FACULTY OF MEDICINE

BLOK KARDIOVASKULER
UNIVERSITAS MUSLIM INDONESIA Makassar, 29 March 2019

“ MODUL 2”

TUTOR :
dr. Rachmawati, Sp.Rad
Created By :
GROUP 15
M. Farizan Atjo (11020160032)
Ainunnisa Muhamma (11020170003)
Miftahul Jannah (11020170042)
Moh. Yusril (11020170052)
Muhammad Fakhri (11020170069)
Muh. Fadil Asrar (11020170055)
Jihan Adjdjibiyan S. Azzubaidi (11020170105)
Indah Setiyani Ulum (11020170134)
Andi Bau Syatirah Ninnong M (11020170138)
Hernita (11020170152)

FACULTY OF MEDICINE
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2019
FOREWORD

We thank Allah for the blessings and blessings of His grace so that the
results of this tutorial can be resolved properly. And do not forget to send
greetings and prayers to the Prophet Muhammad SAW that has brought us from a
world full of ignorance to a nature full of intelligence.

We also thank the parties who helped make this report and the tutors who
guided us during the PBL process.

Hopefully this tutorial report can be useful for everyone who has read this
report and especially for the drafting team itself. Hopefully after reading this
report can expand the knowledge of readers.

Makassar, 29 March 2019

Group 15
SCENARIO 1
A 35-year-old man came to the emergency room with complaints of
sudden shortness of breath 2 hours before entering the hospital. Shortness of
complaint since one day ago weighed 2 hours before entering the hospital.
Shortness accompanied by severe chest pain accompanied by cold sweat.
Everyday the patient works as a pilot. No history of hypertension, diabetes
mellitus and heart disease before.
On examination it was found: cyanosis TD: 160/100 mmHg, Respiratory: 45x
/ minute, S: 37 ° C, pulse: 130 x / minute, SaO2: 85%. EKG examination: sinus
rhythm, 150 x / minute, S I Q III Tinverted III.

DIFFICULT WORDS
-
KEYWORDS
1. A 35 year old man
2. With complaint since the sudden breathing 2 hours before being hospital.
3. Shortness with chest pain and cold sweat’
4. Everyday the patient works as a pilot.
5. On examination it was found:
 cyanosis
 TD: 160/100 mmHg,
 Respiratory: 45x / minute,
 S: 37 ° C,
 pulse: 130 x / minute,
 SaO2: 85%.
 EKG examination: sinus rhythm, 150 x / minute,
 S I Q III Tinverted III
QUESTIONS
1. How is the relationship between patient complaint and activity as a pilot?
2. What is the different between cardiovascular and non cardiovascular
shortness of breath? Explain the pathomecanism of shortness of breath?
3. How diagnose the patient?
4. What is the diagnose in the scenario?

DISCUSSION
1. The relationship between patient complaint and activity as a pilot
Sitting for too long, such as when driving or on an airplane. When our
feet are in a stationary position for quite a long time, our leg muscles do not
contract so that the muscle pump mechanism does not go well. In 1856
virchow first discovered the pathogenesis of DVT and pulmonary embolism
known as Virchow trias (stasis, hypercoagulability and injury).
1. Stasis (the presence of slow blood flow) is a condition of
immobilization of one's activities, for example lying more than 3 days
or legs hanging more than 7 hours (when sitting) slow flowing blood
gives more opportunities for freezing (thrombus), loose thrombus
following venous blood flow to the right heart and after reaching the
pulmonary circulation
2. damage to the vein wall
3. the state of blood easily freezes
so it can be concluded that the effect of patient activity as a pilot patient
lacks leg muscle contractions, causing DVT (deep vein thrombosis) and one
of the complications is that it can cause pulmonary embolism which causes
patients to experience severe tightness and chest pain

