Study Guide Cardio Tayang by Gextha 30 Maret 2015

Study Guide Cardiovascular System
1. PREFACE
The curriculum theme on Cardiovascular System and Disorder is developed
collectively by the academic staff from various departments: Anatomy- Histology,
Physiology, Pharmacology, Pathology, Pediatric, Cardiology, Thorax surgeon, Radiology
and Physiotherapy.
The number of Cardiovascular System credits is five. This book consists of general
information on the learning schedule, block members, facilitators, and the core curriculum,
such as learning outcomes, learning situation, learning task and self-evaluation.
Lecture is only given to emphasize crucial things or objectives of material and to
guide the students before discussion. During discussion, student also has to evaluate their
learning progress independently (self evaluation). For difficult concepts in discussion and
self evaluation, the students are also being asked to discuss several example of case.
More than half of the learning material should be learned independently and in small
group discussion.
Curriculum content, study load and teaching-learning are specified in curriculum
and study guide, student assessment is carried out mainly by objective test at the end of
theme course, and the minimum passing level is set at 70 (70%). A remedial is provided
for those who failed, and later they have to re-sit a second summative test.
Since the integrated curriculum at Faculty of Medicine Udayana University is still in
progress, this guide book will also still have some changes in the future. Regarding that,
we invite readers to give any positive comments for its development.
Planners
Udayana University Faculty of Medicine, DME
2. CONTENTS
1.
Preface .
2.
Contents .............
a. Planners Team .....................................................................
b. Lectures..................
c. Facilitators
3.
Seven General Core Competency
4.
Time Table
-
English Class .
Regular Class ...........
5.
Meeting Students Representatives .................................
13
6.
Assessment ...............
13
7.
Learning program
16
8.
References
75
9.
Standart of Medical Competence
75
10. Evaluation Form
76
11. Item Grid .
80
12. Curriculum Mapping
82
2. a. PLANNERS TEAM
No
NAME
DEPT
PHONE
Anatomy
08123921765
1.
dr. I.G.A. Widianti, M.Biomed (Head)
2.
dr. I Md Junior Rina A, Sp.JP, Fiha (Secretary)
Cardiology
08123814814
3.
dr. Made Muliarta, M.Kes
Physiology
081338505350
4.
dr. I G.N Mayun, PHK
Histology
08155715359
5.
dr. Bajra Nadha, SpJP
Cardiology
0818353925
6.
dr. Eka Guna Wijaya, Sp A
Pediatric
081338599801
b. LECTURERS
No
NAME
DEPT
PHONE
1.
dr. I.G.A. Widianti, M.Biomed
Anatomy
08123921765
2.
dr. I G.N Mayun,PHK
Histology
08155715359
3.
Dr. dr. Adiatmika, M.For
Physiology
08123811019
4.
Physiology
081338505350
5.
Prof. dr. Dewa Putu Sutjana, PFK, M.Erg.

(M.Kes)
Physiology
08123924477
6.
Prof dr. I Gusti Made Aman, SpFK
Pharmacology
081238770650
7.
dr. I G Md Gd Surya Candra Trapika, MSc
Pharmacology
081337991177
8.
dr.Ni Wayan Winarti, SpPA
Patology Anatomy
087862457438
9.
Prof . Dr. Dr. Wita, SpJP
Cardiology
08123809780
10.
Dr. dr. I Ketut Rina, SpPD, SpJP
Cardiology
11.
dr. Bagus Ari Pradnyana Dwi Sutanegara,

SpJP
Cardiology
08123800055
12.
Cardiology
0818353925
13
dr. I Made Junior Rina Artha, Sp.JP
Cardiology
08123814814
14
dr. I Kadek Susila Surya Darma, SpJP
Cardiology
08113853151
08123812808
14.
dr. Eka Guna Wijaya, Sp A
Pediatric
081338599801
15.
Prof. Dr.dr. I Made Wiryana, Sp.An.KIC
Anesthesia
0811392171
16.
dr. Lisna Astuti,Sp.R
Radiology
03617422632
17.
dr. Luh Kamiati, Sp.RM
Physiotherapy
08123998787
18.
dr. Semadi, SpB, SpBTKV
Surgery
08123838654
c. FACILITATORS
REGULAR CLASS (A)
No
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
NAME
dr. Sianny Herawati, Sp.PK
dr. Ni Nengah Dwi Fatmawati,
Sp.MK, Ph.D
dr. Cynthia Dewi Sinardja, Sp.An
dr. Gde Somayana, Sp.PD
dr. I Nyoman Gede Wardana,
M.Biomed
dr. Elysanti Dwi Martadiani,
Sp.Rad
dr. I Wayan Losen Adnyana,
Sp.PD
Dr. dr. I Wayan Suranadi,
Sp.An.KIC
Dr. dr. I Dewa Made Sukrama,
MSi, Sp.MK(K)
dr. Kunthi Yulianti, Sp.KF
GROUP
DEPT
PHONE
A1
Clinical
Pathology
081236172840
A2
Microbiology
087862200814
A3
Anasthesi
08123870037
A4
Interna
081345136913
A5
Anatomy
087860405625
A6
Radiology
081805673099
A7
Interna
08123995536
A8
Anasthesi
08123847575
A9
Microbiology
081338291965
A10
Forensic
081338472005
GROUP
DEPT
PHONE
B1
Biochemistry
081338766244
B2
Forensic
08123988486
Venue
(2rd floor)
2nd floor:
R.2.09
2nd floor:
R.2.11
2nd floor:
R.2.12
2nd floor:
R.2.13
2nd floor:
R.2.14
2nd floor:
R.2.15
2nd floor:
R.2.16
2nd floor:
R.2.20
2nd floor:
R.2.21
2nd floor:
R.2.22
ENGLISH CLASS (B)

No
1.
2.
NAME
dr. Desak Made Wihandani,
M.Kes
dr. Henky, Sp.F., M.BEth,
FACLM
Venue
(2rd floor)
2nd floor:
R.2.09
2nd floor:
R.2.11
3.
4.
5.
6.
7.
8.
9.
10.
dr. Anom Suardika, Sp.OG

dr. Dewa Ayu Agus Sri Laksmi,
M.Sc
dr. Anak Agung Mas Putrawati
Triningrat, Sp.M
dr. Tjokorda Gde Agung
Senapathi, Sp.An
dr. A.A.Bagus Ngurah Nuartha,
SpS.(K)
dr. Ni Gusti Ayu Agung Manik
Yuniawaty Wetan, Sp.B
dr. Tjokorda Gde Dharmayuda,
Sp.PD-KHOM
dr. Putu Yuliawati , Sp.M
B3
Obgyn
0817561966
B4
Parasitology
081392017107
B5
Opthalmology
08123846995
B6
Anasthesi
081337711220
B7
Neurology
08123687288
B8
Surgery
08123214075
B9
Interna
0811394108
B10
Opthalmology
081338601724
2nd floor:
R.2.12
2nd floor:
R.2.13
2nd floor:
R.2.14
2nd floor:
R.2.15
2nd floor:
R.2.16
2nd floor:
R.2.20
2nd floor:
R.2.21
2nd floor:
R.2.22
3. THE SEVEN GENERAL CORE COMPETENCY

1. Patient care
Demonstrate
capability
to
provide
comprehensive
patient
care
that
is
compassionate, appropriate, and effective for the management of health problem,

promotion of health and prevention of disease in primary health care settings.
2. Medical knowledge base

Mastery of a core medical knowledge which includes the biomedical sciences,
epidemiology and statistics, clinical sciences, the sosial aspect of medicine and the
principles of medical ethics, and apply them
3. Clinical skill
Demonstrate capability to effectively apply clinical skill and interpret the findings in
the investigation of patient
4. Communication
Demonstrate capability to communicate effectively and interpersonally to establish
rapport with the patient, family, community at large, and professional associates,
that results in effective information exchange, the creation of a therapeutically and
ethically sound relationship
5. Information management
Demonstrate capability to manager information which includes information access,
retrieval, interpretation, appraisal, and application to patients specific problem, and
maintaining records of his or her practice for analysis and improvement
6. Professionalism
Demonstrate a commitment to carrying out professional responsibilities and to
personal probity, adherence to ethical principles, sensitivity to a diverse patient
population, and commitment to carrying out continual self-evaluation of his or her
professional standart and competence
7. Community-based and health system-based practice

Demonstrate awareness and responsiveness to large context and system of health
care, and ability to effectively use system resources for optimal patient care
4. TIME TABLE
Day
Date
Topic
Learning
situation
English
Class
Regular
Class
PIC
Monday
30th
March
Introduction lecture
Intro. Lecture
08.00 08.15
09.00 09.15
Prof Wita
General anatomy,
Intro. Lecture
08.15 09.00
09.15 10.00
Dr. Widianti
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Pleno
14.00 15.00
15.00 16.00
Intro. Lecture
08.00 08.15
09.00 09.15
Dr Mayun
Intro. Lecture
08.15 09.00
09.15 10.00
Dr. Muliarta
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Team
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Muliarta
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. Muliarta
Intro. Lecture
08.00 09.00
09.00 10.00
Prof Sutjana
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Team
Intro. Lecture
08.00 09.00
09.00 10.00
Prof Sutjana
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
of
topography and
surface anatomy of
the heart and great
vessels.
Tuesday
31st
of
March
Microscopic
Wednesday
1st of April
and valves
Intrinsic Conduction
Thursday
2nd of April
Facilitator
System and Cardiac

Action Potential
Dr. Widianti
structure of the heart
The heart as a pump
Facilitator
Cardiac Out Put and
Facilitator
Regulation of Heart
Pumping
Monday
6th of April
Overview
Circulation
Function
and
of
Its
Facilitator
Facilitator
Tuesday
7th of April
Factors that Affect
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Prof Sutjana
Intro. Lecture
08.00 08.45
09.00 09.45
Dr. Adiatmika
Intro. Lecture
08.45 09.00
09.45 10.00
Dr. Mayun
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Team
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Muliarta
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. Muliarta
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Adiatmika
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. Adiatmika
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Widianti
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. Widianti
Intro. Lecture
08.00 09.00
09.00 10.00
Prof. Wita
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Prof. Wita
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Bajra
Blood Pressure
Microscopic
Anatomy of The
Great Vessel
Wednesday
8th of April
Thursday
9th of April
Friday
10th of April
Myocardial perfusion
Blood Pressure
Facilitator
Facilitator
Regulation
The formation of
Facilitator
anomalies of the
heart and great
vessels.
10
Monday
13rd of April
Approach
to Patient
Facilitator
With Cardiovascular
Disease:
11
Tuesday
CV Physical
Facilitator

14th of April
12
13
Wednesday
15th of April
Thursday
16th of April
Examination I
BCS
10.00 13.00
13.00 16.00
Team Cardio
Practical
AnatomyHistology
13.00 16.00
10.00 13.00
Team
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Bajra
BCS
10.00 13.00
13.00 16.00
Team Cardio
Practical
AnatomyHistology
13.00 16.00
10.00 13.00
Team
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Bajra
BCS
10.00 13.00
13.00 16.00
Team Cardio
Chest Imaging
Intro. Lecture
08.00 08.30
09.00 09.30
Dr. Lisna
Measure Workload
Intro. Lecture
08.30 09.00
09.30 10.00
Dr. Muliarta
BCS
10.00 13.00
13.00 16.00
Team
Intro. Lecture
08.00 09.00
09.00 10.00
Prof Wiryana
BCS
10.00 13.00
13.00 16.00
Prof Wiryana
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Eka Guna
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. Eka Guna
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. K. Rina
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. K. Rina
Intro. Lecture
08.00 08.30
09.00 09.30
Dr. Winarti
Drug used in Angina
Intro. Lecture
08.30 09.00
09.30 10.00
Prof Aman
Pectoris
Ind. Learning
09.00 10.30
12.00 13.30
CV Physical
Examination II
ECG,
Ecocardiografi,
Fonografi
and
USG
Dopler
14
15
16
Friday
17th of April
Monday
20th of April
Tuesday
21st of April
IV line
CVP
Procedure,
Non-cyanotic and
Cyanotic CHD and
Acute Rheumatic
Fever
17
18
Wednesday
22nd of April
Thursday
23rd of April
Ischemic Heart
Facilitator
Disease = ACS
Pathologic aspect of
Facilitator
IHD
19
20
21
22
23
24
Friday
24th of April
Monday,
27th of April
Tuesday
28th of April
Wednesday
29th of April
Thursday,
30th of April
Monday,
4th of May
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Team
Arrhytmias
Intro. Lecture
08.00 08.45
09.00 09.40
Dr. Bajra N
Antiarrhythmic Drugs
Intro. Lecture
08.45 09.00
09.40 10.00
Dr. Surya
Ind. Learning
09.00 10.30
12.00 13.30
Facilitator
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Intro. Lecture
08.00 09.00
09.00 10.00
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. Susila
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Junior R
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. Junior R
Antihypertensive
Intro. Lecture
08.00 08.40
09.00 09.40
Prof Aman
Drugs
Intro. Lecture
08.40 09.00
09.40 10.00
Dr. Surya
Positive Inotropes
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Team
Intro. Lecture
08.00 09.00
09.00 10.00
Dr. Bagus Ari
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Dr. Bagus Ari
Intro. Lecture
08.00 08.45
09.00 09.45
Dr. Bajra N
Hypertension
Heart Failure
Acute and Chronic

Cor-pulmonale
Valvular Heart
Facilitator
Team
Dr. Susila
Facilitator
Facilitator
Facilitator
Facilitator
and Pericardial &

Endocardial
Disease
10
Physiotherapy
patient
Cardiovascular
Disease
25
Tuesday,
5th of May
to
with
Common Peripheral
7th of May
09.45 10.00
Dr. Kamiati
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Team
Intro. Lecture
08.00 09.00
09.00 10.00
Dr Semadi
Ind. Learning
09.00 10.30
12.00 13.30
SGD
10.30 12.00
13.30 15.00
Break
12.00 12.30
11.30 12.00
Student Project
12.30 14.00
10.00 11.30
Pleno
14.00 15.00
15.00 16.00
Facilitator
and
lymphatic disease
Thursday
08.45 09.00
Vascular (artery &

Venous)
26
Intro. Lecture
Facilitator
Team
Evaluation
BASIC CLINICAL SKILL

Day
Date
Topic
Learning
English
Regular
PIC
Place
11
situation
1
Tuesday
14th of April
CV Physical
Intro. Lecture
Wednesday
15th of April
CV Physical
Intro. Lecture
Thursday
16th of April
ECG,
Ecocardiografi,
Fonografi and USG
Dopler
Intro. Lecture
BCS
Friday
17th of April
08.00 09.00
09.00 10.00
10.00 13.00
13.00 16.00
08.00 09.00
09.00 10.00
10.00 13.00
13.00 16.00
08.00 09.00
09.00 10.00
10.00 13.00
13.00 16.00
Dr. Bajra
R.302
Skill
Lab
Dr. Bajra
R.302
Examination II
BCS
Class
Examination I
BCS
Class
Skill
Lab
Dr. Bajra
R.302
Skill
Lab
Chest Imaging
Intro. Lecture
08.00 08.30
09.00 09.30
Dr. Lisna
R.302
Measure Workload
Intro. Lecture
08.30 09.00
09.30 10.00
Dr. Muliarta
R.302
Skill
Lab
BCS
Monday
20th of April
IV Line Procedure
and CVP
Intro. Lecture
BCS
08.00 09.00
09.00 10.00
10.00 13.00
13.00 16.00
Prof
Wiryana
R.302
Skill
Lab
BASIC CLINICAL SKILL
12
Tuesday 14th April 2015

CV Physical Examination I
Anatomy
Histology
English 1-5
English 5-10
Reg 1-5
Reg 5-10
Place
10.00 13.00
13.30 15.30
10.00 13.00
13.00 16.00
10.00 12.00
13.00 16.00
Skill Lab
Lab. Anatomy
Lab. Bersama
13.30 15.30
Wednesday 15th April 2015

CV Physical Examination II
Anatomy
Histology
10.00 13.00
10.00 13.00
13.30 15.30
13.30 15.30
10.00 12.00
13.00 16.00
13.00 16.00
10.00 12.00
Skill Lab
Lab. Anatomy
Lab. Bersama
10.00 12.00
Thursday 16th April 2015

ECG
10.00 13.00
10.00 13.00
13.00 16.00
13.00 16.00
Skill Lab
Friday 17th April 2015

Chest Imaging
Measure Workload
10.00 13.00
13.00 16.00
10.00 13.00
13.00 16.00
13.00 16.00
10.00 13.00
13.00 16.00
10.00 13.00
Skill Lab
Lab. Faal
Monday 20th April 2015

IV line procedure, CVP
10.00 13.00
10.00 13.00
13.00 16.00
13.00 16.00
Skill Lab
5.
MEETING
FACILITATORS
OF
STUDENT
REPRESENTATIVES
AND
Meeting of student representatives and facilitators are designed among the student
representatives of the every small group discussion. The meeting will discuss the on going
teaching learning process, quality of lecturers and facilitators as a feedback to improve the
next process. The purpose of the meeting is to evaluate the teaching learning process of
the block. Feebacks and suggestions are welcome for improvement of the block
educational programs.
6. ASSESSMENT METHOD
Type of assessment is multiple choice questions (MCQ) and fill the blank and OSCE. A
prerequisite condition to follow the assessment is attendance in at least 75% of all
sheculed teaching-learning activities and follows the questionnare test during lecture.
Assessment will be carried out on Thursday 7th of May 2015. There will be 100 question
consisting mostly of Multiple Choice Questions (MCQ) and OSCE will be conducted
together with other block at semester VI.
Assessment in this block consists of: SGD: 5%, student project (review article): 10%,
final exam : 85%. The passing score requirement is 70. The student who does not pass
the passing level should follor remedial. Remedial will be held later.
FORMAT STUDENT PROJECT (article review):
13
TITLE (subject/topic;choose from competency list)

Name
NIM
Faculty of Medicine, Udayana University 2015
1.
2.
3.
4.
Introduction (Pendahuluan)
Content (Isi, sesuai topik yang dibahas)
Summary (Ringkasan)
References (Daftar Pustaka) Van Couver style
Example :
Libby P. The Pathogenesis of Atherosclerosis. In: Braunwald E, Fauci A, Kasper D,
Hoster S, Longo D, Kamason S (eds). Harrison`s Principle of Internal Medicine.
15th ed. New York: McGraw Hill; 2001. p. 1977-82.
5. 6 10 pages, 1,5 spasi, Times New Romance 12.
Article Review Assessment Form

14
Faculty of Medicine, Udayana University

Block
: Cardivascular System and Disorders
Name
:_____________________________________
Student No. (NIM) :_____________________________________

Fasilitator
:_____________________________________
Title
:_________________________________________________
_________________________________________________
_________________________________________________
Time table of consultation

Point of discussion
Week
1. Title
2. References
3. Outline of paper
4. Content
5. Final discussion
Date
Tutor sign
Assessment
A. Paper structure
B. Content
C. Discussion
Total point
:
:
:
7
7
7
8
8
8
9
9
9
10
10
10
: ( A + B + C ) : 3 = _________________
Denpasar, ______________________
Facilitator,
7. LEARNING PROGRAM
Day 1
15
MODULE 1
dr. I Gusti Ayu Widianti, M.Biomed
AIMS:
Describe the general and topography and surface anatomy of the cardiovascular
system
LEARNING OUTCOME:
1. Describe the general and topography anatomy of the cardiovascular system
2. Describe the surface anatomy of the cardiovascular system
CURRICULUM CONTENS:
1. Topography anatomy of the heart and great vessel
2. Mediastinum
3. Pulmonary/lesser and systemic/ greater circulation
ABSTRACT :
The heart is a hollow, fibromuscular organ of a conical or pyramidal form, with a
base, apex and a series of surfaces (sternocostal/anterior, diaphragmatic/inferior and
pulmonaries) and borders (acute and obtuse borders). Enclosed in the pericardium,
occupies the middle mediastinum between the lungs. It is placed obliquely behind the
body of the sternum and adjoining costal cartilage and ribs, one-third lies to the right of the
midline. Because of intimate relation between left atrium, the arch of aorta and
esophagus, enlargement of them resulting compression to each other.
The human heart is a pair of valved muscular pumps combined in a single organ.
Right and left heart pumps is physiologically separate, being interposed in series of
different point in the double circulation: pulmonary/lesser circulation for blood oxygenation
and systemic/greater circulation for tissue perfusion.
Of the four cardiac chambers, the two atria received venous blood for filling of the
two ventricles which then provide the powerful expulsive contraction, forcing blood into the
main arterial trunks: pulmonal trunk and aorta.
On the anterior surface of the chest, the outline of the heart and the sound
produced by the valves can be traced.
Standard References :
1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia,
Lippincott & Wilkins, 2007. p. 26-30, 65-67, 80-115
SELF DIRECTING LEARNING

