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Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
2
STUDY GUIDE THE CARDIOVASCULAR SYSTEM AND DISORDERS
Planners
Komang Januartha Putra Pinatih
I Made Junior Rina Artha
Agung Nova Mahendra
I.B. Rangga Wibuti
I Made Putra Swi Antara
Nyoman Wiryawan
Putu Gede Sudira
Contributors
I Made Junior Rina Artha
I Wayan Wita
Agung Nova Mahendra
Ni Putu Ekawati
A.A. Wiradewi
Luh Kamiati
Hendy Wirawan
A.A. Ayu Dwi Adelia Yasmin
I Kadek Susila Surya Darma
I Nyoman Wiryawan
I Made Putra Swi Antara
I Nyoman Semadi
I.B. Rangga Wibuti
Luh Oliva Saraswati Suastika
Eka Guna Wijaya
Lisna Astuti
Pontisomaya Parami
Editors
Putu Gede Sudira I Made Junior Rina Artha
Layout
Rizky Darmawan
First Edition March 2017
Second Edition February 2018
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system,
or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or
otherwise without prior written permission of the publisher.
Published by Department of Medical Education Medicine Programme, Faculty of Medicine,
Universitas Udayana.
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
3
CONTENTS
STUDY GUIDE THE CARDIOVASCULAR SYSTEM AND DISORDERS ....................................... 2
CONTENTS........................................................................................................................................... 3
PREFACE ............................................................................................................................................. 5
CURRICULUM MAP............................................................................................................................. 6
GENERAL CURRICULUM OF CARDIOVASCULAR SYSTEM AND DISORDERS ...................... 7
PLANNERS AND LECTURERS ........................................................................................................ 10
FACILITATORS .................................................................................................................................. 11
LEARNING ACTIVITY ........................................................................................................................ 12
IMPORTANT INFORMATIONS ......................................................................................................... 12
STUDENT PROJECT ......................................................................................................................... 13
ARTICLE REVIEW ASSESSMENT FORM ...................................................................................... 15
SELF ASSESSMENT ......................................................................................................................... 16
ASSESSMENT METHOD .................................................................................................................. 16
GENERAL TIME TABLE FOR A AND B CLASSES ........................................................................ 16
TIME TABLE OF CLASSES .............................................................................................................. 17
LEARNING PROGRAMS ................................................................................................................... 23
LECTURE 1......................................................................................................................................... 23
LECTURE 3......................................................................................................................................... 28
LECTURE 4......................................................................................................................................... 31
LECTURE 5......................................................................................................................................... 33
LECTURE 6......................................................................................................................................... 35
LECTURE 7......................................................................................................................................... 38
LECTURE 8......................................................................................................................................... 41
LECTURE 9......................................................................................................................................... 43
LECTURE 10 ...................................................................................................................................... 45
LECTURE 12 ...................................................................................................................................... 52
LECTURE 13a .................................................................................................................................... 57
LECTURE 13b .................................................................................................................................... 59
LECTURE 14 ...................................................................................................................................... 61
LECTURE 15 ...................................................................................................................................... 63
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
4
LECTURE 16 ...................................................................................................................................... 66
BASIC CLINICAL SKILLS .................................................................................................................. 70
BASIC CLINICAL SKILL 1 ................................................................................................................. 71
BASIC CLINICAL SKILL 2 ................................................................................................................. 73
BASIC CLINICAL SKILL 3 ................................................................................................................. 75
BASIC CLINICAL SKILL 4 ................................................................................................................. 77
EVALUATION FORM OF THE CARDIOVASCULAR SYSTEM AND DISODERS....................... 79
REFERENCES ................................................................................................................................... 82
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
5
PREFACE
The medical curriculum has become increasingly vertically integrated, with stronger basic
concept and support by clinical examples and cases to help in the understanding of the
relevance of the underlying basic science. Basic science concepts may help in the
understanding of the pathophysiology and treatment of diseases. Cardiovascular system and
disorders block has been written to take account of this trend, and to integrate core aspects of
basic science, pathophysiology, and treatment into a single, easy to use revision aid.
The cardiovascular block will focus on anatomy, histology and physiology of
cardiovascular system, pharmacology of different classes of cardiovascular drugs, symptom and
signs of major cardiovascular disease and its pathophysiology and basic principle concept to
education, prevention, treatment and rehabilitation in cardiovascular system disorder in a
patient, family, and community. This study guide is developed by the academic staffs from
various departments: Pharmacology, Anatomy and Clinical Pathology, Cardiology, Pediatric
Cardiology, Cardiothoracic Surgery, and Medical Rehabilitation, Radiology, and Anesthesia.
The learning process will be carried out for 4 weeks (20 working days) starts from
February 26th, 2018 as shown in the timetable. The final examination will be conducted on April
3rd, 2018 in the form of MCQ. The learning situation includes lecture, individual learning, small
group discussion, plenary session, practice, and clinical skills.
Most of the learning material should be learned independently and discuss in SGD by the
students with the help of a facilitator. The lecture is given to emphasize the most important thing
of the material. In a small group discussion, the students gave learning task to lead their
discussion.
This simple study guide needs more revision in the future so that the planners kindly invite
readers to give any comments and critics for its completion. Thank you.
Planners
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
6
CURRICULUM MAP
Program or curriculum blocks
10 Senior Clerkship
9 Senior Clerkship
8 Senior Clerkship
7
Health System-
based Practice
(3 weeks)
BCS (1 weeks)
Community-
based practice
(4 weeks)
Evidence-based
Medical Practice
(2 weeks)
Special topics :
Health Ergonomy &
Health
Environment
(2 weeks)
Elective Study
IV (evaluation)
(2 weeks)
Compre
Clinic
Orientation
(Clerkship)
+ medical
ethic
(4 weeks)
18
6
The
Cardiovascular
System and
Disorders
(3 weeks)
BCS (1 weeks)
Medical
Emergency
(3 weeks)
BCS (1 weeks)
The Urinary
System and
Disorders
(3 weeks)
BCS (1 weeks)
The Reproductive
System and
Disorders
(3 weeks)
BCS (1 weeks)
Elective Study
III
(3 weeks)
(KKN) 19
5
Neuroscience
and
neurological
disorders
(3 weeks)
BCS (1 weeks)
The Respiratory
System and
Disorders
(3 weeks)
BCS (1 weeks)
The skin &
hearing system
& disorders
(3 weeks)
BCS (1 weeks)
Special Topic :
- Palliative med
- Complemnt &
Alternative Med.
(2 weeks)
Forensic
Medicine and
Medicolegal
(2 weeks)
Elective
Study II
(2 weeks)
18
4
Musculoskeletal
system &
connective
tissue disorders
(3 weeks)
BCS (1 weeks)
Alimentary
& hepatobiliary
systems &
disorders
(3 Weeks)
BCS (1 weeks)
The Endocrine
System,
Metabolism and
Disorders
(3 weeks)
BCS (1 weeks)
Clinical Nutrition
and Disorders
(2 weeks)
BCS (1 weeks)
The Visual
system &
disorders
(2 weeks)
BCS (1weeks)
18
3
Behavior
Change
and disorders
(3 weeks)
BCS (1 weeks)
Basic Infection
& infectious
diseases
(3 weeks)
BCS (1 weeks)
Immune system &
disorders
(2 weeks)
BCS (1 weeks)
Hematologic
system & disorder
& clinical oncology
(3 weeks)
BCS (1 weeks)
Special Topic
(Andro & aging,
Geriatri, Travel
medicine)
(4 weeks)
19
2
BIOMEDIK III
(4 weeks)
Growth
&
development
(2 weeks)
BCS: (1 weeks)
Medical
communication
(2 weeks)
BCS (1 weeks)
Medical
Professionalism
(2 weeks)
BCS (1 weeks)
Basic
Pharmaceutical
medicine &
drug etics
(2 weeks)
Elective
Study I
(2 weeks)
17
1
Studium
Generale and
Humaniora
(2 weeks)
BIOMEDIK I
(8 weeks)
The cell
as biochemical
machinery
(2 weeks)
BCS (1 weeks)
BIOMEDIK II
(6 weeks)
19
Pendidikan Pancasila & Kewarganegaraan ( 3 weeks )
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
7
GENERAL CURRICULUM OF CARDIOVASCULAR SYSTEM AND DISORDERS
Aims:
Comprehend the structure, physiology, and pathology of the cardiovascular system.
Interpret the laboratory and imaging examination of the cardiovascular system disorders.
Diagnose and treat the patient with common cardiovascular system disorders.
Plan education, prevention, management and rehabilitation of cardiovascular system
disorders to patient, family, and community.
Learning outcomes:
Concern about the size of problem and diversity of cardiovascular disease in the
community.
Able to describe the structure and function of the cardiovascular system.
Able to interpret the result of examination (physical, laboratory, electrocardiography and
chest imaging).
Able to explore patients with the cardiovascular problem (chest pain/ discomfort,
palpitation, dyspnea and cyanosis).
Able to manage major cardiac diseases (hypertension, heart failure, coronary artery
disease, cor pulmonale, valvular heart disease and congenital heart disease).
Able to manage common vascular and lymphatic diseases (venous insufficiency,
lymphedema, peripheral artery disease).
Able to implement rehabilitation of cardiovascular diseases.
Curriculum contents:
Structure and function of the cardiovascular system.
Physiology of the heart and blood vessels in related with intrinsic conduction system,
cardiac output regulation and regulation of blood flow.
Symptoms and signs of cardiovascular disease.
Pathophysiology of cardiovascular system disorders.
Basic physical, laboratory, electrocardiography and imaging examination.
Interpretation of examination results.
Drugs that commonly used in cardiovascular system disorders (anti-hypertension, anti-
angina, anti-arrhythmia, and heart failure drugs).
Basic principles of education, prevention, treatment and rehabilitation in cardiovascular
system disorders in patient, family, and community.
Curriculum structure:
Structure of curriculum mainly derives from general competences of Indonesian general
practitioner. Those competencies in diagnosing diseases and doing clinical skills should be
mastered by all the general practitioners here. Local values of our institutions are also
considered as added values in this curriculum.
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
8
NO DAFTAR PENYAKIT SESUAI SKDI 2012 TINGKAT KEMAMPUAN
GANGGUAN DAN KELAINAN PADA JANTUNG
1 Syok (septik, hipovolemik, kardiogenik, neurogenic) 3B
2 Angina pectoris 3B
3 Infark myocard 3B
4 Gagal jantung akut 3B
5 Gagal jantung kronik 3A
6 Cardiorespiratory arrest 3B
7 Takikardi : supraventricular, ventrikular 3B
8 Fibrilasi atrial 3A
9 Fibrilasi ventricular 3B
10 Atrial flutter 3B
11 Ekstrasistol supraventrikuler, ventrikuler 3A
12 Kor pulmonale akut 3B
13 Kor pulmonale kronik 3A
GANGGUAN AORTA DAN ARTERI
14 Hipertensi esensial 4A
15 Hipertensi sekunder 3A
GANGGUAN VENA DAN PEMBULUH LIMFE
16 Tromboflebitis 3A
17 Limfangitis 3A
18 Limfedema (primer, sekunder) 3A
19 Insufiensi vena kronik 3A
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
9
NO KETERAMPILAN KLINIS SESUAI SKDI 2012 TINGKAT KETERAMPILAN
PEMERIKSAAN FISIK
1 Inspeksi Dada 4
2 Palpasi Denyut Apeks Jantung 4
3 Palpasi Arteri Karotis 4
4 Perkusi Ukuran Jantung 4
5 Auskultasi Jantung 4
6 Pengukuran Tekanan Darah 4
7 Pengukuran Tekanan Vena Jugularis (JVP) 4
8 Palpasi Denyut Arteri Ekstremitas 4
9 Penilaian Denyut Kapiler 4
10 Penilaian Pengisian Ulang Kapiler (Capillary Refill) 4
11 Deteksi Bruits 4
PEMERIKSAAN (FISIK) DIAGNOSTIK
12 Tes (Brodie) Trendelenburg 4
13 Elektrokardiografi (EKG): Pemasangan Dan Interpretasi
Hasil EKG Sederhana (VES, AMI, VT, AF) 4
14 Tes Perthes 3
15 Test Homan (Homan’s Sign) 3
16 Uji Postur Untuk Insufisiensi Arteri 3
17 Tes Hiperemia Reaktif Untuk Insufisiensi Arteri 3
18 Test Ankle-Brachial Index (ABI) 3
RESUSITASI
19 Pijat Jantung Luar 4
20 Resusitasi Cairan 4
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
10
PLANNERS AND LECTURERS
NO NAME DEPARTMENT PHONE
1. dr. I Made Junior Rina Artha, Sp.JP(K),
FIHA, FAsCC (Coordinator) Cardiology 08123814814
2. dr. Luh Oliva Saraswati Suastika, Sp.JP,
FIHA (Secretary) Cardiology 081330530247
3. Prof. Dr. dr. I Wayan Wita, Sp.JP(K), FIHA,
FAsCC (member) Cardiology 08123809780
4. dr. Putu Gede Sudira, Sp.S (member) DME 081805633997
5. dr. Agung Nova Mahendra, M.Sc Pharmacology 087861030195
6. dr. Putu Ekawati, M.Repro, Sp.PA Pathology Anatomy 08123958158
7. Dr. dr. AA Wiradewi, Sp.PK Clinical Pathology 08155237937
8. dr. I Kadek Susila Surya Darma, M. Biomed,
Sp.JP, FIHA Cardiology 08113853151
9. dr. I.B. Rangga Wibhuti, M.Biomed,
Sp.JP(K), FIHA, FASE Cardiology 081237287888
10. dr. I Made Putra Swi Antara, Sp.JP(K),
FIHA Cardiology 08123804782
11. dr. A.A. Ayu Dwi Adelia Yasmin, M. Biomed,
SpJP, FIHA Cardiology 087861402169
12. dr. I Nyoman Wiryawan, SpJP(K), FIHA Cardiology 081289053234
13. dr. Hendy Wirawan, SpJP Cardiology 0817352649
14. Dr. dr. Semadi, SpB, SpBTKV Cardiothorac Surgery 08123838654
15. dr. Eka Guna Wijaya, Sp.A(K) Pediatric Cardiology 081338599801
16. dr. Lisna Astuti, Sp.Rad. Radiology 081337934497
17. dr. Luh Kamiati, Sp.KFR Physiotherapy 08123998787
18. dr. Pontisomaya Parami, Sp.An., MARS Anesthesia 08113800107
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
11
FACILITATORS Regular Class (Class A)
No Name Group Departement Phone Venue
(2ndfloor)
1 Dr. dr. Ni Made Linawati, M.Si A1 Histology 081337222567 2nd floor:
R.2.09
2 dr. I Wayan Sugiritama, M.Kes A2 Histology 08164732743 2nd floor:
R.2.10
3 dr. Wayan Citra Wulan Sucipta
Putri, MPH A3 Public Health 087761838141
2nd floor:
R.2.11
4 Dr. dr. Ni Nyoman Sri Budayanti,
Sp.MK (K) A4 Microbiology 08553711398
2nd floor:
R.2.12
5 Prof. Dr. dr. I Made Jawi, M.Kes A5 Pharmacology 08179787972 2nd floor:
R.2.13
6 Dr. dr. Desak Made Wihandani,
M.Kes A6 Biochemistry 081338776244
2nd floor:
R.2.14
7 dr. I Nyoman Gede Wardana,
M.Biomed A7 Anatomy 087860405625
2nd floor:
R.2.15
8 Dr.dr. I Made Muliarta, M.Kes A8 Physiology 081338505350 2nd floor:
R.2.16
9 Dr. dr, I Made Sudarmaja,
M.Kes A9 Parasitology 08123953945
2nd floor:
R.2.20
10 dr. Ni Made Dewi Dian
Sukmawati, Sp.PD A10
Internal
Medicine 08123320380
2nd floor:
R.2.21
English Class (Class B)
No Name Group Departement Phone Venue
(2ndfloor)
1 dr. Putu Gede Sudira Sp.S B1 DME 081805633997 2nd floor:
R.2.09
2 Dr. dr. Bagus Komang
Satriyasa, M.Repro B2 Pharmacology 087777790064
2nd floor:
R.2.10
3 dr. Sari Wulan Dwi Sutanegara,
Sp.T.H.T.K.L (K)., FICS B3 ENT
081237874447/
081338466039 2nd floor:
R.2.11
4 dr. Pontisomaya Parami, Sp. An,
MARS B4 Anesthesia 08113800107
2nd floor:
R.2.12
5 Dr. dr. Susy Purnawati, M.KK B5 Physiology 08123989891 2nd floor:
R.2.13
6 dr. I Wayan Surudarma, Msi B6 Biochemistry 081338486589 2nd floor:
R.2.14
7 dr. Henky, Sp. F, M.Beth,
FACLM B7 Forensics 08123988486
2nd floor:
R.2.15
8 Dr. dr. Cok Bagus Jaya
Lesmana, Sp.KJ (K) B8 Psychiatry 0816295779
2nd floor:
R.2.16
9 dr. I Wayan Gede Sutadarma,
M.Gizi, Sp.GK B9 Biochemistry 082144071268
2nd floor:
R.2.20
10 dr. I.G.A.A. Dwi Karmila, Sp.KK B10 Dermatovenerol
ogy 08123978446
2nd floor:
R.2.21
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
12
LEARNING ACTIVITY
There are several types of learning activity:
Lecture
Plenary session
Independent learning based on the lecture’s topic
Small group discussion to solve the learning task
Practicing
Student project
Clinical skill and demonstration
Self-assessment at the end of every topic
The lecture will be held at room 4.02 (4th floor), while discussion rooms available at 2nd
floor (room 2.09 - 2.16, 2.20, and 2.21).