Reference:
- Disease textbooks in volume II edition VI p. 1692
- Ali Nafiah Nst: Pulmonary Embolism, 2007 for Respiratory 2008
2. Different between cardiovascular and non cardiovascular shortness of
breath, we can found:
Cardiogenic Noncardioenic

Symptoms  When doing activity  Sometimes when doing

 With chest pain activity
  Takipneu  Can be overtaken by
 Fast and deep ISPA
 Not affected by  Dispneu
weather  Affected by weather
 Could hard to eat and and allergen
drink  Sianosis > disappear if
 Orhtopneu given oxygen
 Cold sweat  Pemfis : vesicular
 cyanosis
 physical examination : increase or decrease
 perifer edema  Mengi6

 Pathomecasims of shortness of breath

Dispnea or shortness of breath is a feeling of difficulty breathing and is
the main symptom of cardio pulmonary disease. Dyspnea is caused by
increased respiratory work due to pulmonary congestivascular which reduces
lung flexibility. A person who experiences dyspnea often complains of
shortness of breath or suffocation. The objective symptoms of shortness of
breath include the use of additional respiratory muscles (sternocleidomastoid,
scalenus, trapezius, pectoralis major), nasal lobe breathing, tachypnea and
hyperventilation. The amount of physical energy released to cause dyspnea
depends on age, gender, height of place, type of physical exercise, and
emotional involvement in carrying out the activity. Dispnea that occurs in a
person must be associated with a minimal level of activity that causes dyspnea,
to determine whether dyspnea occurs after moderate or severe activity, or
occurs at rest. The factors that cause shortness of breath are as follows:

• Heart disease: left ventricular failure and mitral stenosis

• Pulmonary disease: obstructive pulmonary disease, asthma, restrictive
pulmonary disease, pulmonary embolism, and pulmonary hypertension
• Emotional: anxiety and depression
• High place exposure: reduced oxygen pressure
• Anemia: reduced oxygen carrying capacity

 The difference between tightness in cardiovascular disease and

 tightness in non-cardiovascular diseases.
The mechanism of congestion due to cardiovascular disease occurs when
an increase in left ventricular filling pressure causes an increase in vascular
permeability. Which causes congestion in the pulmonary vein, which normally
ranges from 5 mmHg to an increase in pressure of around 25 mmHg. So that
plasma contained in the vascular exits from endothelial cells due to
differences in blood vessel pressure with the intertial region and makes the
plasma flood the interticial region. Then the transudate will gather and some
enter into the alveoli which causes less optimal air exchange so that the body
compensates for hyperventilation to meet the lack of oxygen to the tissue, this
is what causes patients to experience congestion.
While the mechanism of tightness due to non-cardiovascular disease
occurs when there is inflammation or resistance to the airway which causes
tissue oxygenation to decrease and makes the need for oxygen increase. The
sudden increase in oxygen demand will require more oxygen for the metabolic
process so that the impulses are sent to the medulla oblongata after which the
impulse is carried on by the effector in the thoracic muscles to contract faster
in compensation for the body to get more oxygen, this is what causes a person
to experience tightness

Reference:
- Florian lang. Stefan silbernagl. 2006. Teks dan atlas berwarna
patofisiolog. Jakarta: EGC hal 218.
- Buku Ajar Ilmu Penyakit Dalam. Edisi 6. Jilid 2
- Price, Sylvia Anderson dan Lorraine MW. Patofisiologi Vol 1. Ed 6.
Jakarta : EGC. 2005.
- Joewono,B.S.2003, ilmu Penyakit Jantung, Airlangga University Press,
Surabaya.
- Bakta, made, dkk., 2000, gawat darurat di bidang penyakit dalam,
Jakarta:EGC, hal 3.

3. What are the steps in the diagnosis of the patient?

A. History:
 From the results of the history it was found that a 35-year-old male
patient came to the Emergency Unit with a sudden complaint of
shortness of breath that was experienced 2 hours earlier. Complaints
felt 1 day ago weighed 2 hours before entering the hospital. Shortness
accompanied by severe chest pain accompanied by cold sweat. A
pilot's passive job. No history of hypertension, diabetes mellitus and
heart disease before.

