2023 Study Guide Kardiovaskular

STUDY GUIDE
STUDY GUIDE THE CARDIOVASCULAR SYSTEM AND DISORDERS
March, 1st 2023 until March, 20th 2023
MEDICAL FACULTY OF UDAYANA UNIVERSITY
2023
Study Guide Cardiovascular System and Disorders
STUDY GUIDE THE CARDIOVASCULAR SYSTEM AND DISORDERS

Planners
AAA Dwi Adelia Yasmin I Dewa Gde Aditya Diprabawa
Luh Oliva Saraswati Suastika Putu Primeriana Nugiaswari
Ni Made Dharma Laksmi I Wayan Sumardika
I Gusti Ayu Harry Sundariyati IGA Sri Darmayani
Contributors
A.A. Ayu Dwi Adelia Yasmin I Made Junior Rina Artha
I.G.A. Widianti Eka Guna Wijaya
I G.A. Dewi Ratnayanti I Nyoman Wiryawan
Indira Vidiari Juhanna I Nyoman Semadi
I Made Muliarta Luh Gede Kamiati
Putu Gede Adiatmika Luh Oliva Saraswati Suastika
I Gusti Made Aman Hendy Wirawan
I Wayan Sumardika Rani Paramita Iswari Maliawan
Agung Nova Mahendra Cyndiana Widia Dewi Sinardja
Ni Wayan Winarti I Dewa Gde Aditya Diprabawa
A.A. Wiradewi Lestarri Ni Made Dharma Laksmi
I Wayan Wita Putu Primeriana Nugiaswari
I Made Putra Swi Antara
Editors
A.A. Ayu Dwi Adelia Yasmin I Dewa Gde Aditya Diprabawa
Ni Made Dharma Laksmi Putu Primeriana Nugiaswari
I Gusti Ayu Harry Sundariyati I Gusti Ayu Sri Darmayani
I Wayan Sumardika
Layout
Rizky Darmawa
March 2023
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 the Department of
Medical Education Medicine Programme, Faculty of Medicine, Universitas Udayana.
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

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Visi Misi Program Studi Sarjana Kedokteran Fakultas Kedokteran

Universitas Udayana
Visi, misi, tujuan pendidikan yang tercantum dalam Rencana Strategis Program Studi Sarjana
Kedokteran dan Profesi Dokter Fakultas Kedokteran Universitas Udayana (Restra PS SKPD FK
UNUD) merupakan dasar utama penyusunan kurikulum program studi tahun 2021.
1. Visi program studi
“Menjadikan Program Studi Sarjana Kedokteran dan Profesi Dokter Fakultas
Kedokteran Universitas Udayana sebagai Lembaga Pendidikan yang Unggul,
Mandiri, Berbudaya dan Beretika, serta Mempunyai Daya Saing di Tingkat Nasional
dan Internasional pada Tahun 2025.”Berdasarkan visi di atas, yang dimaksud dengan
unggul, mandiri, berbudaya dan beretika adalah sebagai berikut:
1. Unggul. Sumber daya manusia yang memiliki kompetensi tinggi, daya saing, dan
bijaksana dalam mengembangkan ilmu pengetahuan yang dimilikinya untuk
meningkatkan martabat bangsa, negara, serta kemanusiaan pada umumnya
(cakra widya prawartana).
2. Mandiri. Sumber daya manusia yang memiliki kepribadian yang tangguh dan
kemampuan berinteraksi dengan lingkungan yang berkembang secara dinamis.
3. Berbudaya. Sumber daya manusia yang memiliki kepekaan dan ketajaman
nurani serta mampu memanfaatkan nilai-nilai luhur budaya lokal yang bersifat
universal untuk berinteraksi di tengah masyarakat.
4. Beretika. Sumber daya manusia yang memiliki perilaku yang sesuai dengan
nilai-nilai dan norma yang dapat menentukan tingkah lakunya dalam bertindak
dan berbuat di kehidupan bermasyarakat.
2. Misi program studi
Untuk mewujudkan visi di atas, PS SKPD FK UNUD memiliki misi untuk
memberdayakan Program Studi Pendidikan Dokter Fakultas Kedokteran Universitas
Udayana sebagai program studi yang melaksanakan Tri Dharma Perguruan Tinggi
berlandaskan pengembangan ilmu pengetahuan dan teknologi di bidang kesehatan,
nilai budaya, serta etika.
3. Tujuan program studi
Program Studi Sarjana Kedokteran dan Profesi Dokter Fakultas Kedokteran
Universitas Udayana memiliki tujuan, antara lain:

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1. Menghasilkan lulusan dokter yang unggul, mandiri, berbudaya, dan beretika yang
memiliki integritas ilmiah di bidang ilmu kedokteran sesuai dengan kompetensi
dan perkembangan ilmu pengetahuan dan teknologi.
2. Meningkatkan akses pelayanan pendidikan kepada peserta didik.
3. Mengembangkan tata kelola organisasi dan meningkatkan tertib administrasi
pengelolaan program studi.
4. Menjalin kerjasama di berbagai bidang dan dengan berbagai pihak dalam
mendukung pelaksanaan Tri Dharma Perguruan Tinggi.
5. Menghasilkan penelitian bermutu bertaraf nasional dan internasional
berlandaskan pengembangan ilmu pengetahuan dan teknologi serta
meningkatkan paten dan publikasi hasil penelitian pada publikasi ilmiah nasional
dan internasional.
6. Melaksanakanpengabdiankepadamasyarakatbaikregionalmaupunnasional dengan
mengaplikasikan ilmu pengatahuan yang dimiliki untuk kepentingan masyarakat.
4. Profil Lulusan
Sebagai lembaga pendidikan yang menghasilkan dokter, Program Studi Sarjana
Kedokteran dan Profesi Dokter Fakultas Kedokteran Universitas Udayana (PS
SKPD FK UNUD) membentuk lulusan dokter dengan profil lulusan sebagai berikut:
1. Dokter yang profesional memberikan layanan pada pusat pelayanan kesehatan
primer.
2. Dokter yang unggul di bidang kedokteran pariwisata/ travel medicine.
3. Dokter peneliti di bidang kesehatan.
4. Dokter pengelola program kesehatan

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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, symptoms
and signs of major cardiovascular disease and its pathophysiology and basic principle concept
to education, prevention, treatment and rehabilitation in cardiovascular system disorder in
patient, family and community. This study guide is developed by the academic staff from various
departments: Anatomy, Physiology, Histology, Pharmacology, Anatomy and Clinical Pathology,
Cardiology and Vascular Medicine, Pediatric Cardiology, Cardiothoracic Surgery, and Medical
Rehabilitation.
The learning process will be carried out for 3 weeks (12 working days) starting from March
1 , 2023 as shown in the time table. The final examination will be conducted on March 16th,
st
2023 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 discussed in SGD by
the students with the help of a facilitator. Lecture is given to emphasize the most important thing
of the material. In small group discussion, the students gave a learning task to lead their
discussion.
This simple study guide need more revision in the future, so that the planners kindly invite
readers to give any comments and critiques for its completion. Thank you.
Planners

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CONTENTS
COVER 1
PLANNER, CONTRIBUTOR, EDITOR 2
VISI MISI PROGRAM STUDI 3
PREFACE 5
TABLE OF CONTENT 6
MAPPING BLOK 8
GENERAL CURRICULUM OF CARDIOVASCULAR SYSTEM AND DISORDERS 9
SKDI 2012 10
RPS, CPL, CPMK 11
LECTURERS 43
FACILITATOR 45
LEARNING ACTIVITY 47
IMPORTANT INFORMATIONS 47
STUDENT PROJECT 48
ASSESSMENT METHOD 50
TIMETABLE OF CLASSES 54
LECTURE 1& 2 63
LECTURE 3 65
LECTURE 4 67
LECTURE 5 69
LECTURE 6 71
LECTURE 7 73
LECTURE 8 75
LECTURE 9 77
LECTURE 10 79
LECTURE 11 81
LECTURE 12 84
LECTURE 13 86
LECTURE 14 102
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LECTURE 15 105
LECTURE 16 110
LECTURE 17 112
LECTURE 18 115
LECTURE 19 118
LECTURE 20 122
LECTURE 21 124
LECTURE 22 127
LECTURE 23 131
LECTURE 24 134
LECTURE 25 136
LECTURE 26-27 139
LECTURE 28 142
LECTURE 29 144
LECTURE 30 147
EVALUATION FORM OF THE CARDIOVASCULAR SYSTEM AND DISORDERS 150
BLUEPRINT ASSESSMENT 156
REFERENCES 158

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MAPPING BLOK

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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 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 is 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 are commonly used in cardiovascular system disorders (antihypertensive, 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 is derive from general competences of Indonesian general
practitioner. Those competences in diagnosing diseases and doing clinical skills should be
mastered by all the general practioners here. Local values of our institutions are also considered
as added values in this curriculum.

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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

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UNIVERSITAS UDAYANA
FAKULTAS KEDOKTERAN
PROGRAM STUDI ILMU PENYAKIT JANTUNG DAN PEMBULUH DARAH
RENCANA PEMBELAJARAN SEMESTER

1 Mata Kuliah Nama Kode Bobot Semester Mata Kuliah Syarat
The Cardiovascular System and Disorders KSN3230AD 4 SKS 6 Tidak ada
2 Dosen 1. dr. A.A. Ayu Dwi Adelia Yasmin, Sp.JP (K), FIHA (Ketua)
Pengampu 2. Prof . Dr. dr. I Wayan Wita, Sp.JP
3. dr. Luh Oliva Saraswati Suastika, Sp.JP (K)
4. Dr. dr. I.G.A. Widianti, M.Biomed
5. dr. I G.A. Dewi Ratnayanti, M.Biomed
6. Prof. Dr. dr. Putu Gede Adiatmika, M.For
7. Dr.dr. Ni Wayan Winarti, Sp.PA (K)
8. Dr. dr. Made Muliarta, M.Kes
9. Prof. dr. I Gusti Made Aman, Sp.FK
10. dr. Agung Nova Mahendra, M.Sc
11. dr. Wayan Sumardika, M.Med.Ed., Ph.D
12. Prof. Dr. dr. Wiradewi Lestari, Sp.PK
13. dr. Indira Vidiari Juhanna, M.Fis
14. dr. I Kadek Susila Surya Darma, Sp.JP, FIHA
15. dr. I Made Putra Swi Antara, Sp.JP(K), FIHA
16. Dr.dr. I Made Junior Rina Artha, SpJP(K), FIHA
17. dr. Hendy Wirawan, Sp.JP, FIHA
18. dr. Nyoman Wiryawan, Sp.JP(K), FIHA
19. dr. Rani Paramita Iswari Maliawan, Sp.JP, FIHA
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20. dr. Eka Guna Wijaya, Sp.A(K)

21. dr. Luh Kamiati, Sp.KFR
22. Dr. dr. I Nyoman Semadi, SpB,SpBTKV
23. dr. Cyndiana Widia Dewi Sinardja, Sp.JP, FIHA
24. dr. I Dewa Gde Aditya Diprabawa, Sp.JP, FIHA
25. dr. Ni Made Dharma Laksmi, Sp.JP, FIHA
26. dr. Putu Primeriana Nugiaswari, Sp.JP, FIHA
Kantor: Lantai 4 Gedung Pusat Jantung Terpadu, RSUP Sanglah Denpasar Ruang Kelas:
Kontak: (0361) 22791115 ● Ruang Kuliah 3.01 dan 3.02 Fakultas
Kedokteran Universitas Udayana
● Ruang Small Group Discussion (SGD) Fakultas
Kedokteran Universitas Udayana
3 Deskripsi Mata The Cardiovascular System and Disorders adalah blok mata kuliah mengenai pengetahuan dasar ilmu penyakit jantung dan
Kuliah pembuluh darah bagi mahasiswa kedokteran semester VI yang telah disesuaikan dengan Standar Kompetensi Dokter Indonesia
(SKDI) tahun 2012. Blok Ilmu Penyakit Jantung dan Pembuluh Darah akan mempelajari anatomi, histologi, dan fisiologi organ jantung
dan pembuluh darah, farmakologi dari berbagai macam kelas obat-obatan jantung, patofisiologi, gejala, dan tanda penyakit jantung
dan pembuluh darah, dan konsep dasar edukasi, pencegahan, penanganan dan rehabilitasi penyakit jantung dan pembuluh darah di
pasien, keluarga, dan masyarakat.
4 CPL yang Kode Rumusan Indikator
dibebankan Mampu bekerja sebagai seorang dokter dan memiliki Mampu bekerja sebagai seorang dokter dan memiliki kompetensi
pada Mata
KU1 kompetensi kerja sesuai dengan standar kompetensi kerja sesuai dengan standar kompetensi dokter Indonesia.
Kuliah
dokter Indonesia.
Mampu membuat keputusan yang independen dalam Mampu membuat keputusan yang independen dalam
menjalankan pekerjaan sebagai seorang dokter menjalankan pekerjaan sebagai seorang dokter berdasarkan
KU2
berdasarkan pemikiran logis, kritis, sistematis, dan pemikiran logis, kritis, sistematis, dan kreatif
kreatif
Mampu memimpin suatu tim kerja untuk memecahkan Menunjukkan Kerjasama dalam tim untuk memecahkan masalah
KU4
masalah pada bidang kesehatan kesehatan pada learning task

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Mampu bertanggung jawab atas pekerjaan di bidang Melaksanakan tugas dan kewajiban di bidang kedokteran sesuai
KU5
kedokteran sesuai dengan kode etik kedokteran kode etik
Mampu mengkomunikasikan pemikiran/argumen atau Menunjukkan kemampuan komunikasi dalam pemirikdan dan
karya inovasi yang bermanfaat bagi pengembangan berargumen yang berlandaskan ilmiah dan etika profesi
KU7 profesi, dan kewirausahaan, yang dapat
dipertanggungjawabkan secara ilmiah dan etika profesi,
kepada masyarakat terutama masyarakat profesi dokter
Mampu bekerja sama dengan profesi lain yang sebidang Mampu bekerja sama dengan profesi lain yang sebidang dalam
KU8 dalam menyelesaikan masalah pekerjaan bidang menyelesaikan masalah pekerjaan bidang kesehatan
kesehatan
Mampu mengembangkan dan memelihara jaringan Mampu mengembangkan dan memelihara jaringan kerja dengan
KU9
kerja dengan masyarakat profesi dan pasien masyarakat profesi dan pasien
Mampu mendiseminasikan informasi dan Kemampuan teknik komunikasi yang efektif kepada pasien dan
pengetahuan secara efektif kepada profesional sesama rekan sejawat dalam melayani pasien
KU11
kesehatan, pasien, masyarakat dan pihak terkait
untuk peningkatan mutu pelayanan kesehatan
CPMK CPL KU1 KU2 KU4 KU5 KU7 KU8 KU9 KU11
Memahami berbagai macam jenis kelainan sistem CPMK-1 X X X X X

jantung dan pembuluh darah
Capaian Mampu menjelaskan struktur dan fungsi organ CPMK-2 X X
Pembelajaran jantung dan pembuluh darah
Mata Kuliah
5 Mampu menjelaskan interpretasi hasil pemeriksaan
(CPMK) dan CPMK-3 X X X X X
kontribusinya fisik, laboratorium, elektrokardiografi, dan imaging
terhadap CPL dada
Mampu melakukan penelusuran terhadap pasien CPMK-4 X X X X
dengan gangguan jantung dan pembuluh darah (nyeri
dada angina, berdebar, sesak, dan sianosis)
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Mampu menjelaskan penanganan dari berbagai CPMK-5 X X X X X X

penyakit dan kelainan di jantung
Mampu menjelaskan penanganan berbagai penyakit CPMK-6 X X X X X
sistem pembuluh darah dan limfa (insufisiensi vena,
lymphedema, dan penyakit arteri perifer)
Mampu menjelaskan edukasi, pencegahan, dan CPMK-7 X X X X X X
penanganan rehabilitasi penyakit jantung dan
pembuluh darah
6 Bahan Kajian/ 1. Anatomy of Cardiovascular System I
Pokok 2. Anatomy of Cardiovascular System II
Bahasan/ Topik 3. Histology of Cardiovascular System: Vascular
4. Physiology of Cardiovascular System: Cardiac Action Potential Intrinsic Conduction System
5. Physiology of Cardiovascular System: Cardiac output regulation
6. Physiology of Cardiovascular System: Function of blood vessels & regulation of blood flow
7. Pharmacology: Antihypertensive drugs
8. Pharmacology: Drugs for ischemic heart disease and heart failure
9. Pharmacology: Antiarrhythmic drugs
10. Pathologic Anatomy of Cardiovascular System: Pathological Aspect of Ischemic Heart Disease
11. Approach to patient with cardiovascular disease
12. Laboratory examination : cardiac marker
13. Chronic heart failure
14. Acute coronary syndrome : STEMI
15. Acute coronary syndrome : NSTE-ACS
16. Laboratory examination: cardiac markers
17. Hypertension : Hypertensive urgency and emergency
18. Chronic Coronary Syndrome
19. Malignant arrhythmias
20. Basic arrhythmias
21. Anatomy 3: Embryology
22. Congenital heart disease and Acute Rheumatic Fever
23. Cardiorespiratory arrest
24. Acute Heart Failure
25. Shock (cardiogenic)

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26. Acute cor pulmonale

27. Chronic cor pulmonale
28. Cardiac Rehabilitation
29. Peripheral Vascular and Aortic Disease
30. Venous Disease and Lymphatic Vessel
7 Rencana Pembelajaran
Pertemuan I-II: Introduction, Anatomy of Cardiovascular System I, Anatomy of Cardiovascular System II, Histology of
Cardiovascular System: Vascular, Physiology of Cardiovascular System: Cardiac Action Potential Intrinsic Conduction
System
Kemampuan akhir ● Mampu menjelaskan topografi dan anatomi umum organ jantung dan pembuluh darah (CPMK-2)
mahasiswa ● Mampu menjelaskan struktur mikroskopis organ jantung (CMPK-2)
● Mampu menjelaskan struktur mikroskopis sistem pembuluh darah arteri dan vena (CMPK-2)
● Mampu menjelaskan perhitungan, regulasi, dan perfusi curah (CPMK-2)
● Mampu menjelaskan fungsi struktural arteri koroner (CPMK-2)
● Mampu menjelaskan struktur fungsional sistem konduksi listrik dan aksi potensial jantung dan implikasi klinisnya (CPMK-1,
CPMK-2)
Kriteria/Indikator ● Ketepatan menjelaskan topografi anatomi dari jantung, mediastinum, pembuluh darah besar, sirkulasi sistemik, dan sirkulasi
Capaian pulmoner
● Ketepatan menjelaskan 3 lapisan jantung, jaringan ikat yang mendukung jantung, dan struktur mikroskopis katup jantung
● Ketepatan menjelaskan Struktur mikroskopis dan klasifikasi pembuluh arteri dan vena
● Ketepatan menjelaskan perhitungan curah jantung, regulasi curah jantung, perfusi jantung, dan fungsi structural arteri coroner
● Ketepatan menjelaskan potensial autoritmik sel jantung, potensial kontraksi sel jantung, dan gelombang elektrokardiografi
jantung
● Kerjasama dalam tim dan tingkat partisipasi dalam kelompok Small Group Discussion, Student Project, dan forum diskusi
Materi Teks Video/Animasi/Audio Slide (PPT)
Pembelajaran
1. Moore KL, Agur AMR: Essential Clinical 1. https://drive.google.com/file/
Anatomy, 3rd ed. Philadelphia, Lippincott& d/1-2orjqsXZPphyyH9qRmle5
Wilkins, 2007. p. 26-30, 65-67, 80-115. MxcqFI02BM/view?usp=shari
2. Gartner LP, Hiatte JL: Color Textbook of ng
Histology, 2nd ed. Philadelphia, WB Saunders 2. https://drive.google.com/file/
Company, 2001. p. 251- 265; 267-268; d/1-3FTUV0xis_iYradA8klFCyO
268-269 L3Yfqc7N/view?usp=sharing
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3. Fowcett DW, Jensh RP: Bloom & Fawcett’s 3. https://drive.google.com/file/

Concise Histology, 2nd ed. London, Arnold. d/1-Br5Vs5loHyDyeZ25AR3ZM
2002. p. 135-136; 136-145; 136-139 fkEugO4pyG/view?usp=sharin
4. Guyton AC: Medical Physiology, 11st ed. g
Philadelphia, Elsevier Saunders Company, 4. https://drive.google.com/file/
2006. p. 104-106, 116-122 d/1-DYLIwp-fC44qG0ubzoo8W
3cZMk3bpra/view?usp=sharin
g
5. https://drive.google.com/file/
d/1-CE88hrLNOaBJUB_CVJoml
h4L70z9vOa/view?usp=sharin
g
6. https://drive.google.com/file/
d/1-MWHbKZwAUijJDoXrLjPEi
UnObVCPltc/view?usp=sharin
g
Bentuk/Metode F2F (Aktivitas Kelas)
Online
Pembelajaran
● Mempelajari materi perkuliahan tentang ilmu ● Belajar mandiri (Self learning & Self Assessment)
penyakit jantung dan pembuluh darah ● Tugas terstruktur melalui penugasan pembuatan Student Project
dengan dengan mendengarkan penjelasan secara berkelompok
kuliah dari dosen pengajar ● Self-Directed Learning dengan pendalaman materi pembelajaran di
● Belajar berkelompok dan berdiskusi media internet melalui Independent Learning
(pengembangan interpersonal skills) dalam
bentuk SGD (Small Group Discussion)
bersama dosen fasilitator SGD
● Pleno membahas pemaparan hasil diskusi
SGD mahasiswa bersama dosen pengajar.
Mempelajari struktur histologi organ jantung
dan pembuluh darah dengan mendengarkan
penjelasan kuliah dari dosen pengajar

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Beban Waktu Online

F2F (Aktivitas Kelas)
Pembelajaran
● 2 x 4 x 50 menit (aktivitas kelas) ● 2 x 4 x 25 menit (Student Project)

● 2 x 4 x 25 menit (Small Group Discussion) ● 2 x 4 x 50 menit (Independent Learning)
Penilaian Metode Instrumen

