REPORT OF PBL 2

“MODUL 2 - CHEST DISCOMFORT”

CARDIOVASCULAR

TUTOR : dr. WISUDAWAN

GROUP 14:

PRIDINA SYADIRA : 110 2011 0006

SITI ABDILLAH MULIADI : 110 2014 0015
AKHMAD FADHIEL NOOR : 110 2014 0033
A.EKA OKTAVIANA B. PUTRI : 110 2014 0049
PRAMULIANSYAH HAQ : 110 2014 0053
ALIFA FAWZIA : 110 2014 0082
NURRAHMAH KADIR : 110 2014 0102
M. RHEZA RIVALDI SALAM : 110 2014 0114
SITI ADANI AYUNDI : 110 2014 0098
MUH. NUR ANSHARI SYAKIR : 110 2014 0150

MEDICAL FACULTY
MUSLIM UNIVERSITY OF INDONESIA
MAKASSAR
2016
Case 2

Scenario 2

male 71 years came to the clinic with complaints of discomfort in the chest
accompanied by a feeling hard to breathe during the last 3 months, especially
when climbing stairs. patients with a history of smoking 30 cigarettes per day. a
family history of father died of a heart attack at the age of 80 years and mother
died by the same causes at the age of 50 years

blood tests obtained glomerulus filtration rate of 25 ml / min / m2, the fasting
blood glucose 11 mmol / liter, LDL cholesterol 5.0 mmol / L, HDL cholesterol of
0.7 mmol / L /

of physical examination found blood pressure is 170/95 mmHg. Pulse 92

times per minute. Other physical examination within normal limits.

1. Difficult Word
No difficult word
2. Key word
 A man 71 yo
 complaints of discomfort in the chest accompanied by a feeling hard to
breathe during the last 3 months, especially when climbing stairs
 history of smoking 30 cigarettes per day
 history of family by heart attack (father died at the age of 80 years and
mother at the age of 50 years)
 GFR 25 ml / min / m2
 fasting blood glucose 11 mmol / liter
 cholesterol 5.0 mmol / L
 HDL cholesterol of 0.7 mmol / L
 blood pressure is 170/95 mmHg
 Pulse 92 times per minute
3. Question
 1. classification of cardiac and non-cardiac chest pain?
2. what is the normal value of blood tests in the scenario above?
3. what the causes of chest pain from the above scenario?
4. what the precipitating factors and risk factors of chest pain in the above
scenario?
5. how is the relationship with the family history of chest pain?
6. how is the relation with smoking history of chest pain?
7. what is the relationship of physical activity with chest pain?
8. measures to determine the diagnosis of disease diagnosis?
9. Basic management to results the diagnosis?
10. explain the differential diagnosis of this scenario!
4. Answer
1. classification of cardiac and non-cardiac chest pain
A. Pleuritic chest pain
Pleuritic chest pain usual posterior or lateral location. Nature sharp
and stabbing. Increased pain when coughing or breathing in and
decreases when holding breath or chest pain side driven. Pain originating
from the chest wall, muscle, ribs, parietal pleura, large airways,
diaphragm, mediastinum and intercostal nerve.
Pleuritic chest pain may be caused by the: Diffusion pelura due to
lung infection, pulmonary embolism, malignancy or inflammation
subdiafragmatik; pneumothorax and penumomediastinum.
B. Non pleuritic chest pain
Pleuritic chest pain usually non-central location, settled or it can spread
to other places. Plaing often caused by abnormalities outside the lungs.
1. Kardial
a. Myocardial ischemia will cause distress or substernal pain
radiating to the axilla and drops down into the inside of the arms,
especially more often to the left arm. Pain can also spread to
epigasterium, neck, jaw, tongue, teeth, mastoid with or without
chest pain substernal. Pain caused by nerve visceral eferan will be
 stimulated during myocardial iskemik, but the cerebral cortex can
not determine whether the pain from myocardial sari. Because of
nerve impulses through the spinal cord T1-T4 which is also a
course of stimulation of sensory nerves from other somatic
systems. Myocardial ischemia occurs when the myocardium 02
needs can not be met by coronary blood flow. At coronary heart
disease blood flow to the heart is reduced due to narrowing of
coronary arteries.
There are 3 ischemic syndromes, namely:
 Stable Angina (Angina classic, Angina of Effort):
Attacks typical chest pain that arises when working. Lasted
only a few minutes and disappear with nitroglycerin or rest.
Chest pain can occur after meals, in cold air, simfatis
excessive reaction or emotional distress.
 Unstable Angina (Angina preinfark, acute coronary
insufficiency):
This type of angina is suspected if the patient has often
repeatedly complained of chest pain that arises when a break
or working light and lasts longer.
 Myocardial infarction: Myocardial ischemia lasting more
than 20-30 minutes can lead to myocardial infarction. Chest
pain lasts longer, radiating to the left shoulder, arm and jaw.
In contrast with angina pectoris, the onset of chest pain has
nothing to do with physical activity and if not treated took
place within a few hours. Besides, patients also complain
dispea, palpitations and sweating. Diagnosis is upheld by the
examiner serioal ECG and cardiac enzymes.
b. Mitral valve prolapse can cause chest pain or Substernal
prekordinal that can last a minute or longer. Sisttolik murmur end
and mid-systolic click the picture of the echocardiogram can help
enforce the diagnosis.
 c. Severe aortic stenosis or aortic substenosis idiopathic hypertrophy
can also cause ischemic chest pain.