Basic knowledge that must be known:
1. Topography anatomy of the heart and great vessel.
2. Mediastinum
3. Pulmonary/lesser and systemic/greater circulation.
16

SCENARIO
CASE:
A student had a motorcycle accident with a bruise in the 4th left intercostals space, just
lateral to the sternum. Her mother consult the physician because she thought that
something bad may be happened with his heart.
LEARNING TASK :
1. What structures may have been injured?
2. Describe the location and functions of the heart.
3. What are the important contents of mediastinum?
4. Identify the major external features of the heart.
5. Comprehend the features of the chambers of the heart.
6. Discuss the surface anatomy of the heart and the great vessels and its clinical
implications.
7. Compare the pulmonary and systemic circulation.
8. Identify the auscultatory point of mitral, aortic, pulmonal, and tricuspid valves.
9. Identify the intercostals space and important lines according to the heart lining.
SELF ASSESSEMENT:
1. Identify the structures that build the arterial system and how the oxygenated blood
flows through the body?
2. Identify on heart specimens: the four chambers of the heart; the atrioventricular,
pulmonary, and aortic valves; papillary muscles and tendinous cords. Discuss their
functions.
3. Identify and list all the openings in and out of each cardiac chamber.
4. Named the three layers of the hearts wall from deep to superficial.
5. Describe the structures, locations and functions of the skeleton of the heart.
6. The heart has an apex, base, surfaces and borders, identify the structures that
formed each of them.
7. Describe how the percussion of the heart performed.
8. Identify the atrioventricular and interventricular grooves and list the structures lie in
them.
9. The surface anatomy of heart: identify in your friend chest the important lines:
midclavicular line, midsternal line, sternal line, parasternal line, axillary line, sternal
angle, jugular notch (incisura jugularis), and intercostals space. Feel and locate the
apex beat of the heart.
Day 2
MODULE 2
17
dr. I G N Mayun, PHK & dr. Made Muliarta M.Kes

AIMS:
1. Describe the microscopic structure of the cardiovascular system
2. Comprehend the basic principles and practical implications of the heart as a
pump
LEARNING OUTCOME:
1. Can describe the microscopic structure of the cardiovascular system
2. Can comprehend the basic principles underlying normal and abnormal
myocardial, endocardial, and pericardial functions, including some common
practical implications (the heart as a pump)
CURRICULUM CONTENS:
1.
2.
3.
4.
5.
The microscopic structure of heart (type of the myocardio cytes and the valves)
The normal and abnormal heart wall and pericardial structures.
Describe Function of the heart
Describe the function of the heart as a pump
Describe cardiac cycle
ABSTRACT I:
The cardiovascular system is a part of the circulatory system that composed of the
heart as a pump and blood vessels. The heart is musculatory organ consist of four
chambers: two atria and two ventricles that separated by atrioventricular septal. The
muscular wall of the heart is composed of cardiac muscle and the heart has three layers:
endocardium, myocardium and epicardium. Myocardium is the thick middle layer of the
heart composed of cardiac muscle cells.
Epicardium is the outhermost layer of the heart and also called the visceral layer of
the pericardium. The subepicardial layer of loose connective tissue contains the coronary
vessels, nerves and ganglia.
The endocardium, a simple squamous epithelium and underlaying subendothelial
connective tissue lines the lumen of the heart. Deep to the endocardium is a
subendocardial layer of loose connective tissue that contains small blood vessels, nerve
and Purkinje fibers.
The atria separated from ventricles by atrioventricular septal in which houses of
atrioventricular orifice at both right and left side of the heart.
At left atrioventricular orifice attached the mitral valves and at right atrioventricular orifice
attached the tricuspidal valves. Both valves attached by chorda tendinae (a dense fibrous
connective tissue) that connect to papillary muscles of ventricles preventing incompetence
of the valves during ventricular contraction (systole).
The vascular components of the the cardiovascular system consist of arteries,
capillaries and veins. The classification of blood vessels (artery and vein) based on their
lumina diameter and composition of tissues in their wall.
The complete microscopic structure of blood vessels presents in muscular type of the
arteries that composed of both the intima, media, adventisia layers with internal and
external elastic membranes.
SA and AV node are specialized cardiac myocytes make up conducting system of
te heart SA and AV node as a pace maker of the heart that impulse begin from SA node
will referred to AV node via internodal pathway, bundle of His and spread to left and right
branches to exite ventricular muscles of the heart
18
ABSTRACT II:
The cardiovascular system serves a number of important functions in the body.
Most of these support other physiological systems. The major cardiovascular functions
divided into five categories: 1.delivery; 2. removal; 3. transport; 4. maintenance; 5.
prevention. Any system of circulation requires three component : 1. a pump (the heart); 2.
a system of channels (the blood vessel); 3. a fluid medium (the blood).
The heart is two pumps in series (the right and left sides) that are connected by
pulmonary and systemic circulations. The heart consists of four chambers : the right
atrium, right ventricle, left atrium, and left ventricle. The right atrium receives oxygen poor
blood from systemic veins; blood moves to the right ventricle and is pump out to the
pulmonary arteries to the lungs. The left atrium receives oxygenated blood from
pulmonary veins; and moves to the left ventricle and is pump out the systemic arteries to
the body tissues.
Each side of the heart consist of two valves that normally maintain one way flow of
blood. Atrioventricular (AV) valves separate the atria from the ventricle.
a. The right AV valve is the tricuspid valve.
b. The left AV valve is the mitral valve
c. These valves open during ventricular relaxation (diastole) to allow blood flow to the
ventricles and close during ventricular contraction (systole) to prevent back flow
(regurgitation) of blood from the ventricles into the atria
Semilunar valves (aortic and pulmonary) open during systole to allow blood flow
from ventricles to the aorta and pulmonary artery. Semilunar valves close to prevent back
flow of blood into the ventricles during diastole.
Closure of the heart valves produce mechanical vibration which are audible at the
chest wall as the heart sound. The first heart sound is caused by closure of the atriaventricular (AV) and the second heart sound is caused by closure of the aortic and
pulmonary valves. A heart murmur is a condition in which abnormal heart sound are
detected with the aid of stethoscope.
The cardiac events that occur from the beginning of one heartbeat to the beginning
of the next are called the cardiac cycle. Each cardiac cycle is initiated by spontaneous
generation of an action potential in the sinus node, in which the normal rhythmical impulse
is generated and spread the cardiac impulse to all parts of the ventricles.
Cardiac cycle consists of a period of relaxation called diastole, the time during
which cardiac muscle relaxes and contraction called systole, the time during which cardiac
muscle is contracting. The atria and ventricles do not contract and relax at the same time.
Standard References:
1. Gartner LP, Hiatte JL: Color Textbook of Histology, 2nd ed. Philadelphia,
WB Saunders Company, 2001. p. 251- 265; 267-268; 268-269
2. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders
Company, 2006. p. 104-106, 116-122
Additional reading:
1. Fowcett DW, Jensh RP: Bloom & Fawcetts Concise Histology, 2nd ed. London,
Arnold. 2002. p. 135-136 ; 136-145; 136-139
19

1. Three layers of the heart, the connective tissue that support the heart and
microscopic of the valves
2. Functions of Heart Valves
3. Blood flow
SCENARIO:
CASE:
A young man who was stabbed (about 5cm depth) in the chest was rushed to a hospital.
The stab wound was in the 3rd left intercostals space, just lateral to the sternum. The
emergency physician noted that the veins of his face and neck were engorged.
LEARNING TASK I:
1. Describe the microscopic structure of the heart?
2. Describe the three types of myocardium(cardiocytes)
3. How do you differentite the myocardium ( mucle of the heart) and purkinje fiber
4. Describe the microscopic structure of the conducting system in the heart (SA, AV,
and bundle of his)
5. Describe microscopic structure of the authoritmic cells fibers and contractile cell
fibers of the myocardium.
6. Descibe the microscopic structure of the heart valves?
LEARNING TASK II:
1.
Describe the general functions of the cardiovascular system
2.
Describe function of the heart provides the driving force for the cardiovascular
system
3.
Why do the ventricles contract as a single unit
4. Describe the pressure changes that occur in the ventricles during the cardiac cycle
and relate these changes to the action of the valves and the blood flow
5. Explain the origin of of the heart sounds and when its produce during cardiac cycle
6.
Name and explain the phases of cardiac cycle
SELF-ASSESSMENT I:
1. What are the basic structures of the heart wall?
2. What structures are form the endocardium?
3. Do you able to describe he relation of the endocardium and endothelium of the
blood vessels that entering and leaving the heart?
4.
5.
6.
7.
Explain the microscopic structure of the purkinje fiber. Where does it location?
What is cardiac skeleton?
What are it components?
Explain the microscopic structure of the heart valves?
SELF-ASSESSMENT II:
1.
2.
3.
4.
What are major function of cardiovascular system?

What are three basic components of the cardiovascular system and its function?
Explain the origin of the heart sound and when its produce during cardiac cycle!
Describe function of the heart provides the driving force for the cardiovascular
system!
20
Day 3
MODULE 3
AIMS:
1. Comprehend the basic principles of Cardiac Action Potential
2. Comprehend the basic principles of Intrinsic Conduction System
LEARNING OUTCOME:
1. Comprehend the functional structure of the conduction system and cardiac
action potensial of the heart and its clinical implications
CURRICULUM CONTENS:
1. Mechanism of action potential
2. Conduction pathway of the heart
.ABSTRACT:
The intrinsic conduction system sets the basic rhythm of the heartbeat. It consists
of auto rhythmic cardiac cell that initiate and distribute impulses (action potentials)
throughout the heart.
The intrinsic conduction system of the heart initiates depolarization impulses.
Action potentials spread throughout the heart (SA node, internodal pathways, AV node,
AV bundle, bundle branches, Purkinje fibers ) causing a coordinated heart contraction
(excitation contraction coupling).
Initiation of action potential in autorhythmic cells :
1. Pacemaker potential due to slow continous influx of sodium and reduced efflux of
potassium
2. Depolarization and reversal of membrane potential
3. Repolarization due to rapid efflux of potassium.
Action potential in contractile cells :
1. Opening of voltage regulated fast sodium channel triggered by entry of positive ion
from adjacent cell depolarization due to rapid influx of sodium
2. Plateau produced by calcium influx balancing potassium efflux.
3. Repolarization due to efflux of potassium.
Plateau has important functional consequences for the mechanical activity of the heart
An ECG wave tracing records the electrical activity of the heart. This is an important
clinical tool, used both in the diagnosis of abnormal cardiac rhythms (arrhythmias) or
defects in the conduction pathways and when investigating possible damage to the bulk of
the myocardium e.g cause by ischemia
Standard Reference :
Company, 2006. p. 104-106, 116-122
1. Autorhythmic cells potential
21

2. Contractile cells potential
3. ECG wave tracing
LEARNING TASK:
1. Describe the excitation contraction process
2. What is the pace maker of the heart in normal condition
3. Describe the pathway of electrical conduction of the heart, starting with the SA
Node
4. Describe the electrical activity of the cells of the SA Node
5. How the SA node functions as the normal pacemaker
SELF-ASSESSMENT :
1. Describe the action potential of the cells of the SA Node
2. Describe the action potential of the cells of the contractile cells
3. Explain the relationship between cardiac cycle and ECG trace wave
Day 4
MODULE 4
Prof. dr. D.P. Sutjana, PFK, Merg
AIMS:
1.
2.
Comprehend the cardiac output

Comprehend the basic principles of cardiac output regulation
LEARNING OUTCOME:
1. Describe how to measure cardiac output
2. Describe the regulation of cardiac output
CURRICULUM CONTENS:
1. Components of cardiac output
2. Factors influence cardiac output
ABSTRACT;
The cardiac out put (COP) is the quantity of blood pumped into the aorta each
minute by the heart. The outputs of the two sides of the heart are normally equal. Cardiac
output is determined by two feature of cardiac function, the heart rate and the volume of
blood ejected during a single contraction of the ventricle (the stroke volume). COP is
defined as the amount of blood pumped per ventricle per unit time. It can be calculated by
multiplying heart rate by stroke volume.
When a person is at rest, the heart pumps only 4 to 6 liters of blood each minute.
During severe exercise, the heart may be required to pump four to seven times this
amount. The basic means by which the volume pumped by the heart is regulated are:
intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing
into the heart and control of heart rate and strength of heart pumping by the autonomic
nervous system.
The intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is
called the Frank-Starling mechanism of the heart. The Frank-Starling mechanism means
that the greate the heart muscle is stretched during filling, the greater is the force of
contraction and the greater the quantity of blood pumped into the aorta.
22

The pumping effectiveness of the heart also is controlled by the sympathetic and
parasympathetic (vagus) nerves, which abundantly supply the heart. The amount of blood
pumped each minute often can be increased more than 100 percent by sympathetic
stimulation. By contrast, the output can be decreased to as low as zero or almost zero by
vagal stimulation.
Company, 2006. p. 111-115, 232-245
1. Components of Cardiac output
2. Factors influence Cardiac output
SCENARIO:
CASE :
A woman, 45 year old, bus passenger from Jakarta to Bali went to see his physician
complained about swelling of ankles and feet.
LEARNING TASK:
1. Why are the ankles and feet swelling?
2. What do you expect of stroke volume in this patient?
3. Describe how the stroke volume is intrinsically regulated by the end-diastolic
volume
4. What should you suggest for this complaint?
SELF-ASSESSMENT :
1. Describe the effects of autonomic nerve stimulation on the cardiac rate and stroke
volume
2. List the factors that affect venous return.
3. Using a flowchart, show how an increased venous return can result in an
increased cardiac out put
4. What is the name of the name of the structure that the margin of the valves
attached?
5. Describe the chorda tendinae?
6. Where are the location of the valves in the heart?
Day 5
MODULE 5
23

AIMS:
1. Comprehend the function of blood vessels
2. Comprehend the regulation of blood flow
LEARNING OUTCOME:
1. Describe the function of blood vessels
2. Describe the regulation of blood flow
CURRICULUM CONTENS:
1. Components of blood vessels
2. Factors influence blood flow
ABSTRACT
The blood vessels of the body form a closed delivery system that begins and ends
at the heart. Of the three types of vessels, arteries have the thickens tunica media
(allowing stretch / recoil and vasoconstriction), vein have relatively thick tunica adventitia
(reservoir vessel) and capillaries are the thinnest (allowing exchanges of material ).
One of the most basic principles of circulatory function is the ability of each tissue
to control its own local blood flow in proportion to its metabolic needs. We shall see that
nervous control the circulation has more global functions, such as redistributing blood flow
to different areas of the body, regulating heart pumping, and providing very rapid control of
systemic arterial pressure. The nervous system controls the circulation almost entirely
through the autonomic nervous system.
Blood flow through individual organs is controlled intrinsically in respons to local
tissue requirements. This phenomenon is called Autoregulation. When true capillaries
are flushed with blood, exchange occurs between the capillary blood and tissue cells.
Arterial system consists of conducting arteries, distributing arteries and arterioles.
Conducting arteries are the largest vessels of the body, begins with the aorta, a single
artery with a large diameter, have generous amount of intramural elastic tissue. Elastic
tissue permits both stretch of the wall during the ejection phase of cardiac systole and a
propulsive elastic recoil during ventricular diastole. Weakness of the aortic wall result in
enlargement of the lumen called aortic aneurysm.
Distributing arteries give off by the aorta, account for the remaining named arteries
of the body and progressively divide into arteries with smaller and smaller diameter.
Arterial anastomoses permit equalization of pressure and alternate channel of supply,
abundant anastomoses occur in the region of joints in which movement might temporary
occlude the main channel. Cerebral arterial cycle equalizes the blood supply to the brain.
End arteries supply discrete regions of tissue that have no direct anastomoses between
them (no collateral supply), found in the heart, kidney, liver, brain, and organs of
gastrointestinal tract. A thrombosis or embolus lodged in an end-artery produces ischemia
and necrosis (infarct) of the tissue.
Arterioles are the smallest arteries, nearly as small as capillaries, regulate the
distribution of blood. Smooth muscle in the walls of arterioles control the size of the vessel
lumen and the sympathetic innervation of vascular musculature regulates blood flow to the
tissues.
Capillaries are exchange sites of the circulatory system and the total crosssectional area is approximately 800 times that of the aorta. The velocity of circulation in
24

the capillaries are very slow, changes from 0,5 m/sec in the aorta to 0,5 mm/sec in the
capillaries.
Sinusoid substitute for capillaries in some organ, such as the liver, spleen, and red bone
marrow, where circulation is slow.
Capillary beds drain into venules, the smallest vein, which come together to form
veins that return blood to the heart at a lower pressure than arteries. Veins
characteristically have large lumina, thin and relatively non muscular walls, relatively
compressible by external forces which aids in blood flow. Valves in many veins limit flow
proximally, toward the heart. Valves occur primarily in veins of limbs and movable viscera,
but not in the cerebral veins. Pressure gradients between the periphery and the right side
of the heart control venous flow.
Arteriovenous anastomoses permit direct transfer of blood from arterial to venous
channels, bypassing the capillary bed. Usually occur in organs that function intermittently
as in gut and skin.
The lymphatic system is composed of an extensive network of extremely variable
lymphatic vessels and nodes, which serve as filters and a source of lymphocytes and
plasma cells. Ascites is the accumulation of lymph (usually from the liver) in the peritoneal
cavity. Pulmonary edema is caused by either increased permeability or a hydrostaticosmotic pressure imbalance in the pulmonary vascular bed, result in fluid accumulation in
the tissue spaces and transudation of fluid into the alveoli.
Company, 2006. p. 161-170, 195-203
1. Components of blood vessels
2. Functions of each blood vessels
Day 6
MODULE 6
25
Dr. dr. I.P.G. Adiatmika, MKes & dr. I G N Mayun, PHK

AIMS:
1. Apply several factors that affecting blood pressure
2. Describe the microscopic structure of the vascular system
LEARNING OUTCOME:
1. Can describe the stroke volume
2. Can describe the heart rate
3. Can describe several factors that affecting blood pressure
4. Can describe the microscopic structure of the vascular system (arterial and
venous)
CURRICULUM CONTENS:
1. Frank Starlink Law
2. Factors influence blood pressure
3. Artery : elastic artery, muscular artery, arteriole and capiller
Venae: large vein, midlle vein, small vein
ABSTRACT I :
The heart pumps blood continually into the aorta, as the blood flows through the
systemic circulation, its mean pressure falls progressively to about 0 mmHg by the time it
reaches the termination of the venae cavae where they empty into the right atrium of the
heart.
Blood pressure (BP) is important indicator of the cardiovascular health. It is
influenced by the contractile activities of the heart and conditions an activities of blood
vessels.
1. Systolic pressure = highest pressure in artery result of ventricular contractions.
2. Diastolic pressure = lowest pressure in artery result of ventricular relaxation.
3. Mean arterial pressure (MAP) = diastolic pressure + 1/3 pulse pressure
When blood pressure is measured first sound indicate systolic pressure, end of sounds
indicate diastolic pressure.
Blood pressure is affected by several factors: peripheral resistance, vessel
elasticity, blood volume and cardiac output. Blood cells and plasma encounter resistance
when they contact blood vessel walls. If resistance increases, then more pressure is
needed to keep blood moving. Smaller blood vessel diameter cause more fluid in contact
with wall and greater resistance, finally greater pressure. In addition, blood volume affects
blood pressure. Greater volume of fluid in blod vessel cause more fluid pressing against
walls and greater pressure. Cardiac output also has direct effect on blood pressure.
Cardiac output = Heart rate x Stroke volume
ABSTRACT II;
The vascular components of the the cardiovascular system consist of arteries,
capillaries and veins. The classification of blood vessels (artery and vein) based on their
lumina diameter and composition of tissues in their wall. The complete microscopic
structure of blood vessels presents in muscular type of the arteries that composed of both
the intima, media, adventisia layers with internal and external elastic membranes. The
coronary vessels are very important artery that serving the myocardium.
Atherosclerotic plaques reduce the lumina of the coronary vessels, may cause
referred pain and pressure known as angina.
Standard Reference:
26

1. Fox S.I.: Human Physiology, 9th ed. New York, McGraw-Hill, 2006. p. 448-454
2. Gartner LP, Hiatte JL: Color Textbook of Histology, 2nd ed. Philadelphia,
WB Saunders Company, 2001. p. 251-262
1. Frank Starlink law
2. Autonomic activation
3. The roles of several ions
4. Microscopic structure and classification the artery and vein
LEARNING TASK:
1. Explain the blood pressure in the various parts of the vascular system
2. Explain how the baroreceptor reflex helps to compensate for a fall in blood
pressure?
3. Why will a person who is severely dehydrated have a rapid pulse?
4. What are the pulse pressure and mean arterial pressure?
5. What is the effect of epinephrine in blood pressure?
6. Explain why a person in hypovolemic shock may have a fast pulse and cold
clammy skin?
7. Describe the microscopic the structure of the coronary artery (muscular type
artery)
8. Diffrentiate the muscular and elastic type artery.
9. Describe the microscopic the structure of the arteriole.
10. Describe the microscopic the structure of the capillary and it classification
SELF-ASSESSMENT :
1. Explain why a person in severe dehydrated may have low blood pressure
2. Why a person with atherosclerosis may have high blood pressure
3. What are the main composition of the tunica media of the elastic artery?
4. Explain the variation of the tunica media of the blood vessel!
Day 7
MODULE 7
AIMS:
Comprehand the basic principles underlying myocard perfusion
LEARNING OUTCOME:
1. Can describe how myocardial perfusion occurs
2. Can describe functional structure of the coronary arteries
CURRICULUM CONTENS:
1. Function of coronary artery
2. The role of diastole
ABSTRACT ;
27