IMPORTANT INFORMATION Meeting of the students’ representative
In the middle of the block schedule, a meeting is designed among the student
representatives of every small group discussions, facilitators, and resource persons. The
meeting will discuss the ongoing teaching-learning process, quality of lecturers and facilitators
as a feedback to improve the next process. The meeting will be taken during student project
presentation.
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
13
STUDENT PROJECT
Title of student project
Group discussion Topic
A1 Endokarditis infeksiosa
A2 Vena varikose
A3 Aneurisma aorta
A4 Kardiomiopati hipertrofi
A5 Koartasio aorta
A6 Trombosis vena dalam
A7 Sindroma Wolff-Parkinson-White (WPW)
A8 Iskemia tungkai akut
A9 Penyakit Raynaud
A10 Hipertensi pulmonal
B1 Perikarditis
B2 Obstructed venous return
B3 Diseksi aorta
B4 Kardiomiopati restriktif
B5 Subclavian steal syndrome
B6 Emboli vena
B7 Sindroma Brugada
B8 Peripheral artery disease (klaudikasio)
B9 Penyakit Buerger
B10 Anomali Ebstein
About Topic, Presentation’s place and schedules, Task rules, Assessment, and Evaluator will
be discussed at a lecture of block introduction on February 26th, 2018.
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
14
TITLE
(subject/ topic: choose from competency list)
Name
NIM
Faculty of Medicine, Udayana University
2018
______________
1. Introduction (Pendahuluan)
2. Content (Isi, sesuai topik yang dibahas)
3. Summary (Ringkasan)
4. References: (Daftar Pustaka) Van Couver style
Example:
Journal
Sheetz MJ, King GL. Molecular understanding of hyperglycemia’s adverse effect for
diabetic complications. JAMA. 2002;288:2579-86.
Textbook
Libby P. The Pathogenesis of atherosclerosis. In: Braunwald E, Fauci A, Kasper D,
Hoster S, Longo D, Jamason S (eds). Harrison’s principles of internal medicine. 15th ed.
New York: McGraw Hill; 2001. p. 1977-82.
Internet
WHO. Obesity: preventing and managing the global epidemic. Geneva: WHO 1998.
[cited 2005 July]. Available from:
http://www.who.int/dietphysicalactivity/publications/facts/ obesity/en.
Student project consists of 6 – 10 pages, 1.5 space, Times new romance 12.
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
15
ARTICLE REVIEW ASSESSMENT FORM
Faculty of Medicine, Udayana University
___________________________________________________________________________
Block : Cardiovascular System and Disorders
Name : ________________________________________
Student No. (NIM) : ________________________________________
Facilitator : ________________________________________
Title : ________________________________________
________________________________________
Time table of consultation
Point of discussion Week Date Tutor sign
1. Title 1
2. References 1
3. Outline of paper 2
4. Content 3
5. Final discussion 4
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/ Evaluator
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
16
SELF ASSESSMENT
Self-assessment of each lecture will be given after each lecture session and will be marked.
This mark can determine whether the student passes this block or not. Any final mark between
62 - 64 will be reconsidered with self-assessment’s mark to see the student’s status. Any
student with self-assessment’s mark 65 or more will pass this block. And for the lower one will
have to attend the remedial examination. It is important to do this self-assessment cautiously,
because this activity may be your ticket to pass this block just at first examination.
ASSESSMENT METHOD
Assessment in this theme consists of:
SGD : 5%
Final Exam : 80%
Student Project : 15%
Final mark 65 or more considered to pass this block. Certain conditions applied for those with a
final mark between 62 – 64. These students will be analyzed using their self-assessment’s
mark. Students with final mark 62 – 64 and self-assessment’s mark equal or more than 65 will
also consider passing this block. The value of marking:
A ≥ 80
B+ >70-79
B 65-70
GENERAL TIMETABLE FOR A AND B CLASSES
CLASS A CLASS B
TIME ACTIVITIES TIME ACTIVITIES
08.00-09.00 Lecture 09.00-10.00 Lecture
09.00-10.30 Independent learning 10.00-11.30 Student project
10.30-12.00 SGD 11.30-12.00 Break
12.00-12.30 Break 12.00-13.30 Independent learning
12.30-14.00 Student project 13.30-15.00 SGD
14.00-15.00 Plenary session 15.00-16.00 Plenary session
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
17
TIMETABLE OF CLASSES
DAY/DATE Class A Class B ACTIVITY VENUE PIC
1
Monday,
February 26
2018
08.00-08.15 09.00-09.15 Introduction Classroom dr. I Made Junior Rina
Artha, SpJP(K)
08.15-09.00 09.15-10.00
Lecture 1 Approach to patient
with cardiovascular
disease
Classroom
Prof. Dr. dr. I Wayan
Wita, SpJP(K)
09.30-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student Project
14.00-15.00 15.00-16.00 Plenary session Classroom Prof. Dr. dr. I Wayan
Wita, SpJP(K)
2
Tuesday,
February 27
2018
08.00-08.30 09.00-09.30 Lecture 2 Cardiovascular
Pharmacology
Classroom dr. Agung Nova
08.30-09.00 09.30-10.00
Lecture 3 Pathologic Anatomy of
Cardiovascular
System: Anomalies
Formation of the heart
and great vessels
Classroom dr. Ni Putu Ekawati,
SpPA
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student Project
14.00-15.00 15.00-16.00 Plenary session Classroom
dr. Agung Nova/dr. Ini
Putu Ekawati, SpPA
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
18
3
Wednesday,
February 28
2018
08.00-08.30 09.00-09.30
Lecture 4 Laboratory
examination: cardiac
markers
Classroom Dr. dr. AA Wiradewi,
SpPK
08.30-09.00 09.30-10.00 Lecture 5 Cardiac Rehabilitation
Classroom dr. Luh Kamiati,
SpRM
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom Dr. dr. AA Wiradewi,
SpPK/ dr. Luh
Kamiati, SpRM
4
Thursday,
March 1
2018
08.00-09.00 09.00-10.00 Lecture 6 Acute coronary
syndrome
Classroom dr. I Made Junior Rina
Artha, SpJP(K)
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary Session Classroom dr. I Made Junior Rina
Artha, SpJP(K)
5
Monday,
March 5
2018
08.00-09.00 09.00-10.00 Lecture 7 Stable coronary artery
disease
Classroom dr. Hendy Wirawan,
SpJP
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
19
14.00-15.00 15.00-16.00 Plenary session Classroom dr. Hendy Wirawan,
Sp.JP
6
Tuesday,
March 6
2018
08.00-09.00 09.00-10.00 Lecture 8 Hypertension part 1
Classroom dr. AAA Adelia
Yasmin, SpJP
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom dr. AAA Adelia
Yasmin, SpJP
7
Wednesday,
March 7
2018
08.00-09.00 09.00-10.00 Lecture 9 Hypertension part 2
Classroom dr. AAA Adelia
Yasmin, SpJP
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom dr. AAA Adelia
Yasmin, SpJP
8
Thursday,
March 8
2018
08.00-09.00 09.00-10.00 Lecture 10 Acute Heart Failure
Classroom
dr. Kadek Susila SD,
SpJP
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom dr. I Kadek Susila SD,
SpJP
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9
Friday,
March 9
2018
08.00-09.00 09.00-10.00 Lecture 11 Chronic Heart Failure
Classroom
dr. I Nyoman
Wiryawan, SpJP(K)
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom dr. I Nyoman
Wiryawan, SpJP(K)
10
Monday,
March 12
2018
08.00-09.00 09.00-10.00 Lecture 12 Arrhythmia
Classroom dr. Putra Swi Antara,
SpJP(K)
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary Session Classroom dr. Putra Swi Antara,
SpJP(K)
11
Tuesday,
March 13
2018
08.00-09.00 09.00-10.00
Lecture 13 Common Peripheral
Vascular and
Lymphatic disease
Classroom Dr. dr. Semadi,
SpBTKV
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom
Dr. dr. Semadi,
SpBTKV
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12
Wednesday,
March 14
2018
08.00-09.00 09.00-10.00 Lecture 14 Valvular Heart Disease
Classroom dr. IB Rangga W,
SpJP(K)
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom dr. IB Rangga W,
SpJP(K)
13
Thursday,
March 15
2018
08.00-09.00 09.00-10.00 Lecture 15 Cor Pulmonale
Classroom
dr. Luh Oliva S
Suastika, SpJP
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom dr. Luh Oliva S
Suastika, SpJP
14
Monday,
March 19
2018
08.00-09.00 09.00-10.00
Lecture 16 Congenital heart
disease and Acute
Rheumatic Fever
Classroom dr. Eka Guna Wijaya,
SpA(K)
09.00-10.30 12.00-13.30 Independent learning
10.30-12.00 13.30-15.00 SGD Disc room Facilitator
12.00-12.30 11.30-12.00 Break
12.30-14.00 10.00-11.30 Student project
14.00-15.00 15.00-16.00 Plenary session Classroom dr. Eka Guna Wijaya,
SpA(K)
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15
Tuesday,
March 20
2018
08.00-15.00 09.00-16.00 Student Project
Presentation
Auditorium/
Classroom* Examiner SP
16
Thursday,
March 22
2018
08.00-11.00 11.00-14.00 Basic Clinical Skill 1: Physical Examination 1
Classroom/
Skill lab
dr. Luh Oliva S
Suastika, SpJP
17
Friday,
March 23
2018
08.00-11.00 11.00-14.00
Basic Clinical Skill 2: ECG
Classroom/
Skill lab
dr. Putra Swi Antara,
SpJP(K)
18
Monday,
March 26
2018
08.00-09.30 09.30-11.00 Basic Clinical Skill 3: Chest radiography
Classroom/
Skill lab
dr. Lisna Astuti,
SpRad
11.00-13.00 13.00-15.00 Basic Clinical Skill 1: Physical Examination 2
Classroom/
Skill lab
dr. IB Rangga W,
SpJP(K)
19
Tuesday,
March 27
2018
08.00-11.00 11.00-14.00
Basic Clinical Skill 4: Cardiopulmonary
resuscitation
Classroom/
Skill lab
dr. I Kadek Susila SD,
SpJP
20
Wednesday,
March 28
2018
08.00-11.00 11.00-14.00 Basic Clinical Skill 5: IV line & venopuncture
Classroom/
Skill lab
dr. Pontisomaya
Parami, Sp.An.,
MARS
22
Friday,
March 30
2018
Pre Evaluation Break
23
Monday,
April 2
2018
Examination
Friday,
July 27
2018
Remedial Examination
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LEARNING PROGRAMS
LECTURE 1
APPROACH TO PATIENT WITH CARDIOVASCULAR DISEASE
Prof dr. I Wayan Wita, SpJP(K), FIHA, FAsCC
Department of Cardiology and Vascular Medicine
AIMS:
Able to do and practice the approach to the 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 Cardiovascular symptoms.