2. Perikardikal
Sensory nerves for pain located on parietal pericardium above the
diaphragm. Pain perikardila location in the sternal region and
preokordinal area, but can spread to the epigastric, neck, shoulders
and back. Pain usually like being stabbed and signage at ime deep
breathing, swallowing, tilted or moved.
Pain disappear when the patient sits and berdandar forward. Certain
movements can increase pain which distinguishes it from the pain of
angina.
Diaphragmatic pericardial inflammation can cause pain epigastrum
lateral and back as pancreatitis or kolesistesis.

3. Aortal
Patients with hypertension, koartasio aorta, chest wall trauma is a
high risk for aortic displacement. Diagnosis is suspected when chest
pain terrific front arise suddenly or pain interskapuler. Chest pain can
mimic myocardial infarction but sharper and more often radiates to
the area interskapuler and down to the bottom depending on the
location and extent of displacement.

4. Gastrointestinal
Geofagitis reflux, kegansan or infection of the esophagus can cause
esophageal pain. Neri esophageal its location in the middle, can
spread to the back, shoulders and sometimes - sometimes down to the
inside of the arm so seangat resemble angina pain. Peptic ulcer
perforation, acute pancreatitis, gastric distention sometimes -
sometimes can cause pain substernal so screwed ischemic pain
cardinal. Burning pain often together - together with dysphagia and
 regurgitation when increases in the recumbent position and berurang
with antacids is typical for disorders of the esophagus,
gastrointestinal photo serially, esofagogram, acid perfusion test, and
inspection esofagoskapi esophageal movement can help enforce the
diagnosis.

5. Mulkuloskletal
Local trauma or inflammation of the chest muscles, bones, cartilage,
often causing chest pain locals. Pain usually occurs after physical
activity, different from angina pain that occurs when exercis. As well
as pleuritic pain. Neri chest can increase the time to breathe in.
Muscle pain may also arise on the movement berpuitar while pleuritic
pain is usually not the case.

6. Functional
Anxiety can cause or prekordinal substernal pain, discomfort in the
chest, palpilasi, dyspnea, using and fear of death. Emotional
disturbances without klealinan objective of the heart organ can
differentiate functional pain with myocardial ischemic pain.

7. pulmonary
Obstruction of upper respiratory tract infections such as those with
chronic larynx can cause chest pain, mainly in swallowing. In acute
pulmonary embolism chest pain resembling acute myocardial
infarction and Substernal. When accompanied by pulmonary
infarction often arise pleuritic pain. In pulmoral primary hypertension
of more than 50% of patients complained of pain precordial occur at
the time of exercise. Chest pain is a symptom of lung cancer that
spread to the pleura, medianal organ or chest wall.

Reference:
 Anwar, T.Bahri. NYERI DADA.2004,1-USU Respository. Hal 1-3

2. normal value of blood tests in the scenario above

a) GFR
stage classification is determined by the value of the glomerular filtration
rate, the higher stage menunjukka n value of the glomerular filtration rate
is lower. The classification divides kidney disease into five stages. Stage 1
is kidney damage with renal function were normal, stage 2 kidney damage
with decreased kidney function are mild, stage 3 kidney damage with the
decline being renal function, stage 4 kidney damage with weight loss of
kidney function, and stage 5 kidney failure (Perazella, 2005).

b) Blood Glucose
Blood glucose is the sugar found in the blood that formed of karbohidr at
the food and stored as glycogen in the liver and skeletal muscle. (Joyce
LeeFever, 2007).
Various blood glucose tests:
  Random blood glucose
Blood sugar tests done at any time of the day regardless of the last
food eaten and the condition of the person's body. (MOH, 1999)
 And fasting blood glucose 2 hours after a meal
Fasting blood glucose tests are glucose tests performed after the
patient has fasted for 8-10 hours, whereas glucose 2 hours after a meal
is an examination conducted 2 hours calculated after patients
completed the meal. (MOH, 1999)
reference value
for fasting blood glucose in serum / plasma is 70-115 mg / dl in adults,
whereas for postprandial blood glucose is <140 mg / dl in adults.
(Joyce Lefever, 2007)

c) cholesterol (LDL and HDL ) (mg/dl)