Blood perfusion to the myocardium build by the reverse flow of blood during
diastole and the autoregulation of the intramyocardial arterioles through the coronary
arteries.
Epicardial coronary arteries serve as conduit, entered deep to the myocardium:
intramyocardial arterioles referred as resistance vessels.
Right and left coronary arteries begin from the sinuses behind the right and left semilunar
cusps of the aortic valve. They distribute blood in large part to their own half of the heart.
Blood flow in the coronary arteries is maximal during diastole and minimal in
systole. During systole, no pressure differential exist between the myocardium and the left
ventricle, flow is not possible. During diastole, a pressure differential does exist and the
elasticity of the aorta propels blood through the coronary circulation.
Standard References
1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott
& Wilkins, 2007. p. 37-38, 95-99, 101
Company, 2006. p. 181-185; 249-256.
Additional reading :
1. Fowcett DW, Jensh RP: Bloom & Fawcetts Concise Histology, 2nd ed. London,
Arnold. 2002. p. 136-141
1. Systole-diastole
2. The function of coronary artery
3. Post exercise hypotension
SCENARIO
CASE 1.
A 45-year-old woman was playing tennis and suddenly fell, complaining of a severe pain
in her chest and down her left arm. Her playing partner rushed her to the hospital.
LEARNING TASK:
1. What likely caused the pain in the womens chest and arm?
2. Name the blood vessels that supply the heart.
3. Where they arised from?
4. List 4 major branches of the right coronary artery.
5. List 3 major branches of the left coronary artery.
6. Is the visceral pain from the chest usually referred to the left arm?
7. Where the most purposeful function of the circulation occur?
8. What the most important function of lymphatic capillaries in the microcirculation?
9. How the cell nutrients from capillaries entered the muscle cells of the heart?
10. How the cell excreta entered the capillaries?
SELF-ASSESSMENT
1. Describe the arterial supply of the heart.
2. What are the symptoms of sudden occlusion of the major coronary artery?
3. Define the terms: arteriole, metarteriole, precapillary sphincter, anastomosis,
collateral circulation, true terminal (end) arteries and functional terminal arteries in
conjunction with coronary arteries.
28

4. Discuss the terms: arteriosclerosis, thrombosis and atheromatous plaque.
5. Which condition stimulates pain endings in the myocardium?
6. Describe the cardiac referred pain
Day 8
MODULE 8
Dr. dr. I.P.G. Adiatmika, MKes
AIMS:
Comprehend the basic principles underlying Blood Pressure Regulation
LEARNING OUTCOME:
1. Can describe the basic principles underlying Blood Pressure Regulation
CURRICULUM CONTENS:
1. Two basic mechanisms for regulating blood pressure.
2. The nervous system controls the circulation.
ABSTRACT:
There are two basic mechanisms for regulating blood pressure.
In short term mechanism, which regulate blood vessel diameter,heart rate, and
contractility. Rising blood pressure stimulates increased parasymphatetic activity which
leads to reduce heart rate (HR), vasodilation and lower blood pressure. Falling blood
pressure stimulates increased sympathetics activity, which leads to increase HR,
contractility, vasoconstriction, and rises blood pressure. Long term regulation, which
regulate blood volume. Long term regulation involves renal regulation of blood volume
(BV) via the rennin angiotensin mechanism and aldosteron mechanism. Increase blood
osmolarity stimulate antidiuretic hormone (ADH) which promote reabsorption of water and
stimulates the thirst center, resulting in increase BV and BP
The nervous system controls the circulation almost entirely through the autonomic
nervous system. The innervation of the small arteries and arterioles allows sympathetic
stimulation to increase resistance to blood flow and thereby to decrease rate of blood flow
through the tissues. The innervation of the large vessels, particularly of the veins, makes it
possible from sympathetic stimulation to decrease the volume of these vessels. The
effects of parasympathetic stimulation on heart function causes decrease heart rate and
slide decrease in heart muscle contractility.
The body also has powerful mechanisms for regulating arterial pressure week after
week and month after month. This long term control of arterial pressure is closely
intertwined with homeostasis of body fluid volume, which is determined by the balance
between the fluid intake and output.
Standard References
Company, 2006. p. 161-170, 205-23.
29

1. Short term mechanism for regulating blood pressure
2. Long term mechanism for regulating blood pressure
3. The nervous system controls the circulation
SCENARIO
CASE :
A woman, British, 30 year old, 60 kg, lie down in the beach under the sun exposure
without drink enough water. Few hours after, she complains about weakness,
dizziness, redness on the skin and feel hot. Pulse rate about 105 x/mnt
LEARNING TASK:
1. Predict the blood pressure in this patient? Why
2. Why the patient may have rapid pulse rate?
3. Explain two basic mechanisms for regulating blood pressure?
4. Describe the baroreceptor reflex and explain its significance in blood pressure
regulation
SELF-ASSESSMENT :
1. Provide an integrated description of how nerves and hormones regulate blood
pressure
2. Explain reflexes that responsible for short term control and long term control
mechanisms to blood pressure
Day 9
MODULE 9
dr. I Gusti Ayu Widianti, M.Biomed
AIMS:
Describe the basic principles underlying the formation of anomalies of the heart
and great vessels
LEARNING OUTCOME:
1. Can describe the basic principles underlying the formation of anomalies of the
heart and its impilcations
2. Can describe the basic principles underlying the formation of anomalies of the
great vessels and its impilcations
CURRICULUM CONTENS:
1. Embryology of the heart
2. Embryology of the great vessels.
ABSTRACT
30

Septal defects are only problematic when the shunt flows from right-to-left.
Anomalies of interventricular septum (VSD) is usually happened at the upper
membranous portion that composed of connective tissue continuous with the annulus
fibrosus. A small VSD may result in an inconsequential left-to-right shunt.
In the presence of pulmonary stenosis, a VSD produces a right-to-left shunt with cyanosis
and the blue-baby syndrome. A large VSD is a principal factor in Tetralogy of Fallot.
Atrial septal defects (ASD) are most common in the vicinity of the fossa ovalis.
Septum secundum defects, the typical patent foramen ovale, account for 10-15% of all
cardiac anomalies. Normal left atrial pressure is slightly greater than right atrial pressure,
a left-to-right shunt occur through an open ASD, oxygenated blood from the left side of the
heart is shunted to the right side, thus not associated with cyanosis. An ASD is usually
compatible with normal life, except at an extreme exercise, cardiac disease, or pulmonary
disease alter chamber pressures, a right-to-left shunt will produce cyanosis.
Patent ductus arteriosus (PDA) is a persistence of the fetal connection (ductus
arteriosus) between the aorta and pulmonary artery after birth, resulting in a left-to-right
shunt. Symptoms may include failure to thrive, poor feeding, tachycardia and tachypneu. A
continous machine-like murmur in the upper left sternal border is common. Diagnosis is by
echocardiography.
1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott
& Wilkins, 2007. p. 91, 93, 94
2. Sadler TW: Langmans Medical Embryology, 10th ed. Philadelphia, Lippincott &
Wilkins, 2006. p. 167-178, 184
1. Embriologi of the heart
2. Embryology of the geart vessel
SCENARIO:
CASE 1;
This baby aged 4 months has been known to have a cardiac murmur since birth. He was
born 8 weeks prematurely and developed respiratory distress requiring high oxygen
concentration for the first week. Since then he has feed satisfactorily but height and weight
growth have been poor even allowing for prematurity.
The diagnosis after examination and investigations: Patent Ductus Arteriosus (PDA).
LEARNING TASK I
1. What factors in the history were of possible importance in causing the ductus
remain open? Why there is no cyanosis in this case?
2. Why is there no cyanosis in this case?
3. Why was the heart murmur audible in diastole as well as systole?
4. Why is there evidence of left ventricular hypertrophy and not right ventricular
hypertrophy?
5. Why is there pulmonary congestion?
6. Why the shunt from aorta to pulmonary artery and not vice versa?
7. After an operation to close the PDA, why is there a risk of the patient becoming
hoarse?
CASE 2 :
This 13 year old girl was recently found to have a cardiac murmur. She has been generally
healthy with good growth, but on questioning her mother admitted she has noticed that girl
tends to tire easily with exercise.
31

The diagnosis after examination and investigations: Atrial Septal Defect (A.S.D.)
LEARNING TASK II:
1. Why is there a mild chest deformity with a bulge in the thoracic cage to the left of
the sternum?
2. Why is there no cyanosis?
3. Why does the right ventricle carry a volume load in A.S.D., while it is the left
ventricle in PDA. Both are left-to-right shunt. Consider the appropriate anatomy
involved.
4. Why is there a systolic murmur over the pulmonary valve and a diastolic murmur
over the tricuspid valve?
CASE 3 :
A 2 year old boy was admitted to the hospital for evaluation of a heart murmur previously
detect at birth. He was less active than other children his age, but although over-exertion
was followed frequently by cyanosis of the lips and nails, there was no history of
unconsciousness. Initial examination revealed a thin, physically retarded, cyanotic child
with no respiratory difficulty. There was moderate clubbing of the fingers. A harsh systolic
murmur was maximal over the mid-precardial area. The first heart sound was normal while
the second was single, distinct and loud.The lungs were clear. X-ray showed a normal
sized heart dominated by a boot-shaped right ventricular outflow tract.
Diagnosis of Tetralogy of Fallot.
LEARNING TASK III:
1. Mention the cardiac abnormality you found in this case.
2. What is the basic defect of this heart malformation?
3. What is the most important abnormality causing cyanosis?
4. Why was he less active than other childres his age?
5. Why is he revealed thin and physically retarded?
6. Why was there clubbing of his fingers?
SELF-ASSESSMENT :
1. Describe the principal normal development of the heart and pericardium.
2. Named the most common congenital anomalies of the heart with their clinical
implications.
3. Describe the abnormities, the hemodynamic changes, the incidence and the
clinical implications in general population of ventricular septal defect (VSD),
Tetralogy of Fallot, and atrial septal defect (ASD).
4. Describe the blood flow before and after birth and changes occur in the vascular
system after birth
Day 10
MODULE 10
32
Prof dr. I Wayan Wita, SpJP

AIMS:
Able to do and practice the approach to patient with cardiovascular disease
(common cardiological symptoms and consultations and investigations in
Cardiology).
LEARNING OUTCOME:
1. Able to do and practice the approach to patient common cardiological
symptoms
2. Able to do and practice the approach to consultations with cardiovascular
disease
3. Able to do and practice the approach to investigations in Cardiology).
CURRICULUM CONTENS:
1. The symptoms of the cardiovascular disease
2. The diagnostic tools to confirm patients with Cardiovascular Diseases
ABSTRACT:
History taking remains the most important component of diagnostic process. Often
diagnosis can be made from the history alone, with examination and investigations only
serving to confirm it. Chest pain is a common symptom. Breathlessness caused by left
ventricle failure may present as orthopnoea and paroxysmal nocturnal dyspnoea.
Palpitation is usually a benign symptom unless it is accompanied by syncope or
presyncope.
Cardiovascular examination begins the moment the patient enters the room. Is the
patient pale, breathless or anxious? Examine the pulse, and check the pulse character.
The blood pressure and auscultation should be performed in appropriate manner. The
electrocardiogram (ECG) and chest-x ray remain the most valuable cardiac investigation
in clinical practice. 24-hour ECG recording is most useful in those with very frequent
arrhythmia symptoms. Stress testing is performed for 2 main reasons: to diagnose
ischaemic heart disease and to assess prognosis. Echocardiography provides both
structural and functional information that assists in the diagnosis of many cardiac
conditions. Cardiac catheterization is an invasive procedure that assess systemic and
pulmonary haemodynamic variables, as well as oxygen saturations and intracardiac
shunts. It assess aortic, valvular, left ventricular and coronary artery structure and
function. The assessment for coronary artery disease is the main indication.
The imaging investigation of the heart may be considered under the following:
1. Chest X-ray
The chest radiograph was one of the first clinical examinations to use the then-new
technology of diagnostic radiography. It remains the most common x-ray examination
and one of the most difficult examinations to interpret. With careful evaluation, it yields
a large amount of anatomic and physiologic information. Chest X-ray remain the
valuable cardiac investigation in clinical practice.
Radiologic method used in the roentgen cardiac examination:
1. Posteroanterior projection, PA/AP
2. Lateral projection
3. Right anterior oblique projection (RAO)
4. Left anterior oblique projection (LAO)
Increase in cardiac size is the most consistent indication of cardiac disease
33

2. Computed tomography (CT-scan)
The basic principle of CT technology is the use of ionizing radiation within a gantry
rotating around the patient in which x-rays are detected on a detector array and
converted through reconstruction algorithms to images. It is these images, acquired at
high spatial and temporal resolution, that have enabled cardiovascular medicine to
enter the CT imaging era
3. Magnetic resonance imaging (MRI)
Over the past decade, cardiac magnetic resonance (CMR) has developed into a
routine clinical imaging tool. With excellent spatial and temporal resolution, unrestricted
tomographic fields, and no exposure to ionizing radiation, CMR offers detailed
morphologic and functional characterization for most types of heart disease
4. Echocardiography
Echocardiography remains the most frequently used and usually the initial imaging
test to evaluate all cardiovascular diseases related to a structural, functional, or
hemodynamic abnormality of the heart or great vessels. Echocardiography uses
ultrasound beams reflected by cardiovascular structures to produce characteristic lines
or shapes caused by normal or altered cardiac anatomy in one, two, or three
dimensions by M (motion)mode, two-dimensional, or three-dimensional
echocardiography, respectively. Doppler examination and color flow imaging provide
reliable assessment of cardiac hemodynamics and blood flow.
5. Angiocardiography
Angiography is a technique used to visualize the lumen, of blood vessels and
organs of the body, with particular interest in the arteries, veins, and the heart
chambers. This is traditionally done by injecting a radio-opaque contrast agent into the
blood vessel and imaging using X-ray based techniques such as fluoroscopy.
6. Cardiac catheterization
Cardiac catheterization is the insertion of a catheter into a chamber or vessel of
the heart. This is done both for diagnostic and interventional purposes. Subsets of this
technique are mainly coronary catheterization, involving the catheterization of the
coronary arteries, and catheterization of cardiac chambers and valves of the Cardiac
System.
7. Nuclear Cardiology
The era of noninvasive radionuclide cardiac imaging in humans began in the early
1970s with the first reports of noninvasive evaluation of resting myocardial blood flow.
Since that time, there have been major advances in the technical ability to image
cardiac physiology and pathophysiology, including that of myocardial blood flow,
myocardial metabolism, and ventricular function.
1. McPhee SJ, Papadakis MA. Current Medical Diagnosis & Treatment. 47th ed. New
York: Lange Mecical Book`s/The McGraw-Hill Companies, 2008.p.
2. Roentgen Signs in Diagnostic Imaging Isadore Meschan

1. History taking
2. Common cardiological symptom and consultation
3. Investigation in Cardiology
LEARNING TASK I:
34

Investigation in pediatric cardiology
1. When you suppose that the patient may be suffering from CHD.
2. Which one who is the most sensitive sign and applied as the best screening of
CHD.
3. What is the most specific sign of CHD.
4. Please explain sign of the left and right heart hypertrophy by inspection and
palpitation.
5. Please mention diagnostic tool in pediatric cardiology.
6. When complete blood count should be perform.
7. Please describe site of classic heart sound and characteristics of that.
LEARNING TASK II:
Investigation in cardiology
1.
2.
3.
4.
Please explain the symptoms in patients with cardiovascular disease

What are the diagnostic tools to confirm patients with Ischaemic Heart Disease?
What is the benefit of 24-hour electrocardiogram?
What is the objective of performing stress testing (treadmill test)?
LEARNING TASK
III:
RADIOLOGY
1. What are the basic projections for cardiac radiography?
2. Explain normal anatomy of the heart on the chest x-rayZ?
3. Explain cardiac enlargement on the chest x-ray?
SELF ASSESSMENT :
1. Please explain the symptoms in patients with cardiovascular disease
2. What are the diagnostic tools to confirm patients with Ischaemic Heart Disease?
3. What is the benefit of 24-hour electrocardiogram?
4. What is the objective of performing stress testing (treadmill test)?
5. Please describe the chest x-ray finding in VSD
6. Differenciated between LVH and RVH on chest x-ray
7. Explain HHD on the chest x-ray
8. Explain tetralogy of Fallot on the chest x-ray
Day 11 & 12
35
MODULE 11 & 12
dr. Bajra Nadha, Sp.JP
AIMS:
Able to physical examination the cardiovasculer system
LEARNING OUTCOME:
1. Able to physical examination and diagnostic the cardiovasculer system.
CURRICULUM CONTENS:
1. Evaluate General Appearance (inspection)
2. Blood Pressure Examination, The Arterial Pulse, The Jugular Venous Pulse
evaluation.
3. Percussion, Palpation, Auscultation
ABSTRACT :
Physical examination is the procedure should be done to obtain any data from the
patient. For cardiovascular system we should do the examination carefully. The physical
examination for cardiovascular system consist of evaluate general appearance, blood
pressure examination, arterial pulse evaluation, the jugular venous pressure, and
percussion, palpation, auscultation, and examination for any edema.
Each of the procedure will reveal specific data from the patient. For cardiovascular
system, auscultation will plays an important role in diagnosing the patient. From
auscultation we should obtain the heart sound quality and identifying any murmur present.
From percussion we should obtain any enlargement of the heart.
Physical examination skills in cardiovascular medicine have declined. Only
minority has recognized classic cardiac finding in relevant disease. Bedside skills has
decreased because on widely use of non invasive imaging technique. But still, cardiac
bedside examination become cornerstone in diagnosis patient with cardiovascular
disease. Physical examination can help determine the cause of given symptom, assess
disease severity and progression, and evaluate the impact of specific therapies. It also
can identify the presence of early stage disease in patients without signs or symptoms.
The examination begins with an appreciation of general appearance of the patient,
including age, posture, demeanor, and general health status. Continue to the skin, looking
for cyanosis, jaundice, ecchymosis, xanthoma and any other specific cardiac sign. On the
head and neck we can assess sign of congenital anomalies, such as hypertelorism, lowset ears, micrognathia, and webbed neck in Noonan, Turner and Down Syndrome. From
extremities find out about clubbing fingers, arachnodactyly, and nail changes, may
accompanying with specific cardiac disease. Cutaneous venous collaterals over the
anterior chest suggest chronic obstruction of the superior vena cava (SVC) or subclavian
vein. Thoracic cage abnormalities, sauch as pectus carinatum (pigeon chest) or pectus
excavatum (funnel chest) may accompany connective tissue disorder; the barrel chest of
emphysema or advanced kyphoscoliosis may be associated with cor pulmonale.
The cardiovascular examination include assessment of jugular venous pressure
(JVP), measuring blood pressure, assessing the pulse and chest using inspection,
palpation, percussion, and auscultation methods. Jugular venous pressure aids in the
estimation of volume status. Superior vena cava syndrome should be suspected if venous
pressure is elevated. Other conditions made increase in JVP such as congestive heart
failure, cor pulmonale, tricuspid stenosis, restrictive cardiomyopathy and constrictive
pericarditis. Blood pressure should be measured with patient in the seated position, with
the arm at the level of the heart, using appropriate-sized cuff. The use of an
36

inappropriately small cuff result in overestimation of the true blood pressure, an issue of
particular relevance in obese patients.
Palpation of arterial pulse include carotid pulse and symmetrically extremities
pulses. The contour of the pulses depends on the stroke volume, ejection velocity,
vascular capacity and compliance, and systemic resistance. Bifid pulse is created by two
distinct pressure peaks can occur normally in person with fever or after exercise. Pulsus
paradoxus termed for fall in systolic pressure of more than 10mmHg with inspiration (this
sign is pathologic of pericardial or pulmonary disease).
Inspection of the heart for apical heartbeat may be visible in thin-chested adults. In
patient with enlarged and hyperdynamic left ventricle, the left anterior chest wall may
heave. Left parasternal lift indicate RV pressure or volume overload. Palpation of the heart
should begin with patient in the supine position inclined at 30 degrees. Left lateral
decubitus position may help to intensify apex beat. Looking for point of maximal impulse
(normally in the midclavicular line at the fifth intercostal space). It is smaller than 2cm in
diameter and moves quickly away from the fingers. Percussion of the heart can be done to
identify heart border on the chest wall. Enlargement of heart will be shown by passing the
normal heart borderline.
Auscultation is one of the important and maybe difficult examination of the heart.
Heart sound component include S1 and S2. S1 indicate the sound produced when mitral
and tricuspid valves are closed in systole, and S2 indicate the sound produced when
aortic and pulmonic valve are closed in diastole. Another S3 and S4 of heart sound can be
audible in several pathologic condition. Heart murmur results from audible vibrations
caused by increased turbulence and are defined by their timing within the cardiac cycle.
There are systolic murmur, diastolic murmur, and continuous murmur. Knowing the type of
murmur and its location are important to identify which cardiac valves problem are exist
and for further management.
Standard Reference:
1. Mann, DL et all. Braunwalds Heart Disease, 10th ed. Philadelphia, Elsevier
Saunders, 2015. p. 118-132
Additional reading:
2. Constant, Jules. Essential of Bedside Cardiology, 2nd ed. New Jersey, Humana
Press Inc. 2003
1. Evaluate General Appearance (inspection)
2. Blood Pressure Examination, The Arterial Pulse, The Jugular Venous Pulse
evaluation.
3. Percussion, Palpation, Auscultation
TRAINING TASK:
CHECK LIST CARDIOVASCULAR PHYSICAL EXAMINATION
37
NO
ITEMS
Evaluate General Appearance