Pembelajaran
F2F Online F2F Online
● Observasi ● Self ● Observasi ● Rubrik Self-Assessment
● Q&A Assessment ● Q&A
● Small Group ● Rubrik Small Group
Discussion Discussion
Pengalaman F2F Online
Belajar/Aktivitas
● Mempelajari materi perkuliahan tentang ● Belajar Mandiri melalui Media Pembelajaran Online
Mahasiswa
penyakit jantung dan pembuluh darah ● Berlatih mengerjakan quiz di rubrik self-assessment
dengan mendengarkan pemaparan dari
dosen pengajar.
● Belajar berkelompok dan berdiskusi
(pengembangan interpersonal skills)
● Berlatih mengaplikasikan teori ilmu ke dalam
bentuk diskusi kasus terstruktur dalam Small
Group Discussion
● Menyatakan pendapat di Forum Diskusi
Student Project
Media Pembelajaran F2F / Online F2F Online
PC/Laptop/Pointer PC/Laptop/Gadget
Fasilitator F2F Kelas A F2F Kelas B
1. dr. I Wayan Gede Sutadarma, M.Gizi, Sp.GK 1. dr. I Ketut Agus Indra Adhiputra, Sp.MK
2. dr.Ni Made Dharma Laksmi,Sp.JP 2. dr. I Gusti Made Gde Surya Chandra Trapika, M.Sc, Ph.D
3. Dr. dr. Bagus Komang Satriyasa, M.Repro 3. dr. Muliani, S.Ked., M.Biomed
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4. dr. Ni Putu Tesi Maratni,S.Ked,M.Biomed 4. dr. Ayu Setyorini M. Mayangsari, M.Sc, Sp.A(K)
5. dr. Gede Wirata, S.Ked, M.Biomed 5. dr. I Gusti Ngurah Pramesemara, S.Ked., M.Biomed., Sp.And
6. dr. I Made Oka Negara, S.Ked, M.Biomed 6. Dr.dr.I G A Widianti, M.Biomed
7. dr. Ida Bagus Amertha Putra Manuaba, 7. dr. I Putu Bayu Mayura, S.Ked, Ph.D
S.Ked.,M.Biomed 8. dr. Cyndiana Widia Dewi Sinardja, M.Biomed., Sp.JP, FIHA
8. Dr.dr.Made Agus Hendrayana,S.Ked,M.Ked 9. Dr.dr.Dewa Ayu Agus Sri Laksemi, M.Sc
9. dr. Putu Primeriana Nugiaswari, Sp.JP, FIHA 10. dr. Luh Oliva Saraswati Suastika, Sp.JP(K), FIHA
10. dr. I Gede Putu Supadmanaba, S.Ked, M.Sc
Pertemuan III-IV: Physiology of Cardiovascular System: Function of blood vessels & regulation of blood flow,
Pharmacology: Antihypertensive drugs, Pharmacology: Drugs for ischemic heart disease and heart failure,
Pharmacology: Antiarrhythmic drugs, Pathologic Anatomy of Cardiovascular System: Pathological Aspect of Ischemic
Heart Disease
Kemampuan akhir ● Mampu menjelaskan stroke volume, heart rate, faktor-faktor yang mempengaruhi tekanan darah, dan prinsip dasar regulasi
mahasiswa tekanan darah (CPMK-2)
● Mampu menjelaskan strategi pengobatan, farmakodinamik, farmakokinetik, aplikasi klinis, interaksi obat, dan toksisitas
obat-obatan dalam terapi hipertensi (CPMK-5, CPMK-6)
obat-obatan dalam penyakit jantung iskemik dan gagal jantung (CPMK-5)
obat-obatan dalam terapi aritmia (CPMK-5)
● Mampu menjelaskan struktur patologi anatomi organ jantung dan pembuluh darah (CPMK-1)
● Mampu menjelaskan perubahan dan kelainan patologi anatomi pada organ jantung dan sistem pembuluh darah di penyakit
jantung iskemik (CPMK-1, CPMK-2)
Kriteria/Indikator ● Ketepatan dalam menjelaskan menjelaskan stroke volume, heart rate, faktor-faktor yang mempengaruhi tekanan darah, dan
Capaian prinsip dasar regulasi tekanan darah
● Ketepatan dalam menjelaskan strategi pengobatan, farmakodinamik, farmakokinetik, aplikasi klinis, interaksi obat, dan
toksisitas obat-obatan dalam terapi hipertensi
● Ketepatan dalam menjelaskan menjelaskan strategi pengobatan, farmakodinamik, farmakokinetik, aplikasi klinis, interaksi obat,
dan toksisitas obat-obatan dalam penyakit jantung iskemik dan gagal jantung
● Ketepatan dalam menjelaskan strategi pengobatan, farmakodinamik, farmakokinetik, aplikasi klinis, interaksi obat, dan
toksisitas obat-obatan dalam terapi aritmia
● Ketepatan dalam menjelaskan struktur patologi anatomi organ jantung dan pembuluh darah
18
● Ketepatan dalam menjelaskan perubahan patologi anatomi pada organ jantung dan system pembuluh darah di penyakit jantung
iskemik
Materi Teks Video/Animasi Slide (PPT)
Pembelajaran th
1. Fox S.I.: Human Physiology, 9 ed. New York, 1. https://drive.google.com/file/d/11mkb5gnlVt6PcS
McGraw-Hill, 2006. p. 448-454. ELs8sQBWsZGJ7I-Q4s/view?usp=sharing
2. Guyton AC: Medical Physiology, 11st ed. 2. https://drive.google.com/file/d/11n9MHQ09_Dm_
Philadelphia, Elsevier Saunders Company, Ocx9PuXm0MCSYVMr8D8F/view?usp=sharing
2006. p. 161-170, 205-23. 3. https://drive.google.com/file/d/11kvXso1KZAvsn4
3. Trevor AJ, Katzung BG, Masters SB: Katzung & cWmJuSLtPGr8LAvGzy/view?usp=sharing
Trevor’s Pharmacology, 7th ed. New York, 4. https://drive.google.com/file/d/11l3gUOk2oNO6u
McGraw-Hill/Lange., 2005. p 66-93, 95-104 MA8VxS7ulyEdDm6y1ex/view?usp=sharing
and p. 114-123. 5. https://drive.google.com/file/d/11i7kORk9EYTCU3
4. Kumar, V., Abbas, A.K. and Aster, J.C. 2015. jFUH34np-mVWE9hy0y/view?usp=sharing
Robbins and Kumar. Pathologic Basis of 6. https://drive.google.com/file/d/11lultINOHRqjQO
Disease, 9 ed. Philadelphia: Elsevier mrqRepHeXczcA7jUfn/view?usp=sharing
Saunders, pp. 491-501, 538-550
5. Wang T, Palluci D, Law K, Yanagawa B, Yam J,
and Butany J. Atherosclerosis: Pathogenesis
and pathology in mini-symposium:
cardiovascular pathology – I. Diagnostic
Histopathology 18:11.2012, Elsevier.
6. Lestari, P., Suastika, L. and Widyadharma, I.,
2019. Relationship Between Medication
Adherence and Hypertension Status in Public
Health Center. International Journal of
Medical Reviews and Case Reports, (0), p.1.
7. Rina,I., Update in Anticoagulant Advance The
Anticoagulant Co-therapy in ACS Patients
Undergoing Fibrinolytic.
8. Rina, I., The Importance of Antiplatelet in
ACS.

19
9. Rina, I., Update in Anticoagulant Advance The

Anticoagulant Co-therapy in ACS Patients
Undergoing Fibrinolytic.

Online
Pembelajaran
Beban Waktu Online

Pembelajaran


Pembelajaran
● Observasi ● Self ● Rubrik Small Group ● Rubrik self assessment
● Q&A Assessment DIscussion

20
● Small Group
Discussion
Belajar/Aktivitas
Mahasiswa
dosen pengajar.
Group Discussion
Student Project
● PC/Laptop/Pointer ● PC/Laptop/Gadget
1. dr. I Wayan Gede Sutadarma, M.Gizi, Sp.GK
1. dr. I Ketut Agus Indra Adhiputra, Sp.MK
2. dr.Ni Made Dharma Laksmi,Sp.JP
2. dr. I Gusti Made Gde Surya Chandra Trapika, M.Sc, Ph.D
3. Dr. dr. Bagus Komang Satriyasa, M.Repro
3. dr. Muliani, S.Ked., M.Biomed
4. dr. Ni Putu Tesi Maratni,S.Ked,M.Biomed
4. dr. Ayu Setyorini M. Mayangsari, M.Sc, Sp.A(K)
5. dr. Gede Wirata, S.Ked, M.Biomed
5. dr. I Gusti Ngurah Pramesemara, S.Ked., M.Biomed., Sp.And
6. dr. I Made Oka Negara, S.Ked, M.Biomed
6. Dr.dr.I G A Widianti, M.Biomed
7. dr. Ida Bagus Amertha Putra Manuaba,
7. dr. I Putu Bayu Mayura, S.Ked, Ph.D
S.Ked.,M.Biomed
8. dr. Cyndiana Widia Dewi Sinardja, M.Biomed., Sp.JP, FIHA
8. Dr.dr.Made Agus Hendrayana,S.Ked,M.Ked
9. Dr.dr.Dewa Ayu Agus Sri Laksemi, M.Sc
10. dr. Luh Oliva Saraswati Suastika, Sp.JP(K), FIHA
Pertemuan V-VI: Approach to patient with cardiovascular disease, Stable coronary artery disease, Acute coronary
syndrome I, Acute coronary syndrome II, Laboratory examination: cardiac markers
Kemampuan akhir ● Mampu menjelaskan keluhan umum dari penyakit jantung dan pembuluh darah (CPMK-1)
mahasiswa ● Mampu menjelaskan pendekatan investigasi kelainan jantung dan pembuluh darah (CPMK-4)
21
● Mampu menjelaskan pendekatan diagnostik dan manajemen penyakit jantung koroner stabil (CPMK-1, CPMK-2)
● Mampu menjelaskan definisi, faktor resiko, dan patofisiologi sindrom arteri koroner (CMPK-1, CPMK-2, CPMK-7)
● Mampu menjelaskan indikasi berbagai jenis-jenis pemeriksaan laboratorium dalam menunjang pemeriksaan penyakit jantung
dan pembuluh darah (CPMK-3)
● Mampu menjelaskan indikasi pemeriksaan laboratorium di penyakit jantung dan pembuluh darah (CPMK-1, CMPK-3)
Kriteria/Indikator ● Ketepatan dalam menjelaskan keluhan umum dan pendekatan investigasi penyakit jantung dan pembuluh darah
Capaian ● Ketepatan dalam menjelaskan pendekatan diagnostik dan manajemen penyakit jantung koroner stabil
● Ketepatan dalam menjelaskan definisi, faktor resiko, dan patofisiologi sindrom arteri koroner
● Ketepatan dalam menjelaskan jenis-jenis pemeriksaan laboratorium
● Ketepatan dalam menejelaskan strategi pemilihan pemeriksaan penunjang laboratorium dalam menunjang diagnosis penyakit
jantung dan pembuluh darah
Pembelajaran
1. McPhee SJ, Papadakis MA. Current Medical 1. https://drive.google.com/file/d/13lheYBbS73ql7kos
Diagnosis & Treatment. 47th ed. New York: yCrbYYGiUAkbxdeH/view?usp=sharing
Lange Mecical Book`s/The McGraw-Hill 2. https://drive.google.com/file/d/13mUWzZr32qkd9f
Companies, 2008.p. 16op9mL44PFyzrvXEz/view?usp=sharing
2. Roentgen Signs in Diagnostic Imaging Isadore 3. https://drive.google.com/file/d/13ybQFUHOWT861
Meschan. Mann, DL et all. Braunwald’s Heart qoBGmcWIc5mX433bWO-/view?usp=sharing
Disease, 10th ed. Philadelphia, Elsevier
4. https://drive.google.com/file/d/13tvpt6x80rjqS73-f
Saunders, 2015.
Yf4Ku-H-X-CXNqm/view?usp=sharing
3. Montalescot G. Et al. 2013 ESC Guidelines on
The Management of Stable Coronary Artery
Disease. Eur H J. 2013:34,2949-3003.
4. Mann, DL et al. Braunwald’s Heart Disease,
10th ed. Philadelphia, Elsevier Saunders,
2015.
5. 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.

22
6. Burtis CA, Bruns DE: Tietz Fundamentals of

Clinical Chemistry and Molecular Diagnostics,
7th ed. St.Louis, MO: Saunders/Elsevier,
2014.
7. Bishop ML, Fody EP, Schoeff LE: Clinical
Chemistry: Principles, Techniques, And
Correlations, 7th ed. Philadelphia: Lippincott
Williams & Wilkins, 2013.D
8. Desai SP, Isa-Pratt S: Clinician’s Guide to
Laboratory Medicine: A Practical Approach,
3rd ed. Michigan: Lexi-Comp, 2004.
9. Surya, I., Wita, I., Iswari, I., Rina Artha, I. and
Sundari, l., 2020. High ratio of monosit:
high-density lipoprotein as a risk factor of
chronic total occlusion in Patients coronary
artery disease. Asian Journal of
Pharmaceutical and Clinical Research,
pp.155-158.
10. Suastika, L., Cardiovascular Comorbidities
Characteristics in COVID-19 Observational
Descriptive Study at Udayana University
Hospital.
11. Prabawa, I., Lestari, A., Muliarta, I., Mardhika,
P., Pertiwi, G., Bhargah, A., Manuaba, I.,
Artha, M., Rina, I. and Rampengan, S., 2020.
The Stromal Cell-derived Factor-1/CXCL12
3’A-gene Polymorphism is Related to the
Increased Risk of Coronary Artery Disease: A
Systematic Review and Meta-analysis. Open

23
Access Macedonian Journal of Medical

Sciences, 8(F), pp.197-202.
12. Surya, I., Wita, I., Iswari, I., Rina Artha, I. And
Sundari, L., 2020. High Ratio of Monosit:
High-Density Lipoprotein As A Risk Factor of
Chronic Total Occlusion In Patients Coronary
Artery Disease. Asian Journal of
Pharmaceutical And Clinical Research,
Pp.155-158.

Online
Pembelajaran
Beban Waktu Online

Pembelajaran


24

Pembelajaran
● Observasi ▪ Self ● Rubrik Self Assesment
● Q&A Assessment ● Rubrik Small Group
● Small Group Discussion
Discussion
Belajar/Aktivitas
Mahasiswa
dosen pengajar.
Group Discussion
Student Project
25
Pertemuan VII-VIII: Hypertension I, Hypertension II, Basic arrhythmias, Malignant arrhythmias, Chronic Heart Failure
Kemampuan akhir ● Mampu menjelaskan pendekatan diagnosis klinis dan manajemen hipertensi (CPMK-1, CPMK-4, CPMK-5)
mahasiswa ● Mampu menjelaskan pendekatan diagnosis dan manajemen hipertensi urgensi dan hipertensi emergensi (CPMK-1, CPMK-4,
CPMK-5)
● Mampu menjelaskan pendekatan diagnosis dan manajemen Arritmia (CPMK-1, CPMK-4)
● Mampu menjelaskan patofisiologi dan kriteria penegakan diagnosis penyakit gagal jantung kronis (CPMK-1, CPMK-3, CPMK-4)
● Mampu menjelaskan pemeriksaan penunjang dan interpretasinya pada penyakit gagal jantung kronis (CPMK-3)
● Mampu menjelaskan penanganan pada penyakit gagal jantung kronis (CPMK-1, CPMK-3, CPMK-4, CPMK-5)
● Mampu menjelaskan definisi, kriteria diagnosis, pemeriksaan penunjang, dan penanganan penyakit gagal jantung akut
(CPMK-1, CPMK-3, CPMK-4, CPMK-5)
Kriteria/Indikator ● Ketepatan dalam menjelaskan pendekatan diagnosis pada pasien hipertensi, hipertensi urgensi, dan hipertensi emergensi
Capaian ● Ketepatan dalam menjelaskan pendekatan diagnosis dan manajemen arritmia
● Ketepatan dalam menjelaskan patofisiologi dan kriteria penegakan diagnosis penyakit gagal jantung kronis
● Ketepatan dalam pemeriksaan menjelaskan penunjang dan interpretasinya pada penyakit gagal jantung kronis
● Ketepatan dalam menjelaskan penanganan pada penyakit gagal jantung kronis
● Ketepatan dalam menjelaskan definisi, kriteria diagnosis, pemeriksaan penunjang, dan penanganan penyakit gagal jantung
akut
● Kerjasama dalam tim dan tingkat partisipasi dalam kelompok dan forum diskusi
Pembelajaran
1. Chobanian A, et al. Seventh Report of the 1. https://drive.google.com/file/d/147TMzeO_DfcK
Joint National Committee On Prevention, z-4fIiMMcl0HZk9LBCib/view?usp=sharing
Detection, Evaluation, And Treatment Of High 2. https://drive.google.com/file/d/13yB7kJLSQcXXl
BVY-JQuXwV_v572Hrhb/view?usp=sharing
Blood Pressure. Hypertension.
3. https://drive.google.com/file/d/13oVVsqRWOSW
2003;42:1206–1252. 1VDLiEroypQ2yxeVG8kVk/view?usp=sharing
2. Mancia G, et al. 2013 ESH/ESC Guidelines for 4. https://drive.google.com/file/d/13y-ONgX4uDLks
the Management of Arterial Hypertension. y1gVVRvsrhJpFsv2Y1f/view?usp=sharing
European Heart Journal. 2013;34:2159-2219.

26
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.
4. 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.
5. Mancia G, et al. 2013 ESH/ESC Guidelines for
the Management of Arterial Hypertension.
European Heart Journal. 2013;34:2159-2219.
6. 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.
7. Evans, JDW et all. Cardiac Electrophysiology
and Arrhythmia. In: Crash Course in
Cardiovascular System 4th Edition. 2012. P
27-42
8. 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

27
9. 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.
10. Miranda D, Lewis GD, Fifer MA. Heart Failure.
In: Lilly LS ed. Pathophysiology of Heart
Disease. 6th ed. Philadelphia: Wolters Kluwer;
2016:220-246
11. Maliawan, R., Suryaguna, S., Maliawan, R.,
Antara, P., Wita, I. and Wardhana, D., 2019.
Paroxysmal ventricular standstill pada pria
berusia 45 tahun dengan manifestasi
Stokes-Adams attack: laporan
kasus. Medicina, 50(1)
12. Nakamura, K., Akagi, S., Ejiri, K., Yoshida, M.,
Miyoshi, T., Sakaguchi, M., Amioka, N.,
Suastika, L., Kondo, M., Nakayama, R., Takaya,
Y., Higashimoto, Y., Fukami, K., Matsubara, H.
and Ito, H., 2021. Inhibitory effects of
RAGE-aptamer on development of
monocrotaline-induced pulmonary arterial
hypertension in rats. Journal of Cardiology,
78(1), pp.12-16.
13. Suastika, L., Hubungan Antara Kriteria
Elektrokardiografi LVH Terhadap Left
Ventricular Mass Index Pada Pasien Hipertensi
Di Rsup Sanglah Denpasar.

Online
Pembelajaran
28
penyakit jantung dan pembuluh darah dengan ● Tugas terstruktur melalui penugasan pembuatan Student Project
dengan mendengarkan penjelasan kuliah dari secara berkelompok
dosen pengajar ● Self-Directed Learning dengan pendalaman materi pembelajaran
● Belajar berkelompok dan berdiskusi di media internet melalui Independent Learning
bentuk SGD (Small Group Discussion) bersama
dosen fasilitator SGD
Beban Waktu Online

Pembelajaran


Pembelajaran
● Observasi ● Self ● Rubrik Small Group ● Rubrik self assesment
● Q&A Assessment Discussion
● Small Group
Discussion
Belajar/Aktivitas
Mahasiswa
penyakit jantung dan pembuluh darah dengan ● Berlatih mengerjakan quiz di rubrik self-assessment
mendengarkan pemaparan dari dosen
pengajar.

29

Group Discussion
Student Project
Pertemuan IX-X: Acute Heart Failure, Anatomy 3: Embryology, Acute cor pulmonale, Chronic cor pulmonale,
Congenital heart disease and Acute Rheumatic Fever
Kemampuan akhir ● Mampu menjelaskan embriologi organ jantung (CPMK-2)
mahasiswa ● Mampu menjelaskan definisi, patofisiologi, diagnosis, dan penanganan Acute Cor Pulmonale (CPMK-1, CPMK-3, CPMK-4,
CPMK-5)
● Mampu menjelaskan definisi, patofisiologi, diagnosis, dan penanganan Chronic Cor Pulmonale (CPMK-1, CPMK-3, CPMK-4,
CPMK-5)
● Mampu menjelaskan definisi, patofisiologi, diagnosis, dan penanganan penyakit jantung kongenital asianotik dan sianotik
(CPMK-1, CPMK-3, CPMK-4, CPMK-5)

30
● Mampu menjelaskan definisi, patofisiologi, diagnosis, dan penanganan Demam Rematik Akut (CPMK-1, CPMK-3, CPMK-4,
CPMK-5)
Kriteria/Indikator ● Ketepatan dalam menjelaskan embriologi organ jantung

Capaian ● Ketepatan dalam menjelaskan definisi, patofisiologi, diagnosis, dan penanganan Acute Cor Pulmonale
● Ketepatan dalam menjelaskan definisi, patofisiologi, diagnosis, dan penanganan Chronic Cor Pulmonale
● Ketepatan dalam menjelaskan definisi, patofisiologi, diagnosis, dan penanganan penyakit jantung kongenital asianotik dan
sianotik
● Ketepatan dalam menjelaskan definisi, patofisiologi, diagnosis, dan penanganan Demam Rematik Akut
Pembelajaran
1. Mann, DL et al. Braunwald’s Heart Disease, 1. https://drive.google.com/file/d/16OSa8EuxPG26
10th ed. Philadelphia, Elsevier Saunders, 2015. qRHmB5ajH7q6WAdPX7f8/view?usp=sharing
p. 429-615 2. https://drive.google.com/file/d/16WUMjaneQ3f
9p6Kf7oztqD7iXeI66ki_/view?usp=sharing
2. Ponikowski et al. 2016 ESC Guidelines For The
3. https://drive.google.com/file/d/1Ar7o8HJ8rF5YJS
Diagnosis and Treatment of Acute and Chronic Es7nGhWxAcS_Kny_76/view?usp=sharing
Heart Failure. European Heart Journal.
2016;ehw128
3. Moore KL, Agur AMR: Essential Clinical
Anatomy, 3rd ed. Philadelphia, Lippincott &
Wilkins, 2007. p. 91, 93, 94
4. Sadler TW: Langman’s Medical Embryology,
10thed. Philadelphia, Lippincott & Wilkins,
2006. p. 167-178, 184
5. Park, MK. Pediatric Cardiology for
Practitioners. 4th Ed. Philadelphia, Mosby.
2002. p 129-144, 185-189, 304-310, 311-318
6. Moore KL, Agur AMR: Essential Clinical
Anatomy, 3rd ed. Philadelphia, Lippincott &
Wilkins, 2007. p. 91, 93, 94

31
7. Sadler TW: Langman’s Medical Embryology,

10thed. Philadelphia, Lippincott & Wilkins,
2006. p. 167-178, 184
8. Suastika, L., Peranan Transesofageal
Ekokardiografi 3 Dimensi (TEE3D) dalam
Penegakan Diagnosis Endokarditis Infektif
dengan Penegakan Diagnosis Endokarditis
Infektif dengan Perforasi AML dan Penentuan
Tatalaksana Lanjutan
9. Suastika, L., Kejadian Katastropik Massa Right
Atrium Efusi Pericard Dengan
TamponadeJantung hingga Obstruksi Tricuspid
Valve Inflow.
10. Suastika,L., Hubungan Antara Kriteria
Elektrokardiografi LVH Terhadap Left
Ventricular Mass Index Pada Pasien Hipertensi
di RSUP Sanglah Denpasar.
11. Suastika, L. and Soesanto, A., 2019.
Echocardiographic Parameters Correlated with
Age in Isolated Severe Rheumatic Mitral
Stenosis Patients in Indonesia. Open Access
Macedonian Journal of Medical Sciences,
7(13), pp.2127-2132.
12. Suastika,L., Patent Foramen Ovale Dengan
Kriptogenik Stroke Perlukah Penutupan
Dengan Alat atau Terapi Medikamentosa.
13. Suastika, L., Karakteristik Ekokardiografi dan
Follow Up Pasien Stenosis Katup Aorta
Bikuspid Berat Setelah Intervensi Balon
Transkateter

Online
Pembelajaran

32
Beban Waktu Online

Pembelajaran


Pembelajaran
● Observasi ● Self ● Rubrik Small Group ● Rubrik Self Assessment
● Q&A Assessment Discussion
● Small Group
Discussion
Pengalaman F2F / Online F2F Online
Belajar/Aktivitas
Mahasiswa
pengajar.