2. Able to do and practice the approach to consultations with Cardiovascular Disease.
3. Able to do and practice the approach to investigations in Cardiology).
CURRICULUM CONTENT:
1. The symptoms of the cardiovascular disease.
2. The diagnostic tools to confirm patients with Cardiovascular Diseases.
ABSTRACT:
History taking remains the most important component of the 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.
The 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 an 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 ischemic 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 assesses systemic and pulmonary hemodynamic variables, as well as oxygen
saturation and intracardiac shunts. It assesses aortic, valvular, left ventricular and coronary
artery structure and function. The assessment of coronary artery disease is the main indication.
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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 remains the valuable cardiac investigation in clinical
practice.Radiologic method used in the roentgen cardiac examination:
a) Posteroanterior projection, PA/AP
b) Lateral Projection
c) Right anterior oblique projection (RAO)
d) Left anterior oblique projection (LAO).
Increase in cardiac size is the most consistent indication of cardiac disease.
2. Computed tomography (CT-scan)
The basic principle of CT technology is the use of ionizing radiation within a gantry rotating
around the patient in which x-rays are detected on a detector array and converted through
reconstruction algorithms to images. It is these images, acquired at high spatial and temporal
resolution, that have enabled cardiovascular medicine to enter the CT imaging era.
3. Magnetic resonance imaging (MRI)
Over the past decade, cardiac magnetic resonance (CMR) has developed into a routine clinical
imaging tool. With excellent spatial and temporal resolution, unrestricted tomographic fields, and
no exposure to ionizing radiation, CMR offers detailed morphologic and functional
characterization for most types of heart disease.
4. Echocardiography
Echocardiography remains the most frequently used and usually the initial imaging test to
evaluate all cardiovascular diseases related to a structural, functional, or hemodynamic
abnormality of the heart or great vessels. Echocardiography uses ultrasound beams reflected by
cardiovascular structures to produce characteristic lines or shapes caused by normal or altered
cardiac anatomy in one, two, or three dimensions by M (motion)–mode, two-dimensional, or
three-dimensional echocardiography, respectively. Doppler examination and color flow imaging
provide a reliable assessment of cardiac hemodynamics and blood flow.
5. Angiocardiography
Angiography is a technique used to visualize the lumen, of blood vessels and organs of the
body, with a particular interest in the arteries, veins, and the heart chambers. This is traditionally
done by injecting a radio-opaque contrast agent into the blood vessel and imaging using X-ray
based techniques such as fluoroscopy.
6. Cardiac catheterization
Cardiac catheterization is the insertion of a catheter into a chamber or vessel of the heart. This
is done both for diagnostic and interventional purposes. Subsets of this technique are mainly
coronary catheterization, involving the catheterization of the coronary arteries, and
catheterization of cardiac chambers and valves of the Cardiac System.
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7. Nuclear Cardiology
The era of noninvasive radionuclide cardiac imaging in humans began in the early 1970s with
the first reports of noninvasive evaluation of resting myocardial blood flow. Since that time, there
have been major advances in the technical ability to image cardiac physiology and
pathophysiology, including that of myocardial blood flow, myocardial metabolism, and
ventricular function.
Standard References :
1. McPhee SJ, Papadakis MA. Current Medical Diagnosis & Treatment. 47th ed. New York:
Lange Medical Book`s/The McGraw-Hill Companies, 2008.p.
2. Roentgen Signs in Diagnostic Imaging Isadore Meschan.
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. History taking
2. Common cardiological symptom and consultation
3. Investigation in Cardiology
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 (a) diagnostic tool(s) in pediatric cardiology!
6. When complete blood count should be performed?
7. Please describe the site of classic heart sound and characteristics of that!
LEARNING TASK II: Investigation in cardiology
1. Please explain the symptoms in patients with cardiovascular disease!
2. What are the diagnostic tools to confirm patients with Ischaemic Heart Disease?
3. What is the benefit of 24-hour electrocardiogram?
4. What is the objective of performing stress testing (treadmill test)?
LEARNING TASK III: RADIOLOGY
1. What are the basic projections for cardiac radiography?
2. Explain normal anatomy of the heart on the chest x-ray!
3. Explain cardiac enlargement on the chest x-ray!
SELF ASSESSMENT :
1. Please explain the symptoms in patients with cardiovascular disease!
2. What are the diagnostic tools to confirm patients with Ischaemic Heart Disease?
3. What is the benefit of 24-hour electrocardiogram?
4. What is the objective of performing stress testing (treadmill test)?
5. Please describe the chest x-ray finding in VSD!
6. Differentiated between LVH and RVH on chest x-ray!
7. Explain HHD on the chest x-ray!
8. Explain tetralogy of Fallot on the chest x-ray!
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LECTURE 2
CARDIOVASCULAR PHARMACOLOGY
dr. Agung Nova Mahendra, M.Sc.
Department of Pharmacology and Therapy
AIMS
The students are expected to know and comprehend the basics and principles of blood
pressure regulation, pathophysiology of angina pectoris, cardiac performance modulation,
arrhythmia mechanisms, and able to apply these knowledges into rational pharmacotherapy of
primary hypertension (HT), angina pectoris, acute and chronic heart failure (HF), and selected
arrhythmias.
LEARNING OUTCOMES
At the end of the lectures, the students are able to:
1. Comprehend and describe therapeutic strategies in HT, angina, HF, and arrhythmias
pharmacy management.
2. Describe important pharmacological features of drugs used in HT, angina, HF, and
arrhythmias.
3. Comprehend clinical applications of drugs used in HT, angina, HF, and arrhythmias.
4. Increase awareness of important or common toxicities and DDIs of drugs used in HT,
angina, HF, and arrhythmias.
CURRICULUM CONTENTS
1. Pathophysiology-based therapeutic strategies in HT, angina, HF, and arrhythmias
pharmacy management.
2. PD and PK of drugs used in HT, angina, HF, and arrhythmias.
3. Clinical applications of drugs used in HT, angina, HF, and arrhythmias.
4. Toxicities and DDIs of drugs used in HT, angina, HF, and arrhythmias.
ABSTRACT
Cardiovascular disorders are leading causes of hospitalization and mortality in the world (Liu et
al., 2010). Among these disorders, hypertension (HT), angina, heart failure (HF), and
arrhythmias are commonly seen in emergency and general clinical practice. Thus, basic
pharmacological knowledge of drugs used in these conditions is the essential pillar of rational
pharmacotherapy to save many lives and improve cardiovascular system health.
STANDARD REFERENCE
Katzung, BG, Trevor AJ. 2015. Basic and Clinical Pharmacology Thirteenth Edition. McGraw-
Hill Education: New York.
SELF-DIRECTED LEARNING
Basic knowledge as the prerequisites of the lecture are:
1. Blood pressure regulation
2. Pathophysiology of angina pectoris
3. Control of normal cardiac contractility
4. Pathophysiology of HF & cardiac performance.
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SCENARIO
Mr. C, 53 years-old, accompanied by his children to an ER, complaining about gasping or
breath every night for about 1-2 weeks. The symptom starts at night and causes him to awake
after several hours of sleep. This symptom is accompanied by an anxious feeling of being
suffocated and persists longer than 30 minutes. History of asthmatic attacks is denied, but he
admits that he is a binge “tuak” and “arak” drinker, shows abnormal lipid profile (during his last
MCU about 3 weeks before), and has a familial history of hypertension and heart attack. After
anamnesis and a set of physical and laboratory examinations, diagnosis of heart failure is
established.
LEARNING TASKS
1. Describe the therapeutic strategies in HT, angina, and HF pharmacy management!
2. What are the classes of drugs used in HT, angina, HF?
3. Describe the classes of antiarrhythmic drugs and their pharmacodynamic characteristics!
4. What are the clinical uses of each class of drugs used in HT, angina, HF, and
arrhythmias?
5. Describe the important/common toxicities & potential drug-drug interactions (DDIs) of
drugs used in HT and angina!
SELF-ASSESSMENT
1. What are the differences between ACEIs and ARBs?
2. What is the rationale of combining β-blocker with nitrate in the therapy of angina?
3. What are the targets of action of amiodarone?
4. Name one anti-HF drug that acts selectively on cardiac β1 adrenoceptor!
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LECTURE 3
PATHOLOGICAL ANATOMY OF CARDIOVASCULAR SYSTEM: ANOMALIC
FORMATION OF THE HEART AND GREAT VESSELS
dr. Ni Putu Ekawati, Sp.PA, M.Repro.
Department of Pathology Anatomy
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 implications
2. Can describe the basic principles underlying the formation of anomalies of the great
vessels and its implications
CURRICULUM CONTENT:
1. Embryology of the heart
2. Embryology of the great vessels.
ABSTRACT
Septal defects are only problematic when the shunt flows from right-to-left. Anomalies of
interventricular septum (VSD) usually happens 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 occurs 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 tachypnea. A continuous machine-
like murmur in the upper left sternal border is common. Diagnosis is by echocardiography.
Standard References:
1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott &
Wilkins, 2007. p. 91, 93, 94
2. Sadler TW: Langman’s Medical Embryology, 10th ed. Philadelphia, Lippincott & Wilkins,
2006. p. 167-178, 184
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SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Embryology of the heart
2. Embryology of the great vessel.
SCENARIO: CASE 1
This baby aged 4 months has been known to have a cardiac murmur since birth. He was born 8
weeks prematurely and developed respiratory distress requiring high oxygen concentration for
the first week. Since then he has feed satisfactorily but height and weight growth have been
poor even allowing for prematurity. The diagnosis after examination and investigations: Patent
Ductus Arteriosus (PDA).
LEARNING TASK I
1. What factors in the history were of possible importance in causing the ductus remains
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 the 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 of examination and investigations: Atrial Septal
Defect (ASD).
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 a 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-precordial area. The first heart sound was normal while the second was single, distinct and
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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 children 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!
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LECTURE 4
LABORATORY EXAMINATION: CARDIAC MARKERS
Dr. dr. Wiradewi, Sp.PK
Department of Clinical Pathology
AIMS:
Can describe various cardiac markers.
LEARNING OUTCOME:
Able to interpret cardiac marker results.
CURRICULUM CONTENTS:
1. Different cardiac markers
2. Mechanisms of each cardiac marker
3. Cardiac marker results
ABSTRACT :
Although many patients with an acute myocardial infarction (AMI) will present with the classic
history of severe chest pain and have ECG findings of ST elevation and pathologic Q waves,
approximately 25% of patients will not. Approximately 50% of patients who come through the
emergency room with a myocardial infarction have nondiagnostic ECGs. It is for this reason that
when a patient is suspected of having myocardial damage, in addition to close hemodynamic
monitoring, a good physical exam, and serial EKGs, a set of cardiac markers should be
obtained.
The cardiac markers include myoglobin, creatine kinase (CK), the MB fraction of creatine kinase
(CK-MB), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and troponin. These
are intracellular cardiac markers normally detectable in the blood at very low levels. As the
myocytes become necrotic, the cardiac markers will leak out of these cells and ultimately into
the vasculature where they can be detected by routine laboratory testing.
Myoglobin is an oxygen-binding protein that is released from myocardial cells when they are
injured. It can be detected 1-4 hours after the insult and peaks at 4-12 hours. Creatine kinase is
another protein that is released from the myocardial cell when it is damaged. Its activity is
greatest in striated muscle, brain and heart tissue. CK-MB levels are detectable at 4-6 hours
postinjury, peak at 24 hours. Aspartate aminotransferase is an enzyme that is also released with
myocardial infarction. Like CK, in acute MI, AST rises to a maximum at 24 hours and declines to
normal levels at about 48 hours postinfarction. Lactate dehydrogenase is an enzyme that is
released during myocardial infarction. AST and LDH are not specific to cardiac diseases.
Troponin is the most specific of the commercially available cardiac markers. Troponin can be
measured as early as 3 hours after the onset of chest pain.
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STANDARD REFERENCES:
1. Burtis CA, Bruns DE: Tietz Fundamentals of Clinical Chemistry and Molecular
Diagnostics, 7th ed. St.Louis, MO: Saunders/Elsevier, 2014.
2. Bishop ML, Fody EP, Schoeff LE: Clinical Chemistry: Principles, Techniques, And
Correlations, 7th ed. Philadelphia: Lippincott Williams & Wilkins, 2013.
3. Desai SP, Isa-Pratt S: Clinician’s Guide to Laboratory Medicine: A Practical Approach,
3rd ed. Michigan: Lexi-Comp, 2004.
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Types of cardiac marker.
2. Mechanisms of each cardiac marker.
LEARNING TASKS
1. A patient came to the emergency room with complaints of chest pain, like being pressed
by a heavy object. The pain is intermittent and reduced if the patient is resting. What
kind of laboratory tests are to be proposed? If the laboratory results are normal and the
ECG was also normal. What is the diagnosis of this patient?
2. A patient came to the emergency room with complaints of chest pain since 5 hours ago.
Patients never feel the same complaint before. Patients had a history of gastric ulcer.
The laboratory results are as follows :
Myoglobin: increased
CK-MB: normal
Troponin normal
What is the diagnosis of this patient?
3. A patient came to the emergency room with complaints of chest pain, like being pressed
by a heavy object. Patients can not say exactly when the pain was beginning. Laboratory
results are as follows:
Myoglobin: normal
CK-MB: increased
Troponin: increased
What is the diagnosis of this patient? Can you estimate when the cell damage occurs?
SELF ASSESSMENTS
1. What are cardiac markers?
2. What other conditions can cause an increase in CK-MB?
3. How does troponin compare with CK?
4. What role do these cardiac markers play in monitoring reperfusion following thrombolytic
therapy?
