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 1


2. CONTENTS

1. Preface ………………………………………………………………………. 1

2. Contents .….…………………………………………………………........... 2

a. Planners Team ..................................................................... 3

b. Lectures……………………………………………….................. 3

c. Facilitators ………………………………………………………… 4

3. Seven General Core Competency ………………………………………… 6

4. Time Table

- English Class ……………………………………………………………. 7

- Regular Class .……………………………………………………….......... 7

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

1. dr. I.G.A. Widianti, M.Biomed (Head) Anatomy 08123921765

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. dr. Made Muliarta, M.Kes 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 08123812808

11. dr. Bagus Ari Pradnyana Dwi Sutanegara, SpJP

Cardiology 08123800055

12. dr. Bajra Nadha, SpJP Cardiology 0818353925



13 dr. I Made Junior Rina Artha, Sp.JP Cardiology 08123814814

14 dr. I Kadek Susila Surya Darma, SpJP Cardiology 08113853151

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. FACILITATORSREGULAR CLASS (A)

No NAME GROUP DEPT PHONE Venue (2rd floor)

1. dr. Sianny Herawati, Sp.PK A1 Clinical Pathology 081236172840

2nd floor: R.2.09

2. dr. Ni Nengah Dwi Fatmawati, Sp.MK, Ph.D A2 Microbiology 087862200814

2nd floor: R.2.11

3. dr. Cynthia Dewi Sinardja, Sp.An A3 Anasthesi 081238700372nd floor:

R.2.12

4. dr. Gde Somayana, Sp.PD A4 Interna 0813451369132nd floor:

R.2.13

5. dr. I Nyoman Gede Wardana, M.Biomed A5 Anatomy 087860405625

2nd floor: R.2.14

6. dr. Elysanti Dwi Martadiani, Sp.Rad A6 Radiology 081805673099

2nd floor: R.2.15

7. dr. I Wayan Losen Adnyana, Sp.PD A7 Interna 08123995536

2nd floor: R.2.16

8. Dr. dr. I Wayan Suranadi, Sp.An.KIC A8 Anasthesi 08123847575

2nd floor: R.2.20

9. Dr. dr. I Dewa Made Sukrama, MSi, Sp.MK(K) A9 Microbiology 081338291965

2nd floor: R.2.21

10. dr. Kunthi Yulianti, Sp.KF A10 Forensic 0813384720052nd floor:

R.2.22



ENGLISH CLASS (B)

No NAME GROUP DEPT PHONE Venue (2rd floor)

1. dr. Desak Made Wihandani, M.Kes B1 Biochemistry 081338766244

2nd floor: R.2.09

2. dr. Henky, Sp.F., M.BEth, FACLM B2 Forensic 08123988486

2nd floor: R.2.11

3. dr. Anom Suardika, Sp.OG B3 Obgyn 08175619662nd floor:

R.2.12

4. dr. Dewa Ayu Agus Sri Laksmi, M.Sc B4 Parasitology 081392017107

2nd floor: R.2.13

5. dr. Anak Agung Mas Putrawati Triningrat, Sp.M B5 Opthalmology 08123846995

2nd floor: R.2.14

6. dr. Tjokorda Gde Agung Senapathi, Sp.An B6 Anasthesi 081337711220

2nd floor: R.2.15

7. dr. A.A.Bagus Ngurah Nuartha, SpS.(K) B7 Neurology 08123687288

2nd floor: R.2.16

8. dr. Ni Gusti Ayu Agung Manik Yuniawaty Wetan, Sp.B B8 Surgery 08123214075

2nd floor: R.2.20

9. dr. Tjokorda Gde Dharmayuda, Sp.PD-KHOM B9 Interna 0811394108

2nd floor: R.2.21

10. dr. Putu Yuliawati , Sp.M B10 Opthalmology 0813386017242nd 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 patient’s 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

1 Monday 30th of March

Introduction lecture

General anatomy,

topography and

surface anatomy of

the heart and great

vessels.

Intro. Lecture

Intro. Lecture

Ind. Learning

SGD

Break

Pleno

08.00 – 08.15

08.15 – 09.00

09.00 – 10.30

10.30 – 12.00

12.00 – 12.30

14.00 – 15.00

09.00 – 09.15

09.15 – 10.00

12.00 – 13.30

13.30 – 15.00

11.30 – 12.00

15.00 – 16.00

Prof Wita

Dr. Widianti

Facilitator

Dr. Widianti

2 Tuesday31st of March

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 Mayun

Dr. Muliarta

Facilitator

Team

3 Wednesday 1st 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 Thursday2nd 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 Monday6th 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

Prof Sutjana

6 Tuesday7th 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. Mayun

Facilitator

Team

7 Wednesday8th 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 Thursday9th 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 Friday10th 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

Dr. Widianti

Facilitator

Dr. Widianti

10 Monday13rd of April

Approach to Patient

With Cardiovascular

Disease:

