Please, refer to the ECG Skills Checklist

a clinician’s physical examination. In our opinion, the appreciation of cardiac anatomy and hemodynamics by bedside echocardiography makes a physician’s clinical evaluation, including physical examination, more relevant to the care of patients. For all physicians who care for patients with a cardiovascular problem, it is essential to know how echocardiographic images are obtained, what type of information echocardiography can provide, and how it should be used for management. Reference: 1. Mann, DL et all. Braunwald’s Heart Disease, 10 th ed. Philadelphia, Elsevier Saunders, 2015. p. 118-132 SELF DIRECTING LEARNING Basic knowledge that must be known: 1. ECG procedure. 2. ECG Interpretation . TRAINING TASK ECG Procedure : Preparation Group should choose one of their members to become a patient for the ECG examination. Ask the patient to lie down on the table. In turn, each the student should perform the ECG Examination; student should start from patient preparation, setup the machine, recording step, and obtaining the result. Instruction: 1. Prepare the patient for ECG examination. 2. Set the electrocardiography appropriately. 3. Place the leads in appropriate position. 4. Start the examination. 5. Obtain the result properly. 6. Explain and give information to the patient.

7. Please, refer to the ECG Skills Checklist

Independent Learning ECG Interpretation Each group will be provided with 10 pieces of electrocardiogram. Student should be familiar with the analyzing step for the ECGram. It is likely that student should start from checking the patient ID, analyze the rhythm, and identify whether there are any abnormality patterns. Student should also be familiar with the writing technique for the ECGram’s interpretation. Instruction 1. Analyze the ECGram given in group. You should refer to the handout given Analyzing the ECG for the interpretation 2. Write down the interpretation made for each ECGram. Discuss the result at wrap up session. Udayana University Faculty of Medicine, DME 43 Day 14 MODULE 14 dr. Lisnawati, Sp.Rad Dr. dr. Made Muliarta, M.Kes AIMS: 1. Able to evaluate and result chest x-rays 2. Able to workload measurement LEARNING OUTCOME: 1. Able to evaluate chest x-rays, including evaluation on heart, lung, diaphragm, skeleton and soft tissues 2. Able to result chest x-rays 3. Able to workload measurement CURRICULUM CONTENS: 1. Able to evaluate chest x-rays, including evaluation on heart, lung, diaphragm, skeleton and soft tissues 2. Able to result chest x-rays 3. Physiologic parameters during activity ABSTRACT I: Chest imaging is important evaluation that supports the diagnosis procedure. Student should be able to evaluate chest x-rays, including evaluation on heart, lung, diaphragm, skeleton and soft tissues. After evaluation, student should be able to write down the result in a given format. Some emergency case, need rapid chest x-rays evaluation. By this training we hope that the student will be able to do such important skill. There are steps in evaluating the chest x-rays, it is systematic steps. The student should be mastered. For cardiovascular system the chest imaging will be posterolateral, lateral, oblique projection. Student should evaluate the heart size; identify any enlargement, the condition of the lung – any edema, arterial and venous hypertension. The imaging investigation of the heart may be considered under the following: 1. Chest X-ray 2. Computed tomography CT-scan 3. Magnetic resonance imaging MRI 4. Echocardiography 5. Angiocardiography 6. Cardiac catheterization 7. Isotope scanning Chest X-ray remain the valuable cardiac investigation in clinical practice. Radiologic method used in the roentgen cardiac examination: 1. Posteroanterior projection, PAAP 2. Lateral projection 3. Right anterior oblique projection RAO 4. Left anterior oblique projection LAO Increase in cardiac size is the most consistent indication of cardiac disease ABSTRACT II: Physiologic parameters will be change during activity, such as heart rate, stroke volume, and cardiac output, blood pressure, peripheral resistance, and oxygen concentration. Some or those parameters could be measure with a very simple technique Udayana University Faculty of Medicine, DME 44 by calculating the arterial pulse, while others could only be measure using specific tools such as ergo meter, ECG, and treadmill. In practice, we could measure the cardiovascular functional capacity by using arterial pulse method, pulse meter, and ECG. Stress test or exercise test should be done for patient with heart disease in special place, in the laboratory. The purposes of stress test are to make quantification of heart disease suffered by the patient and to evaluate the functional capacity of the patient. The arterial pulse in rest condition will reflect the health status of the patient. The working arterial pulse will reflect the workload, and the recovery pulse rate will also reflect the fitness status of the patient. We will use the Karvonen Formula to calculate the heart rate limit on stress test. The ten pulse method is the method for calculating the arterial pulse during activity and recovery period. SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Able to evaluate chest x-rays, including evaluation on heart, lung, diaphragm, skeleton and soft tissues. 