33

Group Discussion
Student Project
Media Pembelajaran F2F Online
Pertemuan XI-XII: Shock (cardiogenic), Cardiorespiratory arrest, Peripheral Vascular and Aortic Disease, Cardiac
Rehabilitation
Kemampuan akhir ● Mampu menjelaskan etiologi, patofisiologi, kriteria diagnosis, penanganan, dan prognosis syok kardiogenik (CPMK-1, CPMK-4,
mahasiswa CPMK-5)
● Mampu menjelaskan kriteria diagnosis dan penanganan henti jantung (CPMK-4, CPMK-5)
● Mampu menjelaskan anatomi pembuluh darah perifer dan limfatik (CPMK-2)
● Mampu menjelaskan patofisiologi dan gejala penyakit pembuluh darah perifer dan limfatik (CPMK-1, CPMK-4)
● Mampu menjelaskan penanganan bedah penyakit pembuluh darah perifer dan limfatik (CPMK-1, CPMK-6)
● Mampu menjelaskan rehabilitasi jantung pada pasien dengan riwayat penyakit jantung (CPMK-7)

34
Kriteria/Indikator ● Ketepatan menjelaskan etiologi, patofisiologi, kriteria diagnosis, penanganan, dan prognosis syok kardiogenik
Capaian ● Ketepatan menjelaskan kriteria diagnosis dan penanganan henti jantung
● Ketepatan menjelaskan anatomi pembuluh darah perifer dan limfatik
● Ketepatan menjelaskan patofisiologi dan gejala penyakit pembuluh darah perifer dan limfatik
● Ketepatan menjelaskan penanganan bedah penyakit pembuluh darah perifer dan limfatik
● Ketepatan dalam menjelaskan proses rehabilitasi jantung pada pasien dengan riwayat penyakit jantung
Pembelajaran
1. Eric R. Bates. Cardiogenic Shock. Cardiac Intensive 1. https://drive.google.com/file/d/16Kt4WNHh_EOUI
Care: Second Edition. 2010. Saunders, Elsevier: w33-tzmXcDWWolztrVy/view?usp=sharing
Chapter 17. 2. https://drive.google.com/file/d/16X3S1NuHdvdaU
xB0qHqwfRG-IKsjVhNY/view?usp=sharing
2. Wolfgang Krüger and Andrew Ludman.
3. https://drive.google.com/file/d/1AjxrbepZ3dDcCO
Cardiogenic Shock. Acute Heart Failure: Putting hrTZ5yBqswna9Ggjj2/view?usp=sharing
the Puzzle of Pathophysiology and Evidence 4. https://drive.google.com/file/d/1AqZkuan-G2LUIS
Together in Daily Practice. Birkhäuser. Basel · 6u423O00Uqq4rLCR85/view?usp=sharing
Boston · Berlin. 2009. Chapter 3. Page 71. 5. https://drive.google.com/file/d/1Ac4W_febG1mW
3. Graham Nichol and David Baker. The epidemiology m4Mjj2OCriJSaRD6fkku/view?usp=sharing
of sudden death. Cardiac Arrest: The Science and
Practice of Resuscitation Medicine: Second
Edition. Cambridge University Press. 2007.
4. Meiso Hayashi, Wataru Shimizu, Christine M.
Albert. The Spectrum of Epidemiology Underlying
Sudden Cardiac Death. Circ Res. 2015 June 5;
116(12): 1887–1906.
doi:10.1161/CIRCRESAHA.116.304521.
5. Matthias L. Riess. New Developments in Cardiac
Arrest Management. Adv Anesth. 2016 ; 34(1):
29–46. doi:10.1016/j.aan.2016.07.003.
6. Rutherford, R., 2014. Vaskular Surgery, Volume 8.
Philadelphia: Elsevier
7. McPhee SJ, Papadakis MA. Current Medical
Diagnosis & Treatment. 47thed. New York: Lange
35
Mecical Book`s/The McGraw-Hill Companies,

2008.p. 287-299, 351-358; 398-416, 360-363;
1241-1246
8. Garrison SJ: Hand Book of Physical Medicine and
Rehabilitation, 2nded, 2003, p. 86
9. Bartels MN: Cardiac Rehabilitation in Grant
Cooper: Essential Physical Medicine and
Rehabilitation, 2006, p. 119.
10. Wita,I. Program rehabilitasi jantung dini pada
pasien diseksi aorta stanford a debakey II Pasca
Operasi Bentall Procedure.

Online
Pembelajaran
Beban Waktu Online

Pembelajaran

36

Pembelajaran
● Observasi ● Self
● Q&A Assesment ● Rubrik Small Group ● Rubrik mall Group
● Small Group Discussion Discussion
Discussion
Belajar/Aktivitas
Mahasiswa
pengajar.
Group Discussion
Student Project
Media Pembelajaran F2F Online
1. dr. I Ketut Agus Indra Adhiputra, Sp.MK
1. dr. I Wayan Gede Sutadarma, M.Gizi, Sp.GK
2. dr. I Gusti Made Gde Surya Chandra Trapika, M.Sc, Ph.D
2. dr.Ni Made Dharma Laksmi,Sp.JP
3. dr. Muliani, S.Ked., M.Biomed
3. Dr. dr. Bagus Komang Satriyasa, M.Repro
4. dr. Ayu Setyorini M. Mayangsari, M.Sc, Sp.A(K)
4. dr. Ni Putu Tesi Maratni,S.Ked,M.Biomed
5. dr. I Gusti Ngurah Pramesemara, S.Ked., M.Biomed., Sp.And
5. dr. Gede Wirata, S.Ked, M.Biomed
6. Dr.dr.I G A Widianti, M.Biomed
6. dr. I Made Oka Negara, S.Ked, M.Biomed
7. dr. I Putu Bayu Mayura, S.Ked, Ph.D
37
7. dr. Ida Bagus Amertha Putra Manuaba, 8. dr. Cyndiana Widia Dewi Sinardja, M.Biomed., Sp.JP, FIHA
S.Ked.,M.Biomed 9. Dr.dr.Dewa Ayu Agus Sri Laksemi, M.Sc
8. Dr.dr.Made Agus Hendrayana,S.Ked,M.Ked 10. dr. Luh Oliva Saraswati Suastika, Sp.JP(K), FIHA
Pertemuan XI-XII: Student Project Presentation
Kemampuan akhir ● Mampu membawakan topik student project yang telah disusun berkelompok berdasarkan topik yang diberikan di awal blok:
mahasiswa Kelas A : Kelas B :
1. Cardiac MRI in coronary artery disease 1. Abdominal Artery Aneurysm
2. Cardiac MRI in myocarditis 2. Hypertrophic Cardiomyopathy
3. Coronary CT angiography 3. Myocardial Infarction with Nonobstructive Coronaries Arteries
4. Myocardial perfusion imaging 4. Air Travel for Acute Coronary Syndrome Patient
5. Ecg stress test 5. Pericarditis in Acute Myocardial Infarction
6. Aortic dissection 6. Patent Ductus Arteriosus
7. Pulmonary embolism 7. Peripartum Cardiomyopathy
8. Takotsubo Cardiomyopathy 8. Atrial Myxoma
9. Acute Limb Ischemia 9. Acute Mitral Regurgitation as a complication of MI
10. Sick Sinus Syndrome 10. Primary Pulmonary Hypertension
Kriteria/Indikator ● Ketepatan dalam menjelaskan topik yang dibawakan
Capaian ● Ketepatan dalam menjawab pertanyaan yang diajukan dalam sesi diskusi
● Kerjasama dalam tim dan tingkat partisipasi dalam kelompok dan forum diskusi
Materi Teks Jurnal Slide (PPT)
Pembelajaran
Materi Student Project masing-masing kelompok - Materi Student Project Kelompok
Bentuk/Metode F2F/Online F2F Online
Pembelajaran
Pemaparan singkat, diskusi, dan presentasi mahasiswa -
berkelompok berdasarkan topik student project
dibagikan di awal blok
Beban Waktu F2F (Aktivitas Kelas)
Online
Pembelajaran
● 1 x 50 menit -

38

Pembelajaran
F2F / Online F2F Online F2F / Online F2F Online
● Presentasi - ● Presentasi masing-masing -
masing-masing kelompok didampingi dosen
kelompok didampingi pembimbing
dosen pembimbing ● Observasi
● Observasi ● Q&A
● Q&A
Belajar/Aktivitas
● Berlatih membawakan materi student project
Mahasiswa
yang telah dibagikan
● Belajar mengaplikasikan teori dalam studi
kasus
● Berlatih mengajukan pertanyaan atau
pendapat di forum diskusi
Fasilitator F2F / Online F2F Online
Tim Blok Ilmu Penyakit Jantung dan Pembuluh Darah -
Pertemuan XIV: Final Exam

Kemampuan akhir ● Mampu menjawab pertanyaan-pertanyaan dalam soal ujian Computer Based Test (CBT)
mahasiswa
Kriteria/Indikator ● Ketepatan dalam menjawab pertanyaan-pertanyaan dalam soal ujian Computer Based Test
Capaian
Materi
Seluruh bahan kajian yang telah diberikan sebelumnya
Pembelajaran
Bentuk/Metode
Belajar mandiri dan evaluasi pembelajaran
Pembelajaran
Beban Waktu Aktivitas di kelas Online
Pembelajaran
● 2 x 50 menit -

39

Pembelajaran
F2F / Online F2F Online F2F / Online F2F Online
● Observasi - ● Rubrik Penilaian ● Pilihan Ganda
● Summative Test
Belajar/Aktivitas
▪ Ujian Summative ▪ Mengerjakan tes summative
Mahasiswa
Fasilitator F2F / Online F2F Online
Tim Blok Ilmu Penyakit Jantung dan Pembuluh Darah -
8. Penilaian
Formative Assessment Proporsi Nilai
Small Group Discussion 15%
Student Project 10%
Quiz 15%
Final Examination (CBT) 60%
100%
Grading Scale
A ≥80
B+ >70-79
B 65-70
C+ 60-64
C 55-60

40
D 45-54
E <45
9. Buku Teks dan Artikel:

1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott & Wilkins, 2007.
2. Sadler TW: Langman’s Medical Embryology, 10thed. 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 R S, 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 Practioners. 4th Ed. Philadelphia, Mosby. 2002.
9. McPhee, S.J., Papadakis, M.A., Current Medical Diagnosis & Treatment. 47th ed. New York, Lange Mecical Book`s/The McGraw-Hill
Companies, 2008.
10. A2: Moore KL, Dalley AF: Clinically Oriented Anatomy, 4th ed. Philadelphia Lippincott & Wilkins, 1999.
11. H2: Fowcett DW, Jensh RP: Bloom & Fawcett’s Concise Histology, 2nd ed. London, Arnold. 2002.
12. Surya, I., Wita, I., Iswari, I., Rina Artha, I. and Sundari, l., 2020. High ratio of monosit: high-density lipoprotein as a risk factor of chronic
total occlusion in Patients coronary artery disease. Asian Journal of Pharmaceutical and Clinical Research, pp.155-158.\
13. Wita,I. Program rehabilitasi jantung dini pada pasien diseksi aorta stanford a debakey II Pasca Operasi Bentall Procedure.
14. Maliawan, R., Suryaguna, S., Maliawan, R., Antara, P., Wita, I. and Wardhana, D., 2019. Paroxysmal ventricular standstill pada pria berusia
45 tahun dengan manifestasi Stokes-Adams attack: laporan kasus. Medicina, 50(1).
15. Suastika, L., Peranan Transesofageal Ekokardiografi 3 Dimensi (TEE3D) dalam Penegakan Diagnosis Endokarditis Infektif dengan
Penegakan Diagnosis Endokarditis Infektif dengan Perforasi AML dan Penentuan Tatalaksana Lanjutan.
16. Suastika, L., Kejadian Katastropik Massa Right Atrium Efusi Pericard Dengan TamponadeJantung hingga Obstruksi Tricuspid Valve Inflow.
17. Suastika,L., Hubungan Antara Kriteria Elektrokardiografi LVH Terhadap Left Ventricular Mass Index Pada Pasien Hipertensi di RSUP Sanglah
Denpasar.
18. Nakamura, K., Akagi, S., Ejiri, K., Yoshida, M., Miyoshi, T., Sakaguchi, M., Amioka, N., Suastika, L., Kondo, M., Nakayama, R., Takaya, Y.,
Higashimoto, Y., Fukami, K., Matsubara, H. and Ito, H., 2021. Inhibitory effects of RAGE-aptamer on development of
monocrotaline-induced pulmonary arterial hypertension in rats. Journal of Cardiology, 78(1), pp.12-16.
19. Suastika, L., Hubungan Antara Kriteria Elektrokardiografi LVH Terhadap Left Ventricular Mass Index Pada Pasien Hipertensi Di Rsup
Sanglah Denpasar.
20. Suastika, L., Cardiovascular Comorbidities Characteristics in COVID-19 Observational Descriptive Study at Udayana University Hospital.

41
21. Lestari, P., Suastika, L. and Widyadharma, I., 2019. Relationship Between Medication Adherence and Hypertension Status in Public Health
Center. International Journal of Medical Reviews and Case Reports, (0), p.1.
22. Suastika, L. and Soesanto, A., 2019. Echocardiographic Parameters Correlated with Age in Isolated Severe Rheumatic Mitral Stenosis
Patients in Indonesia. Open Access Macedonian Journal of Medical Sciences, 7(13), pp.2127-2132.
23. Suastika,L., Patent Foramen Ovale Dengan Kriptogenik Stroke Perlukah Penutupan Dengan Alat atau Terapi Medikamentosa.
24. Suastika, L., Karakteristik Ekokardiografi dan Follow Up Pasien Stenosis Katup Aorta Bikuspid Berat Setelah Intervensi Balon Transkateter.
25. Rina,I., Update in Anticoagulant Advance The Anticoagulant Co-therapy in ACS Patients Undergoing Fibrinolytic.
26. Prabawa, I., Lestari, A., Muliarta, I., Mardhika, P., Pertiwi, G., Bhargah, A., Manuaba, I., Artha, M., Rina, I. and Rampengan, S., 2020. The
Stromal Cell-derived Factor-1/CXCL12 3’A-gene Polymorphism is Related to the Increased Risk of Coronary Artery Disease: A Systematic
Review and Meta-analysis. Open Access Macedonian Journal of Medical Sciences, 8(F), pp.197-202.
27. Surya, I., Wita, I., Iswari, I., Rina Artha, I. And Sundari, L., 2020. High Ratio of Monosit: High-Density Lipoprotein As A Risk Factor of
Chronic Total Occlusion In Patients Coronary Artery Disease. Asian Journal of Pharmaceutical And Clinical Research, Pp.155-158.
28. Rina, I., The Importance of Antiplatelet in ACS.
29. Rina, I., Update in Anticoagulant Advance The Anticoagulant Co-therapy in ACS Patients Undergoing Fibrinolytic.
10. Validasi
Penelaah Penyusun RPS
Penjaminan Mutu Akademik Program Studi Koordinator Mata Kuliah
(I Gusti Ayu Sri Darmayani) (AA. Ayu Dwi Adelia Yasmin)

NIP. 197508172009122001 NIP. 198610082018012001
Disahkan oleh
Ketua Program Studi
(Dr. dr. Komang Januartha Pinatih, M.Kes )

NIP. 1967012219961100

42
LECTURERS
NO NAME DEPARTMENT PHONE

dr. A.A. Ayu Dwi Adelia Yasmin, Sp.JP (K), FIHA
1 Cardiology 087861402169
(Coordinator)
2 Prof . Dr. dr. I Wayan Wita, Sp.JP Cardiology 08123809780
3 dr. Luh Oliva Saraswati Suastika, Sp.JP(K), FIHA Cardiology 081330530247
4 DR. dr. I.G.A. Widianti, M.Biomed Anatomy 08123921765
5 dr. I G.A. Dewi Ratnayanti, M.Biomed Histology 085104550344
6 Prof. Dr. dr. Putu Gede Adiatmika, M.For Physiology 08123811019
7 dr.Indira Vidiari Juhanna, M.Fis Physiology 087861704443
8 Dr. dr. Made Muliarta, M.Kes Physiology 081338505350
9 Prof. dr. I Gusti Made Aman, Sp.FK Pharmacology 081238770650
10 dr. Agung Nova Mahendra, M.Sc Pharmacology 087861030195
11 dr. I Wayan Sumardika, M.Med.Ed., Ph.D Pharmacology 082145952088
Clinical
12 Prof. Dr. dr. Wiradewi Lestari, Sp.PK(K) 08155237937
Pathology
Pathology
13 Dr. dr. Ni Wayan Winarti, Sp.PA (K) 087860990701
Anatomy
14 dr. Kadek Susila Surya Darma, Sp.JP(K) Cardiology 08113853151
15 dr. I Made Putra Swi Antara, Sp.JP(K), FIHA Cardiology 08123804782
16 Dr.dr. I Made Junior Rina Artha, Sp.JP (K), FIHA Cardiology 08123814814
17 dr. Hendy Wirawan, Sp.JP, FIHA Cardiology 0817352649
18 dr. Rani Paramita Iswari Maliawan, Sp.JP, FIHA Cardiology 081805391100
19 dr. Nyoman Wiryawan, Sp.JP(K), FIHA Cardiology 081289053234
20 dr. Eka Guna Wijaya, Sp.A(K) Pediatric 081338599801
21 dr. Luh Kamiati, Sp.KFR Physiotherapy 08123998787
Cardiothoracic
22 Dr. dr. I Nyoman Semadi, SpB,SpBTKV 08123838654
Surgery
23 dr. Cyndiana Widia Dewi Sinardja, Sp.JP, FIHA Cardiology 085100105866
24 dr. I Dewa Gde Aditya Diprabawa, Sp.JP, FIHA Cardiology 082131192377

43
25 dr. Ni Made Dharma Laksmi, Sp.JP, FIHA Cardiology 081805423560

26 dr. Putu Primeriana Nugiaswari, Sp.JP, FIHA Cardiology 081246753864

44
FASILITATOR CARDIOVASCULAR
Class A
Venue
No Name Group Departement Phone
(3ndfloor)
dr. I Wayan Gede Sutadarma, A1 082144071268 3rd floor:
1 Clinical Nutrition
M.Gizi, Sp.GK R.3.11
dr.Ni Made Dharma Laksmi,Sp.JP A2 081805423560 3rd floor:
2 Cardiology
R.3.12
Dr. dr. Bagus Komang Satriyasa, A3 Pharmacology 081237166686 3rd floor:
3
M.Repro R.3.13
dr. Ni Putu Tesi A4 Biochemistry 081916505816 3rd floor:
4 R.3.14
Maratni,S.Ked,M.Biomed
dr. Gede Wirata, S.Ked, M.Biomed A5 Anatomy 081239791628 3rd floor:
5
R.3.15
dr. I Made Oka Negara, S.Ked, A6 Andrology 085935054964 3rd floor:
6
M.Biomed R.3.16
dr. Ida Bagus Amertha Putra A7 Medical & Health 085829295230 3rd floor:
7
Manuaba, S.Ked.,M.Biomed Education R.3.20
Dr.dr.Made Agus A8 08123921590 3rd floor:
8 Microbiology
Hendrayana,S.Ked,M.Ked R.3.21
dr. Putu Primeriana Nugiaswari, A9 Cardiology 081246753864 3rd floor:
9
Sp.JP, FIHA R.3.22
dr. I Gede Putu Supadmanaba, A10 081212479783 3rd floor:
10 Biochemistry
S.Ked, M.Sc R.3.23

45
Class B
Venue
No Name Group Departement Phone
(2ndfloor)
dr. I Ketut Agus Indra Adhiputra, B1 081916166043 2rd floor:
1 Microbiology
Sp.MK R.2.11
dr. I Gusti Made Gde Surya B2 081338367261 2rd floor:
2 Pharmacology
Chandra Trapika, M.Sc, Ph.D R.2.12
dr. Muliani, S.Ked., M.Biomed B3 Anatomy 085103043575 2rd floor:
3
R.2.13
dr. Ayu Setyorini M. Mayangsari, B4 081353286780 2rd floor:
4 Pediatric
M.Sc, Sp.A(K) R.2.14
dr. I Gusti Ngurah Pramesemara, B5 Andrology and 081338605087 2rd floor:
5
S.Ked., M.Biomed., Sp.And Sexology R.2.15
Dr.dr.I G A Widianti, M.Biomed B6 08123921765 2rd floor:
6 Anatomy
R.2.16
dr. I Putu Bayu Mayura, S.Ked, B7 082236165801 2rd floor:
7 Microbiology
Ph.D R.2.20
dr. Cyndiana Widia Dewi Sinardja, B8 085100105866 2rd floor:
8 Cardiology
M.Biomed., Sp.JP, FiHA R.2.21
Dr.dr.Dewa Ayu Agus Sri Laksemi, B9 081392017107 2rd floor:
9 Parasitology
M.Sc R.2.22
dr. Luh Oliva Saraswati Suastika, B10 Cardiology 081330530247 2rd floor:
10 R.2.23
Sp.JP(K), FIHA

46
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
All lectures and SGD will be presented offline and pleno will be held online using Webex
or OASE.
IMPORTANT INFORMATIONS
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 feedback to improve the next process.

47
STUDENT PROJECT
Title and evaluator of student project
Group Evaluator Topic

A1 Dr. Cyndiana Sinardja SpJP Cardiac MRI in coronary artery
disease
A2 Dr. Nugiaswari SpJP Cardiac MRI in myocarditis
A3 Dr. Nugiaswari SpJP Coronary CT angiography
A4 Dr. Cyndiana Sinardja SpJP Myocardial perfusion imaging
A5 Dr. Dwi Adelia SpJP (K) Ecg stress test
A6 Dr. Rani Maliawan SpJP Aortic dissection
A7 Dr. Dharma Laksmi SpJP Pulmonary embolism
A8 Dr. Nyoman Wiryawan SpJP Takotsubo Cardiomyopathy
(K)
A9 Dr. Rani Maliawan SpJP Acute Limb Ischemia
A10 Dr. Putra Antara SpJP (K) Sick Sinus Syndrome
B1 Dr. Dharma Laksmi SpJP Abdominal Artery Aneurysm
B2 Dr. Nyoman Wiryawan SpJP Hypertrophic Cardiomyopathy
(K)
B3 Dr. Susila Surya Darma SpJP Myocardial Infarction with
(K)
Nonobstructive Coronaries Arteries
(MINOCA)
B4 Dr. Aditya Diprabawa SpJP Air Travel for Acute Coronary
Syndrome Patient
B5 Dr. Hendy Wirawan SpJP Pericarditis in Acute Myocardial
Infarction
B6 Dr. Hendy Wirawan SpJP Patent Ductus Arteriosus
B7 Dr. Oliva Saraswati SpJP (K) Peripartum Cardiomyopathy
B8 Dr. Aditya Diprabawa SpJP Atrial Myxoma
B9 Dr. dr. Made Junior Rina A, Acute Mitral Regurgitation as a
SpJP (K) complication of myocardial
infarction
B10 Dr. Oliva Saraswati SpJP (K) Primary Pulmonary Hypertension

48
About Topic, Presentation’s place and schedules, Task rules, Assessment, and Evaluator will be
discussed at the lecture of block introduction on March 1st, 2023. Please make a literature
review with references from the latest five years.

49
TITLE
(subject/topic: choose from competency list)
Name
NIM
Faculty of Medicine, Udayana University

2023
______________
1. Introduction (Pendahuluan)
2. Content (Isi, sesuai topik yang dibahas)
3. Summary (Ringkasan)
4. References: (Daftar Pustaka) Vancouver 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.