Intro. Lecture

Ind. Learning

SGD

08.00 – 09.00

09.00 – 10.30

10.30 – 12.00

09.00 –10.00

12.00 – 13.30

13.30 – 15.00

Prof. Wita

Facilitator



Break

Student Project

Pleno

12.00 – 12.30

12.30 – 14.00

14.00 – 15.00

11.30 – 12.00

10.00 – 11.30

15.00 – 16.00 Prof. Wita

11 Tuesday 14th of April

CV Physical

Examination I

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. Bajra

Team Cardio

Team


CV Physical

Examination II

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. Bajra

Team Cardio

Team


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. Bajra

Team Cardio

14 Friday 17th of April

Chest Imaging

Measure Workload

Intro. Lecture

Intro. Lecture

BCS

08.00 – 08.30

08.30 – 09.00

10.00 – 13.00

09.00 – 09.30

09.30 – 10.00

13.00 – 16.00

Dr. Lisna

Dr. Muliarta

Team


IV line Procedure, CVP

Intro. Lecture

BCS

08.00 – 09.00

10.00 – 13.00

09.00 – 10.00

13.00 – 16.00

Prof Wiryana

Prof Wiryana

16 Tuesday21st of April

Non-cyanotic and

Cyanotic CHD and

Acute Rheumatic

Fever

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. Eka Guna

Facilitator

Dr. Eka Guna

17 Wednesday22nd of April

Ischemic Heart

Disease = ACS

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. K. Rina

Facilitator

Dr. K. Rina



18 Thursday23rd 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. Winarti

Prof Aman

Facilitator

Team

19 Friday24th of April

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 – 09.40

09.40 – 10.00

12.00 – 13.30

13.30 – 15.00

11.30 – 12.00

10.00 – 11.30

15.00 – 16.00

Dr. Bajra N

Dr. Surya

Facilitator

Team

20 Monday, 27th of April

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. Susila

Facilitator

Dr. Susila

21 Tuesday28th of April

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. Junior R

Facilitator

Dr. Junior R


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

Dr. Surya

Facilitator

Team

23 Thursday,30th of April

Acute and Chronic Cor-pulmonale

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. Bagus Ari

Facilitator

Dr. Bagus Ari



24 Monday,4th of May

Valvular Heart

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. Bajra N

Dr. Kamiati

Facilitator

Team

25 Tuesday,5th of May

Common Peripheral

Vascular (artery &

Venous) and

lymphatic disease

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 Semadi

Facilitator

Team

26 Thursday

7th of MayEvaluation



BASIC CLINICAL SKILL

Day Date Topic Learning situation

English Class

Regular Class

PIC Place

1 Tuesday 14th of April

CV Physical

Examination I

BCS

Intro. Lecture 08.00 – 09.00

10.00 – 13.00

09.00 – 10.00

13.00 – 16.00

Dr. Bajra R.302

Skill Lab


CV Physical

Examination II

BCS


10.00 – 13.00

09.00 – 10.00

13.00 – 16.00

Dr. Bajra R.302

Skill Lab


ECG, Ecocardiografi, Fonografi and USG Dopler

BCS


10.00 – 13.00

09.00 – 10.00

13.00 – 16.00

Dr. Bajra R.302

Skill Lab

4 Friday 17th 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.302

R.302

Skill Lab


IV Line Procedure and CVP

BCS


10.00 – 13.00

09.00 – 10.00

13.00 – 16.00

Prof Wiryana

R.302

Skill Lab



BASIC CLINICAL SKILL

English 1-5 English 5-10 Reg 1-5 Reg 5-10 PlaceTuesday 14th April 2015CV Physical Examination I 10.00 – 13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill LabAnatomy 13.30 – 15.30 10.00 – 12.00 Lab. AnatomyHistology 13.30 – 15.30 10.00 – 12.00 Lab. Bersama

Wednesday 15th April 2015CV Physical Examination II 10.00 – 13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill LabAnatomy 13.30 – 15.30 10.00 – 12.00 Lab. AnatomyHistology 13.30 – 15.30 10.00 – 12.00 Lab. Bersama

Thursday 16th April 2015ECG 10.00 – 13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill Lab

Friday 17th April 2015Chest Imaging 10.00 – 13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill LabMeasure Workload 13.00 – 16.00 13.00 – 16.00 10.00 – 13.00 10.00 – 13.00 Lab. Faal

Monday 20th April 2015IV line procedure, CVP 10.00 – 13.00 10.00 – 13.00 13.00 – 16.00 13.00 – 16.00 Skill Lab

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 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):



TITLE (subject/topic;choose from competency list)NameNIMFaculty of Medicine, Udayana University 2015

1. Introduction (Pendahuluan)2. Content (Isi, sesuai topik yang dibahas)3. Summary (Ringkasan)4. 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 FormFaculty of Medicine, Udayana University

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

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 system2. Describe the surface anatomy of the cardiovascular system

CURRICULUM CONTENS: 1. Topography anatomy of the heart and great vessel2. 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


Day 1


SELF DIRECTING LEARNINGBasic knowledge that must be known:

1. Topography anatomy of the heart and great vessel.2. Mediastinum3. Pulmonary/lesser and systemic/greater circulation.

SCENARIOCASE: A student had a motorcycle accident with a bruise in the 4 th 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 2dr. I G N Mayun, PHK & dr. Made Muliarta M.Kes

AIMS: 1. Describe the microscopic structure of the cardiovascular system2. Comprehend the basic principles and practical implications of the heart as a

pump

LEARNING OUTCOME: 1. Can describe the microscopic structure of the cardiovascular system2. 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 heart4. Describe the function of the heart as a pump5. 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.