2. Physiologic parameters during activity. LEARNING TASK I: Chest imaging: Cardiovascular System Preparation There would be 10 set of light cast with a single x-ray film. The group should discuss the x-ray film and write down the result in a piece of A 4 paper. You should notice the time limit for each film. It would be at least 5 – 10 minutes of discussion for each film. Group should move to another x-rays film after complete the discussion and writing down the result. Instruction 1. Group should read the case available before evaluate the x-ray photo. What is the main complaint of the patient? 2. The group should evaluate the x-rays photo systematically 3. Write down the group result on a piece of A4 paper. 4. Move to another x-rays and you should repeat the step 1 till 3 each group should read all photos available. LEARNING TASK II: Home Work: Determine Your Workload by Arterial Pulse Evaluation Question: will be given after the lecture Student should work the task individually. Write down the answer on a piece of A4 paper and make sure you put your name and NIM on it. Collect your work at Lab Bersama on Monday, May 21 st , before 11 am Standard References : 1. Roentgen Signs in Diagnostic Imaging Isadore Meschan Udayana University Faculty of Medicine, DME 45 Day 15 MODULE 15 Prof. Dr. dr. Wiryana, Sp.An KIC Dr. IGN. Mahaalit Aribawa, SpAn.KAR AIMS: 1. Able to skill routine clinical procedure: Intravenous Line IV line 2. Able to LEARNING OUTCOME: 1. Able to two skills should be trained : IV cannulation and venipuncture.. CURRICULUM CONTENS: 1. Technique of venipucture 2. Aseptic procedure . ABSTRACT : Doctor should be able to draw blood in field setting as a part of disease investigation and therapy. Appropriate equipment and supplies should including the following gloves, aseptic kit, bandage, tourniquet, vacutainer tubes or spuit and the container. The complete technique of venipucture is contained in the Venipucture Evaluation Checklist. It will cover the skills in preparation of the doctor and the patient, aseptic procedure, the preparation of the kit, communicate the procedure to the patient, the patient preparation, the insertion technique of the needle, the blood collection, evaluation for any bleeding, and cleaning the work area after the procedure. The checklist will vary from one to another, you should use the checklist as aide- memoir or reminder of the element skills to be done. Basically there would be four main steps in doing the venipuncture and IV line cannulation. It would be explain the procedure, prepare the equipment and positioning the patient, select appropriate site, use standard precaution, and reach the goal obtain adequate specimen and a good technique for cannulation. SELF DIRECTING LEARNING Basic knowledge that must be known: 1. The complete technique of venipucture 2. Aseptic procedure 3. The preparation of the kit 4. Communicate the procedure to the patient 5. The patient preparation 6. The insertion technique of the needle, the blood collection 7. Evaluation for any bleeding 8. Cleaning the work area after the procedure Training Task Venipuncture and IV Line Procedure Preparation Udayana University Faculty of Medicine, DME 46 We will provide the student with Multipurpose Injection Arm and IV line manequin needed for IV line procedure training. It would be at least one mannequin for each two groups. Groups should prepare one infusion set, ringer lactate infusion fluid, antiseptic set, and tape. Each student should bring their own IV needle G-21, syringe 3 cc, and bring glove for antiseptic procedure. Instruction 1. There would be two skills should be trained in this session, IV cannulation and venipuncture. 2. You have to prepare the set for the procedures, prepare the manequin, needle, the infussion set, and the infussion fluid. 3. Demonstrate how will you explain the procedure to the patient, the technique and the complication might be happened. 4. Demonstrate the technique for IV cannulation and venipuncture. Please notice the position of your finger, the angle, and how to evaluate whether the needle inserted properly. 