50
FORM PENILAIAN STUDENT PROJECT
(FASILITATOR)
Blok :
Kelompok :
Fasilitator :
Judul :
Laporan konsultasi
No Hari/Tanggal Topik Diskusi Tanda tangan Fasilitator
Dst
Penilaian
Kriteria Skor
1 2 3 Keterangan
Keaktifan
Sopan santun
Latar Belakang/Pendahuluan dan
Isi SP
Diskusi/pembahasan dan
Simpulan SP
Kualitas SP Secara Umum
Nilai Student Project = Skor Total x 100
15
Denpasar,
Fasilitator
( )

51
FORM PENILAIAN STUDENT PROJECT
(EVALUATOR)
Blok :
Kelompok :
Evaluator :
Judul :
Penilaian
Kriteria Skor
1 2 3 Keterangan
Video Presentasi
Kerja sama dalam Kelompok
Latar Belakang/Pendahuluan dan
Isi SP
Diskusi/pembahasan dan
Simpulan SP
Kualitas SP Secara Umum
Nilai Student Project = Skor Total x 100
15
Denpasar,
Evaluator
( )

52
ASSESSMENT METHOD
Assessment in this theme consists of:
● SGD : 15%
● Final test (CBT) : 60%
● Student Project : 10%
● Quiz : 15%
Final score of 65 or more considered to pass this block. Final test (CBT) mark should be
at least 60 to pass the block. Students with CBT score <60 will not pass the block even though
their total assessment score is >65.
The value of marking:
● A : 80-100 (pass)
● B+ : 70-79.9 (pass)
● B : 65-69.9 (pass)
● C+ : 60-64.9 (fail)
● C : 55-59.9 (fail)
● D : 45-54.9 (fail)
● E : <45 (fail)

53
TIME TABLE OF CLASSES
DAY/DATE Time Class A Class B PIC
Lecture 1 Dr. dr. I Gusti

Anatomy of Ayu Widianti,
08.00-08.50 Independent Learning
Cardiovascular M. Biomed
System I
Dr. dr. I Gusti

Lecture 2
Ayu Widianti,
Anatomy of
09.00-09.50 Independent Learning M. Biomed
Cardiovascular
System II

Anatomy of Ayu Widianti,
Cardiovascular M. Biomed
System I

Ayu Widianti,
11.00-11.50 Break Anatomy of
M. Biomed
Cardiovascular
System II
1
Wednesday, Lecture 3
dr. IGA Dewi
March 1 st Histology of
Ratnayanti, M.
12.00-12.50 Cardiovascular Break
2023 Biomed
System:
Vascular
Lecture 4
Physiology of dr. Indira
Cardiovascular Vidiari
13.00-13.50 System: Cardiac Student Project Juhanna, M.
Action Potential Fis
Intrinsic Conduction
System
Lecture 3
dr. IGA Dewi
Histology of
Ratnayanti, M.
14.00-14.50 Student Project Cardiovascular
System: Biomed
Vascular
dr. Indira
15.00-15.50 Student Project Lecture 4
Vidiari

54
Physiology of Juhanna, M.
Cardiovascular Fis
System: Cardiac
Action Potential
Intrinsic Conduction
System
Lecture 5
Physiology of Dr. dr. Made
08.00-08.50 Cardiovascular Independent Learning Muliarta,
M.Kes
System: Cardiac
output regulation
Lecture 6
Physiology of
Cardiovascular Dr. dr. Made
09.00-09.50 System: Function of Independent Learning Muliarta,
blood vessels & M.Kesr
regulation of blood
flow
Lecture 5
Physiology of Dr. dr. Made
10.00-10.50 Independent Learning Cardiovascular Muliarta,
M.Kes
System: Cardiac
output regulation
2
Lecture 6
Thursday, Physiology of
March 2nd Cardiovascular Dr. dr. Made
2023 11.00-11.50 Break System: Function of Muliarta,
M.Kes
blood vessels &
regulation of blood
flow
Lecture 7
Prof. Dr. dr. I
Pharmacology:
12.00-12.50 Break Gusti Made
Antihypertensive
Aman, Sp. FK
drugs
Lecture 8
Pharmacology: dr. Wayan
Student Project
13.00-13.50 Drugs for ischemic Sumardika, M.
heart disease and Med.Ed, PhD
heart failure
Lecture 7
Prof. Dr. dr. I
Pharmacology:
14.00-14.50 Student Project Gusti Made
Antihypertensive
Aman, Sp. FK
drugs

55
Lecture 8
Pharmacology: dr. Wayan
15.00-15.50 Student Project Drugs for ischemic Sumardika, M.
heart disease and Med.Ed, PhD
heart failure
Lecture 9 dr. Agung

Pharmacology: Nova
08.00-08.50 Student Project
Antiarrhythmic Mahendra,
drugs MSc
dr. Agung
Lecture 9
Nova
09.00-09.50 Student Project Pharmacology:
Mahendra,
3 Antiarrhythmic drugs
MSc
Friday,
10.00-10.50 Independent Learning Independent Learning
March 3rd
2023 11.00-11.50 SGD (Lecture 1-3) SGD (Lecture 1-3) Facilitator
12.00-12.50 SGD (Lecture 4 & 9) SGD (Lecture 4 & 9) Facilitator
Pleno Lecture 1-4 & 9 Pleno Lecture 1-4 & 9

13.00-13.50 Team Lecture
(OASE) (OASE)
14.00-14.50 IPE (Webex) IPE (Webex)
Lecture 10
Pathologic Anatomy
of Cardiovascular Dr. dr. Ni
08.00-08.50 System: Student Project Wayan Winarti,
Pathological Aspect Sp.PA (K)
of Ischemic Heart
Disease
Lecture 10
4
Pathologic Anatomy
Monday, Dr. dr. Ni
of Cardiovascular
09.00-09.50 Student Project Wayan Winarti,
March 6th System: Pathological
Sp.PA (K)
2023 Aspect of Ischemic
Heart Disease
10.00-10.50 Student Project Student Project
11.00-11.50 SGD (Lecture 5-7) SGD (Lecture 5-7) Facilitator
12.00-12.50 SGD (Lecture 8 & 10) SGD (Lecture 8 & 10) Facilitator

56
Pleno Lecture 5-7 Pleno Lecture 5-7

(Webex) (Webex)
Pleno Lecture 8 &10 Pleno Lecture 8 & 10

(Webex) (Webex)
Lecture 11 Prof. Dr. dr. I

Approach to patient WayanWita,
with cardiovascular Sp.JP(K)
disease
Lecture 12 Prof. Dr. dr. AA

Laboratory Wiradewi
examination: Lestari, Sp.PK
cardiac markers (K)
Lecture 11
Prof. Dr. dr. I
Approach to patient WayanWita,
10.00-10.50 Independent Learning Sp.JP(K)
with cardiovascular
disease
5 Lecture 12 Prof. Dr. dr. AA

Tuesday, 11.00-11.50 Break
Laboratory Wiradewi
March 7th examination: cardiac Lestari, Sp.PK
markers (K)
2023
Lecture 13 dr. I Nyoman
12.00-12.50 Chronic Heart Break Wiryawan,
Failure Sp.JP(K)
Dr. dr. I Made

Lecture 14
Junior Rina
13.00-13.50 Acute coronary Student Project
Artha, SpJP(K)
syndrome (STEMI)
Lecture 13 dr. I Nyoman

14.00-14.50 Student Project Wiryawan,
Chronic Heart Failure Sp.JP(K)
Lecture 14 Dr. dr. I Made

Junior Rina
15.00-15.50 Student Project Acute coronary Artha, SpJP(K)
syndrome (STEMI)
dr. Kadek
6 Lecture 15
Acute coronary Susila Surya
Wednesday, 08.00-08.50 Student Project Darma
syndrome
March 8th (NSTE-ACS)
SpJP(K)
2023
57
Lecture 15 dr. Kadek

Acute coronary Susila Surya
09.00-09.50 Student Project syndrome Darma,
(NSTE-ACS) SpJP(K)
10.00-10.50 Student Project Student Project
12.00-12.50 SGD (Lecture 14-15) SGD (Lecture (14-15) Facilitator

(Webex) (Webex)

(Webex) (Webex)
dr. AAA Adelia

Lecture 16 Yasmin,
Hypertension Sp.JP(K)
Lecture 17 dr. Cyndiana

Hypertensive Independent Learning Widia Dewi S,
09.00-09.50
Urgency & Sp.JP
Emergency
dr. AAA Adelia

Lecture 16 Yasmin,
Hypertension Sp.JP(K)
7 Lecture 17 dr. Cyndiana

Thursday, 11.00-11.50 Break
Hypertensive Widia Dewi S,
March 9th Urgency & Sp.JP
Emergency
2023
dr. Dewa Gde
Lecture 18
Aditya
12.00-12.50 Chronic coronary Break
Diprabawa,
syndrome
Sp.JP
Lecture 19 dr. Putra Swi

Student Project
13.00-13.50 Malignant Antara,
arrhythmias Sp.JP(K)
Lecture 18 dr. Dewa Gde

Aditya
Chronic coronary Diprabawa,
syndrome Sp.JP

58
Lecture 19 dr. Putra Swi

15.00-15.50 Student Project Malignant Antara,
arrhythmias Sp.JP(K)
dr. Primeriana
Lecture 20
08.00-08.50 Student Project Nugiaswari,Sp.
Basic arrhythmias
JP
dr. Primeriana
Lecture 20
09.00-09.50 Student Project Nugiaswari,Sp.
Basic arrhythmias
JP
8 10.00-10.50 Independent Learning Independent Learning

Friday,
SGD (Lecture 16-17) Facilitator
March 10th 11.00-11.50 SGD (Lecture 16-17)
2023

13.00-13.50
(OASE) (OASE)
IPE (Webex)
14.00-14.50 IPE (Webex)
Dr. dr. I Gusti

Lecture 21
Ayu Widianti,
08.00-08.50 Anatomy 3: Independent Learning
M. Biomed
Embryology
Lecture 22
dr. Eka Guna
Congenital heart
09.00-09.50 Independent Learning Wijaya,
disease and Acute
Sp.A(K)
Rheumatic Fever
Dr. dr. I Gusti

9 Lecture 21
Ayu Widianti,
Monday, 10.00-10.50 Independent Learning Anatomy 3:
M. Biomed
Embryology
March 13rd
2023 Lecture 22
dr. Eka Guna
Congenital heart
11.00-11.50 Break Wijaya,
disease and Acute
Sp.A(K)
Rheumatic Fever
dr. Rani
Lecture 23
Paramita
12.00-12.50 Cardiorespiratory Break
Maliawan,
arrest
Sp.JP

59
dr. Hendy
Lecture 24
13.00-13.50 Student Project Wirawan,
Acute Heart Failure
Sp.JP
dr. Rani
Lecture 23
Paramita
14.00-14.50 Student Project Cardiorespiratory
Maliawan,
arrest
Sp.JP
dr. Hendy
Lecture 24
15.00-15.50 Student Project Wirawan,
Acute Heart Failure
Sp.JP
Lecture 25 dr. Dharma

Shock (Cardiogenic) Laksmi, Sp.JP
Lecture 25 dr. Dharma

Shock (Cardiogenic) Laksmi, Sp.JP
Student Project Student Project

10.00-10.50
10
Tuesday,
March 14th 12.00-12.50 SGD (Lecture 24-25) SGD (Lecture 24-25) Facilitator
2023

Team Lecture
14.00-14.50 (Webex)
(Webex)

(Webex) (Webex)
dr. L. Oliva
Lecture 26
08.00-08.50 Independent Learning Saraswati S.,
Acute cor pulmonale
Sp.JP(K)
Lecture 27 dr. L. Oliva

Independent Learning
09.00-09.50 Chronic cor Saraswati S.,
11
pulmonale Sp.JP(K)
Wednesday,
March 15th Lecture 26 dr. L. Oliva
10.00-10.50 Independent Learning Acute cor pulmonale Saraswati S.,
2023
Sp.JP(K)
Lecture 27
dr. L. Oliva
11.00-11.50 Break Saraswati S.,
Chronic cor
Sp.JP(K)
pulmonale

60
Lecture 28 dr. Luh

Break Kamiati,
12.00-12.50 Cardiac
Sp.KFR
Rehabilitation
DR. dr. I
Lecture 29 Nyoman
Student Project
13.00-13.50 Peripheral Vascular Semadi,
(Evaluation B1-B5)
and Aortic Disease SpBTKV
Lecture 28 dr. Luh

Student Project
Kamiati,
14.00-14.50 (Evaluation A1-A5)
Cardiac Sp.KFR
Rehabilitation
Dr. dr. I
Lecture 29 Nyoman
Student Project
15.00-15.50 Peripheral Vascular Semadi, Sp.B,
(Evaluation A6-A10)
and Aortic Disease Sp.BTKV
Dr. dr. I
Lecture 30 Student Project Nyoman
08.00-08.50 Venous Disease and
Semadi, Sp.B,
Lymphatic Vessel
Sp.BTKV
Dr. dr. I
Lecture 30
Student Project Nyoman
09.00-09.50 Venous Disease and
Semadi, Sp.B,
Lymphatic Vessel
Sp.BTKV
12 Student Project Student Project

10.00-10.50
(Evaluation B6-B10)
Thursday,
March 16th 11.00-11.50 SGD (Lecture 26-28)
SGD (Lecture 26-28) Facilitator
2023
Independent Learning
Pleno Lecture 26-28

Pleno Lecture 26-28 Team Lecture
14.00-14.50 (Webex)
(Webex)

(Webex) (Webex)

61
13
Friday,
Pre Evaluation Break
March 17th
2023
14
Monday,
Evaluation
March 20th
2023
15
Monday,
Remedial Examination
July 3rd
2023

62
LECTURE 1& 2
ANATOMY OF CARDIOVASCULAR SYSTEM
Dr. dr. I Gusti Ayu Widianti, M.Biomed
AIMS:
Describe the general and topography and surface anatomy of the cardiovascular system.
LEARNING OUTCOME:
1. Describe the general and topography anatomy of the cardiovascular system.
2. Describe the surface anatomy of the cardiovascular system.
3. Describe the basic ground plan of the vascularization of the body.
CURRICULUM CONTENS:
1. Topography anatomy of the heart and great vessel
2. Mediastinum
3. Pulmonary/lesser and systemic/ greater circulation
4. Vascularization of the head and neck, the upper, the trunk, and lower limb.
ABSTRACT I :
The heart is a hollow, fibromuscular organ of a conical or pyramidal form, with a base,
apex and a series of surfaces (sternocostal/anterior, diaphragmatic/inferior and pulmonaries)
and borders (acute and obtuse borders). Enclosed in the pericardium, occupies the middle
mediastinum between the lungs. It is placed obliquely behind the body of the sternum and
adjoining costal cartilage and ribs, one-third lies to the right of the midline. Because of intimate
relation between left atrium, the arch of aorta and esophagus, enlargement of them resulting
compression to each other.
The human heart is a pair of valved muscular pumps combined in a single organ. Right
and left heart pumps is physiologically separate, being interposed in series of different point in
the double circulation: pulmonary/lesser circulation for blood oxygenation and systemic/greater
circulation for tissue perfusion.
Of the four cardiac chambers, the two atria received venous blood for filling of the two
ventricles which then provide the powerful expulsive contraction, forcing blood into the main
arterial trunks: pulmonal trunk and aorta.
On the anterior surface of the chest, the outline of the heart and the sound produced by the
valves can be traced.
ABSTRACT II:
The vascular system of the human components of arteries, capillaries and veins. The
vascular system consist: of the regional vascularization of the head and neck, the upper limb,
the trunk, and the lower limb.
Standard References :
Moore KL, Agur AMR: Essential Clinical Anatomy, 6th ed. Philadelphia, Lippincott& Wilkins,
2018. p. 26-30, 65-67, 80-115.
SELF DIRECTING LEARNING

Basic knowledge that must be known:
1. Topography anatomy of the heart and great vessel.
63
2. Mediastinum
3. Pulmonary/lesser and systemic/greater circulation.
4. Vascularization of the head and neck, the upper, the thrunk, and lower limb
LEARNING TASK I:
CASE:
A 45-year-old woman was playing tennis and suddenly fell, complaining of a severe pain in her
chest and down her left arm. Her playing partner rushed her to the hospital.
1. What likely caused the pain in the women’s chest and arm?
2. Name the blood vessels that supply the heart. Where they arised from?
3. List 4 major branches of the right coronary artery and list 3 major branches of the left
coronary artery.
4. Why did the women feel pain along the medial side of the left arm?
5. Identify on heart specimens: the four chambers of the heart; the atrioventricular,
pulmonary, and aortic valves; papillary muscles and tendinous cords. Discuss their
functions!
LEARNING TASK II:

1. Describe the ground plan of the arterial supply and the venous return and lymphatic
system of the head-neck.
2. List the major branches of the trunk (thorax and abdomen).
3. Describe the ground plan of the arterial supply and the venous return and the lymphatic
system supply of the upper and lower limb .
4. Which superficial veins commonly used for venipuncture of the upper and lower limb?
SELF ASSESSEMENT:
1. Describe the systemic and pulmonary circulation!
2. Named the three layers of the heart’s wall from deep to superficial!
3. Describe the structures, locations and functions of the skeleton of the heart!
4. The heart has an apex, base, surfaces and borders, identify the structures that formed
each of them!
5. Describe how the percussion of the heart performed!
6. Identify the atrioventricular and interventricular grooves and list the structures lie in them!

64
LECTURE 3
HISTOLOGY OF CARDIOVASCULAR SYSTEM
dr. I G.A. Dewi Ratnayanti, M.Biomed
AIMS:
1. Describe the microscopic structure of the cardiovascular system
2. Describe the microscopic structure of the vascular system
3. Describe the microscopic structure of the lymphatic system
LEARNING OUTCOME:
1. Can describe the microscopic structure of the cardiovascular system
2. Can describe the microscopic structure of the vascular system (artery, vein, and capillary)
3. Can describe the microscopic structure of the lymphatic system
CURRICULUM CONTENTS:
1. The microscopic structure of heart (type of the myocardiocytes and the valves)
2. The normal and abnormal heart wall and pericardial structures
3. Arteries : elastic artery, muscular artery, arteriole and capillaries
4. Veins: large vein, middle vein, small vein
5. Capillary: types and characteristic
6. Lymphatic vessels: thoracic duct, small - medium vessels, lymph capillary.
ABSTRACT:
The cardiovascular system is a part of the circulatory system that composed of the heart
as a pump and blood vessels. The heart is musculatory organ consist of four chambers: two
atria and two ventricles that separated by atrioventricular septal. The muscular wall of the heart
is composed of cardiac muscle and the heart has three layers: endocardium, myocardium and
epicardium. The endocardium, a simple squamous epithelium and underlaying subendothelial
connective tissue, lines the lumen of the heart. Deep to the endocardium is a subendocardial
layer of loose connective tissue that contains small blood vessels, nerve, and Purkinje fibers.
Myocardium is the thick middle layer of the heart composed of cardiac muscle cells. Epicardium
is the outermost layer of the heart and also called the visceral layer of the pericardium. The
subepicardial layer of loose connective tissue contains the coronary vessels, nerves and
ganglia. SA and AV node are specialized cardiac myocytes make up conducting system of te
heart SA and AV node as a pace maker of the heart that impulse begin from SA node will
referred to AV node via internodal pathway, bundle of His and spread to left and right branches
to exite ventricular muscles of the heart.
The vascular components of the the cardiovascular system consist of arteries, capillaries
and veins. The classification of blood vessels (artery and vein) based on their lumina diameter
and composition of tissues in their wall. The complete microscopic structure of blood vessels
presents in muscular type of the arteries that composed of the intima, media, adventisia layers
with internal and external elastic membranes. The coronary vessels are very important artery
that serving the myocardium.
Standard References:
Gartner LP, Hiatte JL: Color Textbook of Histology, 2nd ed. Philadelphia, WB Saunders
Company, 2001. p. 251- 265; 267-268; 268-269
Additional reading:

65
Fowcett DW, Jensh RP: Bloom & Fawcett’s Concise Histology, 2nd ed. London, Arnold. 2002. p.
135-136; 136-145; 136-139
SCENARIO:
CASE:
A young man who was stabbed (about 5cm depth) in the chest was rushed to a hospital. The
stab wound was in the 3rd left intercostals space, just lateral to the sternum. The emergency
physician noted that the veins of his face and neck were engorged.
LEARNING TASK:
1. Describe the histologic characteristic of the structure involved in the pathophysiologic of
the case above!
2. Differentiate the muscular and elastic type artery!
3. Describe the microscopic structure of the capillary and it classification!
4. Differentiate between artery, vein, and lymph vessels!
SELF-ASSESSMENT:
1. What are the basic structures of the heart wall?
2. What structures are form the endocardium?
3. Do you able to describe he relation of the endocardium and endothelium of the blood
vessels that entering and leaving the heart?
4. Explain the microscopic structure of the purkinje fiber. Where does it location?
5. What is cardiac skeleton?
6. What are it components?
7. Explain the microscopic structure of the heart valves?
8. What are the main composition of the tunica media of the elastic artery?
9. Explain the variation of the tunica media of the blood vessel!

66
LECTURE 4
PHYSIOLOGY OF CARDIOVASCULAR SYSTEM: CARDIAC ACTION POTENTIAL &

INTRINSIC CONDUCTION SYSTEM
dr. Indira Vidiari Juhanna, M. Fis
AIMS:
1. Comprehend the basic principles of Cardiac Action Potential.
2. Comprehend the basic principles of Intrinsic Conduction System.
LEARNING OUTCOME:
Comprehend the functional structure of the conduction system and cardiac action potensial of
the heart and its clinical implications.
CURRICULUM CONTENS:
1. Mechanism of action potential.
2. Conduction pathway of the heart.
ABSTRACT:
The intrinsic conduction system sets the basic rhythm of the heartbeat. It consists of auto
rhythmic cardiac cell that initiate and distribute impulses (action potentials) throughout the heart.
The intrinsic conduction system of the heart initiates depolarization impulses. Action
potentials spread throughout the heart (SA node, internodal pathways, AV node, AV bundle,
bundle branches, Purkinje fibers ) causing a coordinated heart contraction (excitation
contraction coupling).
Initiation of action potential in autorhythmic cells :
1. Pacemaker potential due to slow continuous influx of sodium and reduced efflux of
potassium
2. Depolarization and reversal of membrane potential
3. Repolarization due to rapid efflux of potassium.
Action potential in contractile cells :
1. Opening of voltage regulated fast sodium channel triggered by entry of positive ion from
adjacent cell depolarization due to rapid influx of sodium
2. Plateau produced by calcium influx balancing potassium efflux.
3. Repolarization due to efflux of potassium.
Plateau has important functional consequences for the mechanical activity of the heart. An
ECG wave tracing records the electrical activity of the heart. This is an important clinical tool,
used both in the diagnosis of abnormal cardiac rhythms (arrhythmias) or defects in the
conduction pathways and when investigating possible damage to the bulk of the myocardium
e.g cause by ischemia
Standard Reference :
Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders Company, 2006. p.
104-106, 116-122

1. Autorhythmic cells potential
2. Contractile cells potential
67
3. ECG wave tracing
CASE:
I Ketut Jering, a new scatterer who was about to go fishing, was found collapsed on the
beach in Sanur, weak and pale with cold hands. Several people who happened to be around
him helped and took him to the HBB Clinic. At the HBB Clinic, the doctor found that he was 45
years old, his temperature was 35.5 degrees Celsius, blood pressure was 105/70 mmHg, pulse
was weak at 120 beats per minute. His ECG showed sinus rhythm, the rate is fast, but all the
ECG waves and complexes are normal. In the anamnesis, Ketut Jering did not consume any
salt for the last one week, he initially planned to stop consuming salt for 2 weeks because he
found that his blood pressure was previously 160/100 mmHg.
LEARNING TASK:
1. Explain the relationship of not consuming salt with the action potential of the heart
muscle!
2. The cardiac muscle action potential formed plateau. Describe which ions contribute to
the formation of plateau!
3. On ECG examination sinus rhythm was recorded within normal limits. Describe the
impuls conduction in sinus rhythm!.
4. I Ketut Jering’s heart rate is 120 per minute, is much more than normal heart rate.
Explain why he looked pale and his hands were cold!
SELF-ASSESSMENT :
1. Describe the excitation – contraction process

2. What is the pace maker of the heart in normal condition
3. Describe the pathway of electrical conduction of the heart, starting with the SA Node
4. Describe the electrical activity of the cells of the SA Node
5. How the SA node functions as the normal pacemaker

68
LECTURE 5
PHYSIOLOGY OF CARDIOVASCULAR SYSTEM: CARDIAC OUTPUT REGULATION
& MYOCARDIAL PERFUSION
Dr. dr. Made Muliarta, M.Kes
AIMS:
1. Comprehend the cardiac output.
2. Comprehend the basic principles of cardiac output regulation.
3. Comprehend the basic principles underlying myocard perfusion.
LEARNING OUTCOME:
1. Can describe how to measure cardiac output.
2. Can describe the regulation of cardiac output.
3. Can describe how myocardial perfusion occurs.
4. Can describe functional structure of the coronary arteries
CURRICULUM CONTENS:
1. Components of cardiac output.
2. Factors influence cardiac output.
3. Function of coronary artery.
4. The role of diastole.
ABSTRACT I:
The cardiac out put (COP) is the quantity of blood pumped into the aorta each minute by
the heart. The outputs of the two sides of the heart are normally equal. Cardiac output is
determined by two feature of cardiac function, the heart rate and the volume of blood ejected
during a single contraction of the ventricle (the stroke volume). COP is defined as the amount of
blood pumped per ventricle per unit time. It can be calculated by multiplying heart rate by stroke
volume.
When a person is at rest, the heart pumps only 4 to 6 liters of blood each minute. During
severe exercise, the heart may be required to pump four to seven times this amount. The basic
means by which the volume pumped by the heart is regulated are: intrinsic cardiac regulation of
pumping in response to changes in volume of blood flowing into the heart and control of heart
rate and strength of heart pumping by the autonomic nervous system.
The intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called
the Frank-Starling mechanism of the heart. The Frank-Starling mechanism means that the
greate the heart muscle is stretched during filling, the greater is the force of contraction and the
greater the quantity of blood pumped into the aorta.
The pumping effectiveness of the heart also is controlled by the sympathetic and
parasympathetic (vagus) nerves, which abundantly supply the heart. The amount of blood
pumped each minute often can be increased more than 100 percent by sympathetic stimulation.
By contrast, the output can be decreased to as low as zero or almost zero by vagal stimulation.
ABSTRACT II:
Blood perfusion to the myocardium build by the reverse flow of blood during diastole and
the autoregulation of the intramyocardial arterioles through the coronary arteries.