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LECTURE 5
REHABILITATION ON CARDIOVASCULAR DISEASE PATIENTS
dr. Luh Kamiati, Sp.KFR
Department of Rehabilitation Medic
AIMS:
Describe cardiac rehabilitation on patient with Cardiovascular Disease.
LEARNING OUTCOME:
Able to describe cardiac rehabilitation in patient with cardiovascular disease.
CURRICULUM CONTENTS:
Cardiac rehabilitation in patient with cardiovascular disease.
ABSTRACT:
Cardiac rehabilitation is a multidisciplinary program of education and exercise established to
assist an individual with heart disease in achieving optimal physical, psychological and
functional status within the limits of the diseased.
The basic goal of cardiac rehabilitation is 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 the decreased length of hospital stay,
more rapid, more complete resumption of usual activities, self-confident, less psychological
distress, and fewer readmissions.
Standard References :
1. McPhee SJ, Papadakis MA. Current Medical Diagnosis & Treatment. 47thed. New York:
Lange Medical 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, 2nded, 2003, p. 86
3. Bartels MN: Cardiac Rehabilitation in Grant Cooper: Essential Physical Medicine and
Rehabilitation, 2006, p. 119.
SCENARIO
CASE:
A 60 years old man admitted to the emergency room because of chest pain. He was diagnosed
with acute heart failure caused by coronary artery disease. He is now stabilized transferred to
the cardiac ward.
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LEARNING TASK:
1. Mention the definition of cardiovascular rehabilitation
2. Explain the objective of cardiovascular rehabilitation
3. Mention the contraindication exercise therapy
4. Explain the beneficial effect of exercise therapy
5. Explain stages of cardiovascular rehabilitation MI
6. Mention effect of exercise to CHF.
SELF DIRECTING LEARNING and SELF-ASSESSMENT
1. Mention definition of cardiovascular rehabilitation
2. Explain the objective of cardiovascular rehabilitation
3. Mention the contraindication exercise therapy
4. Explain the beneficial effect of exercise therapy
5. Explain stages of cardiovascular rehabilitation MI
6. Mention effect of exercise to CHF.
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LECTURE 6
ACUTE CORONARY SYNDROME
dr. I Made Junior Rina Artha, Sp JP (K), FIHA, FAsCC
Department of Cardiology and Vascular Medicine
AIMS:
Describe to diagnose and manage Acute Coronary Syndromes (ACS).
LEARNING OUTCOME:
1. Defining acute coronary syndromes (ACS),
2. Examining ACS Modifiable and non-modifiable risk factors,
3. Describing the pathophysiology of unstable angina (UA), non ST-elevation myocardial
infarction (NSTEMI), and ST-elevation myocardial infarction STEMI).
CURRICULUM CONTENTS:
Pathogenesis of atherothrombosis.
Risk factors for Acute Coronary Syndromes.
Clinical spectrum of Acute Coronary Syndromes.
Interpret laboratory of Acute Coronary Syndromes.
Interpret diagnostic tools for Acute Coronary Syndromes.
Management and its prognosis of Acute Coronary Syndromes.
Post ACS medical rehabilitation and its rehabilitation.
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 increased since the last 10 years in Indonesia (SKRT, 1995 and accounts for one in
seven deaths in the US, killing over 360,000 people a year. For an individual at 40 years old, the
lifetime risk of developing CHD is 49% in men and 32% in women; for those reaching age 70
years, the lifetime risk is 35% in men and 24% in women. Coronary atherosclerosis, the basic
pathogenesis of this disease, is associated with many risk factors such as cigarette smoking,
hyperlipidemia, 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 processes
becomes ‘atherosclerotic plaque’. ACS caused by clots formed in the heart, once the plaque
ruptured, it bleeds and initiates the release of platelets through the clotting process. There is
thrombosis/clot formation which further occludes the diameter of the coronary artery and
decreases blood supply to the heart. 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 an atherosclerotic plaque becomes unstable and either
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ruptures or are eroded. The complicated plaque is a nidus for thrombus formation and may lead
to vessel occlusion.
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 Presenting symptoms when plaque continues to occlude the coronary artery
and/or the coronary artery is contracted, blood carrying the necessary oxygen and nutrients
cannot pass through, thus causing ischemia. Patients present with right or left sided chest pain,
discomfort, pressure or tightness around the chest more than 20 minutes, other symptoms
include pain or discomfort in the shoulder, neck, jaw or back, dyspnea, nausea, vertigo, and
diaphoresis. present with prolonged anginal symptoms that occur at rest. The electrocardiogram
will often show evidence of ischemia that classically takes the form of ST segment shifts, T-
wave inversion, and new bundle branch block. Cardiac enzymes and markers are the principal
determinants that defines 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.
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Risk factors for acute coronary syndromes
2. Clinical spectrum of acute coronary syndromes
3. Interpret laboratory of acute coronary syndromes
4. Interpret diagnostic tools for acute coronary syndromes
5. Management and its prognosis of acute coronary syndromes
6. Post ACS medical rehabilitation and its rehabilitation.
References:
1. Mann, DL et al. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier Saunders,
2015.
2. Ibanez B, et al. 217 ESC Guidelines for management of Acute Myocardial Infarction in
Patients Presenting with ST-Segment Elevation. Eur Heart J. 2017:39,119-177.
SCENARIO 1:
CASE (Acute Coronary syndrome):
A 56-year old male came to Emergency Room due to severe chest pain. The pain was felt since
6-hours prior to admission, it was a heavy sensation and radiating to left arm and jaw, not
relieved by rest, accompanied by shortness of breath since 5 hours PTA that is relieved by
sitting position. He is suffered from uncontrolled DM and Hypertension since 7 years ago. He
appeared severely ill and dyspnea. The blood pressure was 170/90 mmHg; pulse rate was 110
beats-per-minute, regular. There were rales on both lung fields ECG showed:
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LEARNING TASK:
1. What is the most likely diagnosis?
2. What do the next procedure you plan?
3. What is your initial treatment?
4. What is the definitive therapy for this case?
5. What is the could be a complication for this case?
SELF-ASSESSMENT:
1. Please explain the risk factors of acute coronary syndromes!
2. What are the complications of acute myocardial infarction?
3. What is the treatment of choice in ST-elevation myocardial infarction?
4. Please describe the indication and the benefit of CABG (coronary artery bypass graft)!
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LECTURE 7
Stable Coronary Artery Disease
dr. Hendy Wirawan, M.Biomed, Sp JP, FIHA
Department of Cardiology and Vascular Medicine
AIMS:
Describe diagnostic approach and management Stable Coronary Artery Disease (SCAD).
LEARNING OUTCOME:
Be able to describe diagnostic approach and management Stable Coronary Artery Disease.
CURRICULUM CONTENT:
Pathogenesis of atherothrombosis.
Risk factors for Stable Coronary Artery Disease.
Clinical spectrum of Stable Coronary Artery Disease.
Interpret diagnostic tools for Stable Coronary Artery Disease.
Management and its prognosis of Stable Coronary Artery Disease.
ABSTRACT:
Stable Coronary artery disease (SCAD) is most commonly caused by atheromatous plaque that
obstructs or gradually narrows one or more of the epicardial coronary arteries. Other
contributors, such as endothelial dysfunction, microvascular disease, and vasospasm may also
exist alone or in combination with coronary atherosclerosis and may be the dominant cause of
myocardial ischemia in some patients. Thus the concept that coronary artery disease is
synonymous with obstructive coronary atherosclerosis and ischemic heart disease (IHD).
Coronary artery disease (CAD) is a major cause of death and disability in developed countries.
Although the mortality for this condition has gradually declined over the last decades in western
countries, it still causes about one-third of all deaths in people older than 35 years. In
Indonesia, CAD became the second highest cause of death after stroke, which amounted to
12.4% based on System Registration Sample Survey (SRS). It is estimated that 15.400.000
Americans have CAD, 7.800.000 of whom have angina pectoris and 7.600.000 have had MI.
The basic pathogenesis of the disease is coronary atherosclerosis, a chronic process to form
atherosclerotic plaque. 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. Over time, plaque hardens and narrows the
coronary artery, this limits the flow of oxygen-rich blood to the myocardium. Conventional risk
factors that increase the progression of atherosclerosis are hypertension, hypercholesterolemia,
diabetes, sedentary lifestyle, obesity, smoking and family history.
Clinical manifestation of CAD can be either stable angina pectoris/ stable CAD and unstable
angina pectoris/ acute coronary syndrome (ACS). SCAD is generally characterized by episodes
of reversible myocardial demand/supply mismatch, related to ischemia or hypoxia, which are
usually inducible by exercise, emotion or other stress and reproducible—but, which may also be
occurring spontaneously. Such episodes of ischemia/hypoxia are commonly associated with
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transient chest discomfort (angina pectoris). Whereas ACS almost always presents with a
symptom, such as unstable angina, and is frequently associated with myocardial infarction (MI).
The diagnosis and assessment of SCAD involve clinical evaluation, including identifying
significant dyslipidemia, hyperglycemia or other biochemical risk factors and specific cardiac
investigations such as stress testing or coronary imaging. A careful history remains the
cornerstone of the diagnosis of chest pain. The characteristics of discomfort-related to
myocardial ischemia (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 ischemia 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 a
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 ambulatory ECG monitoring (if there is a 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.
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Risk factors for Ischaemic Heart Disease
2. Clinical spectrum of Ischaemic Heart Disease
3. Interpret diagnostic tools for Ischaemic Heart Disease
4. Management and its prognosis of Ischaemic Heart Disease.
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.
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SCENARIO :
CASE (Ischemic Heart Disease) :
A 68-year-old man presents to his new primary care provider for an initial patient visit. His sole
active complaint is mild retrosternal chest pressure that he experiences only after significant
exertion, and the discomfort resolves within minutes of cessation of the provoking activity. The
pattern and the severity of his symptoms have not changed significantly over the last 3 years,
and he denies any episodes of chest pain at rest, dizziness, syncope, dyspnea, palpitations, or
lower extremity edema. Other pertinent medical history includes hypercholesterolemia and long-
standing hypertension. On examination, the patient is comfortable and in no acute distress. The
heart rate is 90 bpm and regular, and the blood pressure 155/85 mmHg. There are no murmurs,
rubs, gallops or clicks on cardiac auscultation and the second heart sound is physiologically
split. A resting ECG is normal.
LEARNING TASK :
1. What is the most likely diagnosis?
2. What is the best next diagnostic step?
3. What is the best next step in therapy?
SELF-ASSESSMENT :
1. Please explain the risk factors for coronary artery disease!
2. Please describe laboratory recommendation for assessment stable angina!
3. What is the noninvasive and invasive recommendation for assessment stable angina?
4. What is the treatment of choice for Stable angina pectoris?
5. Please describe the indication and the benefit of revascularization!
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LECTURE 8
HYPERTENSION
dr. AA Ayu Dwi Adelia Yasmin, M.Biomed, SpJP, FIHA
Department of Cardiology and Vascular Medicine
AIMS:
Describe diagnostic approach and management of Hypertension.
LEARNING OUTCOME:
Be able to describe diagnostic approach and management of Hypertension.
CURRICULUM CONTENTS:
1. Etiology and pathophysiology of Hypertension
2. Clinical criteria and classification of Hypertension
3. Diagnostic approach to Hypertension
4. Management and prognosis of Hypertension
ABSTRACT:
Hypertension is the most common condition seen in primary care and leads to myocardial
infarction, stroke, renal failure, and death if not detected early and treated appropriately.
Hypertension is defined as values ≥140 mmHg Systolic Blood Pressure (SBP) and/or ≥90
mmHg Diastolic Blood Pressure (DBP), based on the evidence from Randomized Controlled
Trials that in patients with these BP values treatment-induced BP reductions are beneficial. The
same classification is used in young, middle-aged and elderly subjects. Overall the prevalence
of hypertension appears to be around 30–45% of the general population, with a steep increase
with aging.
Based on recommendations of the Seventh Report of the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7), the
classification of BP for adults aged 18 years or older has been as follows :
1. Normal: Systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg
2. Prehypertension: Systolic 120-139 mm Hg, diastolic 80-89 mm Hg
3. Stage 1: Systolic 140-159 mm Hg, diastolic 90-99 mm Hg
4. Stage 2: Systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater
Hypertension may be primary, which may develop as a result of environmental or genetic
causes, or secondary, which has multiple etiologies, including renal, vascular, and endocrine
causes. Primary or essential hypertension accounts for 90-95% of adult cases, and secondary
hypertension accounts for 2-10% of cases. Many guidelines exist for the management of
hypertension. Most groups recommend lifestyle modification as the first step in managing
hypertension. If lifestyle modifications are insufficient to achieve the goal BP, there are several
drug options for treating and managing hypertension. Most individuals diagnosed with
hypertension will have increased blood pressure (BP) as they age. Untreated hypertension is
notorious for increasing the risk of mortality and is often described as a silent killer. Mild to
moderate hypertension, if left untreated, may be associated with a risk of atherosclerotic
disease in 30% of people and organ damage in 50% of people within 8-10 years after onset.
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Standard References:
1. 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.
2. Mancia G, et al. 2013 ESH/ESC Guidelines for the Management of Arterial
Hypertension. European Heart Journal. 2013;34:2159-2219.
3. James PA, et al. 2014 Evidence-Based Guideline for the Management of High Blood
Pressure in Adults. Report From the Panel Members Appointed to the Eighth Joint
National Committee (JNC 8). 2014;311(5):507-520.
SCENARIO CASE:
A 60-year-old man decides it is time to have a health check and attends his local GP. As part of
the assessment, the practice nurse takes his blood pressure, which is recorded as 170/90
mmHg. He is 170 m tall, weighs 80 kg and has no past medical history. His basic physical
examination is unremarkable with no audible murmurs on cardiac auscultation. He has no
history of cardiac symptoms or diabetes. His 80-year-old mother is currently on blood pressure
tablets and his father died at the age of 74 years from a heart attack. He stopped smoking 20
cigarettes a day 20 years ago. He drinks 2–3 units of alcohol most days, sometimes more at
weekends. His only exercise is walking the dog. He says he eats well and usually adds salt to
his meals after they are cooked
LEARNING TASK:
1. How do you interpret the patient’s blood pressure reading?
2. What is your advice and management plan for this patient?
3. He asks you why he has high blood pressure. What do you tell him and would you
perform any additional tests or examinations?