1. Inspection of the skin, nails, facies, eyes,
mouth
2. Inspection
neck,
chest
configuration,
extremities
Blood Pressure Examination

1. Determine blood pressure
2. Rule out orthostatic hypotension, coarctatio of
the aorta, cardiac tamponade
The Arterial Pulse

1. Rate and rhythm of the heart
2. Countour of the pulse
3. Amplitude of the pulse
The Jugular Venous Pulse

1. Determine the jugular wave forms
2. Estimate the jugular venous pressure
3. Evaluate the hepatojugular reflux
Percussion
1. Hearts borders
Palpation
1. Palpate the point of maximum impulse
2. Palpate for localized motion
3. Palpate for generalized motion
4. Palpate for thrills
Auscultation
1. Auscultate the cardiac areas
2. The Influence of breathing
3. Describe any murmur present
Examination for Edema

1. Test for Edema
SCORE
1
2
SCORE -------- =
Day 13
38
MODULE 13
dr. Bajra Nadha, Sp.JP
AIMS:
Able to skills for Electrocardiography (ECG), procedure and ECG Interpretation,
Echocardiography, Phonography, and USG Doppler
LEARNING OUTCOME:
1. Able to skills for ECG procedure.
2. Able to ECG interpretation
CURRICULUM CONTENS:
1. ECG procedure
2. ECG Interpretation
ABSTRACT:
Electrocardiogram (ECG) is examination for conduction of hearts electrical impulse. It is
widely used and invaluable clinical tool for the detection and diagnosis of a broad range of
cardiac conditions, as well as a technique that has contributed to the understanding and
treatment of virtually every type of heart disease. Electrocardiography remains the most
direct method for assessing abnormalities of cardiac rhythm. Furthermore, the ECG is
essential in the management of major metabolic abnormalities such as hyperkalemia and
certain other electrolyte disorders, as well as in assessing drug effects and toxicities such
as those caused by digitalis, antiarrhythmic agents, and tricyclic antidepressants. It will
evaluate the impulse made by the pacemaker. The ECG will record any of important
electrical activity of the heart as P wave, QRS complex, and T wave. Each of them reflects
the activity of atrium and ventricle. The ECG changes will associated with any electrical
events occurred in the heart. The standard clinical ECG includes recordings from 12
leads. These 12 leads include three bipolar (leads I, II, and III), six unipolar precordial
leads (leads V1 through V6), and three modified unipolar limb leads (the augmented limb
leads aVr, aVl, and aVf). Students should be able to analyze the printout and interpret the
result as clinical finding for diagnosis. In order to obtain a good result of ECG, student
should be able to demonstrate skills for ECG procedure.
The procedure will consist of the preparation of the equipment and the patient, the
placement of the leads, the recording and the interpretation. Interpretation will be done
through the basic rhythm analysis, the cardiac axis, check the limbs and chest lead for the
wave morphology. There will be some common abnormalities for ECG such as pre
excitation phenomena, bundle branch block, hypertrophy and the most importance the
myocardial ischemia. Student should be able to analyze the cardiogram given in the
course.
Echocardiography remains the most frequently used and usually the initial imaging
test to evaluate all cardiovascular diseases related to a structural, functional, or
hemodynamic abnormality of the heart or great vessels. Echocardiography uses
ultrasound beams reflected by cardiovascular structures to produce characteristic lines or
shapes caused by normal or altered cardiac anatomy in one, two, or three dimensions by
M (motion)mode, two-dimensional, or threedimensional echocardiography, respectively.
Doppler examination and color flow imaging provide reliable assessment of cardiac
hemodynamics and blood flow. Reliable noninvasive hemodynamic evaluation and
confident delineation of cardiovascular structures by echocardiography have dramatically
reduced the clinical necessity for hemodynamic cardiac catheterization. Increasingly,
patients undergo valvular or congenital heart surgery on the basis of an echocardiographic
diagnosis. Echocardiographic units are also being miniaturized to become an extension of
39

a clinicians physical examination. In our opinion, the appreciation of cardiac anatomy and
hemodynamics by bedside echocardiography makes a physicians clinical evaluation,
including physical examination, more relevant to the care of patients. For all physicians
who care for patients with a cardiovascular problem, it is essential to know how
echocardiographic images are obtained, what type of information echocardiography can
provide, and how it should be used for management.
Reference:
Saunders, 2015. p. 118-132
1. ECG procedure.
2. ECG Interpretation
.
TRAINING TASK
ECG Procedure :
Preparation
Group should choose one of their members to become a patient for the ECG examination.
Ask the patient to lie down on the table. In turn, each the student should perform the ECG
Examination; student should start from patient preparation, setup the machine, recording
step, and obtaining the result.
Instruction:
1. Prepare the patient for ECG examination.
2. Set the electrocardiography appropriately.
3. Place the leads in appropriate position.
4. Start the examination.
5. Obtain the result properly.
6. Explain and give information to the patient.
7. Please, refer to the ECG Skills Checklist!
Independent Learning (ECG Interpretation)
Each group will be provided with 10 pieces of electrocardiogram. Student should be
familiar with the analyzing step for the ECGram. It is likely that student should start from
checking the patient ID, analyze the rhythm, and identify whether there are any
abnormality patterns. Student should also be familiar with the writing technique for the
ECGrams interpretation.
Instruction
1. Analyze the ECGram given in group. You should refer to the handout given
(Analyzing the ECG) for the interpretation!
2. Write down the interpretation made for each ECGram.
Discuss the result at wrap up session.
Day 14
40
MODULE 14
dr. Lisnawati, Sp.Rad & dr. Made Muliarta, M.Kes
AIMS:
1. Able to evaluate and result chest x-rays
2. Able to workload measurement
LEARNING OUTCOME:
1. Able to evaluate chest x-rays, including evaluation on heart, lung, diaphragm,
skeleton and soft tissues
2. Able to result chest x-rays
3. Able to workload measurement
CURRICULUM CONTENS:
skeleton and soft tissues
2. Able to result chest x-rays
3. Physiologic parameters during activity
ABSTRACT I:
Chest imaging is important evaluation that supports the diagnosis procedure.
Student should be able to evaluate chest x-rays, including evaluation on heart, lung,
diaphragm, skeleton and soft tissues. After evaluation, student should be able to write
down the result in a given format. Some emergency case, need rapid chest x-rays
evaluation. By this training we hope that the student will be able to do such important skill.
There are steps in evaluating the chest x-rays, it is systematic steps. The student should
be mastered. For cardiovascular system the chest imaging will be posterolateral, lateral,
oblique projection. Student should evaluate the heart size; identify any enlargement, the
condition of the lung any edema, arterial and venous hypertension.
The imaging investigation of the heart may be considered under the following:
1. Chest X-ray
2. Computed tomography (CT-scan)
3. Magnetic resonance imaging (MRI)
4. Echocardiography
5. Angiocardiography
6. Cardiac catheterization
7. Isotope scanning
Chest X-ray remain the valuable cardiac investigation in clinical practice.
Radiologic method used in the roentgen cardiac examination:
1. Posteroanterior projection, PA/AP
2. Lateral projection
3. Right anterior oblique projection (RAO)
4. Left anterior oblique projection (LAO)
Increase in cardiac size is the most consistent indication of cardiac disease
ABSTRACT II:
Physiologic parameters will be change during activity, such as heart rate, stroke
volume, and cardiac output, blood pressure, peripheral resistance, and oxygen
concentration. Some or those parameters could be measure with a very simple technique
41

by calculating the arterial pulse, while others could only be measure using specific tools
such as ergo meter, ECG, and treadmill. In practice, we could measure the cardiovascular
functional capacity by using arterial pulse method, pulse meter, and ECG.
Stress test or exercise test should be done for patient with heart disease in special place,
in the laboratory. The purposes of stress test are to make quantification of heart disease
suffered by the patient and to evaluate the functional capacity of the patient. The arterial
pulse in rest condition will reflect the health status of the patient. The working arterial
pulse will reflect the workload, and the recovery pulse rate will also reflect the fitness
status of the patient. We will use the Karvonen Formula to calculate the heart rate limit on
stress test. The ten pulse method is the method for calculating the arterial pulse during
activity and recovery period.
skeleton and soft tissues.
2. Physiologic parameters during activity.
TRAINING TASK I:
Chest imaging: Cardiovascular System
Preparation
There would be 10 set of light cast with a single x-ray film. The group should discuss the
x-ray film and write down the result in a piece of A4 paper. You should notice the time limit
for each film. It would be at least 5 10 minutes of discussion for each film. Group should
move to another x-rays film after complete the discussion and writing down the result.
Instruction
1. Group should read the case available before evaluate the x-ray photo. What is the
main complaint of the patient?
2. The group should evaluate the x-rays photo systematically!
3. Write down the group result on a piece of A4 paper.
4. Move to another x-rays and you should repeat the step 1 till 3 (each group should
read all photos available).
TRAINING TASK II:
Home Work:
Determine Your Workload by Arterial Pulse Evaluation
Question: will be given after the lecture!
Student should work the task individually. Write down the answer on a piece of A4 paper
and make sure you put your name and NIM on it.
Collect your work at Lab Faal on Monday, April 27th, before 11 am
1. Roentgen Signs in Diagnostic Imaging Isadore Meschan
Day 15
42
MODULE 15
Prof. Dr. dr. Wiryana, Sp.An (KIC)
AIMS:
1. Able to skill routine clinical procedure: Intravenous Line (IV line)
2. Able to
LEARNING OUTCOME:
1. Able to two skills should be trained : IV cannulation and venipuncture..
CURRICULUM CONTENS:
1. Technique of venipucture
2. Aseptic procedure
.
ABSTRACT :
Doctor should be able to draw blood in field setting as a part of disease
investigation and therapy. Appropriate equipment and supplies should including the
following gloves, aseptic kit, bandage, tourniquet, vacutainer tubes or spuit and the
container. The complete technique of venipucture is contained in the Venipucture
Evaluation Checklist. It will cover the skills in preparation of the doctor and the patient,
aseptic procedure, the preparation of the kit, communicate the procedure to the patient,
the patient preparation, the insertion technique of the needle, the blood collection,
evaluation for any bleeding, and cleaning the work area after the procedure.
The checklist will vary from one to another, you should use the checklist as aidememoir (or reminder) of the element skills to be done. Basically there would be four main
steps in doing the venipuncture and IV line cannulation. It would be explain the procedure,
prepare the equipment and positioning the patient, select appropriate site, use standard
precaution, and reach the goal (obtain adequate specimen and a good technique for
cannulation).
1. The complete technique of venipucture
2. Aseptic procedure
3. The preparation of the kit
4. Communicate the procedure to the patient
5. The patient preparation
6. The insertion technique of the needle, the blood collection
7. Evaluation for any bleeding
8. Cleaning the work area after the procedure
TRAINING TASK
Venipuncture and IV Line Procedure
Preparation
43

We will provide the student with Multipurpose Injection Arm and IV line manequin needed
for IV line procedure training. It would be at least one mannequin for each two groups.
Groups should prepare one infusion set, ringer lactate infusion fluid, antiseptic set, and
tape. Each student should bring their own IV needle (G-21), syringe (3 cc), and bring
glove for antiseptic procedure.
Instruction
1. There would be two skills should be trained in this session, IV cannulation and
venipuncture.
2. You have to prepare the set for the procedures, prepare the manequin, needle, the
infussion set, and the infussion fluid.
3. Demonstrate how will you explain the procedure to the patient, the technique and
the complication might be happened.
4. Demonstrate the technique for IV cannulation and venipuncture. Please notice the
position of your finger, the angle, and how to evaluate whether the needle inserted
properly.
5. Refer to the checklists (Venipucture and IV Cannulation) for any details!
6. Ask any comment and score for ypur perfomance from your groups based on the
checlist!
Day 16
MODULE 16
dr. Eka Guna Wijaya, Sp.A
AIMS:
1. Describe Non-cyanotic and Cyanotic Congenital Heart Diseases
2. Describe to diagnose and manage Acute Rheumatic Fever
LEARNING OUTCOME:
1. Can describe to diagnose and manage Non-cyanotic and Cyanotic Congenital
Heart Diseases
2. Can describe to diagnose and manage Cyanotic Congenital Heart Diseases
3. Can describe to diagnose and manage Acute Rheumatic Fever
CURRICULUM CONTENS:
1. Fetal-transitional circulations
2. To diagnose and manage Non-cyanotic Congenital Heart Diseases and its
complications
3. To diagnose and manage Cyanotic Congenital Heart Diseases and its
complications
4. Interpret diagnostic tools of Congenital Heart Diseases
5. The health education and prognosis of Congenital Heart Diseases
6. Interpret diagnostic tool of Acute Rheumatic Fever
7. Management of Acute Rheumatic Fever and its complications
8. Prevention and rehabilitation of Acute Rheumatic Fever
9. Health education and prognosis of Acute Rheumatic Fever
44
ABSTRACT I:
Congenital Heart Disease (CHD) is congenital malformation of the heart including
great vessel that was occur since the baby was delivered.
A lot of kind of CHD has been recognized but ventricular septal defect, atrial septal defect,
patent ductus arteriosus were the most common finding. Tetralogy of Fallot is the
commonest one of cyanotic CHD. Obstructive lesions (pulmonary and aortic stenosis,
coarctatio aorta), transposition of great artery, truncus arteriosus, ebstein anomaly, etc
were relatively rare cases.
CHD is really a dynamic disease. In mild and simple lesion such as VSD and ASD
were usually asymptomatic and half of those may undergoing spontaneous closure after
two years old. Contrassly in severe cases, sign of heart failure, deep cyanosis, acidosis
and other sign express of critical condition may exist in few hours after birth.
Severe pulmonary hypertension is serious longterm complication of large left-toright shunt. Eisenmenger syndrome may slowly develop when pulmonary artery pressure
higher than systemic pressure. The patient appeared cyanotic who previously non
cyanosis.
Left-to-right shunt hemodynamically characterized by increase of pulmonary blood
flow but inversely decrease of systemic blood flow. Under these circumstances may lead
to congestive heart failure due to overcompensated of symphatic and humoral stimulation.
ToF may characterize by four anatomical abnormalities: VSD, overriding of aorta,
right ventricular hypertrophy, and pulmonary stenosis. Right-to-left shunting was seen in
ventricular level. Severity of cyanosis in ToF depends directly on severity of pulmonary
stenosis.
Growth failure is the commonest finding of significant CHD. Screening should be done in
patient with failure of growth and development and certain syndromes to evaluate more
carefully in other to be sure is the patient having or not having of CHD.
Diagnosis investigation of CHD was the following: history taking (antenatal, natal,
and post natal), physical examination, chest radiograph, and ECG. Echocardiography is
needed to evaluate more detail of anatomical defect and cardiac function. Comprehenship
management should be performed in nursing the patient. Dental hygiene, nutritional
support, psychological aspect was a part of integrated management beyond of the
medical and surgical intervention.
ABSTRACT II:
Valvular Heart Disease (VHD) is largely variated disease due to anomaly or
damaged of one or more cardiac valves.
Anomaly most likely congenital in origin include: Tricuspid Atresia, Tricuspid Stenoinsuficiency (Ebstein anomaly) mitral stenosis, mitral insufficiency, pulmonary or aortic
stenosis/atresia.
The most common of VHD is Rheumatic Heart Disease and Mitral Valve Prolaps.
Diagnosis investigation like other disease: History taking, physical examination,
chest X-rays, ECG, and other specific laboratory examination. Echocardiography is
routine procedure to evaluate more detail anatomical abnormality, severity and cardiac
function. Catheterization is needed when valvuloplasty was indicated.
The origin and characteristic of the first and the second heart sound should be
deeply understand before indentified many kind of pathological heart murmur.
Location, timing, quality, intensity, and transmission of heart murmur is the basic
auscultative modality to investigate more advance of specific valvular heart disease.
Management of VHD medically include: digitalis, diuretics, vasodilator, anti
thrombotic agent, endocarditis prophylaxis, dental hygiene and nutritional support.
Rheumatic fever/ Rheumatic Heart Disease was agreed worldwide as an autoimmune
disease.
Tissue hospes has mimic antigenic structure with certain strain of beta hemolytic
streptococcus group a who was infected in the pharing. There is basic pathogenesis
45

concept in development tissue injury/ damage of succeptible host. When autoantibody
was generated in significant number, cross reaction where streptococci causing agent
were killed naturally by humoral and cellular antibody but on the other hand tissue
damage of the hospes was also happen because it was recognized as antigen.
Carditis and arthritis were the most frequent of major symptom of RF/RHD.
Jones criteria was established as definite diagnosis of rheumatic fever. Evolution was
made from the beginning in 1944 and then revised in 1956, modified in 1965, update in
1992, finally recommendation of WHO in 2002.
Bed rest, eradication of causing agent, inflammatory drug and secondary prophylaxis were
the basic management of Rheumatic Fever/ Rheumatic Heart Disease
1. Park, MK. Pediatric Cardiology for Practioners. 4 th Ed. Philadelphia, Mosby.
2002. p 129-144, 185-189, 304-310, 311-318
1. Fetal-transitional circulations
2. Criteria diagnose and manage of the Non-cyanotic Congenital Heart Diseases
and its complications
3. Criteria diagnose and manage of the Cyanotic Congenital Heart Diseases and its
complications
4. The health education and prognosis of Congenital Heart Diseases
5. Interpret diagnostic tool of Acute Rheumatic Fever
6. Management of Acute Rheumatic Fever and its complications
7. Prevention and rehabilitation of Acute Rheumatic Fever
8. Health education and prognosis of Acute Rheumatic Fever.
SCENARIO;
CASE 1:
Putu, 2 years old girl was came to pediatric cardiology clinic with her parent with the main
complain of persistent cough and slight dyspneu.
Physical examination :
HR : 128 x/min, RR : 44 x/min, BW : 9 kg. Positive precordial bulging, cardiac impulse was
displaced to caudolateral associated with lifting. Heart murmur was heard systolic and
diastolic phase at upper left parasternal border.
LEARNING TASK :
1. How to know that patient having continuous murmur.
2. What is the probable complete diagnosis clinically.
3. Is the patient should be given indometasin.
4. What is the best diagnostic tool in this patient.
5. What kind of treatment have been recommended.
CASE 2:
Made, 9 months old baby was referred by GP to pediatric clinic of cardiology due to
cyanosis. Physical examination looked at the baby having cyanotic at the mouth until the
tongue. Cyanotic was also seen at the fingers associated with clubbing. When
auscultation just to be done, the baby suddenly hard crying, uncontrolled for long time and
then hyperapneu and lethargy.
LEARNING TASK:
46

