Study Guide Cardio Semester VI tayang 6 April 2016
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.
(2)
2. CONTENTS
1. Preface ……….
1
2. Contents .….………...
2
a. Planners Team ...
3
b. Lectures………...
3
c. Facilitators ………
5
3. Seven General Core Competency ………
7
4. Time Table
-
English Class ……… 8
-
Regular Class .………... . 8
5. Meeting Students Representatives ...……… 14
6. Assessment ...………. 15
7. Learning program ……….. 16
8. References ……… 80
9. Standart of Medical Competence ……… 81
10. Evaluation Form ……… 81
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2.
a. PLANNERS TEAM
No NAME DEPT PHONE
1. dr. I Made Junior Rina Artha, Sp.JP., Fiha (Head) Cardiology 08123814814 2 dr. A.A. Ayu Dwi Adelia Yasmin, SpJP, FIHA
(Secretary)
Cardiology 087861402169
3. Dr. dr. Made Muliarta, M.Kes Physiology 081338505350 4. dr. I G.A. Dewi Ratnayanti, M.Biomed Histology 087761499889 5. dr I Kadek Susila Surya Darma, SpJP, FIHA Cardiology
08113853151 / 081805584102 6. dr. Eka Guna Wijaya, Sp A Pediatric 081338599801
b.
LECTURERS
No NAME DEPT PHONE
1. Prof. Dr. dr. I Nyoman Mangku Karmaya, M.Repro, PA(K), FIAS
Anatomy 0811387105
2. dr I Nyoman Gede Wardana, M. Biomed Anatomy 087860405625
3. dr. I G.A. Dewi Ratnayanti, M.Biomed Histology 087761499889 4. Prof. Dr. dr. Putu Gede Adiatmika,
M.For
Physiology 08123811019
5. Dr. dr. Made Muliarta, M.Kes Physiology 081338505350 6. Prof. dr. Dewa Putu Sutjana, PFK,
M.Erg. (M.Kes)
Physiology 08123924477
7. Prof dr. I Gusti Made Aman, SpFK Pharmacology 081238770650 8. dr. Ni Putu Ekawati, SpPA Patology Anatomy
08113803933 9. Prof . Dr. dr. I Wayan Wita, SpJP Cardiology 08123809780 10. dr I Kadek Susila Surya Darma, SpJP,
FIHA
Cardiology
08113853151 / 081805584102 11. dr. I B Rangga Wibhuti, M.Biomed,
SpJP, FIHA
Cardiology 081237287888
12. dr. I Made Putra Swi Antara, SpJP, FIHA Cardiology 08123804782 13 dr. I Made Junior Rina Artha, Sp JP (K), Cardiology 08123814814
(4)
FIHA
14 dr. A.A. Ayu Dwi Adelia Yasmin, SpJP, FIHA
Cardiology 087861402169
15. dr I Nyoman Wiryawan, SpJP, FIHA Cardiology 081289053234 16. dr. Eka Guna Wijaya, Sp A Pediatric 081338599801 17. Prof. Dr.dr. I Made Wiryana, Sp.An.KIC Anesthesia 0811392171 18. dr IGN Mahaalit Aribawa, SpAn. KAR Anesthesia 0811396811 19. dr. Lisna Astuti,Sp.R Radiology 03617422632 20. dr. Luh Kamiati, Sp.RM Physiotherapy 08123998787 21. dr. Semadi, SpB,SpBTKV Surgery 08123838654
c. FACILITATORS
(5)
