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Kelompok 15 Modul 2
Kelompok 15 Modul 2
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.
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
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.
Diabetes Melitus
Dislipidemia
Cerebrovascular
Disease VascularPeripheral
DiseaseThyroid
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:
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::
3) Echocardiography of
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.
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
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.
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.
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.
DESCRIPTION:
Laboratory
References:
Epidemiologi
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
DAFTAR PUSTAKA
1. Disease textbooks in volume II edition VI p. 1692
2. Ali Nafiah Nst: Pulmonary Embolism, 2007 for Respiratory 2008
3. Florian lang. Stefan silbernagl. 2006. Teks dan atlas berwarna patofisiolog.
Jakarta: EGC hal 218.
4. Buku Ajar Ilmu Penyakit Dalam. Edisi 6. Jilid 2
5. Price, Sylvia Anderson dan Lorraine MW. Patofisiologi Vol 1. Ed 6. Jakarta :
EGC. 2005.
6. Joewono,B.S.2003, ilmu Penyakit Jantung, Airlangga University Press,
Surabaya.
7. Bakta, made, dkk., 2000, gawat darurat di bidang penyakit dalam,
Jakarta:EGC, hal 3.
8. Sherwood, lauralee. Edition 8. Human Physiology from cell to system.
Jakarta: EGC. Jakarta, 2013.
9. Malcolm S. Thaler. The only ECG book you need. Issue 8. Medical Book
Publishers: ECG.
10. Philip I. Aaronson & Jeremy PT Ward. At a glance. Cardiovascular
system. Third edition. Erlangga Medical Series. 2007.
11. Kapita Selekta Medis, Second edition Editor Junaedi Purnawan and Kawan-
Kawan, Media Publishers Aesculapius Faculty of Medicine UI, 1982.
12. Chu MW, Adams C, et all. Ascending-descending the aorta to the bypass
journal. Medical Faculty