1. What is may be happen to the baby.
2. What must you be done immediately to overcame this condition.
On auscultation, ejection systolic murmur was heard at the upper left parasternal
border line with almost there is no heard of P2.
3. What is the most probable disease may be occur to the baby
4. What does you expected from chest X-ray examination.
5. When phlebotomy should be perform base on routine blood examination
6. Mention a lot of complication may be develop and what is the most hazard
7. When iron preparation should be given in this patient.
CASE 3:
Komang, 10 years old boy come with his parent to pediatric clinic of cardiology with the
main complain of dyspneu on exertion. Coughing and palpitation were also present.
Physical examination revealed: Malnourish boy with slight anemic. Pulse rate : 108 x/ min,
RR : 24 x/min, body temperature 38 degree C. Hyperdinamic of precordium with
displacement of apical impulse caudolaterally with lifting positive. Holosystolic murmur
was heard at cardiac apex referred to axilla. Diastolic murmur was also heard at upper
right parasternal border.
LEARNING TASK
1. Base on those data, what is the most probable diagnosis.
2. What is other history and laboratory examination may be needed to support the
diagnosis.
3. Which of cardiac valve were involve in this patient.
4. How about chest X ray and blood pressure examination.
5. How to manage in short and long time period.
SELF ASSESSMENT
1. Please describe haemodynamic change in PDA.
2. Patten of blood pressure and pulse in PDA.
3. How the chest X-ray in patient with PDA.
4. Is in large PDA you can heard diastolic flow murmur at the apex cordis? Can you
explain about that?
5. Please mention complication of PDA.
6. Please mention a few risk factor in development of cyanotic spell.
7. Can you explain the phatomecanism of cyanotic spell?
8. Please mention differential diagnosis of cyanotic CHD base on increase and
decrease of pulmonary blood flow.
9. Please explain what do you know about pheriperal and central cyanosis.
10. Explain phatomecanism oh tissue injury in acute rheumatic fever
11. Mention etiology, antigenic structure and its cellular product.
12. Please mention mayor and minor manifestation of rheumatic fever.
13. Please mention detail pathology of rheumatic fever.
Day 17
47
MODULE 17
Dr. dr. K. Rina, Sp PD, Sp JP
AIMS:
Describe to diagnose and manage Ischaemic Heart Disease (IHD) and Acute
Coronary Syndromes (ACS)
LEARNING OUTCOME:
1. Can describe to diagnose and manage Ischaemic Heart Disease (IHD)
2. Can describe to diagnose and manage Acute Coronary Syndromes (ACS)
CURRICULUM CONTENS:
1.
2.
3.
4.
5.
Pathogenesis of atherothrombosis
Risk factors of Ischaemic Heart Disease and Acute Coronary Syndromes
Clinical spectrum of Ischaemic Heart Disease and Acute Coronary Syndromes
Interpret laboratory of Acute Coronary Syndromes
Interpret diagnostic tools of Ischaemic Heart Disease and Acute Coronary
Syndromes
6. Management and its prognosis of Ischaemic Heart Disease and Acute Coronary
Syndromes
7. Post ACS medical rehabilitation and its rehabilitations
ABSTRACT:
Coronary artery disease (CAD) is one of the most important causes of premature
death in the developed world, as well in Indonesia. CAD is regarded as a leading cause of
mortality in Province of East Java and Bali, based on the National Household Health
Survey in 1995. Its proportion was reported to be 24.5% of all cause mortality, and its
proportion has been significantly increasing since the last 10 years in Indonesia (SKRT,
1995). Coronary atherosclerosis, the basic pathogenesis of this disease, is associated
with many risk factors such as cigarette smoking, hyperlipidaemia, family history,
hypertension and diabetes mellitus.
Atherosclerosis is a chronic process initiated by lipid deposition and vascular wall
injury that causes increased endothelial permeability, inflammation and recruitment of
monocytes and leucocytes. These cells accumulate oxidized lipids to form macrophages
and foam cells, and lead to the formation of fatty streak and then atheroma. Eventually,
all these process becomes atherosclerotic plaque.
Chronic stable angina is caused by atheroma obstructing coronary artery lumen by
more than 70%. Acute coronary syndromes (ACS = unstable angina and myocardial
infarction) arise when atherosclerotic plaque becomes unstable and either ruptures or are
eroded. The complicated plaque is a nidus for thrombus formation and may lead to vessel
occlusion.
Stable coronary artery disease is generally characterized by episodes of reversible
myocardial demand/supply mismatch, related to ischaemia or hypoxia, which are usually
inducible by exercise, emotion or other stress and reproduciblebut, which may also be
occurring spontaneously. Such episodes of ischaemia/hypoxia are commonly associated
with transient chest discomfort (angina pectoris). SCAD also includes the stabilized, often
asymptomatic, phases that follow an ACS.
A careful history remains the cornerstone of the diagnosis of chest pain. The
characteristics of discomfort-related to myocardial ischaemia (angina pectoris) may be
divided into four categories: location, character, duration and relationship to exertion and
other exacerbating or relieving factors. The discomfort caused by myocardial ischaemia is
48

usually located in the chest, near the sternum, but may be felt anywhere from the
epigastrium to the lower jaw or teeth, between the shoulder blades or in either arm to the
wrist and fingers. The discomfort is often described as pressure, tightness or heaviness;
sometimes strangling, constricting or burning. The duration of the discomfort is briefno
more than 10 min in the majority of cases and more commonly even minutes or less but
chest pain lasting for seconds is unlikely to be due to angina. An important characteristic is
the relationship to exercise, specific activities or emotional stress. Symptoms classically
appear or become more severe with increased levels of exertion and rapidly disappear
within a few minutes when these causal factors abate.
Basic (first-line) testing in patients with suspected SCAD includes standard
laboratory biochemical testing, a resting ECG, possibly ambulatoryECGmonitoring (if there
is clinical suspicion that symptoms may be associated with a paroxysmal arrhythmia),
resting echocardiography and, in selected patients, a chest X-ray (CXR). Such testing can
be done on an outpatient basis. The aim of the management of SCAD is to reduce
symptoms and improve prognosis. The management of CAD patients encompasses
lifestyle modification, control of CAD risk factors, evidence-based pharmacological therapy
and patient education.
The acute coronary syndromes encompass a spectrum of unstable coronary artery
disease that includes unstable angina and myocardial infarction (ST segment elevation
myocardial infarction and non-ST segment elevation myocardial infarction). The history,
electrocardiogram, and cardiac markers determine the presence and the type of ACS.
Patients with an acute coronary syndrome usually present with prolonged anginal
sympoms that occur at rest. Patients with persistent chest pain lasting more than 20
minutes should seek urgent medical attention because of the likelihood of myocardial
amage an dinfarction. The electrocardiogram will often show evidence of ischaemia that
classically takes the form of ST segment shifts, T-wave inversion, and new bundle branch
block. Cardiac enzymes and markers are the principal determinans that define the
category of the acute coronary syndrome. Patients should be given analgesia, oxygen and
transferred to intensive coronary care unit. Treatments consist of aspirin, clopidogrel, lowmolecular weight heparin, beta-blockers and intravenous nitrate infusion. Where available,
percutaneous coronary intervention (PCI) is the treatment of choice. Thrombolytic therapy
is an effective alternative.
1.
2.
3.
4.
Risk factors of Ischaemic Heart Disease and Acute Coronary Syndromes

Clinical spectrum of Ischaemic Heart Disease and Acute Coronary Syndromes
Interpret laboratory of Acute Coronary Syndromes
Interpret diagnostic tools of Ischaemic Heart Disease and Acute Coronary
Syndromes
5. Management and its prognosis of Ischaemic Heart Disease and Acute Coronary
Syndromes
6. Post ACS medical rehabilitation and its rehabilitations
References:
Saunders, 2015.
2. Montalescot G. Et al. 2013 ESC Guidelines on The Management of Stable
Coronary Artery Disease. Eur H J. 2013:34,2949-3003
SCENARIO 1:
CASE:
49

A 70-year old male, came to Emergency Room due to chest pain and shortness of breath.
The pain was felt retro-sternally since 10-hours prior to admission, it was dull pain of 8 of
10 pain scale, not relieved by resting, accompanied by shortness of breath since 5 hours
PTA that is relieved by sitting position. He is suffered from uncontrolled DM and
Hypertension since 10 years ago. He appeared severely ill and dyspnea. The blood
pressure was 80/palp mmHg; pulse rate was 120 beats per-minute, regular. There was
rales on both lung fields and cold extremity. ECG revealed sinus tachycardia 120 beats
per-minute. Elevated ST-segment of ECG was noted at the precordial leads.
LEARNING TASK :
1. What is the most likely diagnosis?
2. What the next procedure do you plan?
3. What is your initial treatment?
4. What is the role of inotropic support in this case?
5. What is the definitive therapy for this case?
SELF-ASSESSMENT :
1. Please explain the risk factors of ischaemic heart disease
2. What are the complications of acute myocardial infarction
3. What is the treatment of choice in ST-elevation myocardial infarction?
4. Please describe the indication and the benefit of CABG (coronary artery bys-pass
graft grafting)?
Day 18
MODULE
MODULE 18
dr Wayan Winarti, SpPA
AIMS:
1. Describe the pathogenesis of atherosclerosis related to Ischemic Heart Disease
(IHD)
2. Describe drug used in Angina Pectoris
LEARNING OUTCOME:
1. Able to explain the pathogenesis of atherosclerosis
2. Able to describe the morphology of atherosclerosis
3. Able to explain the pathogenesis of IHD
4. Able to describe the morphology of myocardial infarction (MI)
5. Able to describe drug used in Angina Pectoris
CURRICULUM CONTENT
1. Pathogenesis of atherosclerosis
2. Morphology of atherosclerosis
50

3. Pathogenesis of IHD
4. Morphology of MI
5. Drug used in Angina Pectoris
ABSTRACT I:
Angina pectoris s characteristically describes as a retrosternal chest discomfort
(constricting, pressing or tight) that has a close relation to physical or emotional stress,
and is rapidly relieved with rest or nitrates. It is commonly, the consequence of obstructive
atheromatous coronary artery disease.
The retrosternal discomfort in angina pectoris is caused by myocardial ischemia.
The myocardial ischemia is due to an imbalance between myocardial oxygen supply and
demand. Decreased myocardial oxygen supply can result from the presence of flowlimiting chronic stenoses in atherosclerotic coronary arteries, or can occur acutely as a
result of vasospasm or thrombosis. The increased in myocardial oxygen demand may
arise as a result of physical exertion or emotional stress, the two common precipitating
factors for angina.
Myocardial oxygen demand is principally determined by heart rate, ventricular
contractility, and by myocardial wall tension, the latter in turn is influenced by cardiac
preload (ventricular filling pressure), ventricular volume, contractility and afterload. Drugs
that ameliorate or prevent angina either decrease myocardial demand (by slowing heart
rate, decreasing ventricular contractility, preload and afterload) or increase myocardial
blood supply (by inducing epicardial coronary artery vasodilatation or preventing epicardial
coronary artery vasoconstriction). Three classes of drugs are used in the treatment of
angina : nitrates, betablockers and calcium channel blockers.
ABSTRACT II:
Ischemic Heart Disease (IHD) is the generic designation for a group of
pathophysiologically related syndromes resulting from myocardial ischemia. In more than
90% of cases, the cause of myocardial ischemia is reduced blood flow due to obstructive
atherosclerotic lesions in the coronary arteries.
Atherosclerosis is characterized by intimal lesions called atheromas (also called
atheromatous or atherosclerotic plaques) that protrude into vessel lumens. Besides
mechanically obstructing blood flow, atherosclerotic plaques can rupture, leading to
catastrophic vessel thrombosis; plaques also weaken the underlying media and thereby
lead to aneurysm formation.
Historically, there have been two dominant hypotheses of atherogenesis: one
emphasizes intimal cellular proliferation, while the other focuses on the repetitive
formation and organization of thrombi. The contemporary view of atherogenesis
incorporates elements of both theories and also integrates the risk factors (constitutional
risk factors, modifiable risk factors and additional risk factors).
The key processes in atherosclerosis are intimal thickening and lipid accumulation.
Atheromatous plaques impinge on the lumen of the artery and grossly appear white to
yellow; superimposed thrombus over ulcerated plaques is red-brown. Plaques vary from
0.3 to 1.5 cm in diameter but can coalesce to form larger masses. Atherosclerotic plaques
have three principal components: (1) cells, including smooth muscle cells, macrophages,
and T cells; (2) ECM, including collagen, elastic fibers, and proteoglycans; and (3)
intracellular and extracellular lipid.
Chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries,
and variable degrees of superimposed acute plaque change, thrombosis, and vasospasm
will lead to vary clinical coronary syndromes such as angina, myocardial infarction (MI),
and even sudden death. Some also fall into chronic ischemic heart disease state.
The distribution of myocardial necrosis correlates with the location of the
decreased perfusion. Most myocardial infarcts are transmural, in which the ischemic
necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of
51

a single coronary artery. In contrast, a subendocardial (nontransmural) infarct constitutes
an area of ischemic necrosis limited to the inner one third to one half of the ventricular
wall.
The gross and microscopic appearance of an infarct depends on the duration of
survival of the patient following the MI. Areas of damage undergo a progressive sequence
of morphologic changes that consist of typical ischemic coagulative necrosis (the
predominant mechanism of cell death in MI, although apoptosis may also occur), followed
by inflammation and repair that closely parallels tissue responses to injury at other sites.
1. McPhee SJ, Papadakis MA. Current Medical Diagnosis & Treatment. 47 th ed. New
York: Lange Mecical Book`s/The McGraw-Hill Companies, 2008.p. 300-324.
2. Kumar V, Cotran R S, Robbins SL: Robbins Basic Pathology, 7th ed. Philadelphia,
Saunders, 2003. p. 328 338; 363 372.
3. Trevor AJ, Katzung BG, Masters SB: Katzung & Trevors Pharmacology, 7th ed.
New York, McGraw-Hill/Lange., 2005. p 105-113
1. Pathogenesis of atherosclerosis
2. Morphology of atherosclerosis (macroscopy and microscopy)
3. Relation between atherosclerosis and IHD
4. Morphology of MI (macroscopy and microscopy)
5. Principles of anti angina pectoris therapy.
6. Classification of anti angina pectoris drugs
7. Important pharmacokinetic properties of anti angina pectoris drugs.
8. Mechanism of actions of anti angina pectoris drugs.
9. Important adverse effects of anti angina pectoris drugs.
SCENARIO:
CASE I:
A 55 year old male experiences crushing substernal chest pain on arriving at work in the
morning. Over the next few hours the pain persists and begins to radiate to his left arm.
He becomes diaphoretic and short of breath. He goes to emergency unit immediately.
Laboratory and ECG findings are consistent with myocardial infarction.
LEARNING TASK I:
1. Important adverse effects of anti angina pectoris drugs
2. Describe the morphology (gross and microscopy) of MI!
3. Explain the morphologic differences between angina and MI!
4. Explain the correlation between atherosclerosis and IHD!
5. Explain about the pathogenesis of atherosclerosis! Mention it risk factors!
6. Describe the morphology (gross and microscopy) of fatty streak
atherosclerotic plaque!
and
LEARNING TASK II:

1. Describe the principles of anti angina pectoris therapy.
2. Describe the classification of anti angina pectoris drugs
3. Describe the important pharmacokinetic properties of anti angina pectoris drugs.
4. Describe the mechanism of actions of anti angina pectoris drugs.
SELF ASSESSMENT:
1. Describe the morphology of 3 days old MI!
52

2.
3.
4.
5.
6.
Mention risk factors of IHD!

Mention the main component of atherosclerotic plaque!
Describe the principles of anti angina pectoris therapy.
Describe the classification of anti angina pectoris drugs
Describe the mechanism of actions and the important pharmacokinetic properties
of anti angina pectoris drugs
Day 19
MODULE 19
AIMS:
Able to diagnose and manage Arrhythmias
LEARNING OUTCOME:
1. Can describe to diagnose Arrhythmias
2. Can describe manage Arrhythmias
CURRICULUM CONTENS:
1.
2.
3.
4.
Etiology and pathophysiology of Arrhythmias

Clinical approach of Arrhythmias
Treatment of Arrhythmias
Prognosis of Arrhythmias
ABSTRACT I:
An arrhythmia (or dysrhythmia) is a disturbance of the electrical rhythm of the heart. Most
arrhythmias are benign and are only troublesome because of the symptoms they cause.
However, some arrhythmias are dangerous and require treatment to prevent
haemodynamic compromise or cardiac arrest, and it is important to recognize these.
In the management of clinical arrhythmias, the physician must evaluate and treat
the whole patient, not just the rhythm disturbance. Some arrhythmias are hazardous to the
patient, regardless of the clinical setting (e.g., ventricular fibrillation, VF), whereas others
are hazardous because of the clinical setting (e.g., rapidly conducted atrial fibrillation in a
patient with severe coronary artery stenoses). Patients with cardiac rhythm disturbances
can present with various complaints, but symptoms such as palpitations, syncope,
presyncope, or congestive heart failure commonly cause them to seek a physicians help.
Their awareness of palpitations and of a regular or irregular cardiac rhythm varies greatly.
A careful drug and dietary history should also be sought; some nasal decongestants can
provoke tachycardia episodes, whereas betaadrenergic blocking eye drops for treatment
of glaucoma can drain into tear ducts, be absorbed systemically, and precipitate syncope
caused by bradycardia.
Examination of the patient during a symptomatic episode can be revealing. Clearly,
heart rate and blood pressure are key measurements to make. Assessment of the jugular
venous pressure and waveform can disclose the rapid oscillations of atrial flutter or
cannon A waves indicative of contraction of the right atrium against a closed tricuspid
valve in patients with AV dissociation in disorders such as complete heart block or VT.
53

Variations in the intensity of the first heart sound and systolic blood pressure have the
same implications.
The ECG is the primary tool in arrhythmia analysis; an EPS, in which intracardiac
catheters are used to record activity from several regions of the heart at one time, is more
definitive. Initially, a 12-lead ECG is recorded. In addition, a long continuous recording with
use of the lead that shows distinct P waves is often helpful for closer analysis; most
commonly, this is one of the inferior leads (2, 3, aVF), V1, or aVR. The ECG obtained
during an episode of arrhythmia may be diagnostic by itself, obviating the need for further
diagnostic testing The following additional tests can be used to evaluate patients who
have cardiac arrhythmias. The physicians choice of which test to use depends on the
clinical circumstances. For example, a patient with multiple daily episodes of presyncope
is likely to have an event recorded on a 24-hour ambulatory electrocardiographic (Holter)
monitor, whereas in a patient who complains of infrequent anxiety- or exercise-induced
palpitations, exercise stress testing may be more likely to provide a diagnosis.
Normal sinus rhythm is arbitrarily limited to impulse formation beginning in the
sinus node at rates between 60 and 100 beats/min. Infants and children generally have
faster heart rates than adults do, both at rest and during exercise. Rates below 50
beats/min are considered to be bradycardia, and rates above 100 beats/min are
considered to be tachycardia.
Tachyarrhythmias are broadly characterized as supraventricular tachycardia (SVT),
defined as a tachycardia in which the driving circuit or focus originates, at least in part, in
tissue above the level of the ventricle (i.e., sinus node, atria, AV node, or His bundle), and
ventricular tachycardia (VT), defined as a tachycardia in which the driving circuit or focus
solely originates in ventricular tissue or Purkinje fibers. Because of differences in
prognosis and management, the distinction between SVT and VT is critical early in the
acute management of a tachyarrhythmia. In general (with the exception of idiopathic VT),
VT often carries a much graver prognosis, usually implies the presence of significant heart
disease, results in more profound hemodynamic compromise, and therefore requires
immediate attention and measures to revert to sinus rhythm. On the other hand, SVT is
usually not lethal and often does not result in hemodynamic collapse; therefore, more
conservative measures can be applied initially to convert to sinus rhythm. Supraventricular
tachycardia (SVTs) are almost benign. Initial management of SVT comprises the Valsalva
manuver, carotid sinus pressure or administration of intra venous adenosine. Beta-blocker
and verapamil reduce symptoms significantly in two-thirds of patients with recurrent SVT.
Radio frequency ablation should be considered for all patients with frequent SVT
Tachycardia in an adult is defined as a rate of 100 beats/min. During sinus
tachycardia, the sinus node exhibits a discharge frequency between 100 and 180
beats/min, but it can be higher with extreme exertion and in young individuals. The
maximum heart rate achieved during strenuous physical activity decreases with age from
about 200 beats/min at 20 years to less than 140 beats/min at 80 years.
Premature complexes are among the most common causes of an irregular pulse.
They can originate from any area in the heartmost frequently from the ventricles, less
often from the atria and the AV junctional area, and rarely from the sinus node. Although
premature complexes arise commonly in normal hearts, they are more often associated
with structural heart disease and increase in frequency with age. The diagnosis of
premature atrial complexes (PACs) is made on the ECG by the presence of a premature P
wave with a PR interval of 120 milliseconds (except in Wolff- Parkinson-White syndrome,
in which case the PR interval is usually shorter than 120 milliseconds). Although the
contour of a premature P wave can resemble that of a normal sinus P wave, it
generally differs.
Atrial fibrillation (AF) is a supraventricular arrhythmia characterized
electrocardiographically by low-amplitude baseline oscillations (fibrillatory or f waves) and
an irregularly irregular ventricular rhythm. AF is the most common arrhythmia treated in
clinical practice and the most common arrhythmia for which patients are hospitalized;
approximately 33% of arrhythmia-related hospitalizations are for AF. The symptoms of AF
54