No Name Group Departement Phone (2&3 Venue rd floor) 1 dr. I G N Sri Wiryawan, M.Repro A1 Histology 08123925104 2nd floor:R.2.09 2 dr. Komang Ayu Kartika Sari, MPH A2 Public Health 082147092348 2nd floor:R.2.10 3 dr.Ni Made Dwi Puspawati,Sp.KK A3 Dermatology 08123766268 2nd floor:R.2.11 4 dr. I Dewa Ayu Inten Dwi Primayanti, M.Biomed A4 Fisiology 081337761299 2nd floor:R.2.12 5 dr. Putu Andrika, Sp.PD-KIC A5 Interna 08123989192 2nd floor:R.2.13 6 dr. I Wayan Niryana, Sp.BS, M. Kes A6 Surgery 08179201958 2nd floor:R.2.14 7 dr. Dewa Gde Mahiswara Suadiatmika, Sp.Rad A7 Radiology 08123846307 2nd floor:R.2.15 8 dr.Siska, Sp.M, M.Kes A8 Opthalmology 0818218210 2nd floor:R.2.16 9 dr. I Komang Arimbawa, Sp.S A9 Neurology 081338226892 2nd floor:R.2.23 10 dr. Ni Putu Sriwidyani , Sp.PA A10 PathologyAnatomy 081337115012 3nd floor:R.3.21 11 dr. I B Rangga Wibhuti, Sp.JP A11 Cardio 081237287888 3nd floor: R.3.22 12 dr. Made Wiranadha, Sp.THT-KL A12 ENT 08123968294 3nd floor:
R.3.23
English Class (Class B)
No Name Group Departement Phone (2&3Venue rd floor)
1 dr. Pontisomaya Parami, Sp.An, MARS B1 Anasthesi 08123661312 2nd floor:R.2.09 2 Dr.dr. G.N. Indraguna Pinatih,M.Sc.AkP, Sp.GK B2 Public Health
08123816424
2nd floor: R.2.10 3 dr. I Wayan Gede Sutadarma, M Gizi B3 Biochemistry
082144071268
2nd floor: R.2.11 4 dr. I Made Pande Dwipayana,Sp.PD-KHOM-FINASIM B4 Interna
08123657130
2nd floor: R.2.12 5 dr. Gede Wirya Kusuma Duarsa, M.Kes, Sp.U B5 Urology
08155753377
2nd floor: R.2.13 6 dr. Made Agus Dwianthara Sueta, Sp.B-KBD B6 Surgery
081338648424
2nd floor: R.2.14 7 dr. Anak Agung Mas Putrawati Triningrat, Sp.M (K) B7 Opthalmology 08123846995 2nd floor:R.2.15 8 dr. Dudut Rustyadi , Sp.F B8 Forensic 08123994234 2nd floor:R.2.16 9 dr. I Gusti Ngurah Purna Putra, Sp.S (K) B9 Neurology 08123915763 2nd floor:R.2.23
(6)
10 dr. I Made Junior Rina Artha, Sp.JP(K) B10 Cardio 08123814814 3nd floor:R.3.21 11 dr. I Wayan Aryabiantara, Sp.An. KIC B11 Anasthesi 08123822009 3nd floor: R.3.22 12 dr. Ida Ayu Putri Wirawati, Sp.PK B12 Clinical
Pathology 082145723828
3nd floor: R.3.23
3. THE SEVEN GENERAL CORE COMPETENCY
(7)
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 baseMastery 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 skillDemonstrate capability to effectively apply clinical skill and interpret the findings in the investigation of patient
4.
CommunicationDemonstrate 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 managementDemonstrate capability to manager information which includes information access, retrieval, interpretation, appraisal, and application to patient’s specific problem, and maintaining records of his or her practice for analysis and improvement
6.
ProfessionalismDemonstrate 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 practiceDemonstrate 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
1 Wednesday 6th of April
Introduction lecture General anatomy, topography and
Intro. Lecture Intro. Lecture
08.00 – 08.15 08.15 – 09.00
09.00 – 09.15 09.15 – 10.00
Prof Wita Dr Wardana
(8)
surface anatomy of the heart and great vessels.