Day 2


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

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 valvec. 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 atriaSemilunar 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; 268-2692. 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


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 system2. Describe function of the heart provides the driving force for the cardiovascular

system3. Why do the ventricles contract as a single unit4. 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

system!

MODULE 3dr. Made Muliarta, M.Kes

AIMS: 1. Comprehend the basic principles of Cardiac Action Potential2. 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 sodium2. 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


Day 3


Standard Reference :1. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders

Company, 2006. p. 104-106, 116-122


1. Autorhythmic cells potential2. Contractile cells potential3. ECG wave tracing

LEARNING TASK:1. Describe the excitation – contraction process2. What is the pace maker of the heart in normal condition3. 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 Node2. Describe the action potential of the cells of the contractile cells3. Explain the relationship between cardiac cycle and ECG trace wave

MODULE 4Prof. dr. D.P. Sutjana, PFK, Merg

AIMS: 1. Comprehend the cardiac output2. Comprehend the basic principles of cardiac output regulation

LEARNING OUTCOME: 1. Describe how to measure cardiac output2. Describe the regulation of cardiac output

CURRICULUM CONTENS:1. Components of cardiac output2. 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


Day 4


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 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


1. Components of Cardiac output2. 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

volume4. What should you suggest for this complaint?

SELF-ASSESSMENT :1. Describe the effects of autonomic nerve stimulation on the cardiac rate and stroke

volume2. List the factors that affect venous return. 3. Using a flowchart, show how an increased venous return can result in an

increased cardiac out put4. 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?




AIMS: 1. Comprehend the function of blood vessels2. Comprehend the regulation of blood flow LEARNING OUTCOME: 1. Describe the function of blood vessels2. Describe the regulation of blood flow

CURRICULUM CONTENS:1. Components of blood vessels2. Factors influence blood flow

ABSTRACTThe 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.


Day 5


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 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


1. Components of blood vessels2. Functions of each blood vessels



MODULE 6Dr. dr. I.P.G. Adiatmika, MKes & dr. I G N Mayun, PHK

AIMS: 1. Apply several factors that affecting blood pressure2. Describe the microscopic structure of the vascular system

LEARNING OUTCOME: 1. Can describe the stroke volume2. Can describe the heart rate 3. Can describe several factors that affecting blood pressure4. Can describe the microscopic structure of the vascular system (arterial and

venous)

CURRICULUM CONTENS:1. Frank Starlink Law2. 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


Day 6


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. 448-4542. Gartner LP, Hiatte JL: Color Textbook of Histology, 2nd ed. Philadelphia,

WB Saunders Company, 2001. p. 251-262


1. Frank Starlink law2. Autonomic activation 3. The roles of several ions4. 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 pressure2. Why a person with atherosclerosis may have high blood pressure3. 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!


AIMS: Comprehand the basic principles underlying myocard perfusion

LEARNING OUTCOME: 1. Can describe how myocardial perfusion occurs2. Can describe functional structure of the coronary arteries


Day 7


CURRICULUM CONTENS:1. Function of coronary artery2. The role of diastole

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, 1012. 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


1. Systole-diastole2. The function of coronary artery3. 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.

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 8Dr. 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.


Day 8


Standard References 1. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders

Company, 2006. p. 161-170, 205-23.


1. Short term mechanism for regulating blood pressure2. Long term mechanism for regulating blood pressure3. 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? Why2. 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

pressure2. Explain reflexes that responsible for short term control and long term control

mechanisms to blood pressure

MODULE 9dr. 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 impilcations2. Can describe the basic principles underlying the formation of anomalies of the

great vessels and its impilcations


Day 9


CURRICULUM CONTENS:1. Embryology of the heart2. Embryology of the great vessels.

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, 942. Sadler TW: Langman’s Medical Embryology, 10th ed. Philadelphia, Lippincott &

Wilkins, 2006. p. 167-178, 184


1. Embriologi of the heart2. 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 I1. 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.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



MODULE 10Prof 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

disease3. Able to do and practice the approach to investigations in Cardiology).

CURRICULUM CONTENS:1. The symptoms of the cardiovascular disease2. 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.


Day 10


Radiologic method used in the roentgen cardiac examination:

1. Posteroanterior projection, PA/AP2. Lateral projection3. Right anterior oblique projection (RAO)4. Left anterior oblique projection (LAO)

Increase in cardiac size is the most consistent indication of cardiac disease2. 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. EchocardiographyEchocardiography 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. AngiocardiographyAngiography 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 catheterizationCardiac 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 CardiologyThe 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


http://en.wikipedia.org/wiki/Coronary_arteries

http://en.wikipedia.org/wiki/Coronary_catheterization

http://en.wikipedia.org/wiki/Heart

http://en.wikipedia.org/wiki/Blood_vessel

http://en.wikipedia.org/wiki/Heart_chamber

http://en.wikipedia.org/wiki/Catheter

http://en.wikipedia.org/wiki/Fluoroscopy

http://en.wikipedia.org/wiki/X-ray

http://en.wikipedia.org/wiki/Radiocontrast



http://en.wikipedia.org/wiki/Vein

http://en.wikipedia.org/wiki/Artery

http://en.wikipedia.org/wiki/Lumen_(anatomy)



1. History taking2. Common cardiological symptom and consultation3. Investigation in Cardiology

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 disease2. 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 disease2. 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 VSD6. Differenciated between LVH and RVH on chest x-ray7. Explain HHD on the chest x-ray8. Explain tetralogy of Fallot on the chest x-ray



MODULE 11 & 12dr. 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, low-set 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.