according to the US National cholesterol Education Program (NCEP) in
2001
1. Cholesterol
 Normal : < 200 mg/dl
 Normal line : 200 – 239 mg/dl
 High : > 239 mg/dl
2. Cholesterol LDL
 Optimal : < 100 mg/dl
 Up to optimal : 100 – 129 mg/dl
 Alarming : 140 – 159 mg/dl
 High : 160 – 190 mg/dl
 Very high : > 190 mg/dl
3. Cholesterol HDL
 Low : < 40 mg/dl
 Alarming : 41 – 59 mg/dl
 Norm : > 60 mg/dl
d) blood pressure
 e) Pulse
 Bradicardi : <60 per minute
 Normal : 60 – 100 per minute
 Takicardi : > 100 per minute

Reference:

1. http://digilib.unimus.ac.id/files/disk1/125/jtptunimus-gdl-chairulper-6215-
2-babii.pdf
2. www.repository.usu.ac.id/bitstream/.../4/Chapter%20II.pdf
3. http://repository.usu.ac.id/bitstream/123456789/23512/5/Chapter
%20II.pdf

3. causes of chest pain from the above scenario

Epicardial coronary arteries are the major site of atherosclerotic

disease. The major risk factors for atherosclerosis (high plasma LDL, low
plasma HDL, cigarette smoking, hypertension and diabetes mellitus) disturb
the normal functions of the vascular endothelium. These functions include
local control of vascular tone, maintenance of an anticoagulant surface, and
defense against inflammatory cells. The loss of these defenses leads to
inappropriate constriction, luminal clot formation, a and abnormal interactions
with blood monocytes and platelets. The latter results in the subintimal
collections of fat, smooth-muscle cells, fibroblasts, and intercellular matrix
(i.e., atherosclerotic plaqus), which develop at irregular rates in different
segments of the epicardial coronary tree and lead eventually to segmental
reduction in cross-sectional area. During episodes of inadequate perfusion
caused by coronary atherosclerosis, myocardial tissue oxygen tension falls and
may cause transient disturbances of the mechanical, biochemical, and
electrical functions of the myocardium.A wide range of abnormalities in cell
metabolism, function and structure underlie these mechanical disturbances
 during ischemia. The normal myocardium metabolizes fatty acids and glucose
to carbondioxide and water. Whith severe oxygen deprivation, fatty acids
cannot be oxidized and glucose is broken down to lactate. The accumulation
of lactate leads to the chest pain (angina).

Reference:

1. T.R. Harrison, etc. Harrison’s Principles of Internal Medicines. 16th

Editon. Pages 1434-1435
2. Pictures: www.google.co.id

4. precipitating factors and risk factors of chest pain in the above scenario
a. factore can change
 Smoking
 Hipertension
 Disiplidemia
 Diabetes Melitus
 Obesity dan metabolic syndrome
 Stress
 Fat diet with high calory
 identity
 b. factor can’t change
 Age
 Gender
 Family history
 Etnes

Reference:

Majid, Abdul. Fakultas Kedokteran Universitas Sumatera Utara.

Repository.usu.ac.id. 2007.

5. relation with the family history of chest pain

Family history of premature coronary artery disease is a risk factor for

development of incident cardiovascular disease. family history for ischemic
heart disease is a significant and independent risk factor for coronary artery
disease. Epidemiological and family studies have repeatedly shown that
genetic predisposition accounts for 40% to 60% of the risk for CAD

In the largest study of its kind to date using cardiac computed tomography
angiography, people with a family history of early signs of coronary artery
disease are at higher risk of developing obstructive coronary artery disease
and plaque in their arteries. Researchers analyzed the data from more than
8,200 patients who underwent cardiac computed tomography angiography
and found that those with a family history of coronary artery disease, or
CAD, have a 28 percent chance of developing the disease themselves than
those with no family history. Family history of CAD also was independently
associated with an increased prevalence of plaque in the arteries.