Ind. Learning SGD
Break Pleno
09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 14.00 – 15.00
12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 15.00 – 16.00
Facilitator
Dr Wardana 2 Thursday
7th of April
Microscopic structure of the heart and valves
The heart as a pump
Intro. Lecture
Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.15
08.15 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.15
09.15 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr Ratnayanti
Dr. Muliarta
Facilitator
Team
3 Friday 8th of
April
Intrinsic Conduction System and Cardiac Action Potential
Intro. Lecture
Ind. Learning SGD
Break
Student Project Pleno
08.00 – 09.00
09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 10.00
12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Muliarta
Facilitator
Dr. Muliarta
4 Monday 11st of April
Cardiac Out Put and Regulation of Heart Pumping
Intro. Lecture
Ind. Learning SGD
Break
Student Project Pleno
08.00 – 09.00
09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 10.00
12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Prof Sutjana
Facilitator
Team 5 Tuesday
12nd of April
Overview of Circulation and Its Function
Intro. Lecture
Ind. Learning SGD
Break
Student Project Pleno
08.00 – 09.00
09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 10.00
12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Prof Sutjana
Facilitator
(9)
6 Wednesday 13rd of April
Factors that Affect Blood Pressure Microscopic Anatomy of The Great Vessel
Intro. Lecture
Intro. Lecture
Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.45
08.45 – 09.00
09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.45
09.45 – 10.00
12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Adiatmika
Dr. Ratnayanti
Facilitator
Team
7 Thursday 14th of April
Myocardial perfusion Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Muliarta
Facilitator
Dr. Muliarta 8 Friday
15th of April
Blood Pressure Regulation
Intro. Lecture
Ind. Learning SGD
Break
Student Project Pleno
08.00 – 09.00
09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 10.00
12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Adiatmika
Facilitator
Dr. Adiatmika
9 Monday 18th of April
The formation of anomalies of the heart and great vessels.
Intro. Lecture
Ind. Learning SGD
Break
Student Project Pleno
08.00 – 09.00
09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 10.00
12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Prof Mangku
Facilitator
Prof Mangku
10 Tuesday 19th of April
Approach to Patient With Cardiovascular Disease
Intro. Lecture
Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.20 08.20 – 08.40 08.40 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.20 09.20 – 09.40 09.40 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Prof. Wita
Facilitator
(10)
11 Wednesday 20th of April
CV Physical Examination
Intro. Lecture
BCS
08.00 – 09.00
10.00 – 13.00
09.00 – 10.00
13.00 – 16.00
Dr. Junior, Susila, Rangga, Adel, Putra Team Cardio
12 Thursday 21st of April
CV Physical Examination Intro. Lecture BCS Practical Anatomy-Histology
08.00 – 09.00
10.00 – 13.00 13.00 – 16.00
09.00 – 10.00
13.00 – 16.00 10.00 – 13.00
Dr. Junior, Susila, Rangga, Adel, Putra Team Cardio Team
13 Friday 22nd
of April
ECG,
Ecocardiografi, Fonografi and USG Dopler
Intro. Lecture
BCS
08.00 – 09.00
10.00 – 13.00
09.00 – 10.00
13.00 – 16.00
Dr. Junior, Susila, Rangga, Adel, Putra
Team Cardio
14 Monday 25th of April
Chest Imaging Measure Workload Intro. Lecture Intro. Lecture BCS Practical Anatomy-Histology
08.00 – 08.30 08.30 – 09.00
10.00 – 13.00 13.00 – 16.00
09.00 – 09.30 09.30 – 10.00
13.00 – 16.00 10.00 – 13.00
Dr. Lisna Dr Muliarta
Team
15 Tuesday 26th of April
IV line Procedure, CVP
Intro. Lecture BCS
Practical Anatomy-Histology
08.00 – 09.00 10.00 – 13.00 13.00 – 16.00
09.00 – 10.00 13.00 – 16.00 10.00 – 13.00
Prof Wiryana/ Mahaalit
Team
16 Wednesday 27th of April
Non-cyanotic and Cyanotic CHD Acute Rheumatic Fever Intro. Lecture Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.30
08.30 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.30
09.30 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Eka Guna
Dr. Eka Guna Facilitator
Dr. Eka Guna
17 Thursday
28th of April Ischemic HeartDisease = ACS
Intro. Lecture Ind. Learning SGD
Break
08.00 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30
09.00 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00
Dr. Junior Rina
(11)
Student Project Pleno