vary widely between patients, ranging from none to severe and functionally disabling
symptoms. The most common symptoms of AF are palpitations, fatigue, dyspnea, effort
intolerance, and lightheadedness.
Atrial flutter is less common than atrial fibrillation. The atrial rate during typical
atrial flutter is usually 250 to 350 beats/min, although it is occasionally slower, particularly
when the patient is treated with antiarrhythmic drugs, which can reduce the rate to about
200 beats/min. In typical atrial flutter, the ECG reveals identically recurring, regular,
sawtooth flutter waves and evidence of continual electrical activity (lack of an isoelectric
interval between flutter waves), often best visualized in leads II, III, aVF, or V1.
Management of atrial fibrillation and flutter is the rate control strategy. It is directed
at limiting the ventricular response to atrial fibrillation by using AV node blocking drugs,
such as digoxin, beta-blockers and verapamil. Cardioversion and anti-arrhythmic drugs
are used to restore and maintain sinus rhythm. Anti-coagulation with warfarin should be
considered for patients with atrial fibrillation and risk factors for stroke.
The prevalence of premature ventricular complexes increases with age; they are
associated with male gender and a reduced serum potassium concentration. Symptoms of
palpitations or discomfort in the neck or chest can result because of the greater than
normal contractile force of the postextrasystolic beat or the feeling that the heart has
stopped during the long pause after the premature complex. A PVC is characterized by the
premature occurrence of a QRS complex that is abnormal in shape and has a duration
usually exceeding the dominant QRS complex, generally longer than 120 milliseconds. In
most patients, PVCs (occurring as single PVCs, bigeminy, or trigeminy but excluding
nonsustained VT) do not need to be treated and treatment is usually dictated by the
presence of symptoms attributable to the PVCs.
In general, the specific type, prognosis, and management of ventricular
tachycardia (VT) depend on whether underlying structural heart disease is present. The
electrocardiographic diagnosis of VT is suggested by the occurrence of a series of three
or more consecutive, abnormally shaped PVCs whose duration exceeds 120 milliseconds,
with the ST-T vector pointing opposite the major QRS deflection. Symptoms occurring
during VT depend on the ventricular rate, duration of tachycardia, and presence and
extent of the underlying heart disease and peripheral vascular disease. VT can occur in
several forms: short, asymptomatic, nonsustained episodes; sustained, hemodynamically
stable events, generally occurring at slower rates or in otherwise normal hearts; or
unstable runs, often degenerating into VF. The dramatic changes in the management of
VT and aborted sudden death during the past decade have been fueled by several large
clinical trials and development of the ICD. Management decisions can be stratified into
those involved in acute management (or termination) and those involved in long-term
therapy (or prevention of recurrence or sudden death.
Ventricular fibrillation (VF) occurs in various clinical situations but most commonly
in association with coronary artery disease and as a terminal event. Ventricular flutter or
VF results in faintness, followed by loss of consciousness, seizures, apnea, and
eventually, if the rhythm continues untreated, death. The blood pressure is unobtainable,
and heart sounds are usually absent. These arrhythmias represent severe derangements
of the heartbeat that usually terminate fatally within 3 to 5 minutes unless corrective
measures are undertaken promptly. Ventricular flutter is manifested as a sine wave in
appearanceregular large oscillations occurring at a rate of 150 to 300 beats/min (usually
about 200). The distinction between rapid VT and ventricular flutter can be difficult and is
usually of academic interest only. Hemodynamic collapse is present with both. VF is
recognized by the presence of irregular undulations of varying contour and amplitude.
Distinct QRS complexes, ST segments, and T waves are absent. Fine-amplitude
fibrillatory waves (0.2 mV) are present with prolonged VF. These fine waves identify
patients with worse survival rates and are sometimes confused with asystole.
Management should follow basic life support and advanced cardiac life support guidelines.
Bradyarrhythmias are arbitrarily defined as a heart rate below 60 beats/min. In
some cases, bradyarrhythmias are physiologic, as in well-conditioned athletes with low
55

resting heart rates or type I AV block during sleep, and in other cases are pathologic. Like
tachyarrhythmias, bradyarrhythmias can be categorized on the basis of the level of
disturbance in the hierarchy of the normal impulse generation and conduction system
(from sinus node to AV node to His-Purkinje system). Sinus bradycardia exists in an adult
when the sinus node discharges at a rate slower than 60 beats/min. P waves have a
normal contour and occur before each QRS complex, usually with a constant PR interval
longer than 120 milliseconds. Sinus arrhythmia often coexists.
Heart block is a disturbance of impulse conduction that can be permanent or
transient, depending on the anatomic or functional impairment. It must be distinguished
from interference, a normal phenomenon that is a disturbance of impulse conduction
caused by physiologic refractoriness resulting from inexcitability caused by a preceding
impulse. Interference or block can occur at any site where impulses are conducted, but
they are recognized most commonly between the sinus node and atrium (SA block),
between the atria and ventricles (AV block), within the atria (intra-atrial block), or within the
ventricles (intraventricular block). An AV block exists when the atrial impulse is conducted
with delay or is not conducted at all to the ventricle when the AV junction is not
physiologically refractory. In some cases of bundle branch block, the impulse may only be
delayed and not completely blocked in the bundle branch, yet the resulting QRS complex
may be indistinguishable from a QRS complex generated by a complete bundle branch
block.
.
1.
Mann, DL et all. Braunwalds Heart Disease, 10th ed. Philadelphia, Elsevier

Saunders, 2015. p. 687-837

1.
2.
3.
4.
5.
Etiology of Arrhythmias
Pathophysiology of Arrhythmias
Clinical approach of Arrhythmias
Treatment of Arrhythmias
Prognosis of Arrhythmias
ABSTRACT II:
ANTIARRHYTHMIC DRUGS
Many factors can precipitate or exacerbate arrhythmias: ischemia, hypoxia,
acidosis or alkalosis, electrolyte abnormalities, excessive catecholamine exposure,
autonomic influences, drug toxicity (eg, digitalis or antiarrhythmic drugs), overstretching of
cardiac fibers, and the presence of scarred or otherwise diseased tissue. However, all
arrhythmias result from (1) disturbances in impulse formation, (2) disturbances in impulse
conduction, or (3) both. Arrhythmias may require treatment because rhythms that are too
rapid, too slow, or asynchronous can reduce cardiac output. Some arrhythmias can
precipitate more serious or even lethal rhythm disturbances. In such patients,
antiarrhythmic drugs may be lifesaving.Arrhythmias can be treated with the drugs and with
nonpharmacologic therapies such as pacemakers,cardioversion, catheter ablation, and
surgery.
The aim of therapy of the arrhythmias is to reduce ectopic pacemaker activity and
modify conduction or refractoriness in reentry circuits to disable circus movement.
Antiarrhythmic drugs decrease the automaticity of ectopic pacemakers more than that of
the sinoatrial node The major mechanisms currently available for accomplishing these
56

goals are (1) sodium channel blockade, (2) blockade of sympathetic autonomic
effects in the heart, (3) prolongation of the effective refractory period, and (4)
calcium channel blockade.Antiarrhythmic drugs and in particular the fact that they can
precipitate lethal arrhythmias in some patients has led to a reevaluation of their relative
risks and benefits. In general, treatment of asymptomatic or minimally symptomatic
arrhythmias should be avoided for this reason.
New York, McGraw-Hill/Lange., 2005. p 124-136
SELF-DIRECTED LEARNING
1. Principles of arrhythmias therapy.
2. Classification of Antiarrhythmic drugs.
3. Important pharmacokinetic properties of Antiarrhythmic drugs.
4. Mechanism of actions of Antiarrhythmic drugs.
5. Important adverse effects of Antiarrhythmic drugs..
SCENARIO
CASE 1 :
A 45-year old gentleman presented with irregular heart beat and dizzy. On physical
examination, the blood pressure was 115/75 mmHg; heart rate was 148 beats per-minute,
irregular and pulse rate was 102 beats per-minute, irregular. S 1 and S2 were single, grade
3/6 rumbling diastolic murmur was heard at apex cordis.
LEARNING TASK I :
1. What is the most likely arrhythmia found in this patient?
2. What is the terminology of differentiation between irregular higher heart rate and
irregular lower pulse rate?
CASE 2 :
A 45-year-old man is noted to have dilated cardiomyopathy with atrial fibrillation and a
rapid ventricular rate. A drug is used to control theventricular rate, but the cardiac
contractility is also affected, placing him in pulmonary edema.
Discuss in your group the following issues.
LEARNING TASK II:
A 65-year-old man is noted to have atrial fibrillation. He also have hospitalized 1 year ago
because of heart failure. A drug is used to control the symptom. After 1 week he come
back to the doctor complain about discoloration of his skin, the colour of his skin become
gray-blue especially in the area exposed to the sun and sometimes it is itchy.
Discuss in your group the following issues.
1. Which antiarrhythmic drug likely is used to the patient?
2. To what class of antiarrhythmic does the drug belong?
3. What is the drugs mechanism of action?
4. Which antiarrhythmic drug should be given to the patient to avoid such event?
5. What is the drugs mechanism of action?
6. List some of the important adverse effects of some important drugs from each
class of antiarrhythmic drug.
SELF ASSESSMENT
57

1. The following adverse effects are associated with amiodarone:
a. Visual disturbances
b. Hyperthyroidism
c. Hypothyroidism
d. Pulmonary fibrosis
e. Photosensitivity
2. Sotalol:
a. Is effective in supraventricular and ventricular arrhythmias
b. Is not effective when given by mounth
c. The dose should be reduced in renal impairment
d. May cause torsades de pointes
e. Is a less potent negative inotropes tha amiodarone
3. Lidocaine
a. Is a class Ib agent that block cardiac Na+ channels, reducing the rate of
rise of the cardiac action potential and increasing the effective refractory
period
b. Is epileptogenic
c. Is a positive inotrope
d. Is usually administered as an intravenous bolus followed by infusion
e. Is the drug of first choice for supraventricular tachycardia
4. Digoxin:
a. Reduces the ventricular rate in atrial fibrilation
b. Is contraindicated in second degree heart block
c. Has narrow theraupetic index
d. Induced arrhytmias may be terminated by magnesium
e. 80% of adminestered digoxin is excreted unchanged in the bile
Day 20
MODULE 20
Dr. Susila Surya Darma, SpJP
AIMS:
Describe to diagnose and manage Hypertension and Vascular disease
LEARNING OUTCOME:
1. Can describe to diagnose and manage the Hypertension
2. Can describe diagnose and manage the Vascular disease
CURRICULUM CONTENS:
1.
2.
3.
4.
Etiology and pathophysiology of Hypertension and Vascular disease

Clinical criteria of Hypertension and Vascular disease
Diagnostic approach of Hypertension and Vascular disease
Management and prognosis of Hypertension and Vascular diseases
58

ABSTRACT I :
Hypertension is one of the most common worldwide diseases afflicting humans
and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic
kidney disease. Despite extensive research over the past several decades, the etiology of
most cases of adult hypertension is still unknown, and control of blood pressure is
suboptimal in the general population. Approximately 75 million adults in the United States
are affected by hypertension. Hypertension is the most important modifiable risk factor for
coronary heart disease (the leading cause of death in North America), stroke (the third
leading cause), congestive heart failure, end-stage renal disease, and peripheral vascular
disease.
Defining abnormally high blood pressure (BP) is extremely difficult and arbitrary.
Furthermore, the relationship between systemic arterial pressure and morbidity appears to
be quantitative rather than qualitative. A level for high BP must be agreed upon in clinical
practice for screening patients with hypertension and for instituting diagnostic evaluation
and initiating therapy. Because the risk to an individual patient may correlate with the
severity of hypertension, a classification system is essential for making decisions about
aggressiveness of treatment or therapeutic interventions.
Based on recommendations of the JNC 7, the classification of BP (expressed in mm Hg)
for adults aged 18 years or older is as follows[3] :
Normal: systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg
Prehypertension: systolic 120-139 mm Hg, diastolic 80-89 mm Hg
Stage 1: systolic 140-159 mm Hg, diastolic 90-99 mm Hg
Stage 2: systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater
Cardiovascular morbidity and mortality rises proportionately with increases in
systolic blood pressure. In 95% of cases, the etiology of hypertension is idiopathic or
essential hypertension. Secondary hypertension (~ 5% of cases) should be identified and
treated. Hypertension is an asymptomatic condition unless associated with hypertensive
crises, and is often an incidental finding on routine examination.
Patients with hypertension should undergo initial basic screening for the secondary
causes of hypertension, and should be assessed for evidence of end-organ damage. All
patients should have urinalysis, serum biochemistry (electrolytes, glucose, urea and
creatinin concentrations and thyroid function tests) and ECG (electrocardiogram) (for
looking signs of left ventricular hypertrophy or ischaemic heart disease).
Treatment of hypertension is associated with primary and secondary preventive
benefits. Selection of anti hypertensive drugs is dependent upon patient choice, side
effects, risk factors profile and co-morbidity.
York: Lange Mecical Book`s/The McGraw-Hill Companies, 2008.p.370-397.
2. Chobanian A. et al. Seventh Report Of The Joint National Committee On
Prevention, Detection, Evaluation, And Treatment Of High Blood Pressure.
Hypertension. 2003;42:12061252

1.
2.
3.
4.
Etiology of Hypertension and Vascular disease

Pathophysiology of Hypertension and Vascular disease
Clinical criteria of Hypertension and Vascular disease
Diagnostic approach of Hypertension and Vascular disease
59

5. Management and prognosis of Hypertension and Vascular diseases
SCENARIO
CASE:
A 65-year old female, came to Emergency Room due to weakness of the left side of the
body, accompanied by confusion and slurred speech since 6 hours PTA when she was
wake up in the morning. She had history of high blood pressure since 5 years PTA and not
took the medicine regularly. The blood pressure at presentation was 230/140 mmHg,
pulse rate 98 beats per minute, regular. The ECG revealed sinus rhythm 98 bpm with LV
High Voltage and LV strain.
LEARNING TASK :
1. What is the diagnosis of the patient?
2. How will you manage the blood pressure of this patient?
3. What is the treatment of choice for this patient?
SELF-ASSESSMENT :
1. What are the complications of hypertension?
2. Please explain the pathogenesis of peripheral arterial disease
3. What are the side effects of hydro-chlorothiazide?
4. Please mention 3 examples of secondary hypertension
Day 21
MODULE 21
Dr. Made Junior Rina Artha, Sp JP
AIMS:
Describe to diagnose and manage Heart Failure
LEARNING OUTCOME:
1. Can describe to diagnose the Heart Failure
2. Can describe manage the Heart Failure
CURRICULUM CONTENS:
1.
2.
3.
4.
Etiology and pathophysiology of Heart Failure

Clinical and diagnostic approach of Heart Failure
Pharmacologic treatment of Heart Failure
Rehabilitation and prognosis of Heart Failure
ABSTRACT I :
Heart failure (HF) is a complex clinical syndrome resulting from structural and functional
impairment of ventricular filling or ejection of blood. Although the clinical syndrome of HF
may arise as consequence of abnormalities or disorder involving all aspects of cardiac
structure and function, most patients have impairment of myocardial performance, with
findings ranging from normal ventricular size and function to marked dilatation and
reduced function.
60

Heart failure is defined, clinically, as a syndrome in which patients have typical
symptoms (breathlessness, ankle swelling, and fatigue) and sign (elevated jugular venous
pressure, pulmonary crackles and displaced apex beat) resulting from abnormality of
cardiac structure and function. Its about 1-2% of the adult population in developed country
has HF, with the prevalence rising to more than 10% among persons 70 years of age or
older. Coronary artery disease (CAD) is the cause of approximately two-third of cases of
systolic HF, although hypertension and diabetes are probable contributing factors in many
cases. There are many other causes of systolic HF, which include previous viral infection
(recognized or unrecognized), alcohol abuse, chemotherapy and idiopathic.
Approximately half of the patients with HF have normal left ventricular function,
that is, HF with preserved ejection fraction (HFpEF), and another half is HF with reduced
ejection fraction (HFrEF). HFpEF generally is defined as a left ventricular ejection fraction
of 50% or grated, whereas HFrEF is defined as an ejection fraction below 40%. These
distinction are crucial because treatment strategies for treating HF is different between
these two entity.
The diagnosis of HF can be difficult, especially in the early stages. Although
symptoms bring patients to medical attention, many of the symptoms of HF are non
specific and do not, therefore, help discriminate between HF and other problems.
Symptoms that are more specific (orthopnea and paroxysmal nocturnal dyspnea) are less
common, especially in patiens with milder disease. Many of the signs of HF results from
sodium and water retention, and are, therefore, also no specific. Elevated jugular venous
pressure, displacement of the apical impuls, are more specific.
A patient who has never exhibited the typical signs or symptoms of HF is described
as having asymptomatic LV systolic dysfunction (or whatever the underlying cardiac
abnormality is). Patients who have had HF for some time are often said to have chronic
HF. A treated patient with symptoms and signs, which have remained generally
unchanged for at least a month, is said to be stable. If chronic stable HF deteriorates, the
patient may be described as decompensated and this may happen suddenly, i.e.
acutely, usually leading to hospital admission, an event of considerable prognostic
importance. New (de novo) HF may present acutely, for example as a consequence of
acute myocardial infarction or in a subacute (gradual) fashion, for example in a patient
who has had asymptomatic cardiac dysfunction, often for an indeterminate period, and
may persist or resolve (patients may become compensated).
When HF is suspected, the goal of the clinical assessments are to determine
whether HF is present, define the underlying cause, assess severity of the disease and
the patients prognosis and identify comorbid condition. When the diagnosis of HF has
already been established, the goal are similar, with a particular focus on optimal
therapeutic intervention. The goals of treatment in patients with established HF are to
relieve symptoms and signs (e.g. oedema), prevent hospital admission, and improve
survival. The relief of symptoms, improvement in quality of life, and increase
in functional capacity are also of the utmost importance to patients. Effective
pharmacological therapies and CRT improve these outcomes, as well as mortality and
hospitalization. Three neurohumoral antagonistsan ACE inhibitor [or angiotensin
receptor blocker (ARB)], a beta-blocker, and an MRAare fundamentally important in
modifying the course of systolic HF and should at least be considered in every patient.
They are commonly used in conjunction with a diuretic given to relieve the symptoms and
signs of congestion.
1.Mann, DL et all. Braunwalds Heart Disease, 10 th ed. Philadelphia, Elsevier Saunders,
2015. p. 429-615
2.McMurray et al. ESC Guidelines For The Diagnosis and Treatment of Acute and Chronic
Heart Failure. European Heart Journal. 2012;33.1787-1847
61

1.
2.
3.
4.
5.
Etiology of Heart Failure

Pathophysiology of Heart Failure
Clinical and diagnostic approach of Heart Failure
Pharmacologic treatment of Heart Failure
Rehabilitation and prognosis of Heart Failure
SCENARIO :
CASE:
A 28-year old female, came to Emergency Room due to shortness of breath since 1 week
PTA, and getting worse since 1 day PTA. The shortness of breath was aggravated by
supine position and alleviated by sitting position. She had history of taking Benzathine
Penicillin intramuscular every month for 2 years due to Rheumatic Heart Disease. The
blood pressure at presentation was 100/70 mmHg, pulse rate 130 beats per minute,
irregular. The physical examination revealed irregular heartbeat, diastolic rumbling
murmur at apex, rales on both lung fields. The ECG revealed atrial fibrillation 130 bpm
with Right axis deviation and right ventricular hyperthropy.
LEARNING TASK :
1. What is the most likely diagnosis of the patient?
2. What is the treatment of choice for this patient?
3. What is the parameters that you should monitor for evaluating the response to
therapy in this patient?
SELF ASSESSMENT:
1. Please describe the Framingham score of heart failure!
2. What are the treatment of chronic heart failure?
3. In heart failure, the heart usually increase doe to hypertrophy and dilatation.
Explain about morphology of concentric and eccentric hypertrophy!
4. Please describe the classification of primary cardiomyopathy
5. A 50 year old man complain from fatigue, short of breath, left chest pain when
walking. This patient is heavy smoker, obesity, and suffering from DM since 10
years ago. The patient is diagnosed myocard infarct (MI)
Check whether the following statement is true or false:
1. The above patient is high risk for exercise therapy
2. Exercise program is starter is after the chest pain is lost or after 2-3 days
3. Rehabilitation has tha aim to recover self confidence, prevent long immobilitation
complication and correct risk factor
4. Exercise can also lost weight and reduce smoking habit
5. After discharge the patient may not do sexual intercourse
6. At thorax surgery case exercise is better to be given after operation
Day 22
MODULE 22
62

AIMS:
1. Describe the anti hypertensive drugs
2. Describe the heart failure drugs
LEARNING OUTCOME:
1. Can describe the anti hypertensive drugs
2. Can describe the heart failure drugs
CURRICULUM CONTENS:
1.
2.
3.
4.
5.
6.
7.
8.
Principles and classification of anti hypertensive drugs