4. He is reluctant to have any treatment. What are the potential consequences of
uncontrolled hypertension? And what are your suggestions to him?
5. What would you prescribe him?
6. What potential are side-effects there from his medication?
SELF-ASSESSMENT:
1. What are the lifestyle modification recommendations for a patient with hypertension
based on guidelines?
2. Please explain the definition of white coat hypertension and masked hypertension, and
how can we diagnose it?
3. What are the side effects of ACE Inhibitor, Diuretic, and Calcium channel blocker?
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LECTURE 9
HYPERTENSIVE URGENCY AND EMERGENCY
dr. AA Ayu Dwi Adelia Yasmin, M.Biomed, SpJP, FIHA
Department of Cardiology and Vascular Medicine
AIMS:
Describe diagnostic approach and management of Hypertensive Urgency and Emergency
LEARNING OUTCOME:
Be able to describe diagnostic approach and management of Hypertensive Urgency and
Emergency.
CURRICULUM CONTENTS:
1. Etiology and pathophysiology of Hypertensive Urgency and Emergency
2. Clinical criteria for Hypertensive Urgency and Emergency
3. Diagnostic approach to Hypertensive Urgency and Emergency
4. Management and prognosis of Hypertensive Urgency and Emergency
ABSTRACT:
Hypertensive emergencies encompass a spectrum of clinical presentations in which
uncontrolled blood pressures lead to progressive or impending end-organ dysfunction. In these
conditions, the blood pressure should be lowered aggressively over minutes to hours.
Neurologic end-organ damage due to uncontrolled blood pressure may include hypertensive
encephalopathy, cerebral vascular accident/ cerebral infarction, subarachnoid hemorrhage,
and/or intracranial hemorrhage. Cardiovascular end-organ damage may include myocardial
ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and/or aortic
dissection. Other organ systems may also be affected by uncontrolled hypertension, which may
lead to acute renal failure/insufficiency, retinopathy, eclampsia, or microangiopathic hemolytic
anemia. The primary goal of the emergency physician is to determine which patients with acute
hypertension are exhibiting symptoms of end-organ damage and require immediate intravenous
parenteral therapy. In contrast, patients presenting with acutely elevated BP (systolic blood
pressure [SBP] >200 mm Hg or diastolic blood pressure [DBP] >120 mm Hg) without symptoms
and whose blood pressure stays significantly elevated to this level on discharge should have
initiation of medical therapy and close follow-up in the outpatient setting. Optimal
pharmacotherapy is dependent upon the specific organ at risk. In patients presenting with
hypertensive emergencies, antihypertensive drug therapy has been shown to be effective in
acutely decreasing blood pressure.
Standard References:
1. 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.
2. Mancia G, et al. 2013 ESH/ESC Guidelines for the Management of Arterial
Hypertension. European Heart Journal. 2013;34:2159-2219.
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3. James PA, et al. 2014 Evidence-Based Guideline for the Management of High Blood
Pressure in Adults. Report From the Panel Members Appointed to the Eighth Joint
National Committee (JNC 8). 2014;311(5):507-520.
SCENARIO CASE:
A 67-year-old woman is brought to the emergency room by her son. He states that she has
been “acting strangely” for the last day or so. According to her records, her usual
antihypertensive regimen consists of lisinopril 10 mg PO every day, HCT 25 mg PO every day,
nifedipine extended-release 90 mg PO every day, and atenolol 50 mg every day. Her son
indicates that she ran out of her medication a week ago. On examination, the patient is
confused, somnolent, and complaining of a headache. Her blood pressure is 230/114 bilaterally.
Funduscopic examination shows arteriolar narrowing and indistinct optic disc margins. The lung
examination reveals no rales; the cardiac examination is significant for an S4 gallop and a grade
2 mid-systolic ejection murmur. The abdomen is soft and non-tender, with no bruits. No
peripheral edema is present.
LEARNING TASK:
1. What is the diagnosis of the patient? Please explain the data that support the diagnosis!
2. What is the appropriate management for the patient?
3. How much the blood pressure goal for this patient?
4. Please give the education for patient and family to prevent this condition in the future!
SELF-ASSESSMENT:
1. Please explain the pathophysiology of hypertensive emergency and urgency!
2. What are the signs and symptoms of hypertensive emergency?
3. What are the drug of choice for treatment of hypertensive urgency?
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LECTURE 10
ACUTE HEART FAILURE
dr. I Kadek Susila Surya Darma, M.Biomed, SpJP, FIHA
Department of Cardiology and Vascular Medicine
AIMS:
Describe to definition, diagnosis, diagnostic test and treatment of Acute Heart Failure.
LEARNING OUTCOME:
1. Can describe definition of Acute Heart Failure
2. Can describe diagnosis of Acute Heart Failure
3. Can describe diagnostic test for Acute Heart Failure
4. Can describe treatment of Acute Heart Failure.
CURRICULUM CONTENT:
Factors triggering Acute Heart Failure
Clinical and diagnostic approach of Acute Heart Failure
Pharmacologic treatment of Acute Heart Failure
Goals of treatment in Acute Heart Failure.
ABSTRACT:
AHF may present as a first occurrence (de novo) or, more frequently, as a consequence of
acute decompensation of chronic HF, and may be caused by primary cardiac dysfunction or
precipitated by extrinsic factors, often in patients with chronic HF. Acute myocardial dysfunction
(ischaemic, inflammatory or toxic), acute valve insufficiency or pericardial tamponade are
among the most frequent acute primary cardiac causes of AHF. Decompensation of chronic HF
can occur without known precipitant factors, but more often with one or more factors, such as
infection, uncontrolled hypertension, rhythm disturbances or non-adherence with drugs/diet.
A large number of overlapping classifications of AHF based on different criteria have been
proposed. The most useful classifications are those based on a clinical presentation at
admission, allowing clinicians to identify patients at high risk of complications, and to manage at
specific targets, which creates a pathway for personalized care in the AHF setting.
The diagnostic workup needs to be started in the pre-hospital setting and continued in the
emergency department (ED) in order to establish the diagnosis in a timely manner and initiate
appropriate management. The greater benefit of early treatment is well established in ACS and
now needs to be considered in the setting of AHF.
In parallel, coexisting life-threatening clinical conditions and/or precipitants that require urgent
treatment/correction need to be immediately identified and managed. Typically, an initial step in
the diagnostic workup of AHF is to rule out alternative causes for the patient’s symptoms and
signs (i.e. pulmonary infection, severe anemia, acute renal failure). AHF is a life-threatening
medical condition, thus rapid transfer to the nearest hospital should be pursued, preferably to a
site with a cardiology department and/or a coronary care/ intensive care unit (CCU/ICU).
Early diagnosis is important in AHF. Therefore, all patients with suspected AHF should have a
diagnostic workup and appropriate pharmacological and non-pharmacological treatment should
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be started promptly and in parallel. Initial evaluation and continued non-invasive monitoring of
the patient’s vital cardiorespiratory functions, including pulse oximetry, blood pressure,
respiratory rate and a continuous ECG instituted within minutes, is essential to evaluate whether
ventilation, peripheral perfusion, oxygenation, heart rate and blood pressure are adequate.
Urine output should also be monitored, although routine urinary catheterization is not
recommended. Patients with respiratory distress/failure or hemodynamic compromise should be
triaged to a location where immediate respiratory and cardiovascular support can be provided
Standard References:
1. Mann, DL et al. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier Saunders,
2015. p. 429-615
2. Ponikowski et al. 2016 ESC Guidelines For The Diagnosis and Treatment of Acute and
Chronic Heart Failure. European Heart Journal. 2016;ehw128
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Factors triggering Acute Heart Failure
2. Clinical and diagnostic approach of Acute Heart Failure
3. Pharmacologic treatment of Acute Heart Failure
4. Goals of treatment in Acute Heart Failure.
SCENARIO: CASE:
A 65-year-old man is hospitalized after he is taken to the emergency department because of
dyspnea and leg edema. He has a longstanding history of hypertension that is treated with
amlodipine. Coronary angiography performed 1 year ago because of chest pain was normal. On
admission, blood pressure is 180/110 mmHg and heart rate is 120/min and regular. Jugular
venous distension is 10 cm while the patient is lying on a stretcher with his head elevated at 45
degrees. He has positive hepatojugular reflex, pitting leg edema, S3 gallop, and rales at basal of
both lungs. No heart murmur is auscultated. Echocardiogram shows left ventricular (LV) ejection
fraction of 20% and LV dilatation. Electrocardiogram shows a left bundle branch block. Serum
electrolytes, hepatic and renal function measurements are normal.
LEARNING TASK :
1. What is the most likely diagnosis of the patient?
2. What is the etiology of the disease?
3. What is the initial treatment for this patient?
SELF ASSESSMENT:
1. Please explain the definition of acute heart failure!
2. What are factors triggering acute heart failure?
3. What is signs and symptoms of heart failure?
4. Please explain clinical profiles of patients with Acute heart failure!
5. Please explain initial treatment for patients with acute heart failure!
6. What is/ are the goal(s) of treatment in acute heart failure?
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LECTURE 11
CHRONIC HEART FAILURE
dr. I Nyoman Wiryawan, SpJP
Department of Cardiology and Vascular Medicine
AIMS:
Describe to pathophysiology, diagnosis, diagnostic test and treatment Heart Failure.
LEARNING OUTCOME:
1. Can describe pathophysiology of Chronic Heart Failure
2. Can describe diagnosis of Chronic Heart Failure
3. Can describe diagnostic test for Chronic Heart Failure
4. Can describe treatment of Chronic Heart Failure
CURRICULUM CONTENT:
1. Etiology and pathophysiology of Chronic Heart Failure
2. Clinical and diagnostic approach to Chronic Heart Failure
3. Pharmacologic treatment of Chronic Heart Failure
4. Prognosis of Chronic Heart Failure.
ABSTRACT:
Heart failure (HF) can be defined as an abnormality of cardiac structure or function leading to
failure of the heart to deliver oxygen at a rate commensurate with the requirements of the
metabolizing tissues, despite normal filling pressures (or only at the expense of increased filling
pressures). HF is defined, clinically, as a syndrome in which patients have typical symptoms
(e.g. breathlessness, ankle swelling, and fatigue) and signs (e.g. elevated jugular venous
pressure, pulmonary crackles, and displaced apex beat) caused by a structural and/or functional
cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac
pressures at rest or during stress.
The current definition of HF restricts itself to stages at which clinical symptoms are apparent.
Before clinical symptoms become apparent, patients can present with asymptomatic structural
or functional cardiac abnormalities [systolic or diastolic left ventricular (LV) dysfunction], which
are precursors of HF.Recognition of these precursors is important because they are related to
poor outcomes, and starting treatment at the precursor stage may reduce mortality in patients
with asymptomatic systolic LV dysfunction. Demonstration of an underlying cardiac cause is
central to the diagnosis of HF. This is usually a myocardial abnormality causing systolic and/or
diastolic ventricular dysfunction. However, abnormalities of the valves, pericardium,
endocardium, heart rhythm and conduction can also cause HF (and more than one abnormality
is often present). Identification of the underlying cardiac problem is crucial for therapeutic
reasons, as the precise pathology determines the specific treatment used (e.g. valve repair or
replacement for valvular disease, specific pharmacological therapy for HF with reduced EF,
reduction of heart rate in tachy-cardiomyopathy, etc).
The main terminology used to describe HF is historical and is based on measurement of the Left
Ventricle Ejection Fraction (LVEF). HF comprises a wide range of patients, from those with
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normal LVEF [typically considered as ≥50%; HF with preserved EF (HFpEF)] to those with
reduced LVEF [typically considered as <40%; HF with reduced EF (HFrEF)]. Patients with an
LVEF in the range of 40–49% represent a ‘grey area’, which we now define as HfmrEF (HF mid-
range EF). Differentiation of patients with HF based on LVEF is important due to different
underlying aetiologies, demographics, co-morbidities, and response to therapies.
The diagnosis of HFpEF is more challenging than the diagnosis of HFrEF. Patients with HFpEF
generally do not have a dilated LV, but instead, often have an increase in LV wall thickness
and/or increased left atrial (LA) size as a sign of increased filling pressures. Most have
additional ‘evidence’ of impaired LV filling or suction capacity, also classified as diastolic
dysfunction, which is generally accepted as the likely cause of HF in these patients (hence the
term ‘diastolic HF’). However, most patients with HFrEF (previously referred to as ‘systolic HF’)
also have diastolic dysfunction, and subtle abnormalities of systolic function have been shown in
patients with HFpEF. Hence the preference for stating preserved or reduced LVEF over
preserved or reduced ‘systolic function’.
Based on ESC guidelines for the diagnosis and treatment of acute and chronic HF 2016, the
term HF is used to describe the symptomatic syndrome, graded according to the New York
Heart Association (NYHA) functional classification, although a patient can be rendered
asymptomatic by treatment. In these guidelines, a patient who has never exhibited the typical
symptoms and/or signs of HF and with a reduced LVEF is described as having asymptomatic
LV systolic dysfunction. Patients who have had HF for some time are often said to have ‘chronic
HF’. A treated patient with symptoms and signs that have remained generally unchanged for at
least 1 month is said to be ‘stable’. If chronic stable HF deteriorates, the patient may be
described as ‘decompensated’ and this may happen suddenly or slowly, often leading to
hospital admission, an event of considerable prognostic importance. New-onset (‘de novo’) HF
may also present acutely, for example, as a consequence of acute myocardial infarction (AMI),
or in a subacute (gradual) fashion, for example, in patients with a dilated cardiomyopathy
(DCM), who often have symptoms for weeks or months before the diagnosis becomes clear.
Although symptoms and signs of HF may resolve, the underlying cardiac dysfunction may not,
and patients remain at the risk of recurrent ‘decompensation’. Congestive HF’ is a term that is
sometimes used and may describe acute or chronic HF with evidence of volume overload. Many
or all of these terms may be accurately applied to the same patient at different times, depending
upon their stage of illness.