5. Refer to the checklists Venipucture and IV Cannulation for any details 6. Ask any comment and score for ypur perfomance from your groups based on the checlist MODULE 16 dr. Eka Guna Wijaya, Sp.A AIMS: 1. Describe Non-cyanotic and Cyanotic Congenital Heart Diseases 2. Describe to diagnose and manage Acute Rheumatic Fever LEARNING OUTCOME: 1. Can describe to diagnose and manage Non-cyanotic and Cyanotic Congenital Heart Diseases 2. Can describe to diagnose and manage Cyanotic Congenital Heart Diseases 3. Can describe to diagnose and manage Acute Rheumatic Fever CURRICULUM CONTENS: 1. Fetal-transitional circulations 2. To diagnose and manage Non-cyanotic Congenital Heart Diseases and its complications 3. To diagnose and manage Cyanotic Congenital Heart Diseases and its complications 4. Interpret diagnostic tools of Congenital Heart Diseases 5. The health education and prognosis of Congenital Heart Diseases 6. Interpret diagnostic tool of Acute Rheumatic Fever 7. Management of Acute Rheumatic Fever and its complications 8. Prevention and rehabilitation of Acute Rheumatic Fever 9. Health education and prognosis of Acute Rheumatic Fever Udayana University Faculty of Medicine, DME 47 Day 16 ABSTRACT I: Congenital Heart Disease CHD is congenital malformation of the heart including great vessel that was occur since the baby was delivered. A lot of kind of CHD has been recognized but ventricular septal defect, atrial septal defect, patent ductus arteriosus were the most common finding. Tetralogy of Fallot is the commonest one of cyanotic CHD. Obstructive lesions pulmonary and aortic stenosis, coarctatio aorta, transposition of great artery, truncus arteriosus, ebstein anomaly, etc were relatively rare cases. CHD is really a dynamic disease. In mild and simple lesion such as VSD and ASD were usually asymptomatic and half of those may undergoing spontaneous closure after two years old. Contrassly in severe cases, sign of heart failure, deep cyanosis, acidosis and other sign express of critical condition may exist in few hours after birth. Severe pulmonary hypertension is serious longterm complication of large left-to- right shunt. Eisenmenger syndrome may slowly develop when pulmonary artery pressure higher than systemic pressure. The patient appeared cyanotic who previously non cyanosis. Left-to-right shunt hemodynamically characterized by increase of pulmonary blood flow but inversely decrease of systemic blood flow. Under these circumstances may lead to congestive heart failure due to overcompensated of symphatic and humoral stimulation. ToF may characterize by four anatomical abnormalities: VSD, overriding of aorta, right ventricular hypertrophy, and pulmonary stenosis. Right-to-left shunting was seen in ventricular level. Severity of cyanosis in ToF depends directly on severity of pulmonary stenosis. Growth failure is the commonest finding of significant CHD. Screening should be done in patient with failure of growth and development and certain syndromes to evaluate more carefully in other to be sure is the patient having or not having of CHD. Diagnosis investigation of CHD was the following: history taking antenatal, natal, and post natal, physical examination, chest radiograph, and ECG. Echocardiography is needed to evaluate more detail of anatomical defect and cardiac function. Comprehenship management should be performed in nursing the patient. Dental hygiene, nutritional support, psychological aspect was a part of integrated management beyond of the medical and surgical intervention. ABSTRACT II: Valvular Heart Disease VHD is largely variated disease due to anomaly or damaged of one or more cardiac valves. Anomaly most likely congenital in origin include: Tricuspid Atresia, Tricuspid Steno- insuficiency Ebstein anomaly mitral stenosis, mitral insufficiency, pulmonary or aortic stenosisatresia. The most common of VHD is Rheumatic Heart Disease and Mitral Valve Prolaps. Diagnosis investigation like other disease: History taking, physical examination, chest X-rays, ECG, and other specific laboratory examination. Echocardiography is routine procedure to evaluate more detail anatomical abnormality, severity and cardiac function. Catheterization is needed when valvuloplasty was indicated. The origin and characteristic of the first and the second heart sound should be deeply understand before indentified many kind of pathological heart murmur. Location, timing, quality, intensity, and transmission of heart murmur is the basic auscultative modality to investigate more advance of specific valvular heart disease. Management of VHD medically include: digitalis, diuretics, vasodilator, anti thrombotic agent, endocarditis prophylaxis, dental hygiene and nutritional support. Udayana University Faculty of Medicine, DME 48 Rheumatic fever Rheumatic Heart Disease was agreed worldwide as an autoimmune disease. Tissue hospes has mimic antigenic structure with certain strain of beta hemolytic streptococcus group a who was infected in the pharing. There is basic pathogenesis concept in development tissue injury damage of succeptible host. When autoantibody was generated in significant number, cross reaction where streptococci causing agent were killed naturally by humoral and cellular antibody but on the other hand tissue damage of the hospes was also happen because it was recognized as antigen. Carditis and arthritis were the most frequent of major symptom of RFRHD. Jones criteria was established as definite diagnosis of rheumatic fever. Evolution was made from the beginning in 1944 and then revised in 1956, modified in 1965, update in 1992, finally recommendation of WHO in 2002. Bed rest, eradication of causing agent, inflammatory drug and secondary prophylaxis were the basic management of Rheumatic Fever Rheumatic Heart Disease Standard References: 1. Park, MK. Pediatric Cardiology for Practioners. 