Day 11 & 12


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 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. Braunwald’s 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

NO ITEMSSCORE

0 1 21 Evaluate General Appearance

1. Inspection of the skin, nails, facies, eyes, mouth

2. Inspection neck, chest configuration, extremities

2 Blood Pressure Examination1. Determine blood pressure 2. Rule out orthostatic hypotension, coarctatio of

the aorta, cardiac tamponade

3 The Arterial Pulse1. Rate and rhythm of the heart2. Countour of the pulse3. Amplitude of the pulse

4 The Jugular Venous Pulse1. Determine the jugular wave forms2. Estimate the jugular venous pressure3. Evaluate the hepatojugular reflux

5 Percussion 1. Heart’s borders

6 Palpation1. Palpate the point of maximum impulse2. Palpate for localized motion 3. Palpate for generalized motion 4. Palpate for thrills

7 Auscultation 1. Auscultate the cardiac areas2. The Influence of breathing3. Describe any murmur present

8 Examination for Edema1. Test for Edema

SCORE -------- =



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 heart’s 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


Day 13


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 a clinician’s physical examination. In our opinion, the appreciation of cardiac anatomy and hemodynamics by bedside echocardiography makes a physician’s 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:1. Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier

Saunders, 2015. p. 118-132


1. ECG procedure.2. ECG Interpretation

.

TRAINING TASK

ECG Procedure :

PreparationGroup 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 ECGram’s 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.



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 tissues2. Able to result chest x-rays3. Able to workload measurement

CURRICULUM CONTENS:1. Able to evaluate chest x-rays, including evaluation on heart, lung, diaphragm,

skeleton and soft tissues2. Able to result chest x-rays3. 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-ray2. Computed tomography (CT-scan)3. Magnetic resonance imaging (MRI)4. Echocardiography5. Angiocardiography6. Cardiac catheterization7. 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/AP2. Lateral projection3. Right anterior oblique projection (RAO)4. Left anterior oblique projection (LAO)

Increase in cardiac size is the most consistent indication of cardiac disease


Day 14


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 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.


1. Able to evaluate chest x-rays, including evaluation on heart, lung, diaphragm, skeleton and soft tissues.

2. Physiologic parameters during activity.

TRAINING TASK I:

Chest imaging: Cardiovascular System PreparationThere 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.

Instruction1. 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 EvaluationQuestion: 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 27 th , before 11 am

Standard References :1. Roentgen Signs in Diagnostic Imaging Isadore Meschan



MODULE 15Prof. 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 venipucture2. 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 aide-memoir (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 venipucture2. Aseptic procedure3. 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


Day 15


TRAINING TASK

Venipuncture and IV Line ProcedurePreparationWe 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.

Instruction1. 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!

MODULE 16dr. Eka Guna Wijaya, Sp.A

AIMS: 1. Describe Non-cyanotic and Cyanotic Congenital Heart Diseases2. Describe to diagnose and manage Acute Rheumatic Fever

LEARNING OUTCOME: 1. Can describe to diagnose and manage Non-cyanotic and Cyanotic Congenital

Heart Diseases2. Can describe to diagnose and manage Cyanotic Congenital Heart Diseases3. Can describe to diagnose and manage Acute Rheumatic Fever

CURRICULUM CONTENS:1. Fetal-transitional circulations2. To diagnose and manage Non-cyanotic Congenital Heart Diseases and its

complications3. To diagnose and manage Cyanotic Congenital Heart Diseases and its

complications4. Interpret diagnostic tools of Congenital Heart Diseases


Day 16


5. The health education and prognosis of Congenital Heart Diseases6. Interpret diagnostic tool of Acute Rheumatic Fever7. Management of Acute Rheumatic Fever and its complications8. Prevention and rehabilitation of Acute Rheumatic Fever9. Health education and prognosis of Acute Rheumatic Fever

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-to-right 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 Steno-insuficiency (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 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

Standard References: 1. Park, MK. Pediatric Cardiology for Practioners. 4th Ed. Philadelphia, Mosby.

2002. p 129-144, 185-189, 304-310, 311-318


1. Fetal-transitional circulations2. Criteria diagnose and manage of the Non-cyanotic Congenital Heart Diseases

and its complications3. Criteria diagnose and manage of the Cyanotic Congenital Heart Diseases and its

complications4. The health education and prognosis of Congenital Heart Diseases5. Interpret diagnostic tool of Acute Rheumatic Fever6. Management of Acute Rheumatic Fever and its complications7. Prevention and rehabilitation of Acute Rheumatic Fever8. 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: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 baby4. What does you expected from chest X-ray examination.5. When phlebotomy should be perform base on routine blood examination6. Mention a lot of complication may be develop and what is the most hazard7. 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 TASK1. 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 ASSESSMENT1. 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 fever11. Mention etiology, antigenic structure and it’s cellular product.12. Please mention mayor and minor manifestation of rheumatic fever.13. Please mention detail pathology of rheumatic fever.