1) General Data (Risk Factors)

a. Age: 35 years
b. Sex: Male
2) Current Disease History
a. Symptoms / signs
b. Functional capacity of the patient (Good, moderate or bad)
c. Shortness of breath
3) History of Fever (is rheumatic fever, diphtheria, endocarditis,
tuberculosis )
4) History of Disease Previously
a. Asking a history of systemic diseases:
 Hypertension

 Diabetes Melitus

 Dislipidemia

 Cerebrovascular

 Disease VascularPeripheral

 DiseaseThyroid

 Bronchial Asthma or Obstructive Lung Disease.

b. Asking for Treatment and Allergies.

 5) Family History (relative to first level)
a. Hypertension
b. Ischemic Heart Disease
c. Diabetes Mellitus
d. Dislipidemia
e. No previous history of heart disease.
6) Personal and Social History
a. His a pilot
b. Alcohol consumption
c. Not allowed to use drugs (especially cocaine,
methamphetamine or "meth"
d. Obesity
e. Sports History (lack of exercise)
f. Intact diet (high in fat or salt)

B. Type A (hard worker and obsessive compulsive type)

C. Physical examination includes:
1) blood pressure of 160/100 mmHg, pulse 130 beats / min with the
impression hypertensive
2) heart Inspection
Inspection of heart means looking for signs that express the state
of the heart in the chest surface by seeing / observing. the signs are

a) form ofprecordium
b) pulseat the apex of the heart
c) Pulse on the chestpulses
d) Venous pulse
3) Palpation of the heart
Palpation can strengthen the results obtained from the
inspection.Invisiblecan also be found by palpation Palpation on the
precordiun must be done with the palm first, then using the tips of
the fingertips .
 throbbing, vibration and traction can be examined by palpation
road either mild or severe The order of palpation in order to
examine the heart is as follows:

a) Examination of the ictus cordis

b) Vibration / thrill
c) examination Examination of the trachea movement.

4) Cardiac Percussion
We do percussion to set the heart boundaries namely the left
heart and the right border of the heart.

5) Cardiac Auscultation
On auscultation, for several blows the heart must try to listen
and focus on the sound I, after there is certainty then focus on the
sound II. On auscultation two things will be considered, namely::

a) Heart SoundsHeart Sounds I and II

b) Heart Noise / Cardiac Murmur: Heart Noise is longer than
heart sounds.
D. Examination Support:
1) Exercise Test
This examination is done if abnormalities of the ECG are
not found. There are several types of tests, namely the Treadmill
test and Bicycleergometer.

This test is considered positive if at the time of the test

there is pain in the chest and an ECG picture shows ST segment
depression more than 1mm. The risk of getting a death or
infarction attack in this test is around 1: 1000.

2) Thalium Ecercise Myocardial lmagingThalium

Radioactive substancesis a substance that is easily absorbed
by normal myocardial tissue. In this test intravenous Thalium 201
 injection was carried out at the peak of the test. Then do heart
scanning immediately and after rest. The ischemic myocardium
contains only a small amount of Thalium compared to the normal
myocardium, so that when undergoing testing in the area of
ischemia this cold spot and coldspot will disappear with rest. If the
cold spot persists for T4 hours, this indicates severe ischemia or the
possibility of myocardial infarction.

3) Echocardiography of

Heart ultrasound) is a method of examination using high

frequency sound waves to capture images of the structure of the
heart organ.

4) Electrocardiogram (ECG)
Outside the attack, the ECG picture in 25% of patients is
still normal. At the time of the attack, depression or ST segment
elevation and negative T wave were found. Other disorders that
may be found are signs of prolonged infarction, left ventricular
enlargement or disruption of delivery.