4 th Ed. Philadelphia, Mosby. 2002. p 129-144, 185-189, 304-310, 311-318 SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Fetal-transitional circulations 2. Criteria diagnose and manage of the Non-cyanotic Congenital Heart Diseases and its complications 3. Criteria diagnose and manage of the Cyanotic Congenital Heart Diseases and its complications 4. The health education and prognosis of Congenital Heart Diseases 5. Interpret diagnostic tool of Acute Rheumatic Fever 6. Management of Acute Rheumatic Fever and its complications 7. Prevention and rehabilitation of Acute Rheumatic Fever 8. Health education and prognosis of Acute Rheumatic Fever. SCENARIO; CASE 1: Putu, 2 years old girl was came to pediatric cardiology clinic with her parent with the main complain of persistent cough and slight dyspneu. Physical examination : HR : 128 xmin, RR : 44 xmin, BW : 9 kg. Positive precordial bulging, cardiac impulse was displaced to caudolateral associated with lifting. Heart murmur was heard systolic and diastolic phase at upper left parasternal border. LEARNING TASK : 1. How to know that patient having continuous murmur. 2. What is the probable complete diagnosis clinically. 3. Is the patient should be given indometasin. 4. What is the best diagnostic tool in this patient. 5. What kind of treatment have been recommended. CASE 2: Made, 9 months old baby was referred by GP to pediatric clinic of cardiology due to cyanosis. Physical examination looked at the baby having cyanotic at the mouth until the tongue. Cyanotic was also seen at the fingers associated with clubbing. When Udayana University Faculty of Medicine, DME 49 auscultation just to be done, the baby suddenly hard crying, uncontrolled for long time and then hyperapneu and lethargy. LEARNING TASK: 1. What is may be happen to the baby. 2. What must you be done immediately to overcame this condition. On auscultation, ejection systolic murmur was heard at the upper left parasternal border line with almost there is no heard of P2. 3. What is the most probable disease may be occur to the baby 4. What does you expected from chest X-ray examination. 5. When phlebotomy should be perform base on routine blood examination 6. Mention a lot of complication may be develop and what is the most hazard 7. When iron preparation should be given in this patient. CASE 3: Komang, 10 years old boy come with his parent to pediatric clinic of cardiology with the main complain of dyspneu on exertion. Coughing and palpitation were also present. Physical examination revealed: Malnourish boy with slight anemic. Pulse rate : 108 x min, RR : 24 xmin, body temperature 38 degree C. Hyperdinamic of precordium with displacement of apical impulse caudolaterally with lifting positive. Holosystolic murmur was heard at cardiac apex referred to axilla. Diastolic murmur was also heard at upper right parasternal border. LEARNING TASK 1. Base on those data, what is the most probable diagnosis. 2. What is other history and laboratory examination may be needed to support the diagnosis. 3. Which of cardiac valve were involve in this patient. 4. How about chest X ray and blood pressure examination. 5. How to manage in short and long time period. SELF ASSESSMENT 1. Please describe haemodynamic change in PDA. 2. Patten of blood pressure and pulse in PDA. 3. How the chest X-ray in patient with PDA. 4. Is in large PDA you can heard diastolic flow murmur at the apex cordis? Can you explain about that? 5. Please mention complication of PDA. 6. Please mention a few risk factor in development of cyanotic spell. 7. Can you explain the phatomecanism of cyanotic spell? 8. Please mention differential diagnosis of cyanotic CHD base on increase and decrease of pulmonary blood flow. 9. Please explain what do you know about pheriperal and central cyanosis. 10. Explain phatomecanism oh tissue injury in acute rheumatic fever 11. Mention etiology, antigenic structure and it’s cellular product. 12. Please mention mayor and minor manifestation of rheumatic fever. 13. Please mention detail pathology of rheumatic fever. Udayana University Faculty of Medicine, DME 50 Day 17 MODULE 17 dr. I Made Junior Rina Artha, Sp JP K, FIHA AIMS: Describeto diagnose and manage Ischaemic Heart Disease IHD and Acute Coronary Syndromes ACS LEARNING OUTCOME: 1. Can describe to diagnose and manage Ischaemic Heart Disease IHD 2. Can describe to diagnose and manage Acute Coronary Syndromes ACS CURRICULUM CONTENS: 1. Pathogenesis of atherothrombosis 2. Risk factors of Ischaemic Heart Disease and Acute Coronary Syndromes 3. Clinical spectrum of Ischaemic Heart Disease and Acute Coronary Syndromes 4. Interpret laboratory of Acute Coronary Syndromes 5. Interpret diagnostic tools of Ischaemic Heart Disease and Acute Coronary Syndromes 6. Management and its prognosis of Ischaemic Heart Disease and Acute Coronary Syndromes 7. Post ACS medical rehabilitation and its rehabilitations ABSTRACT: Coronary artery disease CAD is one of the most important causes of premature death in the developed world, as well in Indonesia. CAD is regarded as a