12.30 – 14.00 14.00 – 15.00
10.00 – 11.30
15.00 – 16.00 Dr. Junior Rina 18 Friday
29th of April
Pathologic aspect of IHD
Drug used in Angina Pectoris
Intro. Lecture
Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.30
08.30 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.30
09.30 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Ekawati
Prof Aman
Facilitator
Team
19 Monday 2nd of May
Arrhytmias Antiarrhythmic Drugs
Intro. Lecture Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.45 08.45 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.45 09.45 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Putra Prof Aman
Facilitator
Team
20 Tuesday, 3rd of May
Hypertension Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
dr . Adelia
Facilitator
dr Adelia
21 Wednesday 4th of May
Heart Failure Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Susila
Facilitator
Dr. Susila 22 Monday
9th of May
Antihypertensive Drugs
Positive Inotropes
Intro. Lecture Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.40 08.40 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.40 09.40 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Prof Aman
Facilitator
Team
23 Tuesday, 10th of May
Acute and Chronic
(12)
Ind. Learning SGD
Break
Student Project Pleno
09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Facilitator
Dr. Wiryawan 24 Wednesday
11st of May Valvular Heart Disease, and
Pericardial & Endocardial Disease
Physiotherapy to patient with Cardiovascular Disease
Intro. Lecture
Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.45
08.45 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.45
09.45 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr. Rangga
Dr. Kamiati
Facilitator
Team 25 Thursday,
12tnd of May
Common Peripheral Vascular Disease Valvuloplasty, valv. replacement
Intro. Lecture
Intro. Lecture Ind. Learning SGD
Break
Student Project Pleno
08.00 – 08.45
08.45 – 09.00 09.00 – 10.30 10.30 – 12.00 12.00 – 12.30 12.30 – 14.00 14.00 – 15.00
09.00 – 09.15
09.15 – 10.00 12.00 – 13.30 13.30 – 15.00 11.30 – 12.00 10.00 – 11.30 15.00 – 16.00
Dr Semadi
Facilitator
Team 26 Mondayday
16th of May
Evaluation
Lecture & Plenary session
: Lecture room 4.01, 4
thfloor
BASIC CLINICAL SKILL
Day
Date
Topic
Learning
situation
English
Class
Regular
Class
PIC
Place
1
Wednesday 20th of AprilCV Physical Examination BCS
Intro. Lecture 08.00 – 09.00
10.00 – 13.00
09.00 – 10.00
13.00 – 16.00
Dr. Bajra R.401
Skill Lab
2
Thursday21st of April
CV Physical Examination
(13)
BCS 10.00 – 13.00 13.00 – 16.00 Skill Lab
3
Friday 22nd ofApril
ECG,
Ecocardiografi, Fonografi and USG Dopler
BCS
Intro. Lecture 08.00 – 09.00
10.00 – 13.00
09.00 – 10.00
13.00 – 16.00
Dr. Bajra R.401
Skill Lab
4
Monday25th of April
Chest Imaging Measure Workload BCS
Intro. Lecture Intro. Lecture
08.00 – 08.30 08.30 – 09.00
09.00 – 09.30 09.30 – 10.00
Dr. Lisna Dr. Muliarta R.401 R.401 Skill Lab
5
Tuesday26th of April
IV Line Procedure and CVP
BCS
Intro. Lecture 08.00 – 09.00
10.00 – 13.00
09.00 – 10.00
13.00 – 16.00 Prof Wiryana
R.401
Skill Lab
BASIC CLINICAL SKILL
English
1-5
English
5-10
Reg 1-5
Reg 5-
10
Place
Wednesday 20th of April CV Physical
Examination 10.00 – 13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill Lab
Thursday 21st of April CV Physical
Examination 10.00 – 13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill Lab
Friday 22nd of April
ECG 10.00 –
13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill Lab
Monday 25th of April
Chest Imaging 10.00 –
13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill Lab
Anatomy 13.30 –
15.30 10.00 – 12.00 Lab. Anatomy
Histology 13.30 –
15.30 10.00 – 12.00 Lab. Bersama
Tuesday 26th of April
IV line procedure, CVP 10.00 –
13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill Lab
Anatomy 13.30 –
15.30
10.00 – 12.00
Lab. Anatomy
Histology 13.30 –
(14)
5. MEETING OF STUDENT REPRESENTATIVES AND
FACILITATORS
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 Monday 16th of May 2016. 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):
TITLE (subject/topic;choose from competency list)
Name
NIM
Faculty of Medicine, Udayana University 2016
1. Introduction (Pendahuluan)2. Content (Isi, sesuai topik yang dibahas) 3. Summary (Ringkasan)
4. References (Daftar Pustaka) Van Couver style Example :
Moore KL, Agur AMR, 2007: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott & Wilkins, p. 26-30, 65-67, 80-115
5. 6 – 10 pages, 1,5 spasi, Times New Romance 12.