69
Epicardial coronary arteries serve as conduit, entered deep to the myocardium:

intramyocardial arterioles referred as resistance vessels.
Right and left coronary arteries begin from the sinuses behind the right and left semilunar
cusps of the aortic valve. They distribute blood in large part to their own half of the heart.
Blood flow in the coronary arteries is maximal during diastole and minimal in systole.
During systole, no pressure differential exist between the myocardium and the left ventricle, flow
is not possible. During diastole, a pressure differential does exist and the elasticity of the aorta
propels blood through the coronary circulation.
Guyton, A. C. and Hall, J. E. (2016) Textbook of Medical Physiology. 13th edn. Phyladelphia:
Elsevier.

1. Components of Cardiac output
2. Factors influence Cardiac output
3. Systole-diastole
4. The function of coronary artery
5. Post exercise hypotension
SCENARIO:
CASE 1:
A man 28 years old, runs for 45 minutes with steady state pulse rate 140 beats/minute. His
pulse rate at rest 60 beats/minute
LEARNING TASK:
1. What do you expect of stroke volume in this patient?
2. Describe how the stroke volume is intrinsically regulated by the end-diastolic volume
3. Describe the change of cardiac output in this men?
CASE 2.
A 45-year-old woman was playing tennis and suddenly fell, complaining of a severe pain in her
chest and down her left arm. Her playing partner rushed her to the hospital. This woman is
suffering from a heart attack (acute myocard infarction)
LEARNING TASK:
1. Why does this happen?
SELF-ASSESSMENT :
1. Describe the effects of autonomic nerve stimulation on the cardiac rate and stroke
volume!
2. List the factors that affect venous return!
3. Using a flowchart, show how an increased venous return can result in an increased
cardiac output!
4. Describe the arterial supply of the heart!

70
LECTURE 6
PHYSIOLOGY OF CARDIOVASCULAR SYSTEM: FUNCTION OF BLOOD VESSELS
& REGULATION OF BLOOD FLOW
Dr. dr. Made Muliarta, M.Kes
AIMS:
1. Apply several factors that affecting blood pressure
2. Comprehend the basic principles underlying blood pressure regulation
LEARNING OUTCOME:
1. Can describe the role of blood vessels in blood pressure.
2. Can describe several factors that affecting blood pressure
3. Can describe the basic principles underlying blood pressure regulation
CURRICULUM CONTENS:
1. Blood vessels as functional parts
1. Factors influence blood pressure
1. Two basic mechanisms for regulating blood pressure.
2. The nervous system controls the circulation.
ABSTRACT
The heart pumps blood continually into the aorta, as the blood flows through the systemic
circulation, its mean pressure falls progressively to about 0 mmHg by the time it reaches the
termination of the venae cavae where they empty into the right atrium of the heart.
Blood pressure (BP) is important indicator of the cardiovascular health. It is influenced by
the contractile activities of the heart and conditions an activities of blood vessels.
1. Systolic pressure = highest pressure in artery result of ventricular contractions.
2. Diastolic pressure = lowest pressure in artery result of ventricular relaxation.
3. Mean arterial pressure (MAP) = diastolic pressure + 1/3 pulse pressure.
When blood pressure is measured first sound indicate systolic pressure, end of sounds indicate
diastolic pressure.
Blood pressure is affected by several factors: peripheral resistance, vessel elasticity, blood
volume and cardiac output. Blood cells and plasma encounter resistance when they contact
blood vessel walls. If resistance increases, then more pressure is needed to keep blood moving.
Smaller blood vessel diameter cause more fluid in contact with wall and greater resistance,
finally greater pressure. In addition, blood volume affects blood pressure. Greater volume of
fluid in blod vessel cause more fluid pressing against walls and greater pressure. Cardiac output
also has direct effect on blood pressure.
There are two basic mechanisms for regulating blood pressure. In short term
mechanism, which regulate blood vessel diameter,heart rate, and contractility. Rising blood
pressure stimulates increased parasymphatetic activity which leads to reduce heart rate (HR),
vasodilation and lower blood pressure. Falling blood pressure stimulates increased
sympathetics activity, which leads to increase HR, contractility, vasoconstriction, and rises blood
pressure. Long term regulation, which regulate blood volume. Long term regulation involves
renal regulation of blood volume (BV) via the rennin – angiotensin mechanism and aldosteron
mechanism. Increase blood osmolarity stimulate antidiuretic hormone (ADH) which promote
reabsorption of water and stimulates the thirst center, resulting in increase BV and BP
The nervous system controls the circulation almost entirely through the autonomic
nervous system. The innervation of the small arteries and arterioles allows sympathetic
71
stimulation to increase resistance to blood flow and thereby to decrease rate of blood flow
through the tissues. The innervation of the large vessels, particularly of the veins, makes it
possible from sympathetic stimulation to decrease the volume of these vessels. The effects of
parasympathetic stimulation on heart function causes decrease heart rate and slide decrease in
heart muscle contractility.
The body also has powerful mechanisms for regulating arterial pressure week after week
and month after month. This long term control of arterial pressure is closely intertwined with
homeostasis of body fluid volume, which is determined by the balance between the fluid intake
and output.
1. Fox S.I.: Human Physiology, 9th ed. New York, McGraw-Hill, 2006. p. 448-454.
2. Guyton AC: Medical Physiology, 11st ed. Philadelphia, Elsevier Saunders Company,
2006. p. 161-170, 205-23.

1. Frank Starling law
2. Autonomic activation
3. The roles of blood vessels
4. Short term mechanism for regulating blood pressure
5. Long term mechanism for regulating blood pressure
6. The nervous system controls the circulation
SCENARIO
A man, 50 years old, come to the general practitioner with the main complaint of headache
since one week ago. On physical examination, blood pressure was 160/100, heart rate 90 bpm
without any physical disorders. On laboratory test, hypercholesterolemia, while the others were
normal.
LEARNING TASK:
1. Explore the factors of hypertension related to the patient ?

2. Discuss several changing of the systems that could as the factors of hypertension ?
3. Explain the mechanim of hypertension related to blood volume ?
4. Explain the mechanism of blood vessel in blood pressure ?
SELF-ASSESSMENT :
1. Provide an integrated description of how nerves and hormones regulate blood pressure
1. Explain reflexes that responsible for short term control and long term control
mechanisms to blood pressure
2. Explain why a person in severe dehydrated may have low blood pressure
3. Why a person with atherosclerosis may have high blood pressure

72
LECTURE 7
ANTIHYPERTENSIVE DRUGS
Prof dr. I Gusti Made Aman, Sp.FK
AIMS:
Describe the anti hypertensive drugs
LEARNING OUTCOME:
Can describe the anti hypertensive drugs
CURRICULUM CONTENS:
1. Principles and classification of anti hypertensivedrugs
2. Important pharmacokinetic properties of anti hypertensive drugs.
3. Mechanism of actions of anti anti hypertensivedrugs.
4. Important adverse effects of anti hypertensive drugs.
ABSTRACT :
Hypertension is important because elevated blood pressure (BP) confers a greater risk of
stroke, heart failure, coronary artery disease (including angina, myocard infarction, and sudden
death), renal disease and peripheral vascular disease. There is a continuous, direct relationship
between elevation in blood pressure and increases the risk. JNC 7, 2003 classification of blood
pressure in adults is as follows: normal, prehypertension, stage I hypertension and stage 2
hypertension.
In general, the higher the blood pressure and the greater the number of risk factors,
indicate higher urgency and stringency in treating hypertension. Lowering blood pressure is just
one way to prevent complications; attention must also be paid to the presence and reversal of
other cardiovascular risk factors such as cigarette smoking, hyperlipidemia and especially in
diabetes mellitus.
Drugs used in lowering blood pressure will decrease peripheral vascular resistance or/and
decrease cardiac output. These can be due to either directly decrease arteriolar smooth muscle
tone (which decrease peripheral resistance), decrease myocardial contractility, heart rate,
venous tone, blood volume (which decrease cardiac output) or indirectly through inhibition of
sympathetic nervous system activity or inhibition of renin-angiotensin-aldosteron system. They
can be used alone or combination to return the blood pressure to target levels with minimal side
effects.
STANDARD REFERENCES:
1. Trevor AJ, Katzung BG, Masters SB: Katzung & Trevor’s Pharmacology, 7th ed. New
York, McGraw-Hill/Lange., 2005. p 66-93, 95-104 and p. 114-123.

1. Principles of anti hypertensive therapy.
2. Classification of anti hypertensive drugs
3. Important pharmacokinetic properties of anti hypertensive drugs.
4. Mechanism of actions of anti anti hypertensivedrugs.
5. Important adverse effects of anti hypertensive drugs
CASE:
SCENARIO
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Mr. A, 50 years-old, complains headache and stiffness in both of his shoulders since 1 week
ago. He went to a GP, and it was revealed that during 3 tandem (serial) BP examinations, his
BP was > 150/90 mmHg. Family history: positive history of hypertension suffered by his father.
LEARNING TASKS
1. Describe the advantages and disadvantages of monotherapy vs. polytherapy in
hypertension pharmacomanagement!
2. Why do ACEIs exert cough?
3. Explain the mechanism of Calcium Channel Blocker-induced constipation!
4. Explain the pharmacodynamics of Reserpine! What side effects may occur in
reserpine-treated individuals!

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LECTURE 8
DRUGS USED IN ISCHEMIC HEART DISEASES AND HEART FAILURE
dr. I Wayan Sumardika, S.Ked., M.Med.Ed, Ph.D
AIMS
The students are expected able to explain and comprehend the basics and principles of cardiac
performance modulation, and able to apply these knowledges into the pharmacotherapy of
ischemic heart disease, acute and chronic heart failure (HF).
LEARNING OUTCOMES
At the end of the lectures, the students are able to:
1. Comprehend therapeutic strategies in IHD and HF pharmacomanagement

2. Describe the pharmacodynamic and pharmacokinetic of drugs used in IHD and HF
3. Comprehend clinical applications of drugs used in IHD and HF
4. Describe the toxicities and drug-drug interaction of drugs used in IHD and HF
CURRICULUM CONTENTS
● Therapeutic strategies in IHD and HF pharmacomanagement

● Pharmacodynamic and pharmacokinetic of drugs used in IHD and HF
● Clinical applications of drugs used in IHD and HF
● Toxicities and drug-drug interaction of drugs used in IHD and HF
ABSTRACT
The primary cause of angina pectoris is an imbalance between the oxygen requirement
of the heart and the oxygen supplied to it via the coronary vessels. In classic angina, the
imbalance occurs when the myocardial oxygen requirement increases, as during exercise, and
coronary blood flow does not increase proportionately. The name denotes chest pain caused by
accumulation of metabolites resulting from myocardial ischemia. Angina pectoris is the most
common condition involving tissue ischemia in which vasodilator drugs are used. The organic
nitrates, eg, nitroglycerin, are the mainstay of therapy for the immediate relief of angina.
Another group of vasodilators, the calcium channel blockers, is also important, especially for
prophylaxis, and beta blockers, which are not vasodilators, are also useful in prophylaxis.
Several newer groups of drugs are under investigation, including drugs that alter myocardial
metabolism and selective cardiac rate inhibitors. The three drug groups traditionally used in
angina (organic nitrates, calcium channel blockers, and beta blockers) decrease myocardial
oxygen requirement by decreasing the determinants of oxygen demand (heart rate, ventricular
volume, blood pressure, and contractility). In some patients, the nitrates and the calcium
channel blockers may cause a redistribution of coronary flow and increase oxygen delivery to
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ischemic tissue. In variant angina, these two drug groups also increase myocardial oxygen
delivery by reversing coronary artery spasm.
Heart failure (HF) is characterized by gradual decrease in cardiac performance and

punctuated by acute decompensations that require hospitalization. Treatment is directed to (a)
reduce symptoms and halt progression of disease during stable periods and to (b) manage of
acute decompensations. Studies have shown that HF pathobiology involves not only defect of
heart contraction machinery but also many other processes and organs, such as baroreceptor
reflex, SANS, kidneys, RAAS, and cardiomyocyte apoptosis. These studies promote the
revolution of novel therapeutic strategies to manage HF cases (Katzung & Parmley, 2009).
SCENARIO
A 55-year-old man is experiencing chest pain in the last 25 minutes ago and comes to primary
health care where you are on duty. He says this is the first time he experiences this kind of chest
pain; it feels burning on the left side of the chest and radiate to left upper arm. He looks pale,
nervous and has difficulty to breath. Based on your examination, his vital sign is as follow
respiratory rate 15 times per minutes, heart rate 130 time per minutes and blood pressure
140/90 mmHg. His Body Mass Index (BMI) is 28.7.
LEARNING TASK 1
1. If the patient took sildenafil, which drug is contraindicated for this patient? And why?
2. Please explain the mechanism of action of drugs that will you used for this patient and
please write the prescription for the drug?
LEARNING TASK 2
1. Please explain some side effects of digoxin and how to treat those side effects?
2. Please explain the use of SGLT2-i in heart failure.
SELF ASSESSMENT
1. Please explain the pharmacokinetic of drugs used in HF
2. Please explain the pharmacodynamic of drugs used in HF
3. Please explain the pharmacokinetic of drugs used in IHD
4. Please explain the pharmacodynamic of drugs used in IHD
5. Please explain some important side effect of drugs used for IHD and HF
1. Katzung, BG, Trevor AJ. 2015. Basic and Clinical Pharmacology Thirteenth Edition.
McGraw-Hill Education: New York.

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LECTURE 9
ANTIARRHYTHMIC DRUGS (AADs) PHARMACOLOGY
dr. Agung Nova Mahendra, S.Ked., M.Sc.
Department of Pharmacology and Therapy
AIMS
Students are expected to comprehend the fundamental and clinical pharmacology of AADs, and
to be able to translate this knowledge into the pharmacotherapy of selected arrhythmias.
LEARNING OUTCOMES
At the end of the lectures, the students are able to:
1. Describe the classification of AADs and their characteristics
2. Describe the pharmacodynamics (PD) and pharmacokinetics (PK) of AADs
3. Comprehend clinical uses of AADs
4. Describe the toxicities of AADs
CURRICULUM CONTENTS
● Classification of antiarrhythmic drugs and their characteristics
● The PD and PK of drugs used in arrhythmias
● Clinical applications of drugs used in arrhythmias
● Toxicities of drugs used in arrhythmias
ABSTRACT
Cardiac arrhythmias are particularly common problem in clinical practice, especially in the field
of general cardiology. These conditions may require treatment because abnormal rhythms can
diminishes cardiac output. Arrhythmias can be treated by drugs that suppress abnormal rhythms
by direct modulation on cardiac syncytium membrane, known as antiarrhythmic drugs (AADs).
The margin of safety is particularly narrow for these drugs, thus therapeutic risks and benefits
must be carefully assessed.
SELF-DIRECTED LEARNING
Basic body of knowledge as the prerequisite of the lecture includes:
● Autonomic Nervous System
● Physiology of Cardiac Conduction System
● Mechanisms of Arrhythmias
REFERENCES
● Dan G, Martinez-Rubio A, Agewall S, Boriani G, Borggrefe M, Gaita F, et al. 2018.
Antiarrhythmic drugs–clinical use and clinical decision making: a consensus document from
the European Heart Rhythm Association (EHRA) and European Society of Cardiology
(ESC) Working Group on Cardiovascular Pharmacology, endorsed by the Heart Rhythm
Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS) and International Society of
Cardiovascular Pharmacotherapy (ISCP) EP Europace. Available at:
https://academic.oup.com/europace/article/20/5/731/4846844 (a correction has been
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published in: EP Europace, Volume 20, Issue 5, May 2018, Page

738, https://doi.org/10.1093/europace/euy119.
● Katzung, BG. 2021. Basic and Clinical Pharmacology 15th Edition. McGraw-Hill. All Rights
Reserved.
● King GS, Goyal A, Grigorova Y, et al. Antiarrhythmic Medications. [Updated 2022 Aug 18].
In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.
SCENARIO:
Mr. KU, 51 years-old, accompanied by his friend, comes to ER complaining about continuous
palpitation and dizziness since + 2 hours before. He also suffers from chest discomfort and is
being anxious of getting suffocated. The signs and symptoms commenced when he was driving
his motorbike to his friend’s home, and did not subside with resting. After conducting
anamnesis, physical examinations, and ECG, the diagnosis of SVT is then applied to this
patient by the ER physician.
LEARNING TASKS
1. Outline the classification of antiarrhythmic drugs (AADs) based on updated
Singh-Vaughan Williams Classification and their general PDs! Name at least 1 drug for
each class!
2. Discuss the PK characteristics of AADs!
3. Discuss the indications and contraindications of AADs!
4. Please describe the adverse effects (toxicities) of AADs!
SELF-ASSESSMENT
1. What are the mechanisms of pro-arrhythmic effects of AADs?
2. What is the drug of choice for paroxysmal SVT?

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LECTURE 10
PATHOLOGICAL ASPECT OF ISCHEMIC HEART DISEASE

Dr. dr. Ni Wayan Winarti, Sp.PA (K)
ABSTRACT
Ischemic heart disease (IHD) represents a group of pathophysiologically related
syndromes resulting from myocardial ischemia—an imbalance between myocardial supply
(perfusion) and cardiac demand for oxygenated blood. In more than 90% of cases, myocardial
ischemia results from reduced blood flow due to obstructive atherosclerotic plaque in the
epicardial coronary arteries.
What is atherosclerosis? Atherosclerosis is hardening of vessel wall in which the lesion
is intimal-based, and composed of a fibrous cap and an atheromatous core. The constituents of
the plaque include smooth muscle cells, extracellular matrices, inflammatory cells, lipids, and
necrotic debris. Atherosclerosis result from chronic inflammatory and healing response of the
arterial wall to endothelial injury. The major risk factors for atherosclerosis are hyperlipidemia,
hypertension, cigarette smoking and diabetes mellitus.
Atherosclerosis may affect any branch of coronary arteries. Ischemia of cardiac muscle
due to atherosclerotic plaque in the coronary arterial walls will lead to many kinds of coronary
syndromes, depend on the site, severity, types (stable or vulnerable plaque) and acute changes
that lead to thrombosis and vasospasm, duration of obstruction and oxygen need of
myocardium.
The coronary syndromes include angina pectoris (stable and unstable), myocardial
infarction (MI), sudden cardiac death and chronic IHD with heart failure. Unstable angina, MI
and sudden cardiac death are known as acute coronary syndrome. It commonly occur due to
acute plaque changes, like hemorrhage, erosion, rupture or fissure of the plaque with thrombus
formation that increase the level of obstruction. Unstable angina is usually characterized by
subendocardial infarction, while MI is transmural. The morphology of infarction is vary depends
on duration of ischemia. Fully developed infarction occur between 1-3 days, grossly m anifested
as pale infarction, and microscopically appeared as coagulative necrosis of myocytes and
neutrophils infiltration in affected area.
LEARNING TASK
1. Explain the morphology of atherosclerosis!
2. Explain the correlation between condition of atherosclerotic plaque with the type of
coronary syndrome that may occur to the patient!
3. Explain the difference between morphology of unstable angina and acute MI!
4. Explain the morphological changes of MI based on duration of cardiac ischemia!
SELF ASSESMENT
1. Mention 4 major modifiable risk factors of atherosclerosis!
2. Describe morphological changes of cardiac muscle in myocardial infarction day 3 and

day 14!
3. Describe the morphological difference between stable and vulnerable plaque!

79
REFERENCES
Kumar, V., Abbas, A.K. and Aster, J.C. 2015. Robbins and Kumar. Pathologic Basis of Disease,
9 ed. Philadelphia: Elsevier Saunders, pp. 491-501, 538-550
Wang T, Palluci D, Law K, Yanagawa B, Yam J, and Butany J. Atherosclerosis: Pathogenesis

and pathology in mini-symposium: cardiovascular pathology – I. Diagnostic Histopathology
18:11.2012, Elsevier

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LECTURE 11
APPROACH TO PATIENT WITH CARDIOVASCULAR DISEASE

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

81
reconstruction algorithms to images. It is these images, acquired at high spatial and temporal
resolution, that have enabled cardiovascular medicine to enter the CT imaging era
3. Magnetic resonance imaging (MRI)
Over the past decade, cardiac magnetic resonance (CMR) has developed into a routine
clinical imaging tool. With excellent spatial and temporal resolution, unrestricted tomographic
fields, and no exposure to ionizing radiation, CMR offers detailed morphologic and functional
characterization for most types of heart disease
4. Echocardiography
Echocardiography remains the most frequently used and usually the initial imaging test to
evaluate all cardiovascular diseases related to a structural, functional, or hemodynamic
abnormality of the heart or great vessels. Echocardiography uses ultrasound beams reflected
by cardiovascular structures to produce characteristic lines or shapes caused by normal or
altered cardiac anatomy in one, two, or three dimensions by M (motion)–mode,
two-dimensional, or three-dimensional echocardiography, respectively. Doppler examination
and color flow imaging provide reliable assessment of cardiac hemodynamics and blood flow.
5. Angiocardiography
Angiography is a technique used to visualize the lumen, of blood vessels and organs of the
body, with particular interest in the arteries, veins, and the heart chambers. This is
traditionally done by injecting a radio-opaque contrast agent into the blood vessel and
imaging using X-ray based techniques such as fluoroscopy.
6. Cardiac catheterization
Cardiac catheterization is the insertion of a catheter into a chamber or vessel of the heart.
This is done both for diagnostic and interventional purposes. Subsets of this technique are
mainly coronary catheterization, involving the catheterization of the coronary arteries, and
catheterization of cardiac chambers and valves of the Cardiac System.
7. Nuclear Cardiology
The era of noninvasive radionuclide cardiac imaging in humans began in the early 1970s with
the first reports of noninvasive evaluation of resting myocardial blood flow. Since that time,
there have been major advances in the technical ability to image cardiac physiology and
pathophysiology, including that of myocardial blood flow, myocardial metabolism, and
ventricular function.
1. McPhee SJ, Papadakis MA. Current Medical Diagnosis & Treatment. 47th ed. New York:
Lange Mecical Book`s/The McGraw-Hill Companies, 2008.p.
2. Roentgen Signs in Diagnostic Imaging Isadore Meschan.

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

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SELF ASSESSMENT :
1. Please explain the symptoms in patients with cardiovascular disease!
2. What are the diagnostic tools to confirm patients with Ischaemic Heart Disease?
3. What is the benefit of 24-hour electrocardiogram?
4. What is the objective of performing stress testing (treadmill test)?
5. Please describe the chest x-ray finding in VSD!
6. Differenciated between LVH and RVH on chest x-ray!
7. Explain HHD on the chest x-ray!
8. Explain tetralogy of Fallot on the chest x-ray!

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LECTURE 12
LABORATORY EXAMINATION : CARDIAC MARKERS

Prof. Dr. dr. AA Wiradewi Lestari, Sp.PK
AIMS:
Can describe various cardiac markers.
LEARNING OUTCOME:
Able to interpret cardiac marker results.
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 streated 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.
STANDARD REFERENCES:
1. Burtis CA, Bruns DE: Tietz Fundamentals of Clinical Chemistryand 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.

1. Types of cardiac marker
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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?