A family history of ischemic events is a major determinant of coronary artery

disease (CAD). Plasma levels of plasminogen activator inhibitor 1 (PAI-1)
modulate this risk. A deletion/insertion polymorphism within the PAI-1 locus
(4G/5G) affects the expression of this gene. There are 50 genetic risk variants
associated with coronary artery disease that are of genome-wide significance
in the discovery population and replicated in an independent population. All
 of these risk variants are extremely common with more than half occurring in
>50% of the general population. They increased only minimally the relative
risk for coronary artery disease. The most striking finding is that 35 of the 50
risk variants act independently of known risk factors, indicating there are
several pathways yet to be appreciated, contributing to the pathogenesis of
coronary atherosclerosis and myocardial infarction. All of the genetic variants
seem to act through atherosclerosis, except for the ABO blood groups, which
show that A and B are associated with increased risk for myocardial
infarction, mediated by a prolonged von Willebrand plasma half life leading
to thrombosis. The potential molecular mechanisms of 9p21, including cell
cycle kinase inhibitors. Discovery of risk variants associated with PCSK9 has
led to the development of novel treatment for plasma low-density lipoprotein
cholesterol. A monoclonal antibody inhibiting PCSK9 has already undergone
phase I and II clinical trials, showing it is a potent inhibitor of low-density
lipoprotein cholesterol and is mediated through more rapid removal of low-
density lipoprotein cholesterol from the plasma. 9p21 in a dose-dependent
relationship was strongly associated with the severity of CAD as determined
by the number of coronary vessels involved. Left main disease also correlated
with the dosage of 9p21 risk allele. The frequency of the 9p21 risk allele was
significantly less in individuals with 1-vessel disease compared to 2- or 3-
vessel disease. 9p21 mediates its risk by acting at the vessel wall to influence
atherosclerosis and is not associated with myocardial infarction. In contrast,
there is not consistent agreement on whether 9p21 relates to the progression
and severity of CAD.

Family history of CVD modifies future CVD risk depending on the number
and age of affected first-degree relatives. Siblings of patients with CVD have
about a 40% risk increase, while offspring of parents with premature CVD
have a 60% to 75% risk increase. Consistent definitions of premature CVD
would allow a better estimate of the true attributable risk.

Reference
  Kruglyak L.; Prospects for whole-genome linkage disequilibrium
mapping of common disease genes. Nat Genet. 1999;22:139-144.
 Slack J, Evans KA. The Increased risk of death from ischemic heart
disease in first degree relatives of 121 men and 96 women with ischemic
heart disease. J Med Genet 1966;3:239-57.
 Phillips RL. Lilltenfeld AM. Diamond EL. Kagan A. Frequency of
coronary heart disease and cerbrovascular accidents In parents and sons of
coronary heart disease Index cases and controls. Am J Epidemiol
1974;100:87-100
 Thordarson O. Fridriksson S Aggregation of deaths from ischaenuc heart
disease among first and second degree relatives of 108 males and 42
females with myocardial infarction. Acta Med Scand 1979;205:493-500.
 Rissanen AM. Familial aggregation of coronary heart disease in a high
incidence area (North Karelta, Finland). Br Heart J 1979;42:294-303.
 Nora 11, Lortscher RH, Spangler RD, Nora AH, Kimberling WJ. Genetic-
epidemiologic study of early-onset ischemic heart disease. Circulation
1980;61 :503-8.

6. relation between smoke and the sympotms

 Yes. Smoke contains many harmful substaces, one of which is the CO
gas. CO gas has the ability to bind to Hb higher than oxygen. So, if there is
smoke inhaled, Hb bring more CO than oxygen. O2 deficient cells will do
compenstate by way of spasm. When the spasm lasts long, the blood vessels
will be damaged and it can be atherosclerosis. Atherosclerosis can cause
hypertension, if hypertension lasts long, it can be grafting blood vessels in
the heart (coronary arteries), and ultimately lead to myocardial infarction.
One of the symptoms of myocardial infarction is chest pain.

Reference: Murray, K Robert, dkk. 2014. Biokimia Harper ed.27. Penerbit Buku
Kedokteran:EGC

7. relationship of physical activity with chest pain

Yes, if the coronary artery stenosis or narrowing of the misbehaving spasme,
coronary artery supply is insufficient so that will happen an imbalance
between the supply and the demand, this will provide a distraction. And at the
time of the activities of an increase in oxygen supply needs, this will cause
hypoxic tissue that will result in increased metabolic results, such as lactic
acid. Deficiency of oxygenation of tissue infarction can cause chest pain

Reference: Rilanto, Lily Ismudiati.dkk. Buku Ajar Kardiologi. FKUI.2003.

Hal.160)

8. measures to determine the diagnosis of disease diagnosis

a. General Situation
Observation of the patient's level of stress. The level of awareness must be
noted and explained. Evaluation of the patient's ability to think logically is
very important because it is a way to determine whether oxygen is able to
reach the brain (brain perfusion). Client awareness needs to be assessed in
 general is compos mentis, apathy, somnolence, sopor, soporokomatous, or
coma.
b. Checking Blood Pressure
Blood pressure is the pressure exerted on the artery wall. This pressure is
influenced by several factors such as cardiac output, arterial tension and
volume, rate and the thickness (viscosity) of blood. Blood pressure is
usually described as the ratio of systolic pressure against diastolic
pressure, with normal adult values ranged from 100/60 to 140/90.
Mechanical penggukuran blood pressure include:
 spignomanometer cuff attached to the upper arm, placed a stethoscope on
the brachial artery on the ventral surface of the elbow slightly below the
cuff spigmomanometer.
 Pressure in spigmomanometer raised by pumping air into the cuff until the
radial and brachial pulse disappeared. Cufflinks developed again by 20 to
30 mmHg above the point of loss of radial pulsations then the pressure
within spigmomanometer sent down slowly.
 When the pulse began to sound again, read the pressure listed on
spigmomanometer scale, this pressure is the systolic pressure.
 Sound denyyutan next pulse rather loud and still sound as loud as it was
until a moment denyutannya weaken or disappear altogether. Last
throbbing sound is the diastolic pressure.
c. Examination