The prevalence of HF depends on the definition applied, but is approximately 1–2% of the adult
population in developed countries has HF, with the prevalence rising to ≥10% among persons
70 years of age or older. Among people >65 years of age presenting to primary care with
breathlessness on exertion, one in six will have unrecognized HF (mainly HFpEF). The lifetime
risk of HF at age 55 years is 33% for men and 28% for women. The proportion of patients with
HFpEF ranges from 22 to 73%, depending on the definition applied the clinical setting (primary
care, hospital clinic, hospital admission), age and sex of the studied population, previous
myocardial infarction. There are many causes of HF, and these vary in different parts of the
world. At least half of patients with HF have a low left ventricular ejection fraction (LVEF).
Coronary artery disease (CAD) is the cause of approximately two-thirds of cases of systolic HF,
although hypertension and diabetes are probably contributing factors in many cases. There are
many other causes of systolic HF, which include previous viral infection (recognized or
unrecognized), alcohol abuse, chemotherapy (e.g. doxorubicin or trastuzumab), and ‘idiopathic’
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dilated cardiomyopathy (although the cause is thought to be unknown, some of these cases
may have a genetic basis).
Data on temporal trends based on hospitalized patients suggest that the incidence of HF may
be decreasing, more for HFrEF than for HFpEF. HFpEF and HFrEF seem to have different
epidemiological and etiological profiles. Compared with HFrEF, patients with HFpEF are older,
more often women and more commonly have a history of hypertension and atrial fibrillation
(AF), while a history of myocardial infarction is less common.
Two key neurohumoral systems activated in HF are the renin–angiotensin–aldosterone system
and sympathetic nervous system. In addition to causing further myocardial injury, these
systemic responses have detrimental effects on the blood vessels, kidneys, muscles, bone
marrow, lungs, and liver, and create a pathophysiological ‘vicious cycle’, accounting for many of
the clinical features of the HF syndrome, including myocardial electrical instability. Interruption
of these two key processes is the basis of much of the effective treatment of HF.
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
(i.e. orthopnea and paroxysmal nocturnal dyspnea) are less common, especially in patients with
milder symptoms, and are, therefore, insensitive. Many of the signs of HF result from sodium
and water retention, and are, therefore, also not specific. Peripheral edema has other causes as
well and is particularly non-specific. Signs resulting from sodium and water retention (e.g.
peripheral edema) resolve quickly with diuretic therapy (i.e. may be absent in patients receiving
such treatment, making it more difficult to assess patients already treated in this way). More
specific signs, such as elevated jugular venous pressure and displacement of the apical
impulse, are harder to detect and, therefore, less reproducible (i.e. agreement between different
doctors examining the same patient may be poor).
Symptoms and signs may be particularly difficult to identify and interpret in obese individuals, in
the elderly, and in patients with chronic lung disease. The patient’s medical history is also
important. HF is unusual in an individual with no relevant medical history (e.g. a potential cause
of cardiac damage), whereas certain features, particularly previous myocardial infarction, greatly
increase the likelihood of HF in a patient with appropriate symptoms and signs. These points
highlight the need to obtain objective evidence of a structural or functional cardiac abnormality
that is thought to account for the patient’s symptoms and signs, to secure the diagnosis of HF.
Once the diagnosis of HF has been made, it is important to establish the cause, particularly
specific correctable causes. Symptoms and signs are important in monitoring a patient’s
response to treatment and stability over time. Persistence of symptoms despite treatment
usually indicates the need for additional therapy, and worsening of symptoms is a serious
development (placing the patient at risk of urgent hospital admission and death) and merits
prompt medical attention.
The echocardiography and electrocardiography (ECG) are the most useful tests in patients with
suspected HF. The echocardiogram provides immediate information on chamber volumes,
ventricular systolic and diastolic function, wall thickness, and valve function. This information is
crucial in determining appropriate treatment (e.g. an ACE inhibitor and beta-blocker for systolic
dysfunction or surgery for aortic stenosis (Valvular Heart Disease)). The ECG shows the heart
rhythm and electrical conduction, i.e. whether there is sinoatrial disease, atrioventricular (AV)
block or abnormal intraventricular conduction. These findings are also important for decisions
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about treatment (e.g. rate control and anticoagulation for AF, pacing for bradycardia, or CRT if
the patient has LBBB). The ECG may also show evidence of LV hypertrophy or Q waves
(indicating loss of viable myocardium), giving a possible clue to the etiology of HF. HF is very
unlikely (likelihood, 2%) in patients presenting acutely and with a completely normal ECG. The
information provided by these two tests will permit an initial working diagnosis and treatment
plan in the majority of patients. Routine biochemical and hematological investigations are also
important, partly to determine whether renin-angiotensin– aldosterone blockade can be initiated
safely (renal function and potassium) and to exclude anemia (which can mimic or aggravate HF)
and because they provide other useful information. Because the signs and symptoms of HF are
so non-specific, many patients with suspected HF referred for echocardiography are not found
to have an important cardiac abnormality. Where the availability of echocardiography is limited,
an alternative approach to diagnosis is to measure the blood concentration of a natriuretic
peptide, a family of hormones secreted in increased amounts when the heart is diseased
(stretched) or the load on any chamber is increased (e.g. by AF, pulmonary embolism, and
some non-cardiovascular conditions, including renal failure). A chest X-ray is of limited use in
the diagnostic workup of patients with suspected HF. It is probably most useful in identifying an
alternative pulmonary explanation for a patient’s symptoms and signs. It may, however, show
pulmonary venous congestion or edema in a patient with HF. It is important to note that
significant LV systolic dysfunction may be present without cardiomegaly on the chest X-ray.
Estimation of prognosis for morbidity, disability, and death helps patients, their families and
clinicians decide on the appropriate type and timing of therapies (in particular, decisions about a
rapid transition to advanced therapies) and assists with the planning of health and social
services and resources. Many variables provide prognostic information, although most of this
can be obtained from readily available data such as age, etiology, NYHA class, LVEF, key co-
morbidities (renal dysfunction, diabetes mellitus, anemia, hyperuricemia), and plasma natriuretic
peptide concentration. Clearly, these variables change over time, as does prognosis so that
precise risk stratification in HF remains challenging. Assessment of prognosis is particularly
important when counseling patients about devices and surgery (including transplantation) and in
planning end-of-life care with patients, their family, and caregivers.
The goals of treatment in patients with established HF are to relieve symptoms and signs (e.g.
edema), prevent hospital admission, and improve survival and finally improved quality of life.
Although the focus of clinical trials was previously mortality, it is now recognized that preventing
HF hospitalization is important for patients and healthcare systems. Reduction in mortality and
hospital admission rates both reflect the ability of effective treatments to slow or prevent
progressive worsening of HF. This is often accompanied by reverse LV remodeling and a
reduction in circulating natriuretic peptide concentrations. The relief of symptoms, improvement
in the quality of life, and increase in functional capacity are also of the utmost importance to
patients, but they have not been the primary outcome in most trials. Three neurohumoral
antagonists— an ACE inhibitor [or angiotensin receptor blocker (ARB)], a beta-blocker, and a
mineralocorticoid receptor antagonist (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.
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Standard References:
1. Libby P, Bonow RO, Mann DL, Zipes DP eds. Heart Failure. In: Braunwald’s Heart
Disease, 10th ed. Philadelphia, Elsevier Saunders, 2015. p. 429-615
2. Ponikowski et al. ESC Guidelines for The Diagnosis and Treatment of Acute and
Chronic Heart Failure. European Journal Heart Failure. 2016 August;18(8): 891-975.
3. Miranda D, Lewis GD, Fifer MA. Heart Failure. In: Lilly LS ed. Pathophysiology of Heart
Disease. 6th ed. Philadelphia: Wolters Kluwer; 2016:220-246
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Etiology of Chronic Heart Failure
2. Pathophysiology of Chronic Heart Failure
3. Clinical and diagnostic approach to Chronic Heart Failure
4. Pharmacologic treatment of Chronic Heart Failure
5. Prognosis of Chronic Heart Failure
SCENARIO: CASE:
A 65 years old man is hospitalized after he is taken to the emergency department because of
dyspnea and leg edema. He has a longstanding history of hypertension that is treated with
amlodipine. Coronary angiography performed 1 year ago because of chest pain was normal. On
admission, blood pressure was 180/110 mmHg and heart rate was 120/min regularly. Jugular
venous distension is 10 cm while the patient is lying on a stretcher with his head elevated at 45
degrees. He has positive hepatojugular reflex, pitting leg edema, S3 gallop, and rales at basal of
both lungs. No heart murmurs are auscultated. Echocardiography examination showed left
ventricular (LV) ejection fraction of 20% and LV dilatation. Electrocardiography result was a left
bundle branch block. Serum electrolytes, hepatic and renal function measurements are normal.
LEARNING TASK:
1. What is the most likely diagnosis of the patient?
2. What is the etiology of the disease?
3. What is the pharmacological treatment for this patient?
SELF ASSESSMENT:
1. Please explain the definition of heart failure!
2. Please explain terminology heart failure related to left ventricular ejection fraction!
3. Please explain terminology heart failure related to the symptomatic severity of heart
failure!
4. What are signs and symptoms of heart failure?
5. Please explain general diagnostic test in patients with suspected heart failure!
6. What are can impact the prognosis of chronic heart failure?
7. Please explain pharmacological treatment for patients with chronic heart failure!
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LECTURE 12 INTRODUCTION TO ARRHYTHMIA
dr. I Made Putra Swi Antara, SpJP(K), FIHA
Department of Cardiology and Vascular Medicine
AIMS:
Able to understand and diagnose arrhythmias.
LEARNING OUTCOME:
Can describe and diagnose arrhythmias.
CURRICULUM CONTENTS:
1. Etiology and pathophysiology of Arrhythmias.
2. Clinical approach to Arrhythmias.
3. Treatment of Arrhythmias.
4. Prognosis of Arrhythmias.
ABSTRACT:
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 hemodynamic
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 stenosis). 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 beta-
adrenergic blocking eye drops for the treatment of glaucoma can drain into tear ducts, be
absorbed systemically, and precipitate syncope caused by bradycardia.
Examination of the patient during a symptomatic episode can be revealing. Clearly, heart rate
and blood pressure are key measurements to make. Assessment of the jugular venous
pressure and waveform can disclose the rapid oscillations of atrial flutter or “cannon” A waves
indicative of contraction of the right atrium against a closed tricuspid valve in patients with AV
dissociation in disorders such as complete heart block or Ventricular Tachycardia/VT. Variations
in the intensity of the first heart sound and systolic blood pressure have the same implications.
The electrocardiogram/ ECG is the primary tool in arrhythmia analysis; an Electrophysiology
Study/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
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further diagnostic 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, an
exercise/treadmill 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.
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.
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, it is critical to
making the distinction between SVT and VT 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 always benign. Initial management of
SVT comprises of the Valsalva maneuver, carotid sinus pressure or administration of
intravenous adenosine. Beta-blocker and verapamil reduce symptoms significantly in two-thirds
of patients with recurrent SVT. Radio-frequency ablation/RFA should be considered for all
patients with frequent SVT.
Atrial fibrillation (AF) is a supraventricular arrhythmia characterized by low-amplitude baseline
oscillations (fibrillatory or F waves) and an irregularly irregular ventricular rhythm on an ECG. 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 generally rate-control strategy. It is directed at
limiting the ventricular response to atrial fibrillation by using AV node blocking drugs, such as
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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 thromboembolic stroke by using a scoring
system (CHA2DS2-VASc).
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, it generally differs.
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 post-extrasystolic 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 non-sustained 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 Implantable
Cardioverter Defibrillator/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
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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.
Bradyarrhythmia is arbitrarily defined as a heart rate below 60 beats/min. In some cases,
bradyarrhythmia is 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,
bradyarrhythmia can be categorized on the basis of the level of disturbance in the hierarchy of
the normal impulse generation and conduction system (from the 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 in excitability 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 the 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.
Main Reference:
Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier Saunders, 2015. p.
687-837
Mandatory Reading:
Evans, JDW et all. Cardiac Electrophysiology and Arrhythmia. In: Crash Course in
Cardiovascular System 4th Edition. 2012. P 27-42
Available at: http://goo.gl/DY79rx
SELF DIRECTED LEARNING
Basic knowledge that must be known:
1. Understanding of Cardiac Electrophysiologic Properties
2. Basic Understanding of ECGs
3. Definition and Mechanisms of Arrhythmias
4. Clinical approach for Arrhythmias
5. Pharmacological and Procedural Treatments for Arrhythmias
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SCENARIO FOR DISCUSSION
CASE 1:
A 45-year old gentleman presented with an irregular heartbeat 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:
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 32-year old gentleman was brought to the emergency department after an out-of-hospital
cardiac arrest (OOHCA) at 4 am on his bed and was successfully resuscitated. No remarkable
health history or precipitating factors were present, nor any risk factors for CAD. Initial rhythm
observed by the emergency response team was VF and was defibrillated twice to convert back
to sinus rhythm. Physical exam was normal. Recorded ECG doesn’t show any apparent
arrhythmia or abnormality.
1. What are the differential cardiac diagnoses for this patient?
2. What abnormality is looked for in the ECG to support the diagnosis?
3. What treatment options are needed for this patient to prevent recurrence of sudden
cardiac death?
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LECTURE 13a COMMON PERIPHERAL VASCULAR AND LYMPHATIC DISEASE
Dr. dr. Semadi, Sp.B, Sp.BTKV
Department of Surgeon
AIMS:
Describe the basic principles of surgery in cardiac diseases
LEARNING OUTCOME:
1. Can describe the basic principles of cardiac surgery
2. Can describe the basic aspect of cardiac surgery
3. Can describe the cardiac diseases who need surgery
CURRICULUM CONTENTS:
1. Surgery of the congenital heart
2. Surgery of the acquired heart diseases
ABSTRACT:
Atrial septal defects (ASD) and ventricular septal defect (VSD) and others are the congenital
cardiac anomaly. The intracardiac defects make the shunt and blood flow through the shunt
from right-to-left or reverse of the heart.