MODULE 17Dr. 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. Pathogenesis of atherothrombosis2. Risk factors of Ischaemic Heart Disease and Acute Coronary Syndromes3. Clinical spectrum of Ischaemic Heart Disease and Acute Coronary Syndromes4. Interpret laboratory of Acute Coronary Syndromes 5. Interpret diagnostic tools of Ischaemic Heart Disease and Acute Coronary

Syndromes6. Management and its prognosis of Ischaemic Heart Disease and Acute Coronary

Syndromes7. 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 reproducible—but, which may also be


Day 17


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 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 brief—no 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, low-molecular 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. Risk factors of Ischaemic Heart Disease and Acute Coronary Syndromes2. Clinical spectrum of Ischaemic Heart Disease and Acute Coronary Syndromes3. Interpret laboratory of Acute Coronary Syndromes 4. Interpret diagnostic tools of Ischaemic Heart Disease and Acute Coronary

Syndromes5. Management and its prognosis of Ischaemic Heart Disease and Acute Coronary

Syndromes6. Post ACS medical rehabilitation and its rehabilitations

References:1. Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier

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: 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 disease2. What are the complications of acute myocardial infarction3. 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)?

MODULE

MODULE 18dr Wayan Winarti, SpPA

Prof dr. I Gusti Made Aman, SpFK

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 atherosclerosis2. Able to describe the morphology of atherosclerosis3. Able to explain the pathogenesis of IHD4. Able to describe the morphology of myocardial infarction (MI)


Day 18


5. Able to describe drug used in Angina Pectoris

CURRICULUM CONTENT1. Pathogenesis of atherosclerosis2. Morphology of atherosclerosis3. Pathogenesis of IHD4. Morphology of MI5. 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 flow-limiting 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 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.

Standard References :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: Robbin’s Basic Pathology, 7th ed. Philadelphia,

Saunders, 2003. p. 328 – 338; 363 – 372.3. Trevor AJ, Katzung BG, Masters SB: Katzung & Trevor’s Pharmacology, 7th ed.

New York, McGraw-Hill/Lange., 2005. p 105-113

SELF DIRECTING LEARNING1. Pathogenesis of atherosclerosis2. Morphology of atherosclerosis (macroscopy and microscopy)3. Relation between atherosclerosis and IHD4. Morphology of MI (macroscopy and microscopy)5. Principles of anti angina pectoris therapy.6. Classification of anti angina pectoris drugs7. 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 drugs2. 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 and

atherosclerotic plaque!

LEARNING TASK II:



1. Describe the principles of anti angina pectoris therapy.2. Describe the classification of anti angina pectoris drugs3. 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!2. Mention risk factors of IHD!3. Mention the main component of atherosclerotic plaque!4. Describe the principles of anti angina pectoris therapy.5. Describe the classification of anti angina pectoris drugs6. Describe the mechanism of actions and the important pharmacokinetic properties

of anti angina pectoris drugs

MODULE 19dr. Bajra Nadha, SpJP

dr. I G Md Gd Surya Candra Trapika, MSc

AIMS: Able to diagnose and manage Arrhythmias

LEARNING OUTCOME: 1. Can describe to diagnose Arrhythmias2. Can describe manage Arrhythmias

CURRICULUM CONTENS:1. Etiology and pathophysiology of Arrhythmias2. Clinical approach of Arrhythmias3. Treatment of Arrhythmias4. 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 physician’s 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


Day 19


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. 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 furtherdiagnostic testing The following additional tests can be used to evaluate patients who have cardiac arrhythmias. The physician’s 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 heart—most 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, itgenerally 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 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 appearance—regular 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 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. .

Standard References :1. Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier

Saunders, 2015. p. 687-837


1. Etiology of Arrhythmias2. Pathophysiology of Arrhythmias3. Clinical approach of Arrhythmias4. Treatment of Arrhythmias5. 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 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.

Standard References :1. Trevor AJ, Katzung BG, Masters SB: Katzung & Trevor’s Pharmacology, 7th ed.

New York, McGraw-Hill/Lange., 2005. p 124-136

SELF-DIRECTED LEARNING1. 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. S1 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 drug’s mechanism of action?4. Which antiarrhythmic drug should be given to the patient to avoid such event?5. What is the drug’s mechanism of action?6. List some of the important adverse effects of some important drugs from each

class of antiarrhythmic drug.