Palpation: Palpation assessment include the frequency, rhythm, quality,

wave configuration, and the blood vessel. Normal heart rate Age cardiac
frequency (beats / min)

o Baby 120-160 / mnt

o School age 75-100 / mnt
o Teens 60-90 / mnt
o Adults 60
 o toddler 90-140 / mnt
o Preschool 80-110 / mnt
o -100 / mnt

 Rhythm
In normal rhythm is regular intervals that occur between each pulse or
heart. When the pulse is irregular rhythm, the heart rate must be calculated
by auscultation apical pulse for a full minute while feeling the pulse. Each
perbadaan between contractions audible and palpable pulse should be
recorded. Rhythm disturbances (dysrhythmias) often result in deficit pulse,
a difference between the apex frequency (frequency heart sounds at the
apex of the heart) and pulse rate. Pulse deficit usually occurs in atrial
fibrillation, atrial flutter, ventricular premature contraction and varying
degrees of heart block.
pulse strength
The strength or the amplitude of the pulse indicates blood volume
diejeksikan to the arterial wall at each contraction of the heart and vascular
system conditions that lead to arterial pulse. Normally, the strength of the
pulse remains the same at every heartbeat.
o 0 no, not palpated
o 1+ pulse is lost, it is very difficult to palpate, easily lost
o 2+ easily palpated, normal pulse
o 3+ full pulse, increased
o 4+ strong, bouncing pulse, can not be lost
4. Hand
In heart patients, the following are the most important findings to be
considered when examining the upper extremity:
 Peripheral cyanosis, where skin appears bluish, indicating a decrease in the
speed of blood flow to the periphery, so it needs a longer time for the
hemoglobin desaturation. Normally occurs in peripheral vasoconstriction
 due to cold air, or a decrease in pathological blood flow, for example,
cardiac shock.
 Pale, may indicate anemia or an increase in systemic vascular resistance.
 capillary refill time (CRT = Capillary Refill Time), is the basis for
estimating the speed of peripheral blood flow. To test capillary refill, press
firmly fingertips and then release it quickly. Normally, reperfusion occurs
almost instantaneously with the return of color on fingers. Reperfusion
slow showing peripheral blood flow velocity slows down, as occurs in
heart failure.
 Temperature and humidity tangandikontrol by the autonomic nervous
system. Normally hands warm and dry. In a state of stress, will feel cold
and damp. In shock the heart, the hand is very cold and wet due to
stimulation of the sympathetic nervous system and cause vasoconstriction.
 Edema stretch the skin and make it difficult to be folded.
 Decreased skin turgor occurs in dehydration and aging.
 Penggadaan (clubbing) of the fingers and toes showed chronic hemoglobin
desaturation, such as congenital heart disease.
5. Examination Jugular Veins
Estimates of right heart function can be made by observing the throb of the
jugular veins in the neck. It is a way of estimating central venous pressure,
reflecting the end diastolic pressure of the right atrium or the right
ventricle (the pressure just before the contraction of the right ventricle).
The jugular vein is inspected to measure the venous pressure is affected by
the volume of blood, the capacity for the right atrium receives blood and
send it to the right ventricle and right ventricle's ability to contract and
push blood into the pulmonary artery.. Technique :
 Ask the client lying on his back with his head is lifted 30 to 45 degrees
(semi-Fowler position)
 Ensure that the neck and upper thoracic already open. Use pillows to
straighten the head. Avoid hyperextension or flexion of the neck to make
sure that the vein does not kink or curl.
 Usually the pulsation is not visible if the client sits. By the time the client
back to the supine position with a slow, high venous pulsations began to
rise high above the manubrium, ie 1 or 2 cm when the client reaches a 45
degree angle. Measure the venous pressure by measuring the vertical
distance between the corner of Louis and the highest level of the internal
jugular vein pulsatility point that can be seen.
 Use two ruler. Create a line from the bottom edge of the ruler usual with
the tip area of the jugular venous pulsation. Then take a centimeter ruler
and create the first ruler perpendicular to the high angle of the sternum.
Measure the distance in centimeters between the ruler and the sternal
angle.
 Repeat the same measurements on the other side. Bilateral pressures in
excess of 2.5 cm are considered the rise and is a sign of right heart failure.
Increasing the pressure on one side can be caused by obstruction.
6. Examination of the Heart
 Inspection
1. Thoracic / chest
The patient lies flat base. In the shape of the chest "Cardiac
Veussure" there is a local protrusion precordium wide area, between
the sternum and the apex CODIS. Sometimes shows cardiac
pulsation.
Voussure their Cardiaque, showed organic heart defects, heart defects
is in progress is long / occurs before the reinforcement perfectly,
hypertrophy or dilatation ventrikel.Benjolan this can be confirmed by
palpation.
Ictus cordis
In normal adults were a bit thin, often appear easily pulsation called
ictus cordis in the fifth intercostal, left medioclavicularis linea. This
pulsation located in accordance with the apex of the heart. Pulsation
diameter of approximately 2 cm, with punctum maximum in the
middle of the area. Pulsation arise at the time sistolis ventricle. When
 ictus cordis shifted to the left and widened, the possibility of an
enlarged left ventricle. In adhesive pericarditis, ictus diastolis out
occurred at the time, and at the time of retraction into sistolis occur.
This condition is called cardiac ictus negative. Strong pulsation in the
left third intercostal space caused by dilatation of the pulmonary
artery. Pulsation in the supra-sternal probably due to the strong
pulsation of the aorta. On the right ventricular hypertrophy, pulsation
appears in IV intercostal space in the sternal edge or epigastric
region. Notice if there intercostalis arterial pulsation which can be
seen on the back. This situation obtained in mitral stenosis. Pulsation
in the neck near the bottom of the scapula was found in coarctatio
aorta.
2. palpation
Apical impulse can sometimes be too palpable. Normlanya felt as a
throbbing light, with a diameter of 1 to 2 cm. Palms originally used to
determine the size and quality. When the apical impulse width and
strong, called sembulan (heave) or a lifting capacity of the left
ventricle. So named because it seemed to "lift" the hands of the chest