85
LECTURE 13
CHRONIC HEART FAILURE
dr. I Nyoman Wiryawan, SpJP(K), FIHA
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 is not a single pathological diagnosis, but a clinical syndrome
consisting of cardinal symptoms (e.g. breathlessness, ankle swelling, and fatigue) that
may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary
crackles, and peripheral oedema). It is due to a structural and/or functional abnormality
of the heart that results in elevated intracardiac pressures and/or inadequate cardiac
output at rest and/or during exercise.
Terminology:
1. Heart failure with preserved, mildly reduced, and reduced ejection fraction
2. Right ventricular dysfunction

Heart failure can also be a result of right ventricular (RV) dysfunction. RV mechanics and
function are altered in the setting of either pressure or volume overload. Although the
main etiology of chronic RV failure is LV dysfunction-induced pulmonary hypertension,

86
there are a number of other causes of RV dysfunction [e.g. MI, arrhythmogenic right
ventricular cardiomyopathy (ARVC), or valve disease]. The diagnosis is determined by a
quantitative assessment of global RV function, most commonly by echocardiography,
using at least one of the following measurements: fractional area change (FAC); tricuspid
annular plane systolic excursion (TAPSE); and Doppler tissue imaging-derived systolic
S0 velocity of the tricuspid annulus.
3. Other common terminology used in heart failure
Heart failure is usually divided into two presentations: chronic heart failure (CHF) and
acute heart failure (AHF). CHF describes those who have had an established diagnosis of
HF or who have a more gradual onset of symptoms. If CHF deteriorates, either suddenly
or slowly, the episode may be described as ‘decompensated’ HF. This can result in a
hospital admission or treatment with intravenous (i.v.) diuretic therapy in the outpatient
setting. In addition, HF can present more acutely. Some individuals with HF may recover
completely [e.g. those due to alcohol-induced cardiomyopathy (CMP), viral myocarditis,
Takotsubo syndrome, peripartum cardiomyopathy (PPCM), or tachycardiomyopathy].
Other patients with LV systolic dysfunction may show a substantial or even complete
recovery of LV systolic function after receiving drug and device therapy.
4. Terminology related to the symptomatic severity of heart failure
The simplest terminology used to describe the severity of HF is the New York Heart
Association (NYHA) functional classification. However, this relies solely on symptoms
and there are many other better prognostic indicators in HF.19 Importantly, patients with
mild symptoms may still have a high risk of hospitalization and death.
5. Etiology of heart failure

87

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6. Key steps in the diagnosis of chronic heart failure

The diagnosis of CHF requires the presence of typical symptoms and/or signs of HF and
objective evidence of cardiac dysfunction.
The following diagnostic tests are recommended for the assessment of patients with
suspected chronic HF:

89
a. Electrocardiogram (ECG). A normal ECG makes the diagnosis of HF unlikely.
b. Measurement of NPs are recommended, if available. A plasma concentration of

B-type natriuretic peptide (BNP) <35 pg/mL, N-terminal pro-B-type natriuretic peptide
90
(NT-proBNP) <125 pg/ mL, or mid-regional pro-atrial natriuretic peptide (MR-proANP) <40
pmol/L make a diagnosis of HF unlikely.
c. Basic investigations such as serum urea and electrolytes, creatinine, full blood
count, liver and thyroid function tests are recommended to differentiate HF from other
conditions, to provide prognostic information, and to guide potential therapy.
d. Echocardiography is recommended as the key investigation for the assessment of
cardiac function. As well as the determination of the LVEF, echocardiography also
provides information on other parameter such as chamber size, eccentric or concentric
LVH, regional wall motion abnormalities (that may suggest underlying CAD, Takotsubo

91
syndrome, or myocarditis), RV function, pulmonary hypertension, valvular function, and

markers of diastolic function.
e. A chest X-ray is recommended to investigate other potential causes of
breathlessness (e.g. pulmonary disease). It may also provide supportive evidence of HF
(e.g. pulmonary congestion or cardiomegaly).
7. The diagnostic algorithm for heart failure

92
8. Pharmacological treatments for patients with heart failure with reduced ejection
fraction
Pharmacotherapy is the cornerstone of treatment for HFrEF and should be implemented
before considering device therapy, and alongside non-pharmacological interventions.
There are three major goals of treatment for patients with HFrEF:
1. Reduction in mortality,
2. Prevention of recurrent hospitalizations due to worsening HF
3. Improvement in clinical status, functional capacity, and QOL
Therapeutic algorithm of Class I Therapy Indications for a patient with heart failure with
reduced ejection fraction.

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95

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9. Heart failure with mildly reduced ejection fraction (HFmrEF)

The diagnosis of HFmrEF requires the presence of symptoms and/or signs of HF, and a
mildly reduced EF (41 49%) The presence of elevated NPs (BNP >_35 pg/mL or
NT-proBNP >_125 pg/mL) and other evidence of structural heart disease [e.g. increased
left atrial (LA) size, LVH or echocardiographic measures of LV filling] make the diagnosis
more likely but are not mandatory for diagnosis if there is certainty regarding the
measurement of LVEF.
There is a substantial overlap of clinical characteristics, risk factors, patterns of cardiac
remodelling, and outcomes among the LVEF categories in HF. Patients with HFmrEF
have, on average, features that are more similar to HFrEF than HFpEF, in that they are
more commonly men, younger, and are more likely to have CAD (50 60%), and less likely
to have AF and non-cardiac comorbidities. However, ambulatory patients with HFmrEF
have a lower mortality than those with HFrEF, more akin to those with HFpEF. Patients
with HFmrEF may include patients whose LVEF has improved from <_40% or declined
from >_50%.
As in other forms of HF, diuretics should be used to control congestion. No substantial
prospective RCT has been performed exclusively in patients with HFmrEF.

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10. Heart failure with preserved ejection fraction (HFpEF)

Clinical characteristics of patients with HFpEF differs from HFrEF and HFmrEF in that
HFpEF patients are older and more often female. AF, CKD, and non-CV comorbidities are
more common in patients with HFpEF than in those with HFrEF.

98
There are numerous potential causes of HFpEF. The pathophysiology of various HFpEF
syndromes differs, and thus they require distinct therapies. Red flags for the potential
presence of Cardiac Amyloidosis include low normal BP in patients with a history of
hypertension, intolerance to beta-blockers or ACE-I, history of bilateral carpal tunnel
syndrome, low voltage on ECG and echocardiographic features such as thickening of the
septum, posterior wall, or RV wall, enlarged atria, a small pericardial effusion, or valve
thickening. Furthermore, it is important to exclude other conditions that might mimic the
HFpEF syndrome (e.g. lung disease, anaemia, obesity, and deconditioning).
The diagnosis of HFpEF remains challenging. More recently, two score-based algorithms
(H2FPEF and HFA-PEFF) have been proposed to aid the diagnosis. Both scores assign a
substantial proportion of suspected HFpEF patients as intermediate likelihood, where in
additional diagnostics are proposed. To facilitate broad clinical application, ESC
guidelines of Acute and Chronic HF 2021 recommends a simplified pragmatic approach
that distils the common major elements in prior diagnostic criteria and emphasizes the
most frequently used variables widely available to clinicians. Some of these variables, in
particular, LA size (LA volume index >32 mL/m2), mitral E velocity <90 cm/s, septal e’
velocity <9 cm/s, E/e’ ratio >9 have been shown to be pivot points beyond which the risk
of CV mortality is increased, underscoring their value. This simplified diagnostic
approach starts with assessment of pretest probability. The diagnosis should include the
following: (1) Symptoms and signs of HF, (2) An LVEF >_50%, (3) Objective evidence of
cardiac structural and/or functional abnormalities consistent with the presence of LV
diastolic dysfunction/ raised LV filling pressures, including raised NPs.
To date, no treatment has been shown to convincingly reduce mortality and morbidity in
patients with HFpEF, although improvements have been seen for some specific
phenotypes of patients within the overall HFpEF umbrella. However, none of the large
RCTs conducted in HFpEF have achieved their primary endpoints. These include
PEP-CHF (perindopril), CHARM-Preserved (candesartan), I-PRESERVE (irbesartan),
TOPCAT (spironolactone), DIG-Preserved (digoxin), and PARAGON-HF
(sacubitril/valsartan). Although nebivolol significantly reduced the combined primary
endpoint of all-cause mortality or CV hospital admission in the SENIORS trial, this trial
included only 15% with an LVEF >50%.

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1. Libby P, Bonow RO, Mann DL, Zipes DP eds. Heart Failure. In: Braunwald’s Heart
Disease, 12th ed. Philadelphia, Elsevier Saunders, 2022. p. 889-1143
2. McDonagh T.A, et al. 2021 ESC Guidelines for The Diagnosis and Treatment of Acute
and Chronic Heart Failure. European Journal Heart Failure. 2021. European Heart
Journal (2021) 00, 1 128
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
4. Heidenreich P.A, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart
Failure. 2022. Circulation. 2022;145:00–00
5. Pedoman Tata Laksana Gagal Jantung. Kelompok Kerja Gagal Jantung dan Penyakit
Karddiometabolik. Perhimpunan Ahli Kardiovaskular Indonesia. 2020

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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 14
ACUTE CORONARY SYNDROME (STEMI)
Dr. dr. I Made Junior Rina Artha, Sp.JP (K), FIHA
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 ST-elevation myocardial infarction STEMI).
● 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 countries, as well as 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). It is 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 a foam cells, and lead to the
formation of ‘fatty streak’ and then ‘atheroma’. The underlying pathophysiology in ACS is
decreased blood flow to the part of myocard which is usually secondary to plaque rupture and
formation of thrombus. The plaque cap tears to expose the lipid core to blood in the arterial
lumen. This core area is highly thrombogenic, containing tissue factor, fragments of collagen,
and crystalline surfaces, which accelerates coagulation. Initially the thrombus forms within the
plaque which may then extend into the arterial lumen causing partial or complete occlusion of
the arterial lumen.
Acute coronary syndrome are a life-threatening conditions that can punctuate the course
of patients with coronary artery disease at any time. The acute coronary syndromes encompass
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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. The
electrocardiogram should be done within 10 minutes of arrival and 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.
Initial therapy of STEMI consist of aspirin, clopidogrel, low-molecular-weight heparin,
beta-blockers and intravenous nitrate infusion. 2017 ESC guideline for STEMI recommend
reperfusion therapy is indicated in all patients with symptoms of ischaemia of ≤12 h duration and
persistent ST-segment elevationan. A primary PCI strategy is recommended over ﬁbrinolysis
within indicated time frames. If timely primary PCI cannot be performed after STEMI diagnosis
within 120 minutes, ﬁbrinolytic therapy is recommended within 12 h of symptom onset in
patients without contraindications. In patients with time from symptom onset >12 h, a primary
PCI strategy is indicated in the presence of ongoing symptoms suggestive of ischaemia,
haemodynamic instability, or life-threatening arrhythmias.

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. 2017 ESC Guidelines for management of Acute Myocardial Infarction in
Patients Presenting with ST-Segment Elevation. Eur Heart J. 2017:39,119-177.
3. Collet et al. 2020 ESC Guidelines for the management of acute coronary syndromes in
patients presenting without persistents ST-segment elevation. Eur Heart J. 2020:00,1-79.
SCENARIO 1:
CASE 1
A 61 year old male came to the emergency room complaining of substernal chest pain while
shoveling 2 hours PTA. He rates the pain as 8 on a scale of 1 - 10. He is slightly diaphoretic. His
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BP is 124/88. His pulse rate is 102 beats-per-minute, regular. His pulse oximetry is 98% on
room air. He had uncontrolled hypertension since 2 years ago and smoking 1 pack/day since he
was young. The ECG showed:
LEARNING TASK:
1. What is the most likely diagnosis?
2. What is your initial treatment?
3. What is the definitive therapy for this case?
4. 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)!

104
LECTURE 15
ACUTE CORONARY SYNDROME
dr. Kadek Susila Surya Darma, Sp.JP (K), FIHA
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 non ST-elevation myocardial infarction (NSTEMI)
· 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:
The pathological correlate for ACS in patients presenting without persistent ST-segment
elevation (NSTE-ACS) at the myocardial level is cardiomyocyte necrosis, measured by troponin
105
release, or, less frequently, myocardial ischemia without cell damage (unstable angina). In
general, individuals with unstable angina have a substantially lower risk of death and derive less
benefit from an aggressive pharmacological and invasive approach. High-sensitivity troponin
(hs-Tn) assay measurements are recommended over less sensitive ones, as they provide higher
diagnostic accuracy at identical low cost. Of note, many cardiac pathologies other than
myocardial infarction (MI) also result in cardiomyocyte injury and, therefore, cardiac troponin
(cTn) elevations.
Other biomarkers may have clinical relevance in specific clinical settings when used in
combination with non–hs-cTn T/I. Creatine kinase-myocardial band (CK-MB) shows a more
rapid decline after MI and may provide added value for detection of early reinfarction. The
routine use of copeptin as an additional biomarker for the early rule-out of MI is recommended
in the very uncommon setting where hs-cTn assays are not available. The time interval to the
second cTn assessment can be shortened with the use of hs-cTn assays due to the higher
sensitivity and diagnostic accuracy for the detection of MI at presentation. It is recommended to
use the 0 h/1 h algorithm (best option, blood draw at 0 h and 1 h) or the 0 h/2 h algorithm
(second-best option, blood draw at 0 h and 2 h). Used in conjunction with clinical and
electrocardiography (ECG) findings, the 0 h/1 h and 0 h/2 h algorithm allows the identification
of appropriate candidates for early discharge and outpatient management. Four clinical variables
significantly affect hs-cTn concentrations including age (differences between healthy very young
vs. ‘healthy’ very old individuals up to 300%), renal dysfunction (differences with very high vs.
very low estimated glomerular filtration rate (eGFR) up to 300%), chest pain onset (>300%), and
sex (~40%).
Initial cTn levels add prognostic information in terms of short- and long-term mortality to
clinical and ECG variables. The higher the hs-cTn levels, the greater the risk of death. Serum
creatinine and eGFR should also be determined in all patients with NSTE-ACS because they
affect prognosis and are key elements of the GRACE risk score, in which assessment is superior
to (subjective) physician assessment for the occurrence of death or MI. In addition, natriuretic
peptides may provide incremental prognostic information.
The use of Academic Research Consortium for High Bleeding Risk (ARC-HBR) assessment is a
pragmatic approach for bleeding risk assessment that includes the most recent trials performed in
high bleeding risk patients, who were previously excluded from clinical trials of dual antiplatelet
therapy (DAPT) duration or intensity. The PRECISE-DAPT score may be used to guide and
inform decision making on DAPT duration with a modest predictive value for major bleeding,
but their value in improving patient outcomes remains unclear.
Clinical assessment may indicate elective noninvasive or invasive imaging even after the rule-out
of MI. Cardiac computed tomography angiography (CCTA) may be an option in patients with
low to- modest clinical likelihood of unstable angina, as a normal scan excludes coronary artery
106
disease (CAD). CCTA has a high negative predictive value to exclude ACS (by excluding CAD)
and predicts an excellent outcome in patients presenting to the emergency department with
low-to-intermediate pretest probability for ACS and a normal CCTA. Stress imaging by cardiac
magnetic resonance imaging (CMR), stress echocardiography, or nuclear imaging may also be an
option based on risk assessment.
An early routine invasive approach within 24 hours of admission is recommended for NSTEMI
based on hs-cTn measurements, GRACE risk score >140, and dynamic new, or presumably new,
ST-segment changes, as it improves major adverse cardiac events and possibly early survival.
Immediate invasive angiography is required in highly unstable patients according to
hemodynamic status, arrhythmias, acute heart failure, or persistent chest pain. In all other clinical
presentation, a selective invasive approach may be performed according to noninvasive testing or
clinical risk assessment.
The principal technical aspects of percutaneous coronary intervention (PCI) in NSTE-ACS

patients do not differ from the invasive assessment and revascularization strategies for other
CAD presentations. Radial access is recommended as the preferred approach in NSTE-ACS
patients undergoing invasive assessment with or without PCI. As multivessel disease is frequent
in NSTE-ACS, timing and completeness of revascularization should be decided according to
functional relevance of all stenoses, age, general patient condition, comorbidities, and left
ventricular function.
MI with nonobstructive coronary arteries (MINOCA) incorporates a heterogeneous group of

underlying causes that may involve both coronary and noncoronary pathological conditions, with
the latter including cardiac and extracardiac disorders. By consensus, myocarditis and Takotsubo
syndrome are excluded. CMR is one of the key diagnostic tools, as it identifies the underlying
cause in >85% of patients and the subsequent appropriate treatment.
Spontaneous coronary artery dissection (SCAD) is a nonatherosclerotic, nontraumatic, or

iatrogenic separation of the coronary arterial tunics secondary to vasa vasorum hemorrhage or
intimal tear, and accounts for up to 4% of all ACS, but the incidence is reported to be much
higher (22-35% of ACS) in women <60 years of age. Intracoronary imaging is very useful for
the diagnosis and treatment orientation. Medical treatment is not well established.
Routine pretreatment with a P2Y12 receptor inhibitor in NSTE-ACS patients in whom coronary
anatomy is not known and an early invasive management is planned is not recommended given
the lack of established benefit. However, it may be considered in selected cases and according to
the bleeding risk of the patient. DAPT consisting of a potent P2Y12 receptor inhibitor in addition
to aspirin is generally recommended for 12 months, irrespective of the stent type, unless there are
contraindications. However, new scenarios have been implemented. DAPT duration can be
shortened (<12 months), extended (>12 months), or modified by switching DAPT or

107
de-escalation. These decisions depend on individual clinical judgment driven by the patient’s
ischemic and bleeding risk, the occurrence of adverse events, comorbidities, comedications, and
the availability of the respective drugs. In at least 6-8% of patients undergoing PCI, long-term
oral anticoagulation is indicated and should be continued. In general, novel oral anticoagulants
(NOACs) are preferred over vitamin K antagonists vitamin K antagonists (VKAs) in terms of
safety when patients are eligible. Dual antithrombotic therapy with a NOAC at the recommended
dose for stroke prevention and single antiplatelet therapy (preferably clopidogrel, chosen in
>90% of cases in available trials) is recommended as the default strategy up to 12 months after a
short period up to 1 week of triple antithrombotic therapy (TAT) (with NOAC and DAPT). TAT
may be prolonged up to 1 month when the ischemic risk outweighs the bleeding risk.
For NSTE-ACS, risk stratification should be done for estimating prognosis and guiding the
treatment. 2020 ESC guideline for NSTE-ACS recommend immediate invasive strategy (<2 h)
for very-high risk NSTE-ACS patients and early invasive strategy (<24 h) for high risk one.
Very-high risk criteria includes at least one citeria of haemodynamic instability, cardiogenic
shock, recurrent/refractory chest pain despite medical treatment, life-threatening arrhythmia,
mechanical complication of MI, acute heart failure clearly related to NSTE-ACS or ST-segment
depression >1mm/6 leads plus ST-segment elevation aVR and/or V1. High risk criteria including
at least one of established NSTEMI diagnosis, dynamic ST/T-segment changes, resuscitated
cardiac arrest without ST-segment elevation or cardiogenic shock and GRACE score >140.

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:
2015.
2. Collet et al. 2020 ESC Guidelines for the management of acute coronary syndromes in
patients presenting without persistents ST-segment elevation. Eur Heart J. 2020:00,1-79.
CASE 1
Eighty-five years old man came to the ER with crushing chest pain since 3 days ago, getting
worsen 4-hours PTA, accompanied by cold sweating. Chest pain was relieved to some extent
with ISDN 5mg SL. No nausea, vomiting nor palpitation. History of stroke (+) and hypertension.

108
His BP is 144/78. His pulse rate is 66 beats-per-minute, regular. He appeared moderately ill and
dyspnea. There were rales on both basal lung fields ECG showed:
LEARNING TASK:
3. How do you do risk stratification for this patient?
4. What is the definitive therapy for this case according to its risk stratification?
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 non ST-elevation myocardial infarction?
4. Please describe the indication and the benefit of CABG (coronary artery bypass graft)!

109
LECTURE 16
HYPERTENSION
dr. AA Ayu Dwi Adelia Yasmin, M.Biomed, SpJP(K), FIHA
AIMS:
Describe diagnostic approach and management of Hypertension.
LEARNING OUTCOME:
Be able to describe diagnostic approach and management of Hypertension.
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:
High Blood Pressure remains the leading cause of death globally, accounting for 10.4 million
deaths per year. When reviewing global figures, an estimated 1.39 billion people had
hypertension in 2010. In accordance with most major guidelines, it is recommended that
hypertension be diagnosed when a person’s systolic blood pressure (SBP) in the office or clinic
is ≥140 mm Hg and/or their diastolic blood pressure (DBP) is ≥90 mm Hg following repeated
examination. The measurement of BP in the office or clinic is most commonly the basis for
hypertension diagnosis and follow-up. Whenever possible, the diagnosis should not be made on
a single office visit. Usually 2–3 office visits at 1–4-week intervals (depending on the BP level)
are required to confirm the diagnosis of hypertension. The diagnosis might be made on a single
visit, if BP is ≥180/110 mm Hg and there is evidence of cardiovascular disease (CVD). If
possible and available, the diagnosis of hypertension should be confirmed by out-of-office BP
measurement.
Hypertension-mediated organ damage (HMOD) is defined as the structural or functional
alteration of the arterial vasculature and/or the organs it supplies that is caused by elevated BP.
End organs include the brain, the heart, the kidneys, central and peripheral arteries, and the
eyes. Patients with hypertension must be treated comprehensively by lifestyle modification
measures and pharmacological therapy. Healthy lifestyle choices can prevent or delay the onset
of high BP and can reduce cardiovascular risk. Lifestyle modification is also the first line of
antihypertensive treatment. Modifications in lifestyle can also enhance the effects of
antihypertensive treatment. Pharmacological treatment for hypertensive patients must be
individualized based on compelling indication and contraindication. Effective management and
treatment of hypertension requires clinicians and patients to work together to balance
pharmacologic and nonpharmacologic interventions and prevent target organ damage.
1. Unger T, Borghi C, Charchar F, et al. 2020 International Society of Hypertension Global
Hypertension Practice Guidelines. Hypertension. 2020; 75; 6 1334-1357
SCENARIO CASE:
A 40-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 140/90
mmHg. He is 170 m tall, weighs 70 kg and has no past medical history. His basic physical

110
examination is unremarkable with no audible murmurs on cardiac auscultation. He has no

history of cardiac symptoms or diabetes.
LEARNING TASK:
1. How do you interpret the patient’s blood pressure reading?
2. He asks you why he has high blood pressure. What do you tell him and would you
perform any additional tests or examinations?
3. What is your advice and management plan for this patient?
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?

111
LECTURE 17
HYPERTENSIVE URGENCY AND EMERGENCY
dr. Cyndiana Widia Dewi Sinardja, M.Biomed, SpJP, FIHA
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.
1. Definition of Hypertensive Urgency and Emergency
2. Etiology and pathophysiology of Hypertensive Urgency and Emergency
3. Clinical criteria for Hypertensive Urgency and Emergency
4. Diagnostic approach to Hypertensive Urgency and Emergency
5. Management and prognosis of Hypertensive Urgency and Emergency
ABSTRACT:
A hypertensive emergency is an acute, marked elevation in blood pressure that is associated

with signs of target-organ damage. These can include pulmonary edema, cardiac ischemia,
neurologic deficits, acute renal failure, aortic dissection, and eclampsia. Various inciting events
can cause hypertensive emergencies. The majority of hypertensive emergencies occur in
patients already diagnosed with chronic hypertension. Noncompliance with antihypertensive
medications and use of sympathomimetics are two of the more common causes. These leading
to a rapid rise in blood pressure beyond the body's innate autoregulation capacity. The
pathophysiology resulting in end-organ dysfunction in hypertensive emergencies is not fully
understood. However, the mechanical stress on vascular walls likely leads to endothelial
damage and a pro-inflammatory response. This result increased vascular permeability, platelet,
and coagulation cascade activation, and fibrin clot deposition leads to hypoperfusion at the level
of the target organ tissue.