Important pharmacokinetic properties of anti hypertensive drugs.
Mechanism of actions of anti anti hypertensive drugs.
Important adverse effects of anti hypertensive drugs
Principles and classification of heart failure drugs
Important pharmacokinetic properties of heart failure drugs.
Mechanism of actions of heart failure drugs.
Important adverse effects of heart failure drugs
ABSTRACT I :
ANTI HYPERTENSIVE DRUGS
Hypertension is important because elevated blood pressure (BP) confers a greater
risk of stroke, heart failure, coronary artery disease (including angina, myocard infarction,
and sudden death), renal disease and peripheral vascular disease. There is a continuous,
direct relationship between elevation in blood pressure and increases the risk. JNC 7,
2003 classification of blood pressure in adults is as follows: normal, prehypertension,
stage I hypertension and stage 2 hypertension.
In general, the higher the blood pressure and the greater the number of risk
factors, indicate higher urgency and stringency in treating hypertension. Lowering blood
pressure is just one way to prevent complications; attention must also be paid to the
presence and reversal of other cardiovascular risk factors such as cigarette smoking,
hyperlipidemia and especially in diabetes mellitus.
Drugs used in lowering blood pressure will decrease peripheral vascular resistance
or/and decrease cardiac output. These can be due to either directly decrease arteriolar
smooth muscle tone (which decrease peripheral resistance), decrease myocardial
contractility, heart rate, venous tone, blood volume (which decrease cardiac output) or
indirectly through inhibition of sympathetic nervous system activity or inhibition of reninangiotensin-aldosteron system. They can be used alone or combination to return the
blood pressure to target levels with minimal side effects.
ABSTRACT II:
Heart failure occurs when the heart is unable to pump blood at a rate sufficient to
meet the metabolic requirements of the tissues. Heart failure is frequently, but not always,
caused by a defect in myocardial contraction that may result from a primary abnormality
in heart muscle, as occurs in the cardiomyopathies or in viral myocarditis. Heart failure
also result from coronary atherosclerosis, which interferes with cardiac contraction by
causing myocardial infarction. Heart failure may also occur in congenital, valvular and
63

hypertensive heart disease in which myocardium is damaged by the long standing
hemodynamic overload.
Drugs used in heart failure include diuretics, vasodilators, nitrate, angiotensin
antagonist, beta blockers and positive inotropes. Positive inotropes increase the
myocardial contractility. They improves the symptoms of heart failure but at the cost of
increasing mortality. They induce arrhythmias, increase myocardial oxygen consumption
and reduced myocardial perfusion (reduction blood flow). They are several classes of
positive inotropes such as beta1 agonis (e.g. dopamine, dobutamine), phosphodiesterase
inhibitors (eg amrinone, milrinone), and digitalis (e.g. digoxin). Beta 1 agonists and
phosphodiesterase inhibitors are not used in chronic heart failure.
New York, McGraw-Hill/Lange., 2005. p 66-93, 95-104 and p. 114-123.
1. Principles of anti hypertensive therapy.
2. Classification of anti hypertensive drugs
3. Important pharmacokinetic properties of anti hypertensive drugs.
4. Mechanism of actions of anti anti hypertensive drugs.
5. Important adverse effects of anti hypertensive drugs
6. Principles of heart failure therapy.
7. Classification of heart failure drugs
8. Important pharmacokinetic properties of heart failure drugs.
9. Mechanism of actions of heart failure drugs.
10. Important adverse effects of heart failure drugs.
CASE 1:
A 60-year-old man was brought to your private practice, and said that he was suffering
from headache since 2 days before. He had gone to many doctors. He brought his ECG,
urine and blood examination results which were appeared normal. He took with him
antihypertensive drugs captopril and hydrochlorthiazide, but they were not taken for the
last 6 days because he had no headache. Aside from his BP 170/95, results of physical
examination appeared normal.
LEARNING TASK I:
1. Compare the mechanism of action of antihypertensive drugs.
2. Describe the compensatory responses, if any, to each types of antihypertensive
drugs
3. List the major sites of action of sympathoplegic drugs and give examples of drugs
that act on each site
4. List the 4 mechanism of action of vasodilator drugs and describe their effects
5. Describe the difference between 2 types of angiotensin antagonists
6. List the major side effects of the prototype antihypertensive drugs
7. Compare the indication and contraindication of antihypertensive drugs
8. Explain the interaction between angiotensin antagonist with potassium sparing
diuretics
CASE 2 :
A 45-year-old woman was admitted to the hospital with shortness of breath when he
walked about 2 meters, for about 6 months on and off , but became worst since 2 days
64

ago. She also suffered from ankle swelling and fatigue. Her symptoms were improved
when she took the prescribed drugs. She had a history of high blood pressure. On
admission her blood pressure was 130/80, heart rate 100/min, regular, raised jugular
venous pressure, dilatation of the heart to the right and left, hepatomegaly, ankle edema,
basal lung rales on the right and left, no murmur. She was diagnosed chronic heart failure.
Digoxin, captopril and furosemide was given to her.
LEARNING TASK II :
1.
2.
3.
4.
Compare the mechanism of action and clinical uses of positive inotropes..

Describe toxic action of digitalis on the heart
Describe the effect of electrolyte imbalance on digitalis effect
Describe the interaction between digitalis and diuretic and quinidine
Explain either the statement is True or False

1. Severe bradycardia may occur after clonidine overdose
2. Captopril decreases sodium and increases potassium in the urine
3. Hemolytic anemia caused by antihypertensive drug clonidine
4. Postural hypotension is a common adverse effect of alfa blocker
5. Losartan most likely causes cough
6. Nitroprusside must be given by intravenous infusion
7. Minoxidil causes vasodilatation by opening potassium channels
Day 23 23
MODULE
dr. Bagus Ari Pradnyana Dwi Sutanegara, SpJP
AIMS:
Describe to diagnose and manage Cor Pulmonale (Pulmonary Heart Disease).
LEARNING OUTCOME:
1. Can describe to diagnose and manage Acute Cor Pulmonale.
2. Can describe to diagnose and manage Chronic Cor Pulmonale.
CURRICULUM CONTENS:
1.
2.
3.
4.
5.
6.
Etiology of Acute and Chronic Cor Pulmonale.

Pathogenesis of Pulmonary Hypertension.
Clinical Manifestation of Cor Pulmonale.
Physical Findings of Cor Pulmonale.
Diagnostic techniques for Cor Pulmonale.
Prevention and Treatment of Cor Pulmonale.
ABSTRACT:
Cor pulmonale is a common complication of pulmonary hypertension. Cor pulmonale
refers to altered structure (eg, hypertrophy or dilatation) and/or impaired function of the
right ventricle that results from pulmonary hypertension that is associated with diseases of
the lung (eg, chronic obstructive pulmonary disease), vasculature (eg, idiopathic lumonary
arterial hypertension), upper airway (eg, obstructive sleep apnea), or chest wall (eg,
kyphoscoliosis). Right sided heart disease due to left sided heart disease is not
65

considered cor pulmonale. Pulmonary hypertension (PH) is defined as PA Pressure > .20
mmHg and is placed in the heterogeneous group of PH associated with disorders of the
respiratory system and/or hypoxaemia. The reason for setting such a threshold is that in
healthy subjects PA Pressure is always < 20 mmHg at rest and, as stated above, a PA
Pressure >20 mmHg is associated with increased morbidity and mortality. However, in
some recent studies PH was defined by PA Pressure > 25 mmHg.
Cor pulmonale tends to be chronic and slowly progressive, but it can be acute.
Acute cor pulmonale occurs when the right ventricle cannot adapt to an increase in the
pulmonary arterial pressure. The increased pulmonary artery pressure may be
consequence of a new acute process, such as pulmonary embolism, or progression of the
chronic disease. The diagnostic evaluation of cor pulmonale is inseparable from the
evaluation for pulmonary hypertension. Cor pulmonale could be diagnosed based on the
clinical manifestation and using chest x-ray, electrocardiography, and echocardiography as
well as magnetic resonance imaging, pulmonary function testing, and right heart
catheterization. Symptoms attributable to cor pulmonale include dyspnea on exertion,
fatigue, lethargy, exertional syncope, and exertional angina. Patients with cor pulmonale
have physical findings related to both pulmonary hypertension and righ-sided heart
disease.
All patients with cor pulmonale should have the underlying cause of the cor
pulmonale and pulmonary hypertension treated. The treatment of cor pulmonale can be
conceptualized as having three major physiological gols: reduction of right ventricular
afterload (eg, pulmonary artery pressure), decrease of right ventricular pressure, and
improvement of right ventricular contractility. In the cor pulmonale condition that leads into
heart failure, diuretics and nitrates may be needed to improve the condition of the patient.
Oxygen supplementation is often required to resolve the shortness of breath. Treatments
of PAH have shown a dramatic change in the past few years. Synthetic prostacyclin
(epoprostenol), prostacyclin analogues, endothelin-1 receptor antagonists and
phosphodiesterase-5 inhibitors were tested in randomised controlled trials, leading to the
approval of several drugs in each class.
1.
2.
3.
4.
5.
6.
Etiology of Acute and Chronic Cor Pulmonale.

Pathogenesis of Pulmonary Hypertension.
Clinical Manifestation of Cor Pulmonale.
Physical Findings of Cor Pulmonale.
Diagnostic techniques for Cor Pulmonale.
Prevention and Treatment of Cor Pulmonale.
SCENARIO:
CASE:
A 70-year old male, came to Emergency Room due to swelling on abdomen and both
legs. The complaints were suffered since 1 month ago and become worsen. He also
complains of shortness of breath and cough, that was experienced since years and
usually could be resolved by nebulizer. He used to be a heavy smoker for 30 years, with
1-2 packs cigarette per day. The blood pressure was 120/80 mmHg; pulse rate was 110
beats per-minute, regular. There were wheezing at both lung field, ascites on abdomen,
and pitting edema on both legs, and increased of jugular venous pressure. ECG revealed
sinus tachycardia 110 beats per-minute with P pulmonale on lead II, III and aVF. The
urinary production is good.
66

LEARNING TASK :
1. What is the most likely diagnosis?
2. What the next procedure do you plan?
3. What is your initial treatment?
SELF-ASSESSMENT :
1. Please explain the risk factors of cor pulmonale.
2. What are the complications of pulmonary hypertension?
3. What is the treatment of choice in acute and chronic cor pulmonale?
Day 24
MODULE 24
dr. Luh Kamiati, SpRM
AIMS:
1.
2.
3.
4.
Able to diagnose and manage Valvular Heart Disease (VHD)

Describe to diagnose and manage Common Peripherial Vascular Disease
Describe diagnose and manage Pericardial disease and Endocardial disease
Decsribe to rehabilitation patient with Cardiovascular Disease
LEARNING OUTCOME:
1. Can describe to diagnose Valvular Heart Disease (VHD)
2. Can describe the manage Valvular Heart Disease (VHD)
3. Can describe to diagnose and manage the Common Peripherial Vascular
Disease
4. Can describe diagnose and manage Pericardial Disease and Endocardial
Disease
5. Can describe to rehabilitation patient with Cardiovascular Disease
CURRICULUM CONTENS:
1.
2.
3.
4.
5.
6.
7.
8.
9.
Etiology, pathophysiology and clinical spectrum of Valvular Heart Disease

Interpret diagnostic tools of Valvular Heart Disease
Management and prognosis and rehabilitation of Valvular Heart Disease
Etiology and pathophysiology of Common Peripherial Vascular Disease
Clinical diagnostic approach, Pharmacologic treatment of Common Peripherial
Vascular Disease
Etiology and pathophysiology of Pericardial and Endocardial disease
Clinical and diagnostic approach of Pericardial and Endocardial diseases
Pharmacologic treatment and Prognosis of Pericardial and Endocardial disease
Rehabilitation and prognosis patient with Cardiovascular Disease
ABSTRACT I:
67

Valvular heart disease is characterized by damage to or a defect in one of the four heart
valves: the mitral, aortic, tricuspid or pulmonary. The mitral and tricuspid valves control the
flow of blood between the atria and the ventricles (the upper and lower chambers of the
heart). The pulmonary valve controls the flow of blood from the heart to the lungs, and the
aortic valve governs blood flow between the heart and the aorta, and thereby the blood
vessels to the rest of the body. The mitral and aortic valves are the ones most frequently
affected by valvular heart disease. Normally functioning valves ensure that blood flows
with proper force in the proper direction at the proper time.
In valvular heart disease, the valves become too narrow and hardened (stenotic) to
open fully, or are unable to close completely (incompetent). A stenotic valve forces blood
to back up in the adjacent heart chamber, while an incompetent valve allows blood to leak
back into the chamber it previously exited. To compensate for poor pumping action, the
heart muscle enlarges and thickens, thereby losing elasticity and efficiency. In addition, in
some cases, blood pooling in the chambers of the heart has a greater tendency to clot,
increasing the risk of stroke or pulmonary embolism. The severity of valvular heart disease
varies. In mild cases there may be no symptoms, while in advanced cases, valvular heart
disease may lead to congestive heart failure and other complications. Valvular heart
disease accounts for 10% to 20% of all cardiac surgical procedure.
The primary causes of valve disease are age-associated calcific valve changes
and inherited or congenital conditions. The prevalence of rheumatic valve disease now is
very low in the United States and Europe because of primary prevention of rheumatic
fever, although rheumatic valve disease remains prevalent in the developing world. In
addition to patients with severe valve disease that eventually requires mechanical
intervention, there is a larger group of patients with mild to moderate disease who need
accurate diagnosis and appropriate medical management.
In developed countries,
valvular heart disease is the most common reason for patients to undergo valve
replacement. But in developing countries, this procedure is rarely performed due to
financial reason. The most prevalent valvular heart disease is the following: 1) mitral valve
disease, 2) aortic valve disease, and 3) tricuspid and pulmonary valve disease.
Most valvular abnormalities can be managed with medical therapy or
percutaneous intervention. One of the management of valvular heart disease is surgical
intervention. Valvular surgery is indicated in patients with limiting symptoms despite
optimal medical therapy, or in those with objective evidence of progressive cardiovascular
deterioration. There are three main surgical approaches to valve disease: a) valvotomy, b)
valve repair, and c) valve replacement
Saunders, 2015.
ABSTRACT II:
Pericardium is composed of two layers, the visceral pericaradium, a monolayer of
mesothelial cells and collagenand elastin fibers that is adherent to the epicardial surface
of the heart and the fibrous parietal layer, which is approximately 2mm thick in normal
humans and surrounds most of the heart. The pericardial space or sac is contained within
these two layers and normally has up to 50ml of serous fluid. Pericardium serves as
barrier to infection, as well as lubrication between the visceral and parietal layers. The
best characterized mechanical function of the pericardium is its restraining effect on
cardiac volume.
The spectrum of pericardial diseas comprises congenital defects, pericarditis (dry,
effusive, effusive-constrictive, constrictive), neoplasm, and cysts. Congenital defect of the
pericardium occure 1 in 10.000 autopsies. It comprises partial left (70%), right (17%) or
total bilateral (extremely rare) pericardial absence. The diagnosis is confirmed by
echocardiography and CT/MRI. Acute pericarditis is either dry, fibrinous or effusive,
independent from its aetiology. A prodrome of fever, malaise, and myalgia is common, but
68

elderly patients may not be febrile. Major symptoms are retrosternal or left precordial
chest pain (radiates to the trapezius ridge, can be pleuritic or stimulate ischemia, and
varies with posture), non-productive cough, and shortness of breath. Pericardial friction
rub and pleural effusion may be present. Diagnosis can be made by history taking,
physical examination, laboratory and imaging. Management include hospitalization, finding
the etiology, observe for tamponade and start anti-inflammatory and symptomatic
treatment.
Endocardium is innermost layer of the heart. Its atrial component is thicker than
ventricular, where purkinje fibers are distributed throughout the ventricular
subendocardium. Primary endocardial diseases are not common, usually non
inflammatory in nature. Endocardial fibroelastosis is familial disease which involve
progressive edema of endocardium, fibroblast proliferation and increased amount of
collagen withing endocardium lead to restrictive cardiomyopathy and interfere cardiac
output.
Secondary cause of endocardial disease usually from infection. Infective
endocarditis (IE) incidence range from 3-10 episodes/100.000 person-years, male to
female ratio is >2:1. Neither the incidence nor the mortality of the disease have decreased
in the past 30 years, this disease still carries poor prognosis and high mortality. IE should
be suspected in some clinical situations, such as fever, new heart murmur, anemia and
embolic events. Up to 90 patient with fever, often associated with systemic symptoms of
chills, poor appetite and weight loss. Transthoracic echocardiography must be performed
rapidly as soos as IE is suspected. Diagnosis of IE based on modified Duke criteria that
composed with mayor and minor criteria. Treatment include supportive therapy based on
sign and symptoms and combination with antibiotic which can be start soon despite
waiting for blood culture result.
Saunders, 2015. p. 1391-1550
2. Habib, Gilbert et al. Guidelines on The Prevention, Diagnosis, and Treatment of
Infective Endocarditis. European Heart Journal. 2009;30.2369-2413
3. Maisch, Bernhard et al. Guidelines on The Diagnosis and Management of
Pericardial Disease. European Heart Journal. 2004; 1-28
Additional reading:
1.Constant, Jules. Essential of Bedside Cardiology, 2nd ed. New Jersey, Humana
Press Inc. 2003
ABSTRACT III:
Cardiac rehabilitation is multidisciplinary program of education and exercise
established to assist individual with heart disease in achieving optimal physical,
psychological and functional status within thw limits of the diseased.
The basic goal of cardiac rehabitation are to restore and improve cardiac function,
reduce disability, identify and cardiac risk factors, increased cardiac conditioning. Cardiac
rehabilitation programs consist primary prevention (education, behavior modification),
secondary prevention, and exercise program.
Cardiac rehabilitation outcomes that can be expected decreased length of hospital stay,
more ripid, more complete resumption of ususal activities, self confident, less
pshychological distress, and fewer readmissions.
York: Lange Mecical Book`s/The McGraw-Hill Companies, 2008.p. 287-299, 351358; 398-416, 360-363; 1241-1246
69

2. Garrison SJ: Hand Book of Physical Medicine and Rehabilitation, 2nd ed, 2003, p.
86
3. Bartels MN: Cardiac Rehabilitation in Grant Cooper: Essential Physical Medicine
and Rehabilitation, 2006, p. 119.
1.
2.
3.
4.
5.
6.
7.
8.
9.
Etiology, pathophysiology and clinical spectrum of Valvular Heart Disease

Interpret diagnostic tools of Valvular Heart Disease
Management and prognosis and rehabilitation of Valvular Heart Disease
Etiology and pathophysiology of Common Peripherial Vascular Disease
Clinical diagnostic approach, Pharmacologic treatment of Common Peripherial
Vascular Disease
Etiology and pathophysiology of Pericardial and Endocardial disease
Clinical and diagnostic approach of Pericardial and Endocardial diseases
Pharmacologic treatment and Prognosis of Pericardial and Endocardial disease
Rehabilitation and prognosis patient with Cardiovascular Disease
SCENARIO:
CASE I:
Using your stethoscope, you would hear single S1 and single S2, and early diastolic
murmur of grade 3/6 at the right 2 ndintercostal-space, radiating to the apical area. Neither
S3 nor S4 noted.
LEARNING TASK:
1. What kind of valvular heart disease is represented by this auscultation findings?
2. Please explain the ECG pattern usually found in this kind of disease
3. Please describe the radiological findings consistent with this disease.
4. Mention definition of cardiovascular rehabilitation
5. Explain the objective of cardiovascular rehabilitation
6. Mention the contraindication exercise therapy
7. Explain the benefit effect of exercise therapy
8. Explain stages of cardiovascular rehabilitation MI
9. Mention effect of exercise to CHF
CASE 2:
A 23-year old gentleman visited the hospital due to chest pain. The chest pain was sharp
in nature. The pain scale was 7 of 10, it was becoming severe when he took a deep
breath and radiating to the neck. He suffered from flu-like syndromes since the last 1
week.
LEARNING TASK:
1. What is the most likely diagnosis of this gentleman?
2. What is the treatment do you plan?
3. What is the common etiology of this situation?
SELF-ASSESSMENT
1. Please describe the etiology of mitral regrugitation
70