The potential for action caused by the activity of the heart

is large enough, so that it can be delivered by tissue around the
heart to the surface of the body. So that the action potential can be
captured by electrodes mounted on the surface of the body. The
tissue around the heart is called "volume conductor".

Electrocardiography (ECG) is a graph that records the

electrical potential of the heart delivered to the surface of the body
and is noted as a potential difference in the electrodes on the skin.
This potential difference occurs because the excitation process
does not occur simultaneously in the entire heart.
Electrocardiography represents total electrical activity in the heart
that is recorded on the surface of the body.
a) Electrical Events in the Heart Cycle
Mechanical events in the heart cycle lag behind the heart's
electrical signal (contraction of the heart muscle follows the
action potential). This is the reason why many leads are used.
The heart cycle starts when the atrium and ventricles are at rest.
While the ECG begins with atrial depolarization.

Picture I. Cardiac Conduction System.

b) Lead (Lead)
When the electrocardiography is connected to two points on
the body, the specific picture of each pair of these relationships
is called the lead. The types of leads that are often used on
ECGs are:

1) Bipolar LeadExtremities
2) Lead ExtremitiesUnipolar
3) precordialLead

c) ECG Interpretation Examination

1) P wave:
a) The duration of the normal P wave
P wave: is a deflection / deviation caused by atrial
depolarization process. The occurrence of the P wave
is due to atrial depolarization spreading radially from
 the SA node to the AV node (atrium conduction
time). Normal P waves meet the criteria:

1) Wavelength not more than 0.12 seconds

2) Height or amplitude not more than 3 mm c.
usually upward deflection (positive) in leads
I, II, aVL and V3-V6 d. usually downward
(negative) deflection on the aVR, often at V1
and sometimes V2
2) PR interval: PR
interval: or more accurately called interval PQ,
measured from the onset of the P wave to the beginning
of the QRS complex. This shows the length of
conduction of ventricular atrios, which includes the time
needed for atrial depolarization and the initial and
repolarization of the atrium. The final atrial
repolarization occurs at the same time as ventricular
depolarization. The normal PR interval value is: 0.12-
0.20 seconds.

3) PR Segment:
The PR segment is the distance between the end of
the P wave and the beginning of the QRS complex. Under
normal circumstances the PR segment is in an isoelectric
or slightly depressed line with a length of no more than
0.8 mm. This PR segment describes the excitation of the
AV node (or delay in transmission of impulses in the AV
node).

4) QRS Complex:
What needs to be considered in the QRS complex is
a) the QRS complex duration: Indicates total
ventricular depolarization, measured from the
onset of the Q wave (or the beginning of R if Q is
invisible), to the end of wave S.
The normal value of the duration of the QRS
complex is 0.08-0.10 seconds. VAT or also called
intrinsic deflection is the time needed for
impulses across the myocardium or from the
endocardium to the epicardium, measured from
the beginning of the Q wave to the RVAT wave
peak should not be more than 0.03 seconds at V1
and V2, and should not be more than 0.05 on V5
and V6.

b) Pathological Q Waves Pathological Q

waves are a sign of an old myocardial
infarction. The pathological Q wave sign, which
is greater than 0.04 seconds and the depth
exceeds one third of the R wave height in the
same QRS complex. Because pathological Q
waves indicate the location of myocardial
infarction, then to diagnose old myocardial
infarction must see at least a pathological Q wave
at two related leads.

Example: a diagnosis of long inferior

myocardial infarction can be established if
pathological Q waves are found in leads II, III,
and aVF (see picture below).
 Picture II. Pathological P waves on leads II, III,
dan aVF.

5) ST segment:
The ST segment is also called the Rs-T segment, is
the measurement of time from the end of the QRS
complex to the beginning of wave T. This shows the time
at which the ventricles are excited before they begin
repolarization. The point that shows where the QRS
complex ends and the ST segment starts, commonly
called J point.