Article Review Assessment Form
Faculty of Medicine, Udayana University
(15)
Block
:
Cardivascular System and Disorders
Name
:_____________________________________
Student No. (NIM) :_____________________________________
Fasilitator
:_____________________________________
Title
:_________________________________________________
_________________________________________________
_________________________________________________
Time table of consultation
Point of discussion
Week
Date
Tutor sign
1. Title
1
2. References
2
3. Outline of paper
3
4. Content
4
5. Final discussion
5
Assessment
A. Paper structure : 7 8 9 10
B. Content : 7 8 9 10
C. Discussion : 7 8 9 10
Total point
: ( A + B + C ) : 3 = _________________
Denpasar, ______________________
Facilitator,
7. LEARNING PROGRAM
(16)
MODULE 1
dr. I Nyoman Gede Wardana, 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 :
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.
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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 heart’s 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.
MODULE 2
dr. I G.A. Dewi Ratnayanti, M.Biomed &
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Dr.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. The microscopic structure of heart (type of the myocardio cytes and the valves) 2. The normal and abnormal heart wall and pericardial structures.
3. Describe Function of the heart
4. Describe the function of the heart as a pump 5. 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
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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 atria-ventricular (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 & Fawcett’s Concise Histology, 2nd ed. London, Arnold. 2002. p. 135-136 ; 136-145; 136-139
SELF DIRECTING LEARNING
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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. Explain the microscopic structure of the purkinje fiber. Where does it location? 5. What is cardiac skeleton?
6. What are it components?
7. Explain the microscopic structure of the heart valves?
SELF-ASSESSMENT II:
1. What are major function of cardiovascular system?
2. What are three basic components of the cardiovascular system and it’s function? 3. Explain the origin of the heart sound and when its produce during cardiac cycle! 4. Describe function of the heart provides the driving force for the cardiovascular
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MODULE 3
Dr. dr. Made Muliarta, M.Kes
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 :
1. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders Company, 2006. p. 104-106, 116-122
SELF DIRECTING LEARNING
Basic knowledge that must be known:
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1. Autorhythmic cells potential 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
CASE:
Chief Complaint: 68-year-old man who collapsed during exertion.
History:Roger Crockett, a 68-year-old man with a 40-pack-year smoking history and recent complaints of angina (sub-sternal chest pressure) upon exercising, collapsed while mowing his lawn. Paramedics arriving at the scene found him unconscious, not breathing, and without a pulse. CPR was successfully performed and Roger was transported to the hospital. An ECG was suggestive of an anterior wall myocardial infarction, and he was given an intravenous solution of tissue plasminogen activator (TPA). Elevated blood creatine phosphokinase (CPK) levels measured over the next 2 days confirmed the diagnosis. Coronary angiography was performed a week later, revealing the following results:
Circumflex artery: 20% blocked Right coronary artery: 15% blocked Left anterior descending artery (LAD): 95% blocked ("Anterior intraventricular artery")
Questions:
1. While listening to his heart with a stethoscope, you notice a high-pitched, blowing, systolic murmur, heard best directly under the left nipple. A review of Roger's medical records shows no prior history of a heart murmur. What is causing this new murmur?