SELF ASSESSMENT1. The following adverse effects are associated with amiodarone:

a. Visual disturbancesb. Hyperthyroidismc. Hypothyroidismd. Pulmonary fibrosise. Photosensitivity

2. Sotalol:a. Is effective in supraventricular and ventricular arrhythmiasb. Is not effective when given by mounthc. The dose should be reduced in renal impairmentd. May cause torsades de pointese. Is a less potent negative inotropes tha amiodarone

3. Lidocainea. 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 epileptogenicc. Is a positive inotroped. Is usually administered as an intravenous bolus followed by infusione. Is the drug of first choice for supraventricular tachycardia

4. Digoxin:a. Reduces the ventricular rate in atrial fibrilationb. Is contraindicated in second degree heart blockc. Has narrow theraupetic indexd. Induced arrhytmias may be terminated by magnesiume. 80% of adminestered digoxin is excreted unchanged in the bile

MODULE 20Dr. 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


Day 20


2. Can describe diagnose and manage the Vascular disease

CURRICULUM CONTENS:1. Etiology and pathophysiology of Hypertension and Vascular disease2. Clinical criteria of Hypertension and Vascular disease3. Diagnostic approach of Hypertension and Vascular disease4. Management and prognosis of Hypertension and Vascular diseases

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;42:1206–1252




1. Etiology of Hypertension and Vascular disease 2. Pathophysiology of Hypertension and Vascular disease3. Clinical criteria of Hypertension and Vascular disease4. Diagnostic approach of Hypertension and Vascular disease5. 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 disease3. What are the side effects of hydro-chlorothiazide?4. Please mention 3 examples of secondary hypertension

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 Failure2. Can describe manage the Heart Failure

CURRICULUM CONTENS:1. Etiology and pathophysiology of Heart Failure 2. Clinical and diagnostic approach of Heart Failure


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3. Pharmacologic treatment of Heart Failure 4. 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.

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 increasein 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 antagonists—an ACE inhibitor [or angiotensin receptor blocker (ARB)], a beta-blocker, and an MRA—are 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.

Standard References:1.Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier Saunders, 2015. p. 429-6152.McMurray et al. ESC Guidelines For The Diagnosis and Treatment of Acute and Chronic Heart Failure. European Heart Journal. 2012;33.1787-1847


1. Etiology of Heart Failure 2. Pathophysiology of Heart Failure 3. Clinical and diagnostic approach of Heart Failure 4. Pharmacologic treatment of Heart Failure 5. 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 cardiomyopathy5. 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 therapy2. Exercise program is starter is after the chest pain is lost or after 2-3 days3. 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 habit5. After discharge the patient may not do sexual intercourse6. At thorax surgery case exercise is better to be given after operation

MODULE 22Prof dr. I Gusti Made Aman, SpFK

dr. I G Md Gd Surya Candra Trapika, MSc

AIMS: 1. Describe the anti hypertensive drugs2. Describe the heart failure drugs

LEARNING OUTCOME: 1. Can describe the anti hypertensive drugs2. Can describe the heart failure drugs

CURRICULUM CONTENS:1. Principles and classification of anti hypertensive drugs2. Important pharmacokinetic properties of anti hypertensive drugs.3. Mechanism of actions of anti anti hypertensive drugs.4. Important adverse effects of anti hypertensive drugs5. Principles and classification of heart failure drugs6. Important pharmacokinetic properties of heart failure drugs.7. Mechanism of actions of heart failure drugs.8. 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


Day 22


indirectly through inhibition of sympathetic nervous system activity or inhibition of renin-angiotensin-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 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.

Standard References:1. Trevor AJ, Katzung BG, Masters SB: Katzung & Trevor’s Pharmacology, 7th ed.

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 drugs3. Important pharmacokinetic properties of anti hypertensive drugs.4. Mechanism of actions of anti anti hypertensive drugs.5. Important adverse effects of anti hypertensive drugs6. Principles of heart failure therapy.7. Classification of heart failure drugs8. 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 effects5. Describe the difference between 2 types of angiotensin antagonists6. List the major side effects of the prototype antihypertensive drugs7. Compare the indication and contraindication of antihypertensive drugs8. 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 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. Compare the mechanism of action and clinical uses of positive inotropes..2. Describe toxic action of digitalis on the heart3. Describe the effect of electrolyte imbalance on digitalis effect4. Describe the interaction between digitalis and diuretic and quinidine

Explain either the statement is True or False1. Severe bradycardia may occur after clonidine overdose2. Captopril decreases sodium and increases potassium in the urine3. Hemolytic anemia caused by antihypertensive drug clonidine4. Postural hypotension is a common adverse effect of alfa blocker5. Losartan most likely causes cough6. Nitroprusside must be given by intravenous infusion7. Minoxidil causes vasodilatation by opening potassium channels

MODULE 23

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. Etiology of Acute and Chronic Cor Pulmonale.2. Pathogenesis of Pulmonary Hypertension.


Day 23


3. Clinical Manifestation of Cor Pulmonale.4. Physical Findings of Cor Pulmonale.5. Diagnostic techniques for Cor Pulmonale.6. 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 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. Etiology of Acute and Chronic Cor Pulmonale.2. Pathogenesis of Pulmonary Hypertension.3. Clinical Manifestation of Cor Pulmonale.4. Physical Findings of Cor Pulmonale.5. Diagnostic techniques for Cor Pulmonale.6. 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.

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?