ST segments that are not isoelectric (not parallel to

the PR segment or baseline), up or down to 2 mm in
precordial leads (Dr. R. Mohammad Saleh mentions 1
mm above or below the line) are considered abnormal. If
the ST segment rises is called ST elevation and if it goes
down is called ST depression, both are signs of coronary
heart disease. The normal ST segment length is between
0.05-0.15 seconds (ST interval).
 Picture V. Normal segment ST on ECG

Picture III. ST depression and ST Elevation

on ECG

6) T wave: T
wave is a deflection produced by the repolarization of the
heart ventricle. T wavelengths are usually 0.10-0.25
seconds. On a normal ECG, the T wave is as follows: -
positive in leads I and II, and horizontal, biphasic or
negative in lead III - negative in aVR, and positive,
negative or biphasic in aVL or aVF. - negative at V1, and
positive at V2 to V6.
 Picture IV. T Wave on ECG

7) U Wave: U
waves usually follow the T wave, which process is not
known to be produced. U waves are positive and small
deflections after the T wave before the P wave, also called
after potential. Negative U waves are always abnormal.

8) QT interval The QT interval is

the beginning of the Q wave to the end of the T wave,
describing the duration of the electrical process during
ventricular systolic (duration of electrical systole) or
ventricular depolarization and its repolarization. This QT
interval changes depending on the frequency of the heart,
so it must be corrected according to the frequency of the
heart (QTc). For this correction use a normogram that
gives Q-Tc for heart frequencies 60x / minute. Normal Q-
Tc in men should not exceed 0.42 seconds and in women
it should not be more than 0.45 seconds.
/

DESCRIPTION:

A. P wave: atrial activation.

1) Width <0.12 seconds
2) High <0.3 millivolts
3) Always positive in lead II and negative at lead aVR
B. PR interval: duration of AV conduction
1) From the start of the P wave to the beginning of the QRS complex
2) Normal duration is 0.12-0.20 seconds
C. QRS complex: right and left ventricular activation
1) Width 0.06–0.12 seconds The
2) length varies between each lead
3) Q wave -> first negative deflection
4) R wave -> first positive deflection
5) S wave -> negative deflection after wave R
6) Complex duration QRS: duration of ventricular muscle
depolarization
 7) PP interval: duration of atrial cycle
8) RR interval: ventricular cycle duration
9) QT interval: duration of ventricular depolarization and
repolarization
D. ST Segment
1) From the end of the S wave to the beginning of the T wave
2) Normal: isoelectric
E. T waves
1) Positivein lead I, II, V3-V6 and negative at aVR
Small box size: 1 mm and large box size: 5 mm. Paper recording speed is
25 mm / second, meaning that one small box is 0.04 seconds.
Standard amplitude of 1 millivolt.

 Laboratory

examination On examination it was found: Cyanosis TD: 160/100

mmHg, Respiratory: 45x / minute, S: 37 ° C, pulse: 130 x / minute, SaO2:
85%. ECG examination: sinus rhythm, 150 x / minute, SIQ III Tinverted
III.

References:

1. Sherwood, lauralee. Edition 8. Human Physiology from cell to system.

Jakarta: EGC. Jakarta, 2013.
2. Malcolm S. Thaler. The only ECG book you need. Issue 8. Medical
Book Publishers: ECG.
3. Philip I. Aaronson & Jeremy PT Ward. At a glance.
Cardiovascular system. Third edition. Erlangga Medical Series.
2007.
4. Kapita Selekta Medis, Second edition Editor Junaedi Purnawan and
Kawan-Kawan, Media Publishers Aesculapius Faculty of Medicine
UI, 1982.
 5. Chu MW, Adams C, et all. Ascending-descending the aorta to the
bypass journal. Medical Faculty

4. What is the diagnose in the scenario?

 PULMONARY EMBOLISM (PE)

 Definition
Pulmonary Embolism (PE) is a blood clot that lodges in the lung arteries.
The blood clot forms in the leg, pelvic, or arm veins, then breaks off from the
vein wall and travels through the heart into the lung arteries. Most PEs are due to
pelvic and upper leg blood clots that first grow to a large size in the vein before
detaching and traveling to the lungs. PE can cause death or chronic shortness of
breath from high lung artery pressures (“pulmonary hypertension”). PE can
impair heart muscle function, especially the right ventricle, which pumps blood
into the lung arteries.