Atrial septal defects (ASD) are most common in the vicinity of the fossa ovalis. Septum
secundum defects, the typical patent foramen ovale, account for 10-15% of all cardiac
anomalies. Normal left atrial pressure is slightly greater than right atrial pressure, a left-to-right
shunt occurs 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) usually happens 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 tachypnea due to a lung infection.
Others cardiac diseases are more common as coronary arterial diseases (CAD), Acquired Valve
diseases of rheumatic heart disease and congenital valve anomaly
Standard References:
Stuart W. Jamieson and Norman E Shumway: Cardiac Surgery in Rob & Smith’s Operative
Surgery, 4th edition. Butterworths London, 2004.
SELF DIRECTING LEARNING
Basic knowledge that must be known is cardiac surgery in principles
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SCENARIO:
CASE 1;
This baby aged 4 months has been known to have a cardiac murmur since birth. He was born 8
weeks prematurely and developed respiratory distress requiring high oxygen concentration for
the first week. Since then he has feed satisfactorily but height and weight growth have been
poor even allowing for prematurity. The diagnosis after examination and investigations: Patent
Ductus Arteriosus (PDA).
LEARNING TASK I
1. How to prepare if the patient has surgery?
2. What is cardiac surgery category for PDA closure?
3. PDA commonly concomitant with a congenital anomaly. Is it every PDA have surgery to
close the shunt?
4. After an operation to close the PDA, why is there a risk of the patient becoming hoarse?
CASE 2 :
This 13-year-old girl was recently found to have a cardiac murmur. She has been generally
healthy with good growth, but on questioning her mother admitted she has noticed that girl
tends to tire easily with exercise. The diagnosis of examination and investigations: Atrial Septal
Defect (ASD)
LEARNING TASK II:
1. What is cardiac surgery category for ASD closure?
2. What the difference between close and open cardiac surgery?
3. After ASD was closed, why the patient getting good growth of the body?
4. And why is the patient after ASD closure getting arrhythmia?
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-precordial 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 is PS, VSD, Overriding aorta and RVH. How do repair it?
2. Why is the patient becoming worse after the surgical repair of the defect?
SELF-ASSESSMENT:
1. Describe the principle cardiac surgery!
2. Describe the principle coronary heart surgery!
3. Describe the principle of Valve surgery!
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LECTURE 13b TREATMENT OF AORTA AND ARTERIAL DISEASES
Dr. dr. Semadi, Sp.B, Sp.BTKV
Department of Surgeon
AIMS:
Describe the basic principles of surgery in aorta and arteries.
LEARNING OUTCOME:
1. Can describe the basic principles of aorta and arteries.
2. Can describe the basic aspect of aorta arteries.
3. Can describe the aorta and arteries diseases who need surgery.
CURRICULUM CONTENTS:
1. Surgery of the aneurysm of the aorta.
2. Surgery of the peripheral artery diseases.
ABSTRACT:
Atherosclerosis is the usual cause of vascular diseases. The aneurysm of the aorta is dilated of
aorta lumen over one and a half size of the normal lumen of the aorta. The aorta can
enlargement, elongated and tortuous with or without thrombus in the lumen of the aorta. It can
be found in thoracic region or abdominal region or both. The patient got the pain in the chest or
abdominal pain depend on the aneurysm position. If you found the abdominal aortic aneurysm
(triple A), the large pulsatile tumor was found on central topographic of the abdomen. The
patient becomes dangerous if an aortic aneurysm ruptured and the patient getting haemorrhagic
shock.
Atherosclerosis can cause the peripheral artery diseases. The artery becomes aneurysm,
stenosis and occluded. If the artery got occlusion on middle size of that, the distal part of the
organ will ischemic and become the death of the tissue that calls gangrene.
Standard References:
Allan D. Callow, Calvin B. Erust.: Vascular surgery, Theory, and Practice, Prentice- Hall
International Inc.London, 1995
SELF DIRECTING LEARNING
Basic knowledge that must be known is vascular surgery in principles.
SCENARIO: CASE 1;
Old man, he was a pain on the abdomen and the tumor was found on abdomen palpation. The
tumor was pulsatile 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 hemodynamically
LEARNING TASK I:
a) How to diagnose the patient?
b) How to prepare if the patient has surgery?
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c) How to do to enlargement of the aorta?
d) What are the complications of aorta surgery?
CASE 2 :
This 43-year-old man was recently found to have a cold of feet. He has been generally healthy
with pain on both legs if he walking for while he was heavy smoking from teenager. The
diagnosis after physical examination that concludes: peripheral artery diseases of both popliteal
artery
LEARNING TASK II:
1. What will you do to investigate the patient for definitive diagnosis?
2. What will you do to improve the blood flow to the distal end of feet?
3. How the prognosis and recurrent rate?
SELF-ASSESSMENT:
1. Describe the principle of vascular surgery!
2. Describe the principle arterial repair!
3. Describe the principle of care after vascular surgery!
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LECTURE 14 VALVULAR HEART DISEASE
dr. I B Rangga Wibhuti, M.Biomed, SpJP, FIHA, FASE
Department of Cardiology and Vascular Medicine
AIMS:
Able to diagnose and manage Valvular Heart Disease (VHD).
LEARNING OUTCOME:
1. Able to combine history taking, physical examination, and supportive examinations to
make initial/working diagnosis of VHD patients, and able to suggest further
examination(s) needed to diagnose VHD.
2. Able to manage VHD patients in short term and long-term management.
3. Able to combine history taking, physical examination, and supportive examinations to
diagnose the patients.
CURRICULUM CONTENT:
1. Etiology, pathophysiology, and clinical spectrum of VHD.
2. Indication and interpretation of supportive examination(s)for VHD.
3. Management of VHD patients.
ABSTRACT:
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
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mild to moderate disease who need an accurate diagnosis and appropriate medical
management. 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, percutaneous intervention, or surgical
intervention.
Standard References:
Mann, DL et al. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier Saunders, 2015.
Additional reading:
Constant, Jules. Essential for Bedside Cardiology, 2nded. New Jersey, Humana Press Inc. 2003
SCENARIO:
CASE:
A 30-year-old woman complained of progressive exertional shortness of breath in the past one
year. Physical examination revealed a loud first heart sound, an opening snap and a mid-
diastolic rumbling murmur with an irregularly irregular pulse.
LEARNING TASK:
1. What diagnosis do these findings suggest?
2. What is the underlying etiology?
3. What investigation is useful and describe the findings that are consistent with the initial/
working diagnosis?
4. What pharmacological treatment does she need? Describe the mechanism of action for
the medicine(s) and why she needs it/them?
5. What other treatment does she (might) need? Please describe the indication, procedure,
and complication that might occur!
SELF DIRECTING LEARNING and SELF-ASSESSMENT
1. Describe the etiology and clinical sign and symptoms for each valvular heart disease
(aortic valve regurgitation/stenosis, mitral valve regurgitation/stenosis, tricuspid valve
regurgitation/stenosis, pulmonic valve regurgitation/stenosis)!
2. Please explain the complication of mitral stenosis!
3. Please describe the ECG findings in aortic stenosis!
4. What is the Austin-Flint murmur?
5. Please explain the indication of mitral valve replacement procedure?
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LECTURE 15
ACUTE AND CHRONIC COR PULMONALE
dr. Luh Oliva Saraswati Suastika, Sp.JP, FIHA
Department of Cardiology and Vascular Medicine
AIMS:
Define the diagnosis and management of Cor Pulmonale (Pulmonary Heart Disease).
LEARNING OUTCOME:
1. Able to define the diagnosis and management of Acute Cor Pulmonale.
2. Able to define the diagnosis and management of Chronic Cor Pulmonale.
CURRICULUM CONTENT:
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.
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 pulmonary 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 a mean pulmonary artery (PA) Pressure >20 mmHg and is
placed in the heterogeneous group of PH associated with disorders of the respiratory system
and/or hypoxemia.
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 a sudden increase in the pulmonary
arterial pressure. The increased pulmonary artery pressure may be a consequence of a new
acute process, such as pulmonary embolism, acute respiratory distress syndrome, or
progression of the chronic disease. The diagnostic evaluation of cor pulmonale is inseparable
from the evaluation of 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 right-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 goals: reduction of right ventricular afterload (eg, pulmonary
artery pressure), a decrease of right ventricular pressure, and improvement of right ventricular
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contractility. In the cor pulmonale condition that leads to 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 analogs, endothelin-1 receptor
antagonists and phosphodiesterase-5 inhibitors were tested in randomized controlled trials,
leading to the approval of several drugs in each class.
SELF DIRECTING LEARNING
Basic knowledge that must be known:
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 1:
A 70-year old male came to Emergency Room due to swelling on the abdomen and both legs.
The complaints were suffered since 1 month ago and become worse. 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 the abdomen, and pitting edema on both legs, and
increased of jugular venous pressure. ECG revealed sinus tachycardia 110 beats-per-minute
with P pulmonal on lead II, III and aVF. The urinary production is good.
LEARNING TASK :
1. What is the most likely diagnosis?
2. Which further examinations would you recommend to support your diagnosis?
3. What is your initial treatment?
CASE 2:
A 60-year old female with obesity and cervical cancer who had undergone chemotherapy
presented to the emergency room with dyspnea on exertion, chest pain, and syncope. Initial
assessment of vital signs as follows: blood pressure 90/50, heart rate 120x/min, respiratory rate
30x/min and SaO2 86%. Her jugular venous pressure was 10 cmH2O. Laboratory work was
notable for troponin-I of 0.172 (normal <0.04 ng/mL) and NT-proBNP of 8603 (normal <125
pg/mL). Her ECG showed a S1Q3T3 pattern with large S wave in lead I and both prominent Q
waves and inverted T waves in lead III.
LEARNING TASK :
1. What is the most likely diagnosis?
2. Which further examinations would you recommend to support your diagnosis?
3. What is your initial treatment?
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SELF-ASSESSMENT :
1. Please explain the risk factors of cor pulmonale!
2. What are the complications of pulmonary hypertension?
3. What is the treatment choice for acute and chronic cor pulmonale?
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LECTURE 16
CONGENITAL HEART DISEASE AND ACUTE RHEUMATIC FEVER
dr. Eka Guna Wijaya, Sp.A (K)
Department of Pediatric
AIMS:
1. Describe Non-cyanotic and Cyanotic Congenital Heart Diseases.
2. Describe to diagnose and manage Acute Rheumatic Fever.
LEARNING OUTCOME:
1. Can describe, diagnose, and manage Non-cyanotic and Cyanotic Congenital Heart
Diseases.
2. Can describe, diagnose, and manage Cyanotic Congenital Heart Diseases.
3. Can describe, diagnose, and manage Acute Rheumatic Fever.
CURRICULUM CONTENS:
1. Fetal-transitional circulations.
2. To diagnose and manage Non-cyanotic Congenital Heart Diseases and its
complications.
3. To diagnose and manage Cyanotic Congenital Heart Diseases and its complications.
4. Interpret diagnostic tools for Congenital Heart Diseases.
5. The health education and prognosis of Congenital Heart Diseases.
6. Interpret diagnostic tool for Acute Rheumatic Fever.
7. Management of Acute Rheumatic Fever and its complications.
8. Prevention and rehabilitation of Acute Rheumatic Fever.
9. Health education and prognosis of Acute Rheumatic Fever.
ABSTRACT I:
Congenital Heart Disease (CHD) is a congenital malformation of the heart including a great
vessel that occurred 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, coarctation 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 undergo spontaneous closure after two years old. The
contrast in severe cases, a sign of heart failure, deep cyanosis, acidosis and another sign
express of the critical condition may exist in few hours after birth.
Severe pulmonary hypertension is a serious long-term complication of the 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 an 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 sympathetic and humoral stimulation.
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ToF may characterize by four anatomical abnormalities: VSD, overriding of the aorta, right
ventricular hypertrophy, and pulmonary stenosis. Right-to-left shunting was seen in ventricular
level. The severity of cyanosis in ToF depends directly on the severity of pulmonary stenosis.
Growth failure is the commonest finding of significant CHD. Screening should be done in a
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 CHD.
Diagnosis investigation of CHD was the following: history taking (antenatal, natal, and
postnatal), 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 an anomaly or damaged of one
or more cardiac valves.
Anomaly most likely congenital in origin include Tricuspid Atresia, Tricuspid Steno-insufficiency
(Ebstein anomaly) mitral stenosis, mitral insufficiency, pulmonary or aortic stenosis/atresia.
The most common of VHD is Rheumatic Heart Disease and Mitral Valve Prolapse.
Diagnosis investigation like another disease: History taking, physical examination, chest X-rays,
ECG, and other specific laboratory examination. Echocardiography is a 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
understood before identified many kinds of a pathological heart murmur.
Location, timing, quality, intensity, and transmission of heart murmur is the basic auscultatiion
modality to investigate more advance of specific valvular heart disease.
Management of VHD medically includes digitalis, diuretics, vasodilator, antithrombotic agent,
endocarditis prophylaxis, dental hygiene and nutritional support.
Rheumatic fever/ Rheumatic Heart Disease was agreed worldwide as an autoimmune disease.
Tissue hospes has a mimic antigenic structure with a certain strain of beta-hemolytic
streptococcus group a who was infected in the sharing. There is basic pathogenesis concept in
development tissue injury/ damage of susceptible host. When autoantibody was generated
insignificant number, a cross-reaction where streptococci causing agent were killed naturally by
humoral and cellular antibody but on the other hand tissue damage of the houses was also
happen because it was recognized as antigen.
Carditis and arthritis were the most frequent of a major symptom of RF/RHD.