2. Is the cause of the murmur in any way related to his heart attack? Explain.
3. While listening to his breathing with a stethoscope, you hear some wheezing and inspiratory rales ("crackling noises"). Explain these findings.
4. A chest X-ray taken two weeks after his collapse shows a markedly enlarged cardiac silhouette and generalized haziness at the bases of the lungs.
a. Why is the heart enlarged?
b. Why are the lungs "hazy" on chest X-ray?
5. Roger is stabilized and ultimately discharged from the hospital. Three months after the heart attack, he comes back to his physician for a checkup. He
complains of dyspnea ("shortness of breath") at rest and difficulty breathing while lying down ("orthopnea"). He says he can only sleep when he is propped up by two large pillows. Why is he having these symptoms?
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7. Which term more accurately describes the stress placed upon Roger's heart -- increased pre-load or increased aferload?
8. Why does it help Roger to sleep with pillows under his head?
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
MODULE 4
Prof. dr. D.P. Sutjana, PFK, M.Erg
AIMS:
1. Comprehend the cardiac output
2. 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.
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
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stimulation. By contrast, the output can be decreased to as low as zero or almost zero by vagal stimulation.
Standard References :
1. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders Company, 2006. p. 111-115, 232-245
SELF DIRECTING LEARNING
Basic knowledge that must be known: 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?
5. If a myocardial contractile cell is placed in interstitial fluid and depolarized, the cell will contract. If Ca2+ is removed from the fluid surrounding the myocardial cell, and the cell is depolarized, it will not contract. If the experiment is repeated with a skeletal muscle fibre the skeletal muscle will contract when depolarized, whether Ca2+ is present or not. What conclusion can you draw from the result of this experiment?
6. A drug that blocks all Ca2+ channels in the myocardial cell membrane is placed in the solution around the cell . What will happen to the force of contraction in that cell?
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?
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MODULE 5
Prof. dr. D.P. Sutjana, PFK, M.Erg
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
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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 cross-sectional area is approximately 800 times that of the aorta. The velocity of circulation in 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 hydrostatic-osmotic pressure imbalance in the pulmonary vascular bed, result in fluid accumulation in the tissue spaces and transudation of fluid into the alveoli.
Standard References :
1. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders Company, 2006. p. 161-170, 195-203
SELF DIRECTING LEARNING
Basic knowledge that must be known: 1. Components of blood vessels 2. Functions of each blood vessels
MODULE 6
Prof. Dr. dr. I.P.G. Adiatmika, M.Kes &
dr. I G.A. Dewi Ratnayanti, M.Biomed
AIMS:
1. Apply several factors that affecting blood pressure
2. Describe the microscopic structure of the vascular system
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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:
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,
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SELF DIRECTING LEARNING
Basic knowledge that must be known: 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!
MODULE 7
Prof. dr. D.P. Sutjana, PFK, Merg
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
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ABSTRACT ;
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
2. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders Company, 2006. p. 181-185; 249-256.
Additional reading :
1. Fowcett DW, Jensh RP: Bloom & Fawcett’s Concise Histology, 2nd ed. London, Arnold. 2002. p. 136-141
SELF DIRECTING LEARNING
Basic knowledge that must be known: 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 women’s 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.
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4. Discuss the terms: arteriosclerosis, thrombosis and atheromatous plaque. 5. Which condition stimulates pain endings in the myocardium?
6. Describe the cardiac referred pain
MODULE 8
Prof. Dr. dr. I.P.G. Adiatmika, M.Kes
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
1. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders Company, 2006. p. 161-170, 205-23.
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SELF DIRECTING LEARNING
Basic knowledge that must be known:
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
MODULE 9
Prof. Dr. dr. I Nyoman Mangku Karmaya, M.Repro, PA(K), FIAS
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.
(32)
ABSTRACT
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.
Standard References:
1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott & Wilkins, 2007. p. 91, 93, 94
2. Sadler TW: Langman’s Medical Embryology, 10th ed. Philadelphia, Lippincott &
Wilkins, 2006. p. 167-178, 184
SELF DIRECTING LEARNING
Basic knowledge that must be known: 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?