 Epidemiologi

Pulmonary embolism is a common complication of hospitalization and

contrib-utes to 5 to 10 percent of deaths in hospitalized patients, making it one of
the leading causes of preventable hospital deaths. Despite it being an enormous
health problem, the true incidence of pulmonary embolism is uncertain. The
diagnosis of venous thrombi and pulmonary emboli can be difficult and requires
specialized imaging techniques that are not available in all hospitals or
healthcare settings. In the United States, the estimated incidence of diagnosed
pulmonary embolism is 71 to 117 per 100,000 person-years, but the true
incidence is likely to be much more than this rate because studies show that for
every case of diagnosed, non-fatal pulmonary embolism, there are 2.5 cases of
fatal pulmo-nary embolism diagnosed only after death. Other studies have
estimated that more than one million people in the United States are affected by
pulmonary embolism per year, with 100,000 to 200,000 of these events being
fatal .

 Risk factors
 Inlude immobility, smoking cigarettes, being overweight, and having high
blood pressure all of which can be potentially controlled with a heart healthy
lifestyle. A recent study showed that eating fruits and vegetables can be
protective against developing PE. However, people who frequently eat red meat
had double the risk of developing PE. Other risk factors for PE include cancer,
long airline flights, surgery and trauma. PE is also associated with women ’s
health issues such as use of birth control pills, pregnancy and hormone
replacement therapy. Certain genetic mutations predispose to PE, such as “factor
V Leiden” and the “prothrombin gene mutation.”

 Symptoms
The most common symptom is unexplained shortness of breath and/or chest
pain with difficulty breathing. However, PE can be difficult to diagnose and has
been called “the Great Masquerader.” It can mimic pneumonia, congestive heart
failure, and a viral illness known as pleurisy.
• Shortness of breath
• Chest pain, often worse when taking a breath
• A feeling of apprehension • Sudden collapse
• Coughing • Sweating
• Bloody phlegm (coughing up blood)
The signs and symptoms of these disorders can vary by individual and
event. Some individuals may also experience uncommon symptoms such as
dizziness, back pain or wheezing. Because PE can be fatal, if you experience
these signs or symptoms seek medical attention right away.

 Patofisiologi
Increased pulmonary vascular resistance caused by obstruction,
neurohumoral, or pulmonary artery baroreceptors or increased pulmonary
arterial pressure 2. Disrupted gas exchange due to increased alveolar dead
space from the impact of vascular obstruction and hypoxemia due to alveolar
hypoventilation, low ventilation-perfusion unit and shunt from the right to the
left and also carbon monoxide transfer disorders 3. Alveolar hyperventilation
due to reflex stimulation by receptor irritation 4. Increased airway resistance
due to bronchoconstriction 5. Reduced pulmonary compliance caused by
 pulmonary edema, pulmonary bleeding and loss of surfactant.

 Diagnosis
A definitive diagnosis of PE must be made in a hospital or clinic with
radiology facilities. A chest CT scan (“CAT scan”) or a nuclear medicine scan
are the most common tests to diagnosis PE. The most crucial point is for
patients and their health care providers to consider the possibility of PE. Prior
to a chest CT scanning or a nuclear medicine scan, doctors may determine the
likelihood of PE through screening tests such as a chest X-ray,
electrocardiogram and a blood test called a “D-dimer” (low D-dimer levels
virtually exclude PE).