MODULE 24

dr. Bajra Nadha, SpJP dr. Luh Kamiati, SpRM

AIMS: 1. Able to diagnose and manage Valvular Heart Disease (VHD)2. Describe to diagnose and manage Common Peripherial Vascular Disease 3. Describe diagnose and manage Pericardial disease and Endocardial disease4. 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

Disease4. Can describe diagnose and manage Pericardial Disease and Endocardial

Disease5. Can describe to rehabilitation patient with Cardiovascular Disease

CURRICULUM CONTENS:


Day 24


1. Etiology, pathophysiology and clinical spectrum of Valvular Heart Disease2. Interpret diagnostic tools of Valvular Heart Disease3. Management and prognosis and rehabilitation of Valvular Heart Disease4. Etiology and pathophysiology of Common Peripherial Vascular Disease 5. Clinical diagnostic approach, Pharmacologic treatment of Common Peripherial

Vascular Disease 6. Etiology and pathophysiology of Pericardial and Endocardial disease7. Clinical and diagnostic approach of Pericardial and Endocardial diseases8. Pharmacologic treatment and Prognosis of Pericardial and Endocardial disease9. Rehabilitation and prognosis patient with Cardiovascular Disease

ABSTRACT I: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

Standard References:1. Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier

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 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.

Standard References:1. Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier

Saunders, 2015. p. 1391-15502. Habib, Gilbert et al. Guidelines on The Prevention, Diagnosis, and Treatment

of Infective Endocarditis. European Heart Journal. 2009;30.2369-24133. 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, 351-358; 398-416, 360-363; 1241-1246

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. Etiology, pathophysiology and clinical spectrum of Valvular Heart Disease2. Interpret diagnostic tools of Valvular Heart Disease3. Management and prognosis and rehabilitation of Valvular Heart Disease4. Etiology and pathophysiology of Common Peripherial Vascular Disease 5. Clinical diagnostic approach, Pharmacologic treatment of Common Peripherial

Vascular Disease 6. Etiology and pathophysiology of Pericardial and Endocardial disease7. Clinical and diagnostic approach of Pericardial and Endocardial diseases8. Pharmacologic treatment and Prognosis of Pericardial and Endocardial disease9. 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 2ndintercostal-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 disease3. Please describe the radiological findings consistent with this disease.4. Mention definition of cardiovascular rehabilitation5. Explain the objective of cardiovascular rehabilitation6. Mention the contraindication exercise therapy7. Explain the benefit effect of exercise therapy8. Explain stages of cardiovascular rehabilitation MI9. 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-ASSESSMENT1. Please describe the etiology of mitral regrugitation2. Please explain the complication of mitral stenosis3. Please describe the ECG findings in aortic stenosis4. 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 rehabilitation10. Explain the objective of cardiovascular rehabilitation11. Mention the contraindication exercise therapy12. Explain the benefit effect of exercise therapy13. Explain stages of cardiovascular rehabilitation MI14. Mention effect of exercise to CH

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 surgery2. Can describe the basic aspect in cardiac surgery3. Can describe the cardiac diseases who need surgery

CURRICULUM CONTENTS:1. Surgery of the congenital heart2. 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.


Day 25


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.

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

Standard References:1. Stuart W. Jamieson and Norman E Shumway: Cardiac Surgery in Rob & Smith’s

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 arteries2. Can describe the basic aspect in aorta arteries3. Can describe the aorta and arteries diseases who need surgery

CURRICULUM CONTENTS:1. Surgery of the aneurysm of aorta2. 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.

Standard References:1. Allan D. Callow, Calvin B. Erust. : Vascular surgery, Theory and Practice,

Prentice- Hall International Inc.London , 1995


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 I1. How to prepare if the patient have surgery2. What is cardic surgery category for PDA closure3. PDA commonly concomittent with congenital anomaly. Is it every PDA have

surgery to close the shunt4. 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 closure2. What the different between close and open cardiac surgery3. After ASD was closured, why the patient getting good growing of the body4. 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 surgery2. Describe the principle coronary heart surgery3. Describe the principle of Valve surgery

SCENARIO:

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 surgery3. How to do to enlargement of aorta4. 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 diagnosis2. What will you do to improve the blood flow to the distal end of feet3. How the prognosis and reccurent rate

SELF-ASSESSMENT :1. Describe the principle of vascular surgery2. Describe the principle arterial repair3. Describe the principle of care after vascular surgery



8. REFERENCESA. Student Standard References :

1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott & Wilkins, 2007.

2. Sadler TW: Langman’s Medical Embryology, 10th ed. Philadelphia, Lippincott & Wilkins, 2006.

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, 20066. Kumar V, Cotran R S, Robbins SL: Robbin’s Basic Pathology, 7th ed.

Philadelphia, Saunders, 20037. Trevor AJ, Katzung BG, Masters: Katzung & Trevor’s Pharmacology, 7th ed.

New York, Lange Medical Book’s/Mc.Graw-Hill, 2005.8. Park MK. Pediatric Cardiology for Practioners. 4th Ed. Philadelphia, Mosby.