112
In patients who present with markedly elevated blood pressure, a careful history and exam are
necessary to determine which of these patients is having a true hypertensive emergency.
Symptoms such as a headache, dizziness, altered mental status, shortness of breath, chest
pain, decreased urine output, vomiting, or changes in vision warrant further evaluation. The
source of the abrupt onset of hypertension should also be investigated to direct treatment.The
expected exam findings vary depending on the specific target organ most affected.
While the specific target organ that is affected may dictate some specifics of treatment, rapid
lowering of blood pressure is the mainstay of therapy for hypertensive emergencies. The goal
would be to lower the mean arterial pressure by 20% to 25% within the first 1 to 2 hours.
Several agents can be used, but the unifying characteristics are that they are rapidly acting and
easily titratable.
Hypertensive urgency, on the contrary, is characterized by an acute increase in BP in the

absence of symptoms suggesting acute organ damage. Hospitalization is not necessary and
this condition may be managed effectively with close outpatient follow-up. The decrease in BP
may be obtained in hours or even days by oral antihypertensive treatment
1. Unger T, Borghi C, Charchar F, et al. 2020 International Society of Hypertension Global
Hypertension Practice Guidelines. Hypertension. 2020; 75; 6 1334-1357
SCENARIO CASE #1:
A 50 - year - old man is admitted via Emergency Department with a history of a sudden onset of
central chest pain. On examination pulse is 110 bpm, blood pressure is 200/130 mmHg, heart
sounds are reported as normal, and there is evidence of mild left ventricular failure. Oxygen
saturations are 100% on room air. He has longstanding hypertension history, with his last
treatments on medical record were Amlodipine 10 mg OD, Bisoprolol 10 mg OD, Thiazide 2 5
mg OD, Candesartan 32 mg OD, but he didn’t take his medication since 1 week. The ECG
shows left ventricular hypertrophy and strain. During the course of the clinical examination the
patient reports increasingly severe pain, travelling through to the back.
LEARNING TASK:
1. What is the differential diagnosis of this patient?
2. What would be your immediate management for this patient?
SCENARIO CASE #2:
A 74-year-old man came for a routine clinic appointment and a physical examination,
complaining of a moderate posterior cervical headache for a few days. There was no history of
medical problems. He rarely saw a physician and could not recall any prior blood pressure (BP)
determinations. His headache had occurred off and on for the past couple of months, but had
become more bothersome during the past week. He was not taking any prescription
medications, but had been taking two to three tablets of over-the-counter ibuprofen daily for the

113
past week for his headache. The patient denied any chest discomfort or breathing difficulty. He
was a nonsmoker and a nondrinker. His mother had hypertension. On examination, he was
comfortable but complaining of headache. there were minimal physical findings: fundi were
normal; there was an S4 gallop but no heart murmurs and no bruits. All pulses were present,
and his lungs were clear. There was trace bipedal edema. Cervical range of motion was slightly
reduced, without elicitation of any tenderness. Laboratory results revealed a blood urea nitrogen
level of 13 mg/dL (normal, 7–18 mg/dL), creatinine level of 0.7 mg/dL (normal, 0.4–1.2 mg/dL),
and potassium of 3.8 mEq/L (normal, 3.5–5.0 mEq/L). Urinalysis showed no protein or cells, and
a 12-lead ECG and Head CT was normal.
LEARNING TASK:
1. What is the differential diagnosis of this patient?
2. What would be your immediate management for this patient?
SELF-ASSESSMENT:
1. Please explain the pathophysiology of hypertensive emergency and urgency!
2. What are the signs and symptoms of hypertensive emergency and urgency?
3. What are the drug of choice for treatment of hypertensive emergency and urgency?

114
LECTURE 18
Chronic Coronary Syndrome
dr. I Dewa Gde Aditya Diprabawa, Sp.JP, FIHA
AIMS:
Describe diagnostic approach and management Chronic Coronary Syndrome (CCS)
LEARNING OUTCOME:
Be able to describe diagnostic approach and management of Chronic Coronary Syndrome.
CURRICULUM CONTENT:
● Pathogenesis of atherothrombosis.
● Risk factors for Chronic Coronary Syndrome.
● Clinical spectrum of Chronic Coronary Syndrome.
● Interpret diagnostic tools for Chronic Coronary Syndrome.
● Management and its prognosis of Chronic Coronary Syndrome.
ABSTRACT:
Coronary artery disease (CAD) is a pathological process characterized by atherosclerotic
plaque accumulation in the epicardial arteries, whether obstructive or non-obstructive. 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, most often progressive, and hence serious, even in clinically apparently
silent periods. Initiated by lipid deposition and vascular wall injury that causes increased
endothelial permeability, inflammation and recruitment of monocytes and leukocytes. 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/ chronic coronary syndrome
(CCS) and unstable angina pectoris/ acute coronary syndrome (ACS) due to an acute
atherothrombotic event caused by plaque rupture or erosion. CCS 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
115
may also be occurring spontaneously. Such episodes of ischemia/hypoxia are commonly

associated with 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 most frequently encountered clinical scenarios in patients with suspected or
established CCS are: (i) patients with suspected CAD and ‘stable’ anginal symptoms, and/or
dyspnoea; (ii) patients with new onset of heart failure (HF) or left ventricular (LV) dysfunction
and suspected CAD; (iii) asymptomatic and symptomatic patients with stabilized symptoms <1
year after an ACS, or patients with recent revascularization; (iv) asymptomatic and symptomatic
patients >1 year after initial diagnosis or revascularization ; (v) patients with angina and
suspected vasospastic or microvascular disease ; and (vi) asymptomatic subjects in whom CAD
is detected at screening.
The diagnosis and assessment of CCS 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 CCS 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 CCS 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.

1. Risk factors for Coronary Artery Disease
2. Clinical spectrum of Coronary Artery Disease
3. Diagnostic modalities for Coronary Artery Disease
4. Management and prognosis of Coronary Artery Disease
References:
1. Mann, DL et all. Braunwald’s Heart Disease, 10th ed. Philadelphia, Elsevier Saunders,
2015.
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2. Knuuti, J. et al. 2019 ESC Guidelines for the diagnosis and management of chronic
coronary syndromes. Eur H J. 2019:00,1-7.
SCENARIO :
A 70-year-old woman presents to her new primary care provider for an initial patient visit. Her
sole active complaint is mild retrosternal chest pressure that she experiences when she climbing
up the stairs or walking about 200 meters, and the discomfort resolves within minutes after she
rest. The pattern and the severity of her symptoms have not changed significantly over the last
1 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. Describe characteristic of chest discomfort related to myocardial ischemia?
2. What is severity grading according the Canadian Cardiovascular Society?
3. What is patient risk factor for coronary artery disease?
4. What is next management (further diagnostic tests and medical therapy) for the patient?
SELF-ASSESSMENT :
1. Please explain the risk factors for coronary artery disease!
2. Please describe laboratory recommendation for assessment stable angina/CCS!
3. What is the noninvasive and invasive recommendation for assessment stable
angina/CCS?
4. What is the treatment of choice for Stable angina pectoris/CCS?
5. Please describe the indication and the benefit of revascularization.

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LECTURE 19
MALIGNANT ARRHYTHMIAS
dr. I Made Putra Swi Antara, Sp.JP(K), FIHA
AIMS:
Able to understand and diagnose arrhythmias.
LEARNING OUTCOME:
Can describe and diagnose arrhythmias.
Able to identify and manage malignant arrhythmias
1. Clinical approach to Arrhythmias.
2. Treatment of Arrhythmias.
3. Prognosis of Arrhythmias.
ABSTRACT:
Tachyarrhythmias are broadly characterized as supraventricular tachycardia (SVT),

defined as tachycardia where the driving circuit or focus originates, at least in part, in tissue
above the level of the ventricle (i.e., the sinus node, atria, AV node, or His bundle). The other is
ventricular tachycardia (VT), defined as 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 distinguish between SVT and VT in the acute management of a
tachyarrhythmia. In general (except for idiopathic VT), VT diagnosis 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 options for SVT comprise Valsalva maneuver, carotid sinus pressure, or
intravenous adenosine administration. 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 in the ECG by

low-amplitude baseline oscillations (fibrillatory or f-waves) in the atria paired with an
irregularly-irregular ventricular rhythm. AF is the most common arrhythmia treated in clinical
practice and the most common arrhythmia for which patients are hospitalized; approximately
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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, mainly when the patient is
treated with antiarrhythmic drugs, reducing the rate down 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 a rate-control strategy. It is

directed at limiting the ventricular response to atrial fibrillation using AV node blocking drugs,
such as digoxin, beta-blockers, and verapamil. Cardioversion and antiarrhythmic drugs are used
to restore and maintain sinus rhythm. Anticoagulation with warfarin should always be
considered for patients with atrial fibrillation and risk factors for thromboembolic stroke by using
a scoring system (i.e., 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 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/PVCs increases with age; they are
associated with the 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-extra systolic 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.
Bradyarrhythmia is arbitrarily defined as a heart rate below 60 beats/min. Bradyarrhythmia

can be physiologic, as in well-conditioned athletes with low resting heart rates or type I AV block
during sleep, and in some other cases, be pathologic. Like tachyarrhythmias, bradyarrhythmia
can be categorized based on 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
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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 with young
and healthy individuals.
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 where 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 delay or is not conducted at all to the ventricle
when the AV junction is not physiologically refractory. In some bundle branch block cases, the
impulse may only be delayed and not completely blocked in the bundle branch. The resulting
QRS complex may be indistinguishable from a QRS complex generated by a complete bundle
branch block.
In general, the specific type, prognosis, and management of ventricular tachycardia (VT)
depend on whether underlying structural heart disease is present. VT's electrocardiographic
diagnosis 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. VT symptoms 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 VT
management and aborted sudden death during the past decade have been fueled by several
large clinical trials and the 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 and most commonly
associated with coronary artery disease 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 heartbeat derangements that usually terminate
fatally within 3 to 5 minutes unless corrective measures are undertaken promptly. Ventricular
flutter is manifested as a sine wave in appearance—regular large oscillations occurring at a rate
of 150 to 300 beats/min (usually about 200). The distinction between rapid VT and ventricular
flutter can be difficult and is usually of academic interest only. Hemodynamic collapse is present
with both. VF is recognized by the presence of irregular undulations of varying contour and
amplitude. Distinct QRS complexes, ST segments, and T waves are absent. Fine-amplitude
fibrillatory waves (0.2 mV) are present with prolonged VF. These fine waves identify patients

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with worse survival rates and are sometimes confused with asystole. Management should follow
basic life support and advanced cardiac life support guidelines.
Malignant arrhythmias can also occur due to rare diseases that fall into a category called
cardiac channelopathies. These abnormalities cause an increased chance of arrhythmias such
as VT/VF to occur spontaneously, leading to sudden cardiac arrest. Some of the more common
ones are Brugada syndrome, Long-QT syndrome, Arrhythmogenic Right Ventricular
Cardiomyopathy (ARVC), and Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT).
Most of these diseases are treated by preventing sudden cardiac arrest with the implantation of
an ICD.
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://bit.ly/aritmiakv
SELF DIRECTED LEARNING
The basic knowledge that must be known:

1. Clinical approach for Arrhythmias
2. Pharmacological and Procedural Treatments for Arrhythmias
CASE 1:
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 was present, nor any risk factors for CAD. The emergency
response team's initial rhythm finding was VF and was defibrillated twice to convert back to
sinus rhythm. The physical exam was normal. Recorded ECG does not 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 the recurrence of sudden
cardiac death

121
LECTURE 20
BASIC ARRHYTHMIAS
dr. Putu Primeriana Nugiaswari, SpJP, FIHA
AIMS:
Able to understand and diagnose arrhythmias.
LEARNING OUTCOME:
Can describe and diagnose arrhythmias.
1. Etiology and pathophysiology of Arrhythmias.
2. Clinical approach to 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 vital to recognize these dangerous ones.
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). In contrast, others are
hazardous because of the clinical setting (e.g., rapidly conducted atrial fibrillation/AF 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. The level of
awareness of palpitations and whether 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 glaucoma treatment 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. 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 the use of the lead that shows distinct P waves is
often helpful for closer analysis; most commonly, this is one of the inferior leads (II, III, aVF), V1,
or aVR. The ECG obtained during an episode of arrhythmia may be diagnostic by itself,
obviating the need for further lengthy and costly diagnostic testing. The physician's choice of
122
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. In contrast, for patients who complain 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 tachycardia. The sinus node
exhibits a discharge frequency between 100 and 180 beats/min during sinus tachycardia, 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.
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://bit.ly/aritmiakv
SELF DIRECTED LEARNING

The basic knowledge that must be known:
1. Understanding of Cardiac Electrophysiologic Properties
2. Basic Understanding of ECGs
3. Definition and Mechanisms of Arrhythmias
SCENARIO FOR DISCUSSION

CASE 1:
A 45-year old gentleman presented with an irregular heartbeat and dizziness. 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?

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LECTURE 21
EMBRYOLOGY OF THE HEART AND THE GREAT VESSELS
Dr.dr. I.G.A. Widianti, M.Biomed
AIMS:
Describe the basic principles underlying the formation of anomalies of the heart and great
vessels.
LEARNING OUTCOME:
1. Can describe the basic principles underlying the formation of anomalies of the heart and
its implications
2. Can describe the basic principles underlying the formation of anomalies of the great
vessels and its implications
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) is usually happened at the upper membranous portion that
composed of connective tissue continuous with the annulus fibrosus. A small VSD may result in
an inconsequential left-to-right shunt.
In the presence of pulmonary stenosis, a VSD produces a right-to-left shunt with cyanosis and
the blue-baby syndrome. A large VSD is a principal factor in Tetralogy of Fallot.
Atrial septal defects (ASD) are most common in the vicinity of the fossa ovalis. Septum
secundum defects, the typical patent foramen ovale, account for 10-15% of all cardiac
anomalies. Normal left atrial pressure is slightly greater than right atrial pressure, a left-to-right
shunt occur through an open ASD, oxygenated blood from the left side of the heart is shunted to
the right side, thus not associated with cyanosis. An ASD is usually compatible with normal life,
except at an extreme exercise, cardiac disease, or pulmonary disease alter chamber pressures,
a right-to-left shunt will produce cyanosis.
Patent ductus arteriosus (PDA) is a persistence of the fetal connection (ductus arteriosus)
between the aorta and pulmonary artery after birth, resulting in a left-to-right shunt. Symptoms
may include failure to thrive, poor feeding, tachycardia and tachypneu. A continous machine-like
murmur in the upper left sternal border is common. Diagnosis is by echocardiography.

124
1. Moore KL, Agur AMR: Essential Clinical Anatomy, 6th ed. Philadelphia, Lippincott
& Wilkins, 2018. p. 91, 93, 94
2. Sadler TW: Langman’s Medical Embryology, 14thed. Philadelphia, Lippincott &
Wilkins, 2014. p. 167-178, 184

1. Embryology of the heart
2. Embryology of the great vessel
SCENARIO:
CASE 1;
A 2 year old boy was admitted to the hospital for evaluation of a heart murmur previously detect
at birth. He was less active than other children his age, but although over-exertion was followed
frequently by cyanosis of the lips and nails, there was no history of unconsciousness. Initial
examination revealed a thin, physically retarded, cyanotic child with no respiratory difficulty.
There was moderate clubbing of the fingers. A harsh systolic murmur was maximal over the
mid-precardial area. The first heart sound was normal while the second was single, distinct and
loud.The lungs were clear. X-ray showed a normal sized heart dominated by a boot-shaped
right ventricular outflow tract.
Diagnosis of Tetralogy of Fallot.
LEARNING TASK:
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 is he revealed thin and physically retarded?
CASE 2:
This baby aged 3 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:
1. What factors in the history were of possible importance in causing the ductus remain
open? Why there is no cyanosis in this case?
2. Why is there evidence of left ventricular hypertrophy and not right ventricular
hypertrophy?

125
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. Compare the circulation: after and before birth!

126
LECTURE 22
CONGENITAL HEART DISEASE AND ACUTE RHEUMATIC FEVER
dr. Eka Guna Wijaya, Sp.A(K)
AIMS:
1. Describe Non-cyanotic and Cyanotic Congenital Heart Diseases.
2. Describe Acute Rheumatic Fever.
LEARNING OUTCOME:
1. Can describe and diagnose Non-cyanotic and Cyanotic Congenital Heart Diseases.
2. 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. Interpretation for diagnostic tool of Acute Rheumatic Fever.
7. Management of Acute Rheumatic Fever and its complications.
8. Prevention and rehabilitation of Acute Rheumatic Fever.
9. Health education and prognosis of Acute Rheumatic Fever.
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.
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.

127
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
1. Park, MK. Pediatric Cardiology for Practitioners. 4th Ed. Philadelphia, Mosby. 2002. p
129-144, 185-189, 304-310, 311-318

128

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. Interpretion for diagnostic tool of Acute Rheumatic Fever
6. Management of Acute Rheumatic Fever and its complications
7. Prevention and rehabilitation of Acute Rheumatic Fever
8. Health education and prognosis of Acute Rheumatic Fever.
SCENARIO: CASE 1:
Putu, 2 years old girl 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 continuous heart murmur has heard at the
upper left parasternal border.
LEARNING TASK :
1. What kind of complications might experience in this case if the patient didn’t got
adequate treatment?
CASE 2:
Made, 9 months old baby was referred by GP to the pediatric cardiology clinic 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 is the emergency and comprenhensive treatment should be given to save the
patient?
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 380C. 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
129
1. What is the working diagnosis?

2. 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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LECTURE 23
SUDDEN CARDIAC ARREST
dr. Rani Paramita Iswari Maliawan, M.Biomed, Sp.JP

AIMS:
Describe diagnostic and initial management of sudden cardiac arrest
LEARNING OUTCOME:
Be able to describe diagnostic and initial management of sudden cardiac arrest.
1. Etiology and pathophysiology of sudden cardiac arrest.

2. Recognition of sudden cardiac arrest
3. Initial and quick management of sudden cardiac arrest
4. Prognostication of sudden cardiac arrest
ABSTRACT:
An international consensus workshop classified cardiac arrest as the “cessation of

cardiac mechanical activity, as confirmed by the absence of signs of circulation.”5 This definition
emphasizes that cardiac arrest is a clinical syndrome that involves the sudden (usually less than
1 hour from onset of first symptoms until death) loss of detectable pulse, or cessation of
spontaneous breathing. If an EMS provider or physician did not witness the event, then it may
be uncertain as to whether a cardiac arrest has occurred.
Cardiac arrest is a major international public health problem accounting for an estimated
15–20% of all deaths. Although resuscitation rates are generally improving throughout the
world, the majority of individuals who suffer a sudden cardiac arrest will not survive. SCD most
often develops in older adults with acquired structural heart disease, but it also rarely occurs in
the young, where it is more commonly due to inherited disorders. Coronary heart disease (CHD)
is known to be the most common pathology underlying SCD, followed by cardiomyopathies,
inherited arrhythmia syndromes, and valvular heart disease.
Even when a strict definition and multiple sources of ascertainment are used, other non-
cardiac conditions that evolve rapidly such as acute cerebral hemorrhage, aortic rupture, and
pulmonary embolism cannot be excluded without a carefully performed autopsy. Autopsy rates
are generally low and vary widely across countries with rates as low as 10 % of all deaths within
the United States compared to 23.8% in Finland , and the protocols for the performance of
autopsies in the cases of suspected SCD vary widely as well, even within regions of countries.
The presumed mechanism underlying an abrupt, unheralded death in these conditions is

electrical instability leading to a lethal arrhythmia triggered by ischemia or other arrhythmogenic
stimuli resulting in acute hemodynamic collapse. This hypothesis is difficult to prove as most
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deaths are not monitored, and those that are comprise a highly selected population. Studies in
epidemiologic cohorts of men and women from the 1970s to 1990s suggest that 88 to 91
percent of deaths that occur within one hour of symptom onset are arrhythmic in nature. Since
ventricular fibrillation (VF) degenerates to asystole over the course of several minutes, the
majority of SCD victims demonstrate asystole or Pulseless Electrical Activity (PEA) when first
examined by rescue teams. In cases of SCD where there has been a relatively short delay
between collapse and the initial determination of rhythm, the proportion of cases with
documented ventricular tachyarrhythmias increases to 75–80%. However, as mentioned
previously, VF is less often and PEA is more commonly encountered in recent Out-of Hospital
Cardiac Arrest (OHCA) series. Therefore, a proportion of SCD is likely due to abrupt
hemodynamic collapse in the absence of preceding fatal arrhythmia, and this proportion may be
growing in the population.
Management of SCD depend of quick recognition and quick decision to do high quality
cardiopulmonary resuscitation (CPR) based on the latest guidelines available. American Heart
Association (AHA) developed the first CPR guidelines, which since then have been updated
regularly. The process of generating CPR guidelines has evolved over several decades. The
AHA, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, the
Australian Resuscitation Council, and others have been comprehensively evaluating the
available resuscitation science and collaborating extensively for decades, which has led to
similar CPR guidelines published in different regions of the world.
The most current (2015) AHA Advanced Cardiac Life Support (ACLS) guidelines stress
several key points: (1) early defibrillation and early chest compressions; (2) high-quality
compressions, that is, a rate of 100–120 compressions per minute, a compression depth of at
least 2 inches, and complete chest recoil; (3) no unnecessary interruptions of chest
compressions; and (4) a ventilation rate no greater than 8 to 10 breaths per minute.
1. Graham Nichol and David Baker. The epidemiology of sudden death. Cardiac Arrest:
The Science and Practice of Resuscitation Medicine: Second Edition. Cambridge
University Press. 2007.
2. Meiso Hayashi, Wataru Shimizu, Christine M. Albert. The Spectrum of Epidemiology
Underlying Sudden Cardiac Death. Circ Res. 2015 June 5; 116(12): 1887–1906.
doi:10.1161/CIRCRESAHA.116.304521.
3. Matthias L. Riess. New Developments in Cardiac Arrest Management. Adv Anesth. 2016
; 34(1): 29–46. doi:10.1016/j.aan.2016.07.003.

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SCENARIO
CASE:
A 60 year-old man suddenly collapsed while have a mild jogging. A local bystander
quickly respond by checking his consciousness and then immediately performing CPR with 15:2
(15 compression and 2 ventilations); after 3 minutes bystander is exhausted and cannot
continue CPR. Patient known to have history of recurrent syncope but never check to any
medical practitioners. His father died of sudden cardiac arrest while sleeping 20 years ago at
age 45 yo.
LEARNING TASK:
1. Do you think the bystander did the CPR in right order? If it’s not, derscribe the CPR
algorithm according to ACLS guidelines.
2. If the monitor attached and it shows ventricular fibrillation (VF), what is the prognosis of
this patient? Is it better than asystole or pulseless electrical activity (PEA)?
3. What is most likely the cause/etiology of sudden cardiac arrest in this case?
4. Describe the high quality CPR that should be done in this patient.
SELF-ASSESSMENT:
1. Describe the risk stratification of sudden cardiac arrest

2. Describe the prognosis of cardiac arrest survivor with and without significant cardiovascular
disease
3. Describe the high quality CPR

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LECTURE 24
ACUTE HEART FAILURE
dr. Hendy Wirawan, M.Biomed, SpJP, FIHA
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
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

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 25
CARDIOGENIC SHOCK
dr. Ni Made Dharma Laksmi, Sp.JP, FIHA

AIMS:
Describe diagnostic and initial management of cardiogenic shock
LEARNING OUTCOME:
Be able to describe etiology and pathophysiology of cardiogenic shock
Be able to describe diagnostic and initial management of cardiogenic shock
Be able to describe prognosis of cardiogenic shock
1. Etiology and pathophysiology of cardiogenic shock

2. Clinical diagnostic criteria of cardiogenic shock
3. Initial management of cardiogenic shock
4. Prognostication of cardiogenic shock
ABSTRACT:
Cardiogenic shock is a hemodynamically complex syndrome characterized by a low

cardiac output that often culminates in multiorgan system failure and death. Despite recent
advances, clinical outcomes remain poor, with mortality rates exceeding 40%. In the absence of
adequately powered randomized controlled trials to guide therapy, best practices for shock
management remain nonuniform. Emerging data from North American registries, however,
support the use of standardized protocols focused on rapid diagnosis, early intervention,
ongoing hemodynamic assessment, and multi- disciplinary longitudinal care. It is characterized
by the inability of tissue blood flow and oxygen delivery to meet metabolic demands.
Cardiogenic shock is a type of circulatory shock resulting from severe impairment of ventricular
pump function rather than from abnormalities of the vascular system or blood volume.
Clinical trials and societal guidelines have employed a variety of definitions of CS.
Patient eligibility for the SHOCK trial was based on both clinical and hemodynamic criteria,
whereas other trials relied on clinical criteria, including sustained hypotension and evidence of
end-organ malperfusion. Building on the Diamond-Forrester classification system using cardiac
index and pulmonary capillary wedge pressure, CS profiles initially focused on pulmonary
congestion and systemic perfusion. Modern CS phenotyping is more nuanced, encompassing a
broader spectrum of clinical and hemodynamic presentations beyond the classic “cold and wet”
construct. In general, there is a profound depression of myocardial contractility resulting in a
potentially deleterious spiral of reduced cardiac output, low blood pressure, and further coronary
ischemia, followed by additional reductions in contractility. This cycle may lead to death. This

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classic paradigm also includes compensatory, although pathological, systemic vasoconstriction

that results from acute cardiac injury and ineffective stroke volume.
The most common causes of cardiogenic shock are acute impairment of myocardial
pump function from: acute myocardial infarction and associated complications, including rupture
of a papillary muscle or septum, severe MR and pericardial tamponade, acute valvular disease,
acute decompensated chronic heart failure, acute right heart failure, persistent severe rhythm
disturbances, and other cardiac diseases.
1. Behnam N. Tehrani, a Alexander G. Truesdell, Mitchell A. Psotka, et al. A Standardized and

Comprehensive Approach to the Management of Cardiogenic Shock. JACC Heart Failure
2020;8:879-91.
2. Eric R. Bates. Cardiogenic Shock. Cardiac Intensive Care: Second Edition. 2010. Saunders,
Elsevier: Chapter 17.
3. Wolfgang Krüger and Andrew Ludman. Cardiogenic Shock. Acute Heart Failure: Putting the
Puzzle of Pathophysiology and Evidence Together in Daily Practice. Birkhäuser. Basel ·
Boston · Berlin. 2009. Chapter 3. Page 71.
SCENARIO
CASE 1:
A 57 year-old man was admitted to ER with chest discomfort for 2 days and getting
worse 3 hours prior to admission. He also feels breathlessness and cold sweat. He looks
severely ill and diaphoretic, blood pressure is 70 over palpation, heart rate times per minute,
cold extremities and bibasilar rales heard over lung auscultation. He has history of DM Type 2
and hypertension before and currently not controlled by medication. ECG and chest x-ray are
shown below:

137
LEARNING TASK:
1. What is the main diagnosis of the case above? Describe your reasoning.
2. What is the most probable etiology of the case above? Describe your reasoning.
3. Describe the pathophysiology of shock condition above
4. What is the initial management in this patient?
SELF-ASSESSMENT:
1. Describe the complications following cardiogenic shock

2. Describe clinical data and additional examinations for confirming cardiogenic shock
3. Learn about quick diagnosis and initial stabilization of cardiogenic shock patients
4. Learn about treatment targets of cardiogenic shock

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LECTURE 26-27
ACUTE AND CHRONIC COR PULMONALE
dr. Luh Oliva Saraswati Suastika, Sp.JP(K), FIHA
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.