 Physical Examination
Suspicion of pulmonary embolism is the basis for determining a diagnostic
test. Dyspnoea is the most common symptom, and tachypnoe is the most
characteristic sign of pulmonary embolism. In general, severe dyspnoea,
syncope or cyanosis are the main signs of life-threatening pulmonary
embolism. Pleuritic pain indicates that the pulmonary embolism is small and is
located in the distal pulmonary artery, adjacent to the pleural line

 Treatment
The foundation of treatment is thinning the blood with anticoagulants such
as heparin, low molecular weight heparin, fondaparinux, direct thrombin
inhibitors (argatroban, lepirudin, or bivalirudin) or the oral blood thinner,
warfarin. Immediately acting intravenous or injected blood thinner must be
administered right away. The oral blood thinner, warfarin, takes about five days
to become effective to prevent the development of a recurrent PE. In addition
to blood thinners, more aggressive therapies include “clot buster” drugs such as
TPA or catheter-based or surgical embolectomy to remove the PE. The
duration of treatment with the oral blood thinner will vary from 6 months to
lifelong, depending upon the circumstances of the PE and other individual risk
factors
 Referensi :
- Ischemia, C. L. (n.d.). Pulmonary Embolism What is Pulmonary
Embolism ( PE )? Surgeon General ’ s Call to Action.

 COR PULMONAL
 Definition
Pulmonary cast is often referred to as pulmonary heart disease, defined as
right ventricular dilatation and hypertrophy due to pulmonary artery disease
and or pulmonary parenchyma. Historically this definition has excluded
heart disease and right heart failure due to left-sided heart dysfunction.

 Etiology
Pulmonary cast is caused by acute or chronic changes in pulmonary and /
or parenchymal blood vessels which are sufficient to cause pulmonary
hypertension. Actual cor pulmonary prevalence is difficult to ascertain for
two reasons, first, not all patients with chronic pulmonary disease will
experience cor pulmonary and secondly the ability to diagnose pulmonary
hypertension and cor pulmonary through physical examination and
laboratory examination is relatively insensitive. However, the advancement
of Doppler / 2-D echo imaging and biomarkers (BNP) makes screening and
detection of cor pulmonary easier.

 Epidemiology
Chronic obstructive pulmonary disease (COPD) and chronic bronchitis
causes around 50% of cor pulmonary cases in North America any disease
that attacks the pulmonary arteries or parenchyma can cause cor pulmonary.
In contrast to COPD, the increase in pulmonary arterial pressure seems to be
significantly higher in intertial lung disease; in this case, there is a good
correlation between pulmonary arterial pressure and carbon monoxide
diffusion capacity, and patient survival. If cor pulmonary coincides with
obstruction of sleep apnea, COPD or hypoventilation syndrome such as
hypoventilation obesity pub syndrome can occur at the same time.
  Pathophysiology
The pathophysiological mechanism in general in each case is
pulmonary hypertension in a degree that is sufficient to cause dilatation of
the RV, with or without RV hypertrophy at the same time. Systemic cor
pulmonary consequences are changes in cardiac output and salt and water
homeostasis. Automatically, an RV is a thin, thin elastic heart space that is
more suitable for handling volume overload than pressure overload. Based
on this, continuous pressure overload due to pulmonary hypertension and
increased pulmonary vascular resistance ultimately lead to RV failure.
The RV response to pulmonary hypertension depends on the severity
and acute absence of pressure overload. Acute pulmonary cast occurs due to
sudden and severe stimuli, for example (massive pulmonary embolism)
accompanied by RV dilatation and failure but without R. hypertrophy,
meanwhile, chronic cor pulmonary is caused by progressively progressing
pulmonary hypertension which causes mild RV hypertrophy initially and
followed by RV dilation.
Chronic cor pulmonary decompensation can be aggravated by events
that induce intermittent pulmonary vasoconstriction and RV afterload, such
as hypoxemia and especially hypercarbia-induced repiratoric acidosis such
as OHS and continuous events, including exacerbations of COPD acute
pulmonary embolism positive (mechanical) pressure ventilation. RV failure
can also be triggered by changes in the volume of RVs that occur in a
variety of conditions, including increased fatigue and fluid retention, atrial
arrhythmias, polycythemia, sepsis. The most common mechanism that
causes pulmonary hypertension, namely vasoconstriction activation of the
blood clotting cascade and damage to the pulmonary arteries.