2. Please explain the complication of mitral stenosis
3. Please describe the ECG findings in aortic stenosis
4. What is the Austin-Flint murmur?
5. Please explain the indication of mitral valve replacement procedure?
6. What is the treatment of constrictive pericarditis?
7. What is the management of pericardial effusion?
8. What is the most accurate diagnostic tool of pericardial effusion?
9. Mention definition of cardiovascular rehabilitation
10. Explain the objective of cardiovascular rehabilitation
11. Mention the contraindication exercise therapy
12. Explain the benefit effect of exercise therapy
13. Explain stages of cardiovascular rehabilitation MI
14. Mention effect of exercise to CH
Day 25
MODULE 25
dr. I Nyoman Semadi, SpB, SpBTKV
SURGERY IN CARDIAC DISEASES
AIMS:
Describe the basic principles of surgery in cardiac diseases
LEARNING OUTCOME:
1. Can describe the basic principles of cardiac surgery
2. Can describe the basic aspect in cardiac surgery
3. Can describe the cardiac diseases who need surgery
CURRICULUM CONTENTS:
1. Surgery of the congenital heart
2. Surgery of the acquired heart diseases
ABSTRACT:
Atrial septal defects (ASD) and ventricular septal defect (VSD) and others are the
congenital cardiac anomaly. The intracardiac defects makes the shunt and blood flows
through the shunt from right-to-left or reverse of the heart.
Atrial septal defects (ASD) are most common in the vicinity of the fossa ovalis.
Septum secundum defects, the typical patent foramen ovale, account for 10-15% of all
cardiac anomalies. Normal left atrial pressure is slightly greater than right atrial pressure,
a left-to-right shunt occur through an open ASD, oxygenated blood from the left side of the
heart is shunted to the right side, thus not associated with cyanosis. An ASD is usually
compatible with normal life, except at an extreme exercise, cardiac disease, or pulmonary
disease alter chamber pressures, a right-to-left shunt will produce cyanosis.
Ventricular septal defect (VSD) is usually happened at the upper membranous
portion that composed of connective tissue continuous with the annulus fibrosus. A small
VSD may result in an inconsequential left-to-right shunt.
71

In the presence of pulmonary stenosis, a VSD produces a right-to-left shunt with
cyanosis and the blue-baby syndrome. A large VSD is a principal factor in Tetralogy of
Fallot.
Patent ductus arteriosus (PDA) is a persistence of the fetal connection (ductus
arteriosus) between the aorta and pulmonary artery after birth, resulting in a left-to-right
shunt. Symptoms may include failure to thrive, poor feeding, tachycardia and tachypneu
due to lung infection.
Others cardiac diseases are more common as a coronary arterial diseases (CAD),
Acquierd Valve diaseses of rheumatic heart disease and congenital valve anomaly
1. Stuart W. Jamieson and Norman E Shumway: Cardiac Surgery in Rob & Smiths
Operative Surgery, 4th edition. Butterworths London, 2004
1. Cardiac surgery in principles
TREATMENT FOR AORTA AND ARTERIAL DISEASES

AIMS:
Describe the basic principles of surgery in aorta and arteries
LEARNING OUTCOME:
1. Can describe the basic principles of aorta and arteries
2. Can describe the basic aspect in aorta arteries
3. Can describe the aorta and arteries diseases who need surgery
CURRICULUM CONTENTS:
1. Surgery of the aneurysm of aorta
2. Surgery of the peripheral artery diseases
ABSTRACT:
Atherosclerosis is the usual cause of vascular diseases. The aneurysm of aorta is
dilated of aorta lumen over one and half size of normal lumen of aorta. The aorta can
enlargement, elongated and tortous with or without thrombus in the lumen of aorta. It can
be found on thoracic region or abdominal region or both. The patient got pain of the chest
or abdominal pain depend the aneurysm posotion. If you found the abdominal aortic
aneurysm (triple A), the large pulsatil tumor was found on central topographic of abdomen.
The patient become dengerous if aortic aneurysm ruptured and the patient getting
haemorhagic shock.
Atherosclerosis can cause the peripheral artery diseases. The artery become
aneurysm, stenosis and occluded. If the artery got occlusion on midle size of that, the
distal part of organ will ischemic and become death of the tissue that call ganggrene.
1. Allan D. Callow, Calvin B. Erust. : Vascular surgery, Theory and Practice,
Prentice- Hall International Inc.London , 1995
72

1. Vascular surgery in principles
SCENARIO:
CASE 1;
This baby aged 4 months has been known to have a cardiac murmur since birth. He was
born 8 weeks prematurely and developed respiratory distress requiring high oxygen
concentration for the first week. Since then he has feed satisfactorily but height and weight
growth have been poor even allowing for prematurity.
The diagnosis after examination and investigations: Patent Ductus Arteriosus (PDA).
LEARNING TASK I
1. How to prepare if the patient have surgery
2. What is cardic surgery category for PDA closure
3. PDA commonly concomittent with congenital anomaly. Is it every PDA have
surgery to close the shunt
4. After an operation to close the PDA, why is there a risk of the patient becoming
hoarse?
CASE 2 :
This 13 year old girl was recently found to have a cardiac murmur. She has been generally
healthy with good growth, but on questioning her mother admitted she has noticed that girl
tends to tire easily with exercise.
The diagnosis after examination and investigations: Atrial Septal Defect (A.S.D.)
LEARNING TASK II:
1. What is cardic surgery category for ASD closure
2. What the different between close and open cardiac surgery
3. After ASD was closured, why the patient getting good growing of the body
4. And why is the patient after ASD closure getting arrythmia
CASE 3 :
A 2 year old boy was admitted to the hospital for evaluation of a heart murmur previously
detect at birth. He was less active than other children his age, but although over-exertion
was followed frequently by cyanosis of the lips and nails, there was no history of
unconsciousness. Initial examination revealed a thin, physically retarded, cyanotic child
with no respiratory difficulty. There was moderate clubbing of the fingers. A harsh systolic
murmur was maximal over the mid-precardial area. The first heart sound was normal while
the second was single, distinct and loud.The lungs were clear. X-ray showed a normal
sized heart dominated by a boot-shaped right ventricular outflow tract.
Diagnosis of Tetralogy of Fallot.
LEARNING TASK III:
1. The cardiac anomaly are PS, VSD, Overriding aorta and RVH. How do repair it
2. Why the patient becoming worse after the surgery repair of the defect
SELF-ASSESSMENT :
1. Describe the principle cardiac surgery
2. Describe the principle coronary heart surgery
3. Describe the principle of Valve surgery
SCENARIO:
73

CASE 1;
Old man, he was pain on abdomen and the tumor was found on abdomen palpation. The
tumor was pulsatil and 7 cm in diameter and fixed. The blood pressure of the patient got
high. The diagnose of the disease is triple A with stable hemodinamically
LEARNING TASK I:
1. How to diagnose the patient
2. How to prepare if the patient have surgery
3. How to do to enlargement of aorta
4. Any complication to surgery of aorta
CASE 2 :
This 43 year old man was recently found to have cold of feet. He has been generally
healthy with pain on both leg if he walking for while, he was heavy smoking from teeneger.
The diagnosis after phisical examination that conclude: peripheral artery diseases of both
popliteal artery
LEARNING TASK II:
1. What will you do to investigate the patient for difinitive diagnosis
2. What will you do to improve the blood flow to the distal end of feet
3. How the prognosis and reccurent rate
SELF-ASSESSMENT :
1. Describe the principle of vascular surgery
2. Describe the principle arterial repair
3. Describe the principle of care after vascular surgery
8. REFERENCES
A. Student Standard References :
1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia,
Lippincott & Wilkins, 2007.
2. Sadler TW: Langmans Medical Embryology, 10th ed. Philadelphia, Lippincott &
Wilkins, 2006.
74

3. Gartner LP, Hiatte JL: Color Textbook of Histology, 2nd ed. Philadelphia, WB
Saunders Company, 2001.
4. Guyton AC: Textbook of Physiology, 11st ed. Philadelphia, WB.Saunders
Company, 2006
5. Fox S.I.: Human Physiology, 9th ed. New York, McGraw-Hill, 2006
6. Kumar V, Cotran R S, Robbins SL: Robbins Basic Pathology, 7th ed.
Philadelphia, Saunders, 2003
7. Trevor AJ, Katzung BG, Masters: Katzung & Trevors Pharmacology, 7th ed.
New York, Lange Medical Books/Mc.Graw-Hill, 2005.
8. Park MK. Pediatric Cardiology for Practioners. 4 th Ed. Philadelphia, Mosby.
2002.
9. McPhee, S.J., Papadakis, M.A., Current Medical Diagnosis & Treatment. 47 th
ed. New York, Lange Mecical Book`s/The McGraw-Hill Companies, 2008.
10. Allan D. Callow, Calvin B. Erust. : Vascular surgery, Theory and Practice,
Prentice- Hall International Inc.London , 1995
Saunders, 2015. p. 1391-1550
12. Habib, Gilbert et al. Guidelines on The Prevention, Diagnosis, and Treatment of
Infective Endocarditis. European Heart Journal. 2009;30.2369-2413
13. Maisch, Bernhard et al. Guidelines on The Diagnosis and Management of
Pericardial Disease. European Heart Journal. 2004; 1-28
14. McPhee SJ, Papadakis MA. Current Medical Diagnosis & Treatment. 47 th ed.
New York: Lange Mecical Book`s/The McGraw-Hill Companies, 2008.p. 287299, 351-358; 398-416, 360-363; 1241-1246
15. Garrison SJ: Hand Book of Physical Medicine and Rehabilitation, 2 nd ed, 2003,
p. 86
16. Bartels MN: Cardiac Rehabilitation in Grant Cooper: Essential Physical
Medicine and Rehabilitation, 2006, p. 119.
17. Stuart W. Jamieson and Norman E Shumway: Cardiac Surgery in Rob &
Smiths Operative Surgery, 4th edition. Butterworths London, 2004
B. Additional Student References :
1. A2: Moore KL, Dalley AF: Clinically Oriented Anatomy, 4th ed. Philadelphia
Lippincott & Wilkins, 1999.
2. H2: Fowcett DW, Jensh RP: Bloom & Fawcetts Concise Histology, 2nd ed.
London, Arnold. 2002.
9. STANDART OF MEDICAL COMPETENCE
Expected level of competence:

1. Able to recognize and organized clinical features of disease. In case, it appeared
in literature or correspondence, he know how to organize these clinical features
and how to get further information. This level indicates an overview level. If these
clinical features found on patient, doctor able to recognize it, suspect the diagnosis
and reffered immediately
75

2. Able to make clinical diagnosis based on physical examination and additional
investigation requested by doctor e.g. routine laboratory assay or X-ray. Doctor
able to refer patient to relevant specialist immediately and capable to follow up
afterward.
3. A. Able to make clinical diagnosis based on physical examination and additional
able to decide and give initial treatment also refer to relevan specialist for nonemergency cases.
3. B. Able to make clinical diagnosis based on physical examination and additional
able to decide and give initial treatment also refer to relevan specialist for
emergency cases.
4. Able to make clinical diagnosis based on physical examination and additional
able to decide and manage the case independently.
10. EVALUATION FORM

Evaluation form of The Cardiovascular System and Disoders
Please fill the form according to the real condition. This evaluation will not influence your
final block result.
Please cross on the score column that suitable with your judgment
Score
No.
Point being evaluated
Topic
1.
General anatomy, topography and surface

anatomy of the heart and great vessels.
Microscopic structure of the heart

pericardial
The heart as a pump
Intrinsic Conduction System

Action
wall and
and Cardiac
Potential
6
Heart Valves and Heart Sounds
Microscopic Anatomy of The Valves of The
76
Heart
8
Cardiac Out Put and Regulation of Heart

Pumping
Factors that Affect Blood Pressure

Microscopic Anatomy of The Great Vessel
10
Microscopic Anatomy of The Great Vessel
11
12
Blood Pressure Regulation
13
The formation of anomalies of the heart and

great vessels.
14
Approach to Patient With

Disease
15
Non-cyanotic & Cyanotic CHD
16
Acute Rheumatic Fever
17
Ischemic Heart Disease = ACS
18
Pathologic aspect of IHD
19
Drug used in Angina Pectoris
20
Arrhytmias
21
22
Hypertension
23
Antihypertensive Drugs
24
Heart Failure
25
Positive Inotropes
26
Common Peripheral Vascular

disease
27
Cardiomyopathi
28
Valvular
Heart
Disease
Endocardial Disease
29
Measure Workload
30
CV Physical Examination
Cardiovascular
and lymphatic
Pericardial
&
77
31
ECG
32
Chest Imaging
33
IV line Procedure
Learning strategy
Lecture
Independent learning
Small group discussion
Practical
Case based learning
Problem based learning
Learning task
Self assessment
Lecturer
1.
DR. dr. Ketut Rina, Sp PD, Sp JP
2.
Dr. I G.N Mayun, PHK
3.
Dr. I Gusti Ayu Widianti, M.Biomed
4.
Dr. Made Muliarta, M.Kes
5.
Prof. dr. Dewa Sutjana, M
DR. Dr. Adiatmika, M.For
7.
Prof dr. I G M. Aman
DR. Wayan Sumardika
Dr. IGM Gd Surya Candra Trapika,MSc
10
Dr W. Winarti, SpPA
11
Dr. Eka Guna Wijaya, Sp A
12
Prof dr. Wita, SpJP
13
Dr. Susila Surya Darma
14
Dr. Bajra Nadha, SpJP
15
Dr. Junior Rina A, SpJP
16
Dr. Bagus Ari D, SpJP
17
Dr. Lisna Astuti,Sp.R
78
18
Dr. Luh Kamiati, SpRM
19
Dr. N. Semadi, SpB
Facilitator
Name of your group facilitator:
Assessment
Time provide
Suitability of question with topic given
Score:
1. Bad or not suitable with expectation
2. Insufficient or inadequate with expectation
3. Sufficient or inadequate with expectation
4. Good or suitable with expectation
5. Excellent or exceed expectation
Problem you found during Block Cardiovascular System and Disorders for each point
evaluated above:
Topic
Learning strategy
Lecturer
Facilitator
Assessment
Your suggestion/input:
Topic
79

Learning strategy
Lecturer
Facilitator
Assessment
11. ITEM GRID

Question type: MCQ with vignette
No
Topic
Number of
question
PIC
1.
Prof dr. Wita
General anatomy, topography and

surface anatomy of the heart and
great vessels.
Dr. IGA Widianti
Microscopic structure of the heart

wall and pericardial
Dr. IGN Mayun
The heart as a pump
Dr. Made Muliarta,
Intrinsic Conduction System and

Cardiac Action Potential
Dr. Made Muliarta,
Heart Valves and Heart Sounds
Prof. Dewa Sutjana
Microscopic Anatomy
Valves of The Heart
Dr. I G N Mayun
Cardiac Out Put and Regulation

of Heart Pumping
Prof. Dewa Sutjana
Factors that
Pressure
DR. Dr. Adiatmika,
10
Microscopic
Great Vessel
11
Dr. Made Muliarta
12
Blood Pressure Regulation
DR. Dr. Adiatmika,
13
The formation of anomalies of

the heart and great
Dr. IGA Widianti
of
Affect
The
Blood
Anatomy of The
Vignette
Dr. IGN Mayun
80
vessels.
14
Approach
to
Patient
Cardiovascular Disease
With
Prof Dr. dr. Wita,
15
Non-cyanotic & Cyanotic CHD &

Acute Rheumatic Fever
Dr. Eka Guna W
16
Acute and Chronic Cor-pulmonale
Dr Bagus Ari S
17
Ischemic Heart Disease = ACS
Dr. Ketut Rina
18
Pathologic aspect of IHD
Dr W. Winarti
19
Drug used in Angina Pectoris
Prof dr. IGM Aman
20
Valvular
Heart
Disease
&
Pericardial & Endocardial Disease
Dr. Bajra Nadha
21
Arrhytmias
Dr. Bajra Nadha
22
Dr. W. Sumardika
23
Hypertension
Dr. Susila Surya D
24
Antihypertensive Drugs
Dr. IGM Gd Surya

Candra Trapika,
25
Heart Failure
Dr. Junior Rina
26
Positive Inotropes
Prof dr. IGM Aman
27
Common Peripheral Vascular

disease and lymphatic disease
Dr. Nyoman Semadi
28
Cardiomyopathi
Dr. Luh Kamiati,
29
CV Physical Examination
Dr. Bajra
30
ECG
Dr. Bajra
31
Measure Workload
Dr. Muliarta
32
IV line procedure
Prof Wiryana
33`
Chest Imaging
Dr Lisna Astuti
100
question
TOTAL
~ CURRICULUM MAP ~
Smstr
Program or curriculum blocks
10
Senior Clerkship
81
Senior Clerkship
Senior clerkship
Medical
Emergency
(3 weeks)
Special Topic:
-Travel medicine
(2 weeks)
Elective Study III

(6 weeks)
Clinic
Orientation
(Clerkship)
(6 weeks)
BCS (1 weeks)
The Respiratory
System and
Disorders
(4 weeks)
The Cardiovascular
System and
Disorders
(4 weeks)
The Urinary System

and Disorders
(3 weeks)
The Reproductive
System and Disorders
(3 weeks)
BCS (1 weeks)
Alimentary
& hepatobiliary systems
& disorders
(4 Weeks)
BCS (1 weeks)
The Endocrine
System, Metabolism
and Disorders
(4 weeks)
BCS (1 weeks)
Clinical Nutrition and
Disorders
(2 weeks)
BCS (1 weeks)
Elective Study II
(1 weeks)
BCS (1 weeks)
BCS (1 weeks)
BCS (1 weeks)
Musculoskeletal
system &
connective
tissue disorders
(4 weeks)
Neuroscience
and
neurological
disorders
(4 weeks)
Behavior Change
and disorders
(4 weeks)
BCS (1 weeks)
Hematologic
system & disorders & clinical
oncology
(4 weeks)
BCS (1 weeks)
Immune
system &
disorders
(2 weeks)
BCS(1 weeks)
Infection
& infectious
diseases
(5 weeks)
BCS
(1 weeks)
The skin & hearing
system
& disorders
(3 weeks)
BCS (1 weeks)
Medical
Professionalism
(2 weeks)
BCS(1 weeks)
Evidence-based
Medical Practice
(2 weeks)
BCS (1 weeks)
Health System-based
Practice
(3 weeks)
BCS(1 weeks)
Community-based
practice
(4 weeks)
BCS (1 weeks)
Studium
Generale and
Humaniora
(3 weeks)
Medical
communication
(3 weeks)
BCS (1 weeks)
The cell
as biochemical machinery
(3 weeks)
Growth
&
development
(4 weeks)
BCS (1 weeks)
BCS(1 weeks)
BCS: (1 weeks)
Special Topic :
- Palliative
medicine
-Compleme
ntary &
Alternative
Medicine
- Forensic
(3 weeks)
Elective
Study II
(1 weeks)
Special Topic
- Ergonomi
- Geriatri
(2 weeks)
Elective
Study I
(2 weeks)
The Visual
system &
disorders
(2 weeks)
Pendidikan Pancasila & Kewarganegaraan (3 weeks)
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Study Guide Cardio Tayang by Gextha 30 Maret 2015

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Study Guide Cardiovascular System

Udayana University Faculty of Medicine, DME

Study Guide Cardiovascular System

a. Planners Team .....................................................................

Seven General Core Competency

Regular Class ...........

Meeting Students Representatives .................................

Standart of Medical Competence

10. Evaluation Form

11. Item Grid .

12. Curriculum Mapping

Udayana University Faculty of Medicine, DME

Study Guide Cardiovascular System

dr. I.G.A. Widianti, M.Biomed (Head)

dr. I Md Junior Rina A, Sp.JP, Fiha (Secretary)

dr. Made Muliarta, M.Kes

dr. I G.N Mayun, PHK

dr. Bajra Nadha, SpJP

dr. Eka Guna Wijaya, Sp A

dr. I.G.A. Widianti, M.Biomed

dr. I G.N Mayun,PHK

Dr. dr. Adiatmika, M.For

dr. Made Muliarta, M.Kes

Prof. dr. Dewa Putu Sutjana, PFK, M.Erg.

Prof dr. I Gusti Made Aman, SpFK

dr. I G Md Gd Surya Candra Trapika, MSc

dr.Ni Wayan Winarti, SpPA

Prof . Dr. Dr. Wita, SpJP

Dr. dr. I Ketut Rina, SpPD, SpJP

dr. Bagus Ari Pradnyana Dwi Sutanegara,

dr. Bajra Nadha, SpJP

dr. I Made Junior Rina Artha, Sp.JP

dr. I Kadek Susila Surya Darma, SpJP

Udayana University Faculty of Medicine, DME

Study Guide Cardiovascular System

dr. Eka Guna Wijaya, Sp A

Prof. Dr.dr. I Made Wiryana, Sp.An.KIC

dr. Lisna Astuti,Sp.R

dr. Luh Kamiati, Sp.RM

dr. Semadi, SpB, SpBTKV

ENGLISH CLASS (B)

Udayana University Faculty of Medicine, DME

Study Guide Cardiovascular System

dr. Anom Suardika, Sp.OG

3. THE SEVEN GENERAL CORE COMPETENCY

compassionate, appropriate, and effective for the management of health problem,

2. Medical knowledge base

Udayana University Faculty of Medicine, DME

Study Guide Cardiovascular System

7. Community-based and health system-based practice

Udayana University Faculty of Medicine, DME

Study Guide Cardiovascular System

System and Cardiac

structure of the heart

The heart as a pump

Cardiac Out Put and

Udayana University Faculty of Medicine, DME

Study Guide Cardiovascular System

Factors that Affect

Udayana University Faculty of Medicine, DME

Study Guide Cardiovascular System

Dr. Eka Guna

Dr. Eka Guna

Drug used in Angina