wall during palpation.
PMI abnormal. When PMI V intercostal space located below or
adjacent to the lateral line medioklavikularis, the cause is an enlarged
left ventricle because of left heart failure. Normally, PMI only
palpable in the intercostal space. If PMI can be palpable in two
separate areas and denyutannya paradoxical movement (not
simultaneously), should be suspected ventricular aneurysm.
In addition to the pulsation note frisson "thrill" that feels in the palm
of the hand, a result of abnormal heart valves. These vibrations
correspond to a heart murmur (murmur) is strong at a time so that it
can at palpation auscultation. Thrill also palpable on the blood vessels
when there is a significant obstruction to blood flow, and will be on
 when the carotid artery narrowing (stenosis) of the aortic valve.
Decide on what phase of the vibration was felt, as well as its location.
3. percussion
Usefulness of percussion is to determine the boundaries of the heart.
In patients with pulmonary emphysema there is difficulty percussion
boundaries of the heart. Besides percussion boundaries of the heart,
also must diperkusi large blood vessels in the basal part of the heart.
In normal circumstances between the left and right sternal edge in the
region are deaf manubrium sterni which is an area of the aorta. When
the area is widened, possibly as a result of aortic aneurysm.
To determine the limits of the heart left to do percussion from lateral
to medial. Left heart border extends from the line in the intercostal
space medioklavikularis III to V. The change between the resonant
sounds from the lungs to the relatively dim we designate as the left
heart border.
Border-right is located under the right border of the sternum and not
be detected. Enlargement of the heart either to the left or right would
normally be seen. In some people whose breasts are very dense or
obese or suffering from emphysema, heart lies far below the surface
of the chest so that even the left boundary was not clear except when
enlarged.
Cardiac auscultation
Inspection includes examination cardiac auscultation of heart sounds,
heart murmurs and friction pericard.
4. Heart sounds
To hear heart sounds, note the localization and origin of heart sounds,
heart sounds specify S1 and S2, the sound intensity and quality, the
presence or absence of heart sounds S3 and S4 heart sounds, rhythm
and frequency heart sounds, and other heart sounds that accompany
heart sounds.
 Localization and origin of heart sounds
Auscultation of the heart performed at places as follows:
1. Ictus cordis to hear heart sounds originating from the mitral
valve
2. Intercostal II left to hear heart sounds originating from the
pulmonary valve.
3. Intercostal III right to hear heart sounds emanating from the
aorta
4. Intercostal IV and V in the right and left edges of the sternum
or the end of the sternum to hear heart sounds coming from the
valve trikuspidal.
Places auscultation above is not in accordance with the place and
the anatomical location of the valves in question. This is due to
conduction of
 heart sounds to the chest wall.
Determine the heart sound I and II, In a healthy person can be
heard two kinds of heart sounds:
1. The first heart sound (S1), caused by the closure of mitral
valves and trikuspidal. This sound is a sign of the onset of
ventricular systole phase. I heart sounds heard coincided with a
palpable pulse in the carotid artery pulsation.
2. The second heart sound (S2), caused by closing the valves of
the aorta and pulmonary and mark the beginning of ventricular
diastole phase.
3. The intensity of tubes and Sound Quality
The intensity of the heart sounds heavily influenced by the
thickness of the chest wall and the presence of fluid in the
cavity pericard.
The intensity of the heart sounds should be determined
according to the severity pelannya or sound she heard. Heart
sounds I generally louder than heart sound II at the apex of the
 heart, whereas in the basal part II heart sound heart sound
bigger than I.
4. Note also the quality of heart sounds
In the state splitting (broken heart sounds), the heart sound I
broke due to the closure of the mitral and tricuspid valves are
not concurrent. It may be found in normal circumstances. Heart
sound to 2 ruptured, under normal circumstances discovered
during inspitasi where P 2 is slower than A 2. In circumstances
where the splitting of heart sounds do not disappear on
respiration (fixed splitting), then this condition is usually found
on the pathological and ASD and Right Bundle branch Block
(RBBB).
5. The presence or absence of heart sounds III and IV heart sound
3rd heart sound with low intensity occasionally heard at the end
of rapid ventricular filling, low-pitched, most clearly at the apex
of the heart. Under normal circumstances is found in children
and young adults. In pathological conditions found in severe
cardiac abnormalities eg heart failure and myocarditis. Heart
sounds 1, 2 and 3 provide a sound like hoofbeats, referred to as
protodiastolik gallop.
Heart sounds to 4 occurs because of ventricular distention imposed
due to the contraction of the atria, most clearly heard in the apex
cordis, normal in children and in adults found in pathological
conditions, namely the A - V block and systemic hypertension.
Heart rhythm that occurs by the 4th called presistolik gallop.
6. The rhythm and frequency heart sounds
Rhythm and frequency heart sounds should be compared with the
pulse frequency. Normal heart rhythm was regular and irregular when
called arrhythmia cordis.
Frequency heart sounds must be determined in a minute, and then
compared with the frequency of the pulse. When the frequency of the
 pulse and heart sounds each more than 100 times per minute is called
tachycardi and when the frequency is less than 60 beats per minute is
called bradycardia.
Sometimes the heart rhythm changed by respiration. At slower
expiratory time, a condition called sinus arrhythmias. This is due to
changes in the autonomic nervous system stimulation in S - A node as
the pacemaker. If the heart rhythm is not at all regularly referred
fibrillation. Sometimes a normal heart rhythm is occasionally
punctuated by a heart rate accelerates called extrasystole, followed by
a longer phase of diastole (compensatoir pause). Opening snap,
caused by the opening of the mitral valve in stenosa aorta or
pulmonary stenosa.
Reference: Candrawati, Susiana. Physical examination Cardiovascular System. In
http: //www.scribd.com/doc/16636735/Pemeriksaan-Fisik-kardiovaskuler [2 April
2016]