 Clinical Symptoms
Chronic pulmonary cast symptoms are usually associated with
underlying pulmonary disorders. Dispneu, the most common symptom is
usually caused by increased breathing due to changes in elastic lung recoil
(fibrosis lung disease). Changes in respiratory mechanics (eg
 overinflammation of COPD) or inefficient ventilation. Syncope due to
coughing or heavy activity can occur due to the inability of the RV to drain
blood adequately to the left side of the heart. Abdominal pain and ascites
that occurs in the cor pulmonary are the same as right heart failure in
chronic HF. Lower extremity edema can occur due to neurohormoral
activation, increased RV filling pressure, or increased carbon monoxide and
hypoxemia levels, which can cause peripheral vasodilation and edema
formation.

 Physical Examination
Tachypneu, increased jugular venous pressure, hepatomegaly and edema
of the lower extremities. Other cardiovascular signs include heave of the RV
that is felt along the edge of the left sternum or epigastrium. Increased
intensity of holosystolic murmurs in tricuspid regurgitation when inspiring
(carvallo sign). Cyanosis is a finding in advanced cor pulmonary and is
caused by low cardiac output associated with systemic vasoconstriction and
incompatibility of perfusion ventilation in the lung.

 Diagnosis
The ECG in severe pulmonary hypertension shows P pulmonary deviasis,
the right axis and RV hypertrophy. A chest diagnosis can show enlargement
of the main pulmonary artery, hilar vessels, and descending right pulmonary
artery. Spirometry and lung volume can identify obstruction and / or
restrictive defects that identify lung parenchymal arterial blood gas can
show hypoxemia and or hypercapnia. Chest chest CT scan is useful in
diagnosing acute thromboembolic disease, but scans of pulmonary perfusion
ventilation remain the most suitable examination for diagnosing chronic
thromboembolic disease. High-resolution chest CTscans can identify
intertial lung disease.
Two-dimensional echocardiography is useful for measuring the thickness
of the RV and the dimensions of the heart space and the anatomy of the
tricuspid and pulmonary valves. Doppler echocardiography can be used to
 assess pulmonary arterial pressure. MRI is also useful for assessing RV
structure and function, especially in patients who have difficulty imaging
with 2D electrocardiography due to severe lung disease. Right heart
cancerization is useful for diagnosing pulmonary hypertension and to rule
out increased cardiac pressure as a cause of right heart failure. BNP and N-
terminal BNP levels increase in patients with cor pulmonary due to RV
stretching and can increase dramatically in acute pulmonary embolism.

 Treatment
The general principle of therapy involves decreasing breathing work
by using noninvasive mechanical ventilation and bronchodilation, and
dealing with the underlying infection. Adequate oxygenation (oxygen
saturation> 90-92%) and correction of respiratory acidosis are very
important to reduce pulmonary vascular resistance. The patient must be
transfused if anemic and phlebotomy can be considered in cases of extreme
polycythemia. Duiretics is an effective therapy for RV failure, which must
be considered in the use of long-term diuretics is to avoid induction of
alkalosis contractions. Vasodilators can improve symptoms effectively by
decreasing pulmonary pressure and RV afterload if there is only pulmonary
arterial hypertension.

Refernsi :
- Harrisons cardiovascular medicine. LOscalzo, Joseph ED 2 page
183-185 EGC : 2015
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