2002.9. McPhee, S.J., Papadakis, M.A., Current Medical Diagnosis & Treatment. 47th

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 , 199511. Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier

Saunders, 2015. p. 1391-155012. Habib, Gilbert et al. Guidelines on The Prevention, Diagnosis, and Treatment

of Infective Endocarditis. European Heart Journal. 2009;30.2369-241313. Maisch, Bernhard et al. Guidelines on The Diagnosis and Management of

Pericardial Disease. European Heart Journal. 2004; 1-2814. McPhee SJ, Papadakis MA. Current Medical Diagnosis & Treatment. 47 th ed.

New York: Lange Mecical Book`s/The McGraw-Hill Companies, 2008.p. 287-299, 351-358; 398-416, 360-363; 1241-1246

15. Garrison SJ: Hand Book of Physical Medicine and Rehabilitation, 2nd 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 & Smith’s 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 & Fawcett’s 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

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 investigation requested by doctor e.g. routine laboratory assay or X-ray. Doctor able to decide and give initial treatment also refer to relevan specialist for non-emergency cases.

3. B. 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 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 investigation requested by doctor e.g. routine laboratory assay or X-ray. Doctor 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 1 2 3 4 5

A Topic

1. Introduction lecture

2 General anatomy, topography and surface anatomy of the heart and great vessels.

3 Microscopic structure of the heart wall and



pericardial

4 The heart as a pump

5 Intrinsic Conduction System and Cardiac Action

Potential

6 Heart Valves and Heart Sounds

7 Microscopic Anatomy of The Valves of The Heart

8 Cardiac Out Put and Regulation of Heart Pumping

9 Factors that Affect Blood Pressure

Microscopic Anatomy of The Great Vessel

10 Microscopic Anatomy of The Great Vessel

11 Myocardial perfusion

12 Blood Pressure Regulation

13 The formation of anomalies of the heart and great vessels.

14 Approach to Patient With Cardiovascular 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 Antiarrhythmic Drugs

22 Hypertension

23 Antihypertensive Drugs

24 Heart Failure

25 Positive Inotropes

26 Common Peripheral Vascular and lymphatic



disease

27 Cardiomyopathi

28 Valvular Heart Disease Pericardial & Endocardial Disease

29 Measure Workload

30 CV Physical Examination

31 ECG

32 Chest Imaging

33 IV line Procedure

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. 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

6 DR. Dr. Adiatmika, M.For

7. Prof dr. I G M. Aman

8 DR. Wayan Sumardika

9 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

18 Dr. Luh Kamiati, SpRM

19 Dr. N. Semadi, SpB

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 expectation2. Insufficient or inadequate with expectation3. Sufficient or inadequate with expectation4. Good or suitable with expectation5. 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

Learning strategy

Lecturer

Facilitator

Assessment

11. ITEM GRID

Question type: MCQ with vignette

No Topic Number of question

PIC Vignette

1. Introduction lecture Prof dr. Wita

2 General anatomy, topography and surface anatomy of the heart and great vessels.

Dr. IGA Widianti

3 Microscopic structure of the heart wall and pericardial

Dr. IGN Mayun

4 The heart as a pump Dr. Made Muliarta,

5 Intrinsic Conduction System and Cardiac Action Potential

Dr. Made Muliarta,

6 Heart Valves and Heart Sounds Prof. Dewa Sutjana

7 Microscopic Anatomy of The Valves of The Heart

Dr. I G N Mayun

8 Cardiac Out Put and Regulation of Heart Pumping

Prof. Dewa Sutjana

9 Factors that Affect Blood Pressure

DR. Dr. Adiatmika,



10 Microscopic Anatomy of The Great Vessel

Dr. IGN Mayun

11 Myocardial perfusion Dr. Made Muliarta

12 Blood Pressure Regulation DR. Dr. Adiatmika,

13 The formation of anomalies of the heart and great

vessels.

Dr. IGA Widianti

14 Approach to Patient With Cardiovascular Disease

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 Antiarrhythmic Drugs 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

TOTAL 100question



~ CURRICULUM MAP ~Smstr Program or curriculum blocks

10 Senior Clerkship

9 Senior Clerkship

8 Senior clerkship

7

Medical Emergency(3 weeks)

BCS (1 weeks)

Special Topic:-Travel medicine(2 weeks)

Elective Study III(6 weeks)

Clinic Orientation (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-Complementary & Alternative Medicine - Forensic(3 weeks)

Elective Study II(1 weeks)

4

Musculoskeletal system &connectivetissue disorders(4 weeks)

BCS (1 weeks)

Neuroscienceandneurologicaldisorders(4 weeks)

BCS (1 weeks)

Behavior Changeand disorders(4 weeks)

BCS(1 weeks)

The Visualsystem &disorders(2 weeks)

BCS(1 weeks)

3

Hematologicsystem & disor-ders & clinical oncology(4 weeks)

BCS (1 weeks)

Immune system &disorders(2 weeks)

BCS(1 weeks)

Infection & infectiousdiseases(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(2 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

StudiumGenerale and Humaniora(3 weeks)

Medicalcommunication(3 weeks)

BCS (1 weeks)

The cellas bioche-mical machinery(3 weeks)

BCS(1 weeks)

Growth&development(4 weeks)

BCS: (1 weeks)

Pendidikan Pancasila & Kewarganegaraan (3 weeks)


Study Guide Cardio Tayang by Gextha 30 Maret 2015

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