(33)
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. 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(34)
MODULE 10
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 assesss 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)
(35)
4. Left anterior oblique projection (LAO)
Increase in cardiac size is the most consistent indication of cardiac disease 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.
Standard References :
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
SELF DIRECTING LEARNING
Basic knowledge that must be known: 1. History taking
2. Common cardiological symptom and consultation 3. Investigation in Cardiology
(36)
LEARNING TASK I:
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. 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)?
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
MODULE 11
dr. I Made Junior Rina Artha, Sp JP (K), FIHA & Team
AIMS:
Able to physical examination the Cardiovasculer System
LEARNING OUTCOME:
1. Able to physical examination the Cardiovasculer System.
(37)
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.
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Evaluate General Appearance (inspection)
2. Blood Pressure Examination, The Arterial Pulse, The Jugular Venous Pulse evaluation.
(38)
CHECK LIST:
CARDIOVASCULAR PHYSICAL EXAMINATION
NO
ITEMS
0
SCORE
1
2
1 Evaluate General Appearance
1. Inspection of the skin, nails, facies, eyes, mouth 2. Inspection neck, chest configuration, extremities
2 Blood Pressure Examination
1. Determine blood pressure
2. Rule out orthostatic hypotension, coarctatio of the aorta, cardiac tamponade
3 The Arterial Pulse
1. Rate and rhythm of the heart 2. Countour of the pulse
3. Amplitude of the pulse
4 The Jugular Venous Pulse
1. Determine the jugular wave forms 2. Estimate the jugular venous pressure 3. Evaluate the hepatojugular reflux
5 Percussion
1. Heart’s borders
6 Palpation
1. Palpate the point of maximum impulse 2. Palpate for localized motion
3. Palpate for generalized motion 4. Palpate for thrills
7 Auscultation
1. Auscultate the cardiac areas 2. The Influence of breathing 3. Describe any murmur present
8 Examination for Edema
1. Test for Edema
(1)
29 Antihypertensive Drugs 30 Heart Failure
31 Positive Inotropes 32 Valvular Heart Disase 33 Cor Pulmonale 34 Cardiomyopathi
35 Common Peripheral Vascular disease B Learning strategy
1 Lecture
2 Independent learning 3 Small group discussion 4 Practical
5 Case based learning 6 Problem based learning 7 Learning task
8 Self assessment C Lecturer
1. Prof. Dr. dr. I Nyoman Mangku Karmaya, M.Repro, PA(K), FIAS
2. Dr I Nyoman Gede Wardana, M. Biomed 3. dr. I G.A. Dewi Ratnayanti, M.Biomed 4. Dr. dr. Putu Gede Adiatmika, M.For 5. Dr. dr. Made Muliarta, M.Kes
6. Prof. dr. Dewa Putu Sutjana, PFK, M.Erg. (M.Kes)
7. Prof dr. I Gusti Made Aman, SpFK
8. dr. I G Md Gd Surya Candra Trapika, MSc 9. dr. Ni Putu Ekawati, SpPA
(2)
11. dr I Kadek Susila Surya Darma, SpJP, FIHA 12. dr. I B Rangga Wibhuti, M.Biomed, SpJP, FIHA 13. dr. I Made Putra Swi Antara, SpJP, FIHA 14 dr. I Made Junior Rina Artha, Sp JP (K), FIHA 15 dr. A.A. Ayu Dwi Adelia Yasmin, SpJP, FIHA 16. Dr I Nyoman Wiryawan, SpJP, FIHA
17. dr. Eka Guna Wijaya, Sp A
18. Prof. Dr.dr. I Made Wiryana, Sp.An.KIC 19. Dr IGN Mahaalit Aribawa, SpAn. KAR 20. dr. Lisna Astuti,Sp.R
21. dr. Luh Kamiati, Sp.RM 22. dr. Semadi, SpB,SpBTKV D Facilitator
1 Name of your group facilitator:
E Assessment
1 Time provide
2 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
(3)
Facilitator
Assessment
Your suggestion/input:
Topic
Learning strategy
Lecturer
Facilitator
Assessment
11. ITEM GRID
Question type: MCQ with vignette
No
Topic
Number of
question
PIC
Vignette
(4)
surface anatomy of the heart and great vessels.