9. Basic management to results the diagnosis

All of the patients with stable angina gave nitrat and antipalatelet, except thera
are some contraindications to increase the supply of blood. If both of
medicines still can not to reduce the pain, it can be added with B-Blockers or
calcium channel blockers to decrease the pain. If patients have coronary
stenosis it can be added with Trimetazidie or ACE-inhibitor (small dosage).
 Nitrat : can cause vasodilatation so it can be headache and hypotension.
Nitrogliserin (GTN 2,5 mg) or ISDN (10 mg or 20 mg) gave peroral, 2-3
times a day, it can decrease the frequency of angina. Sublingual nitrat,
such as GTN 2,5 mg or ISDN 5 mg diberikan if it needed when it
suddenly attack.
 Antiplatelet or Antiagregation : to keep if the plack rupture not
cause atherotrombosis that can become acute coronary syndrome.Such as
aspirin (80-100 mg) orclopidogrel.
  B-Blockers and Calcium Channel Blocker : If nitrat and antiplatelet had
been gave ans still have a pain, hypertension, so it can be added with B-
Blockers and Calcium Channel Blockers. And if the angina still unstable
so it can be gave triple theraphy combine nitrat, B-Blockers and Calcium
Channel Blockers.

Reference :

1. Prof. Dr. dr. Peter Kabo, PhD, MD. 2010. Bagaimana Menggunakan Obat-
Obat Kardiovaskular Secara Rasional. Jakarta : Badan Penerbit FK UI. Hal
132-138.
2. I Rilantono, Lily. 2012. Penyakit Kardiovaskular. Jakarta : Badan Penerbit
FK UI. Hal 136.

10. differential diagnosis of this scenario

A. ACUTE MYOCARDAL INFARCTION
Acute Myocardial Infarction (AMI) is an interruption of blood flow to the
heart which causes the heart muscle cells undergo hypoxia. Blood vessel The
coronary blockage so that the blood flow to the heart muscle stops, except for
a small amount of collateral flow from the surrounding blood vessels. Muscle
areas that did not receive blood flow or current is very little that can not
maintain muscle function heart, said experience is the development of
myocardial infark.Infark
rapid necrosis of the heart muscle caused by the imbalance between supply
and oxygen demand

What causes myocardial infarction?