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 40-year old male came to the outpatient clinic with chief complaint of dyspnea on exercise
and bilateral ankle swelling since one month ago that worsen since three days before. He had
history of Tuberculosis infection three years ago and only took his TB therapy for 3 months and
he stopped taking his pills after that. On examination, his blood pressure was 100/60 mmHg,
pulse rate of 90 beats per minute, regular. There was vesicular sound in both lungs, but
decreased in the right side. There was also grade 2/6 systolic murmur in ICS IV left parasternal
line, bilateral ankle edema, minimal ascites and distended jugular vein. ECG showed sinus
rhythm of 90 beats per minute with tall P wave (amplitude of 3 mm) most prominent seen in the
lead II.
LEARNING TASK :
2. Which further examinations would you recommend to support your
diagnosis?
CASE 2:
A 30-year old man was brought to emergency room with chief complaint of sudden dyspnea
since 12 hours before admission. He had history of fever and cough since one day before. He
also had chest pain since two hours before admission. Initial examination included: blood
pressure 80/50 mmHg, heart rate 140x/min, respiratory rate 30x/min, and SaO2 86% initially that
increased to 95% with 15 lpm oxygen with non-rebreathing mask. Laboratory work was notable
for troponin-I of 0.172 (normal <0.04 ng/mL), NT-proBNP of 8603 (normal <125 pg/mL), D-dimer
level of 6083 μg/mL. His rapid covid-19 antigen was positive. His ECG showed sinus

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tachycardia with non specific T inversion in all leads, chest x-ray showed consolidation typical of
covid-19 infection in both lungs.
LEARNING TASK :
2. Which further (laboratory or imaging) examinations would you recommend to support
your diagnosis?
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 28
REHABILITATION ON CARDIOVASCULAR DISEASE PATIENTS

dr. Luh Kamiati, Sp.KFR
AIMS:
Describe cardiac rehabilitation on patient with Cardiovascular Disease.
LEARNING OUTCOME:
Able to describe cardiac rehabilitation in patient with cardiovascular disease
Cardiac rehabilitation in patient with cardiovascular disease
ABSTRACT:
Cardiac rehabilitation is the process which persons with cardiovascular disease (including but
not limited to patients with coronary heart disease [CHD]) undergo to restore and maintain their
optimal physiological, psychological, social, vocational, and emotional status. (American
Association of Cardiovascular and Pulmonary Rehabilitation–AACPR). The overall goal is to
improve and maintain a good level of cardiovascular fitness, thereby returning the individual to
as normal and productive of a life as possible. For those able to return to work: Return to
productive employment as soon as possible. ,Improve and maintain good cardiovascular fitness.
For those not able to return to work: Maintain as active of a life as possible. And Establish new
areas of interest to improve quality of life. Patient education and reduction of coronary risk factor
( modifiable or reversible factor ). Comprehensive cardiac rehabilitation should include
components are clinical evaluation, optimization of pharmacotherapy, physical exercise,
psychological rehabilitation, evaluation and reduction of CHD risk factors, lifestyle modification
and patient education .Outcome cardiac rehabilitation can decreased length of hospital stay,
more rapid and complete resumption of usual activities, increased self confident, fewer
readmission, less psychological distress and can improve quality of life. The phases of cardiac
rehabilitation are phase 1( inpatient period ),phase2 ( immediate out patient period ), phase 3 (
maintenance period).
1. American College of Sports Medicine. (2018). Guidlines for Exercise Testing and
Prescription Tenth Edition. Wolters Kluwer.
2. Curccurullo, S. J. (2015). Physical Medicine and Rehabilitation Board Review Third
Edition. New York: demons MEDICAL.
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.
LEARNING TASK:
1. Mention the definition of cardiovascular rehabilitation

2. Explain the objective of cardiovascular rehabilitation
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3. Mention the contraindication exercise therapy

4. Explain the benefit effect of exercise therapy
SELF DIRECTING LEARNING and SELF-ASSESSMENT

1. Mention the definition of cardiovascular rehabilitation
2. Explain the objective of cardiovascular rehabilitation
3. Mention the contraindication exercise therapy
4. Explain the benefit effect of exercise therapy

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LECTURE 29
PERIPHERAL ARTERY AND AORTIC DISEASES
DR. dr. I Nyoman Semadi SpB., SpBTKV(K)VE
AIMS:
Describe to diagnose and manage peripheral artery and aortic diseases
LEARNING OUTCOME:
1. Defining peripheral artery diseases (PAD) and aortic diseases

2. Describing the pathophysiology of PAD and aortic diseases
3. Examining PAD and aortic diseases, clinical and pathological aspect, risk factor,
epidemiology, imaging procedures and surgical management
● Pathogenesis of atherosclerosis and thrombosis.

● Risk factors for PAD and aortic diseases
● Clinical spectrum of peripheral artery diseases (PAD) and aortic diseases
● Interpret the imaging or laboratory result (or diagnostic tools) of peripheral artery
diseases (PAD) and aortic diseases
● Clinical diagnosis and complication
● Management and its prognosis of peripheral artery diseases (PAD) and aortic diseases
● Medical rehabilitation and its rehabilitation after limb amputation.
ABSTRACT:
Peripheral artery diseases (PAD) and aortic diseases were increases in the world, especially in
developed countries, as well as in Indonesia recent decade. The most important causes of
morbidity and mortality of the diseases due to atherosclerosis of the artery, and aorta. In
Indonesia, Peripheral artery diseases (PAD) is regarded as a leading cause of morbidity with
limb amputation and mortality due to septic condition. Arterial atherosclerosis, is 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 a foam cells, and lead to the
formation of ‘fatty streak’ and then ‘atheroma’.
The underlying pathophysiology in PAD is decreased blood flow to the part of limb, which is
usually secondary to plaque rupture and formation of thrombus. The plaque cap tears to expose
the lipid core to blood in the arterial lumen. This core area is highly thrombogenic, containing
tissue factor, fragments of collagen, and crystalline surfaces, which accelerates coagulation.
Initially the thrombus forms within the plaque which may then extend into the arterial lumen
causing partial or complete occlusion of the arterial lumen.

144
Peripheral Arterial Diseases (PAD) and aortic diseases are a life-threatening conditions that can
cause morbidity and mortality of patients at any time.
The spectrum of the syndrome of PAD and aortic diseases are diminished of blood flow to the
limb and distal organ. Ischemia due to hypoperfusion can makes limb threatening or dead limb.
Sometimes the the patient look good, but in severe condition the patient getting worse and died.
In this condition; the history, physical examination, procedural tool, laboratory examination will
helping the doctor to know the condition, Some procedure will be done to evaluate severity of
the diseases and prognosis.
Management of the diseases depend on limb threatening or dead limb. Surgery will help the
patient to release obstruction of the artery or arterial repair. But many of the patient got limb
amputation for any level. Medical therapy for any kind, usually use to reduced complication and
pain relief. Rehabilitation will giving to the patient to helping mobilization and good or normal
activity by the prosthesis.
1. Risk factors for PAD and Aortic diseases

2. Clinical spectrum of PAD and Aortic diseases
3. Interpret laboratory of PAD and Aortic diseases
4. Interpret diagnostic tools for PAD and Aortic diseases
5. Medical therapy and surgery or surgical intervention and its prognosis of PAD and Aortic
diseases
6. Medical rehabilitation and its rehabilitation.
References:
1. Rutherford’s Vascular Surgery, 8th edition.

2. Cronenwett J.L, Johnston K.W. 2014. Rutherford’s Vascular Surgery. 8th Ed.
3. Moore, Vascular and Endovascular Surgery. A Comprehensive Review, 8th edition.
4. Ehrin Armstrong. 2017. Endovascular Treatment of Peripheral Artery Disease and
Critical Limb Ischemia, An Issue of Interventional Cardiology Clinics
5. Ian Loftus , Robert Hinchliffe. 2018. Vascular and Endovascular Surgery : A Companion
th
to Specialist Surgical Practice, 6 edition
6. Ho JP, Cho KJ, Po P-J, Chu S-Y, Gopinathan A. 2016. Practical Guide to Surgical and
Endovascular Hemodialysis Access Management.
7. Morgan Mcmonagle , Matthew Stephenson. 2014. Vascular and Endovascular Surgery
at a Glance.
SCENARIO 1:
CASE :
A 55 year old male came to the emergency department complaining of right foot become bluish
and painful since 2 days ago. He got the pain as 8 on a scale of 1-10. He has no pulse on right
popliteal artery. His blood pressure is 120/82 mmHg. His pulse rate of right radial artery is 92
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beats-per-minute, irregularly. His pulse oximetry of left finger of foot 98% and no blood
saturation detected on right foot. He had uncontrolled hypertension since 3 years ago. He got
diabetic since 5 years ago, blood sugar level high and he is no smoking patient.
LEARNING TASK:

2. What is procedure of plan will you do?
3. What is your initial treatment and the definitive therapy for this case?
4. What is the could be a complication for this case?
SELF-ASSESSMENT:
1. Please explain the risk factors of PAD and Aortic diseases ?.

2. What are the complications of PAD ?
3. What is the treatment of choice in dead limb ?
4. Please describe the indication and the benefit of vascular repair !

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LECTURE 30
VENOUS DISEASES AND LYMPHATIC VESSEL
DR. Dr. I Nyoman Semadi SpB., SpBTKV(K)VE
AIMS:
Describe to diagnose and manage venous diseases and lymphatic vessel
LEARNING OUTCOME:
1. Defining venous diseases of peripheral vascular diseases

2. Describing the pathophysiology of venous diseases
3. Examining venous diseases, clinical and pathological aspect, risk factor, edpidemiology,
imaging procedures and surgical management
● Pathogenesis of venous diseases

● Risk factors for venous diseases
● Clinical spectrum of venous and lymphatic vessel diseases
● Interpret the imaging or laboratory result (or diagnostic tools) of venous diseases
● Clinical diagnosis and complication of venous diseases
● Management and its prognosis of venous diseases
● Medical treatment and its rehabilitation of venous diseases
ABSTRACT:
Venous diseases are very common affecting the women. But venous diseases can also affect
men, although epidemiologically not as much as women. Statistically, women experience
varicose veins 3 times more than men. The risk factors that have been identified as the cause of
varicose veins in the legs are: gender, hormonal, occupation, long standing position. No race
was found to have an effect on the presence of varicose veins. The pathology of varicose veins
in the legs is caused by the failure of the venous valves to hold the blood flowing upward in the
veins when standing up to the heart. So that in a standing state, the blood refluxes into the leg
veins below. The clinical picture that occurs is that the veins appear dilated, elongated, winding,
swollen feet can even experience tissue damage and skin changes in the form of ulcers that
bleed easily. These chronic ulcers continue to bleed for a while, and those who heal have
fibrotic skin and a whitish colour. The complaints experienced were swollen legs, tortuous veins,
heavy legs, ulcers that were difficult to heal and bleeding, unable to stand for long and were
painful. Physical examination can be performed in a standing position to see dilated leg veins in
the branches of a small vein called the rete reticular vein (telangiectasia), a medium vein
branch, namely the reticular vein (reticular varicose veins) and large veins under the skin
surface (the saphenous vein magna and the saphenous vein parva). ) are often called truncal
varicose veins. Examination with several medical devices such as Doppler Ultrasound,
Venography and others can show pathological abnormalities that occur, hemodynamics and the
presence of thrombosis.

147
Treatment of patients with varicose veins can be done conservatively at an early stage,
sclerotherapy can be done on telengiectasia, and reticular varicose veins, but sometimes
aggressive action is needed even surgery at an advanced stage. Surgical treatment can be
done with open surgery or endovascular ablation. Nowadays, many people use ablation
technique as a therapy option because there are no surgical scars. There are no reports that
cause fatal conditions / death due to varicose veins, but varicose veins are very annoying and
can be suffered throughout his life. It is necessary to use tight dressings or stockings to hold
refluxed blood in the legs, reduce swelling of the legs, prevent worsening. Rehabilitation by
exercising, riding a bicycle and swimming can provide optimal therapeutic results.

1. Risk factors for venous diseases
2. Clinical spectrum of venous diseases
3. Interpret diagnostic tools venous diseases
4. Medical therapy, surgery or surgical intervention and its prognosis of venous diseases 5.
Rehabilitation.
References:
1. Rutherford’s Vascular Surgery, 8th edition.

2. Cronenwett J.L, Johnston K.W. 2014. Rutherford’s Vascular Surgery. 8th Ed.
3. Moore, Vascular and Endovascular Surgery. A Comprehensive Review, 8th edition. 4. Ehrin
Armstrong. 2017. Endovascular Treatment of Peripheral Artery Disease and Critical Limb
Ischemia, An Issue of Interventional Cardiology Clinics
5. Ian Loftus , Robert Hinchliffe. 2018. Vascular and Endovascular Surgery : A Companion to
th
Specialist Surgical Practice, 6 edition
6. Ho JP, Cho KJ, Po P-J, Chu S-Y, Gopinathan A. 2016. Practical Guide to Surgical and
Endovascular Hemodialysis Access Management.
7. Morgan Mcmonagle , Matthew Stephenson. 2014. Vascular and Endovascular Surgery at a
Glance.
SCENARIO:
CASE :
A 43 year old, female came to the outpatient department, complaining of right leg become
swollen and pain since 3 weeks ago. She got venous enlargement and tortous on right leg.
Good pulse all of arteries, skin is worm and redness above the right ankle. Blood pressure level
is 110/82 mmHg. Patient pulse rate of left radial artery is 92 beats-per-minute, regularly. The
patient bring her doppler ultrasound examination of the right leg. She had hypertension since 1
years ago. Her job in supermart as attendant of any person who coming to the market.
LEARNING TASK:
1. What is the most likely diagnosis and write the grade of CVI?

148
2. What is the diagnosis of plan will you do?

3. What is your kind definitive therapy for this case?
4. What is could be a complication for this case?
SELF-ASSESSMENT:
1. Please explain the risk factors of venous diseases ?.

2. What are the complications of venous diseases ?
3. What is the treatment of choice in truncle venous diseases ?
4. Please describe the indication and the benefit of venous ablation !

149
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 score column that suitable with your judgment
Scor
e
No. Point being evaluated
1 2 3 4 5
A Topic
1. Introduction lecture
2 General anatomy, topography and surface

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

valves and great vessels
4 Embryology of the heart
5 Intrinsic conduction system and cardiac action

potential
6 Cardiac output and regulation of heart pumping
7 Myocardial perfusion
8 Blood pressure regulation
9 Factors that affect blood pressure
10 The formation of anomalies of the heart and

great vessels.
11 Antihypertensive drugs
12 Drugs used in angina pectoris
13 Antiarrhythmic drugs
14 Drugs for heart failure
15 Cardiac markers
16 Approach to patient with cardiovascular disease

150
17 Common peripheral vascular disease
18 Hypertension
19 Hypertensive urgency & emergency
20 Cardiac rehabilitation
21 Ischemic Heart Disease & ACS
22 Acute & chronic heart failure
23 Arrhythmias
24 Cor Pulmonale
25 Non-cyanotic & Cyanotic CHD&Acute Rheumatic

Fever
26 Pathologic Anatomy of Cardiovascular System
B Learning strategy
Lecture
1
2 Independent learning
3 Small group discussion
4 Practical
5 Case based learning
6 Problem based learning
7 Learning task
8 Self assessment
C Lecturer
1. Dr. dr. I.G.A. Widianti, M. Biomed
2. dr. I G.A. Dewi Ratnayanti, M.Biomed

151
3. Prof. Dr. dr. Putu Gede Adiatmika, M.For
4. Dr. dr. Made Muliarta, M.Kes
5. dr. Indira Vidiari Juhanna, M.Fis
6. Prof dr. I Gusti Made Aman, Sp.FK
7. dr. Agung Nova Mahendra, M.Sc
8. dr. Wayan Sumardika, M.Med.Ed., Ph.D
9. Dr. dr. Ni Wayan Winarti, Sp.PA (K
10. Prof. Dr. dr. AA Wiradewi Lestari, Sp.PK
11. Prof . Dr. dr. I Wayan Wita, Sp.JP(K), FIHA
12. dr Kadek Susila Surya Darma, Sp.JP(K), FIHA
13. Dr. dr. I Nyoman Semadi, Sp.B, Sp.BTKV
14. dr. I Made Putra Swi Antara, Sp.JP(K), FIHA
15 Dr.dr. I Made Junior Rina Artha, Sp.JP(K), FIHA
16 dr. A.A. Ayu Dwi Adelia Yasmin, Sp.JP (K), FIHA
17. dr. Luh Oliva Saraswati Suastika, Sp.JP(K),

FIHA
18. dr. Hendy Wirawan, M.Biomed, Sp.JP, FIHA
19. dr. I Nyoman Wiryawan, Sp.JP(K), FIHA
20. dr. Rani Paramita Iswari Maliawan, Sp.JP, FIHA
21. dr. Eka Guna Wijaya, Sp.A(K)
22. dr. Luh Kamiati, Sp.KFR
23. dr. Cyndiana Widia Dewi Sinardja, Sp.JP, FIHA
24. dr. I Dewa Gde Aditya Diprabawa, Sp.JP, FIHA
25. dr. Ni Made Dharma Laksmi, Sp.JP, FIHA

152
D Facilitator
1 Name of your group facilitator:
E Assessment
1 Time provide
2 Suitability of question with topic given
Score:
1. Bad or not suitable with expectation
2. Insufficient or inadequate with expectation
3. Sufficient or inadequate with expectation
4. Good or suitable with expectation
5. Excellent or exceed expectation

153
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

154
Blueprint Assessment
No. Topic Jumlah Soal
1. Anatomy of Cardiovascular System I and II 8
2. Histology of Cardiovascular System 4
3. Physiology of Cardiovascular System: Cardiac Action 4

Potential Intrinsic Conduction System
4. Physiology of Cardiovascular System: Cardiac output 4

regulation
5. Physiology of Cardiovascular System: Function of 4

blood vessels & regulation of blood flow
6. Pharmacology: Antihypertensive drugs 4
7. Pharmacology: 4
Drugs for ischemic heart disease and heart failure
8. Pharmacology: Antiarrhythmic drugs 4
9. Pathologic Anatomy of Cardiovascular System: 3

Pathological Aspect of Ischemic Heart Disease
10. Approach to patient with cardiovascular disease 3
11. Laboratory examination: cardiac markers 3
12. Chronic Heart Failure 3
13. Acute coronary syndrome (STEMI) 3
14. Acute coronary syndrome (NSTE-ACS) 3
15. Hypertension 4
16. Hypertensive Urgency & Emergency 3
17. Chronic coronary syndrome 3
18. Malignant arrhythmias 3
19. Basic arrhythmias 3
20. Anatomy 3: Embryology 3
21. Congenital heart disease and Acute Rheumatic Fever 3

155
22. Cardiorespiratory arrest 3
23. Acute Heart Failure 3
24. Shock (Cardiogenic) 3
25. Acute cor pulmonale 3
26. Chronic cor pulmonale 3
27. Cardiac Rehabilitation 3
28. Peripheral Vascular and Aortic Disease 3
29. Venous Disease and Lymphatic Vessel 3

156
REFERENCES
A. Student Standard References :

1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott &
Wilkins, 2007.
2. Sadler TW: Langman’s Medical Embryology, 10thed. 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 R S, 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 Practioners. 4th Ed. Philadelphia, Mosby. 2002.
9. McPhee, S.J., Papadakis, M.A., Current Medical Diagnosis & Treatment. 47th ed. New
York, Lange Mecical Book`s/The McGraw-Hill Companies, 2008.
B. Additional Student References :

1. A2: Moore KL, Dalley AF: Clinically Oriented Anatomy, 4th ed. Philadelphia Lippincott &
Wilkins, 1999.
2. H2: Fowcett DW, Jensh RP: Bloom & Fawcett’s Concise Histology, 2nd ed. London,
Arnold. 2002.

157

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STUDY GUIDE

STUDY GUIDE THE CARDIOVASCULAR SYSTEM AND DISORDERS

March, 1st 2023 until March, 20th 2023

MEDICAL FACULTY OF UDAYANA UNIVERSITY

STUDY GUIDE THE CARDIOVASCULAR SYSTEM AND DISORDERS

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

Visi Misi Program Studi Sarjana Kedokteran Fakultas Kedokteran

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

The cardiovascular block will focus on anatomy, histology and physiology of

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

GENERAL CURRICULUM OF CARDIOVASCULAR SYSTEM AND DISORDERS

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

NO DAFTAR PENYAKIT SESUAI SKDI 2012 TINGKAT KEMAMPUAN

GANGGUAN DAN KELAINAN PADA JANTUNG

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

RENCANA PEMBELAJARAN SEMESTER

20. dr. Eka Guna Wijaya, Sp.A(K)

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

Memahami berbagai macam jenis kelainan sistem CPMK-1 X X X X X

Mampu menjelaskan penanganan dari berbagai CPMK-5 X X X X X X

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

26. Acute cor pulmonale

3. Fowcett DW, Jensh RP: Bloom & Fawcett’s 3. https://drive.google.com/file/

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

Beban Waktu Online

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Penilaian Metode Instrumen

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9. Rina, I., Update in Anticoagulant Advance The

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Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

6. Burtis CA, Bruns DE: Tietz Fundamentals of

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Access Macedonian Journal of Medical

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3. James PA, et al. 2014 Evidence-Based

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2023

9. Ponikowski et al. ESC Guidelines for The

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Kriteria/Indikator ● Ketepatan dalam menjelaskan embriologi organ jantung

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7. Sadler TW: Langman’s Medical Embryology,

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