aminotransferase; AST Test: Aspartate Aminotransferase; SGOT; GOT;
Serum Glutamic-Oxaloacetic Transaminase; Aspartate Transaminase | Lab Tests Online".
https://labtestsonline.org/understanding/analytes/ast/tab/test. N.p., 2016. Web. 5 June 2016.

Aulia, Rizky, 2009. Gagal Jantung. Tinjauan Pustaka. [online] Available at: http://lib.ui.ac.id/file?
file=digital/122491-S09004fk-Hubungan%20antara-Literatur.pdf [Accessed 29 May 2016].
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Beckerman, J. (2016). What Is an Enlarged Heart (Cardiomegaly)?. [online] WebMD. Available at:
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May 2016].

Dokudok.com. 2015. ISTILAH PADA SUARA NAFAS | | dokudok. [online] Available at:
http://dokudok.com/ilmu-dasar/istilah-pada-suara-nafas/ [Accessed 5 Jun. 2016].

FARMER, B., HARRIS, R., JOLLY, W. and VAIL, W. (1974). Studies on the Cardiomegaly of the
Spontaneously Hypertensive Rat. Circulation Research, 35(1), pp.102-110.

Guyton, A. and Hall, J. (2006). Textbook of medical physiology. Philadelphia: Elsevier Saunders.

Imaligy, Ervina U., 2014. Gagal Jantung Pada Geriatri. CDK-212/vol. 41 no. 1. [online] Available
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[Accessed 29 May 2016].

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Jun. 2016].

Rachma, N. (2014). Enlarged Heart atau Kardiomegali. | Jurnal Biodiversity Warriors. [online]
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Silverman, M. 1990. The Third Heart Sound. Butterworths. [online] Available at:
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Sovari, A. (2015). Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis. [online]

Emedicine.medscape.com. Available at: http://emedicine.medscape.com/article/157452-
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Thaler, M. (2012). The only EKG book you'll ever need. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins.

Updated by: Laura J. Martin, and the A.D.A.M. Editorial team. "Aspartate Aminotransferase (AST)
Blood Test: Medlineplus Medical Encyclopedia".
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Updated by: Neil K. Kaneshiro, a. 2016. Wheezing: MedlinePlus Medical Encyclopedia [online]
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44
WebMD. 2016. Causes and Treatments of Heart Murmurs. [online] Available at:
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Wolf, A D., Lavine, J E. (2000). Hepatomegaly in Neonates and Children. [online] Available
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%20Review-2000-Wolf-303-10.pdf [Accessed 26 May 2016].

Job Description:

1. Compile file: Nabila Izzati

2. Editor: Nabila Izzati
3. PPT: Andi Lestari Rahman
4. LI1 : All members included
5. LI2: All members included
6. Concept Mapping I: Erlin Rosmilah
7. Concept Mapping II: Liofelita C and Sandhilino
8. Final Hypothesis and Conclusion: Nabila Izzati
9. Journal Appraisal and Critical Appraisal: Abdulrahman

45