Thrombosis - the most common cause
 The common cause of an MI is a blood clot (thrombosis) that forms inside a
coronary artery, or one of its branches and blocks the blood flow to a part of
the heart.Blood clots do not usually form in normal arteries. However, a clot
may form if there is some atheroma within the lining of the artery. Atheroma
is the technical term for fatty patches or ’plaques’ (This is similar to water
pipes that get ’furred up’). Plaques of atheroma may gradually form over a
number of years in one or more places in the coronary arteries. Each plaque
has an outer firm shell with a soft inner fatty core.What happens is that a
’crack’ (’plaque rupture’) develops in the outer shell of the atheroma plaque.
This exposes the softer inner core of the plaque to blood and can trigger the
clotting mechanism in the blood to form a blood clot. Therefore, a build up of
atheroma is the root problem that leads to most cases of MI.
Treatment with a procedure called angioplasty (see below) can break up the
clot and restore blood flow through the artery. If treatment is given quickly
enough this prevents damage to the heart muscle, or limits the extent of the
damage.

Amal Kumar Banerjee, Et all. Guidelines for Management of Acute Myocardial

Infarction. Vol 59.2011

B. ANGINA
Angina–also sometimes called angina pectoris, is a symptom of an underlying
heart condition. It means that the heart is not getting enough blood and as a
result, not enough oxygen. This decrease of oxygen being delivered to the
muscle of the heart happens if one or more coronary arteries are narrowed or
blocked, a condition called atherosclerosis.
This type of blockage may result in chest pain. And while angina does not
usually damage the heart, and the pain might only last a few minutes, it is a
warning sign that you should not ignore. Your body is telling you that your
risk for a heart attack or cardiac arrest is increased. Very simply, angina is
 your heart’s way of getting your attention. An angina attack is not the same as
a heart attack, although many of the symptoms are the same. An angina attack
may be provoked by extremes in emotion (being very angry or upset), eating a
large meal or eating it very quickly, doing more exercise than usual
(overexerting yourself), being exposed to extremes in temperature (too hot or
too cold), or smoking. If the angina is a result of physical activity, stopping
the activity generally stops the pain. But no matter what the cause of the chest
pain or discomfort, it is important that you get medical attention as soon as
possible.
CLASSIFICATION
Stable angina
occurs when the heart has to work harder than normal, during exercise, for
example. It has a regular pattern, and if you already know that you have stable
angina, you will be able to predict the pattern. Once you stop exercising, or
take medication (usually nitroglycerin) the pain goes away, usually within a
few minutes.
Unstable angina
is more serious, and may be a sign that a heart attack could happen soon.
There is no predictable pattern to this kind of angina; it can just as easily occur
during exercise as it can while you are resting. It should always be treated as
an emergency. People with unstable angina are at increased risk for heart
attacks, cardiac arrest, or severe cardiac arrhythmias (irregular heartbeat or
abnormal heart rhythm).

Gilles Montalescot. 2013 ESC Guidelines On The Management Of Stable

Coronary Artery Disease Addenda. Esc Guidelines Addenda. European Heart
Journal.2013

C. CORONARY ARTERY DISEASE

 Atherosclerosis is the main cause of coronary artery disease. The process
begins as disruption of endothelial function due to the accumulation of
lipoprotein droplets in the intima of the coronary vessels. Water insoluble
lipids are carried in the bloodstream attached to water soluble apolipoproteins
(lipoproteins). High concentrations of low density lipoprotein (LDL) can
permeatean already disrupted or dysfunctional endothelium where it
undergoes oxidation and, in diabetics, glycation. Modified LDL attracts
leukocytes into the intima and can be scavenged by macrophages leading to
the formation of foam cells. These cells replicate giving rise to one of the
earliest.
Smooth muscle cells are then recruited and migrate to the site of the foamy
cells. Smooth muscle cells proliferate and manufacture extracellular matrix. A
large volume of the plaque is occupied by extracellular matrix (collagen and
proteoglycan) secreted by the smooth muscle cells. The fatty streak is now
transformed into the fibrous plaque. At this point the lesion begins to encroach
on the lumen of the vessel. Small blood vessels form in these plaques
(angiogenesis) and these plaques can subsequently calcify. Inflammation plays
an important role in promoting smooth muscle cell migration and
proliferation. The final lesion, the advanced complicated lesion, consists of a
fibrous capoverlying a lipid rich core which also contains necrotic material,
this core is highly thrombogenic.

Munther K. Homoud, et all. Coronary Artery Disease.Tufts-New England Medical

CenterSpring.2008.

11.