3 Microscopic structure of the heart wall and pericardial
dr. Rtanayanti
4 The heart as a pump Dr. dr Made Muliarta, 5 Intrinsic Conduction System and
Cardiac Action Potential Dr. dr Made Muliarta, 6 Heart Valves and Heart Sounds Prof. Dewa Sutjana 7 Microscopic Anatomy of The
Valves of The Heart Dr Ratnayanti 8 Cardiac Out Put and Regulation
of Heart Pumping Prof. Dewa Sutjana 9 Factors that Affect Blood
Pressure
Prof Adiatmika, 10 Microscopic Anatomy of The
Great Vessel dr. Ratnayanti 11 Myocardial perfusion Dr. dr Made Muliarta 12 Blood Pressure Regulation Prof Dr dr Adiatmika, 13 The formation of anomalies of
the heart and great vessels. Prof Dr dr MangkuKarmaya 14 Approach to Patient With
Cardiovascular Disease Prof Dr. dr. Wita, SpJP 15 Non-cyanotic & Cyanotic CHD,
Acute Rheumatic Fever
Dr. Eka Guna W, SpA 16 Ischemic Heart Disease = ACS Dr. Juniort Rina, SpJP 17 Pathologic aspect of IHD Dr Putu Ekawati, SpPA 18 Drug used in Angina Pectoris Prof dr. IGM Aman 19 Arrhytmias Dr Putra, SpJP 20 Antiarrhythmic Drugs Prof dr Aman 21 Hypertension Dr. Adelia, SpJP 22 Antihypertensive Drugs Prof Aman 23 Heart Failure Dr. Susila, SpJP 24 Positive Inotropes Prof Aman 25 Valvular Heart Disase Dr Rangga, SpJP
(5)
26 Cor Pulmonale Dr. Wiryawan, SpJP 27 Common Peripheral Vascular
disease Dr. Nyoman Semadi, SpB 28 Cardiomyopathi Dr. Luh Kamiati,SpRM
TOTAL
100
question
~ CURRICULUM MAP ~
Smstr
Program or curriculum blocks
10
Senior Clerkship
9
Senior Clerkship
(6)
Emergency (3 weeks) BCS (1 weeks)
-Travel medicine
(2 weeks) (6 weeks) (Clerkship)(6 weeks)
6
The Respiratory System and Disorders (4 weeks) BCS (1 weeks)
The
Cardiovascular System and Disorders (4 weeks) BCS (1 weeks)
The Urinary System and Disorders (3 weeks) BCS (1 weeks)
The Reproductive System and Disorders (3 weeks) BCS (1 weeks)
5 Elective Study II (1 weeks) Alimentary & hepato-biliary 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)
Special Topic : - Palliative medicine -Compleme ntary & Alternative Medicine - Forensic (3 weeks) Elective Study II (1 weeks) 4 Musculoskeletal system & connective tissue disorders (4 weeks) BCS (1 weeks)
Neuroscience and
neurological disorders (4 weeks) BCS (1 weeks)
Behavior Change and disorders (4 weeks) BCS(1 weeks) The Visual system & disorders (2 weeks) BCS (1 weeks)
3
Hematologic system & disor-ders & 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)
2
Medical Professionalism (2 weeks) BCS (1 weeks)
Evidence-based Medical Practice (3 weeks) Health System-based Practice (3 weeks) BCS (1 weeks)
Community-based practice (4 weeks) Special Topic - Ergonomi - Geriatri (2 weeks) Elective Study I (2 weeks) 1 Stadium Generale and Humaniora (3 weeks) Medical communication (3 weeks) BCS (1 weeks)
The cell as bioche-mical machinery (3 weeks) BCS(1 weeks) Growth & development (4 weeks) BCS: (1 weeks)