Jones criteria were established as a definite diagnosis of rheumatic fever. Evolution was made
from the beginning in 1944 and then revised in 1956, modified in 1965, updated 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 Practitioners. 4th Ed. Philadelphia, Mosby. 2002. p
129-144, 185-189, 304-310, 311-318
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SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Fetal-transitional circulations
2. Criteria diagnose and manage the Non-cyanotic Congenital Heart Diseases and its
complications
3. Criteria diagnose and manage the Cyanotic Congenital Heart Diseases and its
complications
4. The health education and prognosis of Congenital Heart Diseases
5. Interpret diagnostic tool for Acute Rheumatic Fever
6. Management of Acute Rheumatic Fever and its complications
7. Prevention and rehabilitation of Acute Rheumatic Fever
8. Health education and prognosis of Acute Rheumatic Fever.
SCENARIO: CASE 1:
Putu, 2 years old girl came to pediatric cardiology clinic with her parent with the main complain
of a persistent cough and slight dyspnea.
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. A heart murmur has heard systolic and diastolic
phase at the upper left parasternal border.
LEARNING TASK :
1. How to know that patient having a continuous murmur?
2. What is the probable complete diagnosis clinically?
3. Is the patient should be given indomethacin?
4. What is the best diagnostic tool in this patient?
5. What kind of treatment has been recommended?
CASE 2:
Made, 9 months old baby was referred by GP to the 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 a long time and then hypercapnia
and lethargy.
LEARNING TASK:
1. What may happen to the baby?
2. What must you be done immediately to overcome this condition?
3. On auscultation, ejection systolic murmur was heard at the upper left parasternal
borderline with almost there is no heard of P2. Why?
4. What is the most probable disease may occur in the baby?
5. What do you expect from chest X-ray examination?
6. When should phlebotomy be performed base on routine blood examination?
7. Mention a lot of complication may be developed and what is the most hazard!
8. When should iron preparation be given to this patient?
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CASE 3:
Komang, 10 years old boy comes with his parent to the pediatric clinic of cardiology with the
main complain of dyspnea on exertion. Coughing and palpitation were also present. Physical
examination revealed: a Malnourish boy with slight anemic. Pulse rate: 108 x/ min, RR: 24
x/min, body temperature 38 degrees C. Hyperdynamic of precordium with a displacement of
apical impulse caudolaterally with lifting positive. Holosystolic murmur was heard at cardiac
apex referred to the axilla. Diastolic murmur was also heard at the upper right parasternal
border.
LEARNING TASK
1. Base on those data, what is the most probable diagnosis?
2. What are other history and laboratory examination may be needed to support the
diagnosis?
3. Which of the cardiac valve were involved in this patient?
4. How about chest X-ray and blood pressure examination?
5. How to manage in short and long time period?
SELF ASSESSMENT
1. Please describe the hemodynamic change in PDA!
2. Please describe the pattern of blood pressure and pulse in PDA!
3. How the chest X-ray in a patient with PDA?
4. Is in large PDA you can hear 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 the development of cyanotic spell!
7. Can you explain the pathomechanism of cyanotic spell?
8. Please mention the differential diagnosis of cyanotic CHD base on increase and
decrease of pulmonary blood flow!
9. Please explain what do you know about peripheral and central cyanosis!
10. Explain pathomechanism oh tissue injury in an acute rheumatic fever!
11. 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!
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BASIC CLINICAL SKILLS
Topik BCS PIC
Pemeriksan fisik kardiovaskular 1 dr. Luh Oliva S Suastika, SpJP
Pemeriksan fisik kardiovaskular 2 dr. IB Rangga W, SpJP(K)
Elektrokardiografi dr. Putra Swi Antara, SpJP(K)
Chest imaging dr. Lisna Astuti, Sp.Rad
Resusitasi jantung paru dr. Kadek Susila SD, SpJP
IV line procedure dr. Pontisomaya Parami, SpAn, MARS
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BASIC CLINICAL SKILL 1 CARDIOVASCULAR PHYSICAL EXAMINATIONS
dr. Luh Oliva Saraswati Suastika, Sp.JP, FIHA
dr. I.B. Rangga Wibhuti, Sp.JP(K), FIHA, FASE
AIMS:
Able to do a physical examination of the Cardiovascular System.
LEARNING OUTCOME:
Able to do a physical examination of the Cardiovascular System.
CURRICULUM CONTENT:
1. Evaluate general appearance
2. Blood pressure examination, the arterial pulse, the jugular venous pulse evaluation.
3. Inspection, 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
the cardiovascular system consists of evaluating 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 play an important role in diagnosing the patient. From auscultation, we should
obtain the heart sound quality and identify any murmur present. From percussion, we should
obtain any enlargement of the heart.
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. Evaluate general appearance.
2. Blood pressure examination, the arterial pulse, the jugular venous pulse evaluation.
3. Inspection, palpation, auscultation.
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CHECKLIST:
CARDIOVASCULAR PHYSICAL EXAMINATION
NO ITEMS SCORE
0 1 2
1 Evaluate General Appearance
Inspection of the skin, nails, faces, eyes, mouth
2 Blood Pressure Examination
Determine blood pressure
Rule out orthostatic hypotension, coarctation of the aorta, cardiac
tamponade
3 The Arterial Pulse
Rate and rhythm of the heart
Contour of the pulse
Amplitude of the pulse
4 The Jugular Venous Pulse
Estimate the jugular venous pressure
Evaluate the hepatojugular reflux
5 Inspection
Chest configuration
Ictus cordis
6 Palpation
Palpate the point of maximum impulse
Palpate for thrills
7 Auscultation
Auscultate the cardiac areas
The Influence of breathing
Describe any murmur present
8 Examination of Edema
Test for Edema
Score:
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BASIC CLINICAL SKILL 2
ELECTROCARDIOGRAPHY
dr. I Made Putra Swi Antara, SpJP(K), FIHA
AIMS:
Able to skills for Electrocardiography (ECG), procedure of, and ECG Interpretation,
Echocardiography, Phonography, and USG Doppler.
LEARNING OUTCOME:
1. Able to do the ECG procedure.
2. Able to do ECG interpretation.
CURRICULUM CONTENS:
1. ECG procedure
2. ECG Interpretation.
ABSTRACT:
Electrocardiogram (ECG) is an examination of 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 be associated with any electrical events occurring 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, all, 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, the 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. The 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
three-dimensional echocardiography, respectively. Doppler examination and color flow imaging
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provide a reliable assessment of cardiac hemodynamics and blood flow. Reliable noninvasive
hemodynamic evaluation and confident delineation of cardiovascular structures by
echocardiography have dramatically reduced the clinical necessity for hemodynamic cardiac
catheterization. Increasingly, patients undergo valvular or congenital heart surgery on the basis
of an echocardiographic diagnosis. Echocardiographic units are also being miniaturized to
become an extension of 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: Mann, DL et al. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier
Saunders, 2015. p. 118-132
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. ECG procedure.
2. ECG Interpretation
Preparation ECG Procedure
The group should choose one of their members to become a patient for the ECG examination.
Ask the patient to lie down on the table. In turn, each the student should perform the ECG
Examination; the student should start with patient preparation, set up 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 the electrocardiogram. The student should be
familiar with the analyzing step for the ECGram. It is likely that student should start by checking
the patient ID, analyze the rhythm, and identify whether there are any abnormality patterns. The
student should also be familiar with the writing technique for the ECGram’s interpretation.
Instruction
1. Analyze the ECGram given in a 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 the wrap-up
session!
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
75
BASIC CLINICAL SKILL 3
CHEST RADIOLOGY IMAGING
dr. Lisnawati Astuti, Sp.Rad
AIMS:
Able to evaluate and result in chest x-rays.
LEARNING OUTCOME:
1. Able to evaluate chest x-rays, including evaluation of heart, lung, diaphragm, skeleton
and soft tissues.
2. Able to result in chest x-rays.
CURRICULUM CONTENT:
1. Able to evaluate chest x-rays, including evaluation of heart, lung, diaphragm, skeleton
and soft tissues.
2. Able to result in chest x-rays.
ABSTRACT:
Chest imaging is an important evaluation that supports the diagnosis procedure. The student
should be able to evaluate chest x-rays, including evaluation of heart, lung, diaphragm, skeleton
and soft tissues. After evaluation, the 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 the cardiovascular system, the
chest imaging will be posterolateral, lateral, oblique projection. The student should evaluate the
heart size; identify any enlargement, the condition of the lung – any edema, arterial and venous
hypertension.
The imaging investigation of the heart may be considered under the following:
1. Chest X-ray
2. Computed tomography (CT-scan)
3. Magnetic resonance imaging (MRI)
4. Echocardiography
5. Angiocardiography
6. Cardiac catheterization
7. Isotope scanning
Chest X-ray remains the valuable cardiac investigation in clinical practice.
The radiologic method used in the roentgen cardiac examination:
1. Posteroanterior projection, PA/AP
2. Lateral Projection
3. Right anterior oblique projection (RAO)
4. Left anterior oblique projection (LAO)
Increase in cardiac size is the most consistent indication of cardiac disease.
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
76
SELF DIRECTING LEARNING
Basic knowledge that must be known:
Able to evaluate chest x-rays, including evaluation of heart, lung, diaphragm, skeleton and soft
tissues.
LEARNING TASK I:
Chest imaging: Cardiovascular System
Preparation
There would be 10 set of the 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. The group should
move to another x-rays film after complete the discussion and write down the result.
Instruction
1. The 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-ray and you should repeat the step 1 till 3 (each group should read all
photos available).
Standard References:
Roentgen Signs in Diagnostic Imaging Isadore Meschan
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
77
BASIC CLINICAL SKILL 4
dr. Pontisomaya Parami, SpAn, MARS
AIMS:
1. Able to practice skill routine clinical procedure: Intravenous line (IV line).
2. Able to practice skill routine clinical procedure: venipuncture.
LEARNING OUTCOME:
Able to two skills should be trained: IV cannulation and venipuncture.
CURRICULUM CONTENS:
1. Technique of venipuncture.
2. Aseptic procedure.
ABSTRACT :
The doctor should be able to draw blood in a 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
venipuncture is contained in the Venipuncture 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 explain the procedure, prepare the equipment
and position the patient, select an appropriate site, use standard precaution, and reach the goal
(obtain the adequate specimen and a good technique for cannulation).
SELF DIRECTING LEARNING
Basic knowledge that must be known:
1. The complete technique of venipuncture
2. Aseptic procedure
3. The preparation of the kit
4. Communicate the procedure to the patient
5. The patient preparation
6. The insertion technique of the needle, the blood collection
7. Evaluation of any bleeding
8. Cleaning the work area after the procedure.
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
78
Training Task
Venipuncture and IV Line Procedure
Preparation
We will provide the student with Multipurpose Injection Arm and IV line mannequin needed for
IV line procedure training. It would be at least one mannequin for every 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), a syringe (3 cc), and bring a glove for the
antiseptic procedure.
Instruction
1. There would be two skills should be trained in this session, IV cannulation and
venipuncture.
2. You have to prepare the set for the procedures, prepare the mannequin, needle, the
infusion set, and the infusion fluid.
3. Demonstrate how will you explain the procedure to the patient, the technique and the
complication might happen.
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 (Venipuncture and IV Cannulation) for any details!
6. Ask any comment and score for your performance from your groups based on the
checklist!
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
79
EVALUATION FORM OF THE CARDIOVASCULAR SYSTEM AND DISORDERS
Please fill the form according to the real condition. This evaluation will not influence your final
block result.
Please cross on the scoring column that suitable with your judgment.
No. Point being evaluated Score
1 2 3 4 5
A Topic
1. Approach to patient with cardiovascular disease
2 Cardiovascular Pharmacology
3 The formation of anomalies of the heart and great
vessels.
4 Cardiac markers
5 Cardiac rehabilitation
6 Acute Coronary Syndrome
7 Stable Angina Pectoris
8 Acute heart failure
9 Chronic Heart Failure
10 Hypertension
11 Hypertensive urgency & emergency
12 Arrhythmias
13 Valvular Heart Disease
14 Cor Pulmonale
15 Non-cyanotic & Cyanotic CHD & Acute Rheumatic
Fever
16 Common peripheral vascular disease
17 CV Physical Examination
18 ECG
19 Chest Imaging
20 CV Physical Examination 2
21 Cardiopulmonary resuscitation
22 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
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
80
C Lecturer
1. Prof. Dr. dr. I Wayan Wita, Sp.JP(K), FIHA,
FAsCC
2. dr. Ni Putu Ekawati, Sp.PA, M.Repro
3. Dr. dr. Wiradewi, Sp.PK
4. dr. Agung Nova Mahendra, M.Sc
5. dr. I Made Junior Rina Artha, Sp.JP(K), FIHA,
FAsCC
6. dr. I.B. Rangga Wibhuti, M.Biomed, Sp.JP(K),
FIHA, FASE
7. dr. I Made Putra Swi Antara, Sp.JP(K), FIHA
8 dr. I Kadek Susila Surya Darma, M. Biomed,
Sp.JP, FIHA
9 dr. A.A. Ayu Dwi Adelia Yasmin, M. Biomed,
Sp.JP, FIHA
10. dr. Nyoman Wiryawan, SpJP(K), FIHA
11. dr. Luh Oliva Saraswati Suastika, Sp.JP, FIHA
12. dr. Hendy Wirawan, SpJP
13. dr. Eka Guna Wijaya, Sp.A(K)
14. dr. Pontisomaya Parami, Sp.An. MARS
15. dr. Luh Kamiati, Sp.KFR
16. Dr. dr. Semadi, Sp.B, Sp.BTKV
D Facilitator
1 Name of your group facilitator:
E Assessment
1 Time provides
2 Suitability of question with topic given
Score:
1. Bad or not suitable for expectation
2. Insufficient or inadequate with expectation
3. Sufficient or inadequate with expectation
4. Good or suitable with expectation
5. Excellent or exceed expectation
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
81
The 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
Study Guide Cardiovascular System and Disorders
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2018
82
REFERENCES
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, 2006
6. Kumar V, Cotran RS, Robbins SL: Robbin’s Basic Pathology, 7th ed. Philadelphia, Saunders,
2003
7. 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 Practitioners. 4th Ed. Philadelphia, Mosby. 2002.
9. McPhee, S.J., Papadakis, M.A., Current Medical Diagnosis & Treatment. 47th ed. New York,
Lange Medical Book`s/The McGraw-Hill Companies, 2008.
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.