leading cause of mortality in Province of East Java and Bali, based on the National Household Health Survey in 1995. Its proportion was reported to be 24.5 of all cause mortality, and its proportion has been significantly increasing since the last 10 years in Indonesia SKRT, 1995. Coronary atherosclerosis, the basic pathogenesis of this disease, is associated with many risk factors such as cigarette smoking, hyperlipidemia, family history, hypertension and diabetes mellitus. Atherosclerosis is a chronic process initiated by lipid deposition and vascular wall injury that causes increased endothelial permeability, inflammation and recruitment of monocytes and leucocytes. These cells accumulate oxidized lipids to form macrophages and foam cells, and lead to the formation of ‘fatty streak’ and then ‘atheroma’. Eventually, all these process becomes ‘atherosclerotic plaque’. Chronic stable angina is caused by atheroma obstructing coronary artery lumen by more than 70. Acute coronary syndromes ACS = unstable angina and myocardial infarction arise when atherosclerotic plaque becomes unstable and either ruptures or are eroded. The complicated plaque is a nidus for thrombus formation and may lead to vessel occlusion. Stable coronary artery disease is generally characterized by episodes of reversible myocardial demandsupply mismatch, related to ischaemia or hypoxia, which are usually inducible by exercise, emotion or other stress and reproducible—but, which may also be occurring spontaneously. Such episodes of ischaemiahypoxia are commonly associated with transient chest discomfort angina pectoris. SCAD also includes the stabilized, often asymptomatic, phases that follow an ACS. A careful history remains the cornerstone of the diagnosis of chest pain. The characteristics of discomfort-related to myocardial ischaemia angina pectoris may be Udayana University Faculty of Medicine, DME 51 divided into four categories: location, character, duration and relationship to exertion and other exacerbating or relieving factors. The discomfort caused by myocardial ischaemia is usually located in the chest, near the sternum, but may be felt anywhere from the epigastrium to the lower jaw or teeth, between the shoulder blades or in either arm to the wrist and fingers. The discomfort is often described as pressure, tightness or heaviness; sometimes strangling, constricting or burning. The duration of the discomfort is brief—no more than 10 min in the majority of cases and more commonly even minutes or less— but chest pain lasting for seconds is unlikely to be due to angina. An important characteristic is the relationship to exercise, specific activities or emotional stress. Symptoms classically appear or become more severe with increased levels of exertionand rapidly disappear within a few minutes when these causal factors abate. Basic first-line testing in patients with suspected SCAD includes standard laboratory biochemical testing, a resting ECG, possibly ambulatoryECGmonitoring if there is clinical suspicion that symptoms may be associated with a paroxysmalarrhythmia, resting echocardiography and, in selected patients, a chest X-ray CXR. Such testing can be done on an outpatient basis. The aim of the management of SCAD is to reduce symptoms and improve prognosis. The management of CAD patients encompasses lifestyle modification, control of CAD risk factors, evidence-based pharmacological therapy and patient education. The acute coronary syndromes encompass a spectrum of unstable coronary artery disease that includes unstable angina and myocardial infarction ST segment elevation myocardial infarction and non-ST segment elevation myocardial infarction. The history, electrocardiogram, and cardiac markers determine the presence and the type of ACS. Patients with an acute coronary syndrome usually present with prolonged anginal sympoms that occur at rest. Patients with persistent chest pain lasting more than 20 minutes should seek urgent medical attention because of the likelihood of myocardial amage an dinfarction. The electrocardiogram will often show evidence of ischaemia that classically takes the form of ST segment shifts, T-wave inversion, and new bundle branch block. Cardiac enzymes and markers are the principal determinans that define the category of the acute coronary syndrome. Patients should be given analgesia, oxygen and transferred to intensive coronary care unit. Treatments consist of aspirin, clopidogrel, low- molecular weight heparin, beta-blockers and intravenous nitrate infusion. Where available, percutaneous coronary intervention PCI is the treatment of choice. Thrombolytic therapy is an effective alternative. SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Risk factors of Ischaemic Heart Disease and Acute Coronary Syndromes 2. Clinical spectrum of Ischaemic Heart Disease and Acute Coronary Syndromes 3. Interpret laboratory of Acute Coronary Syndromes 4. Interpret diagnostic tools of Ischaemic Heart Disease and Acute Coronary Syndromes 5. Management and its prognosis of Ischaemic Heart Disease and Acute Coronary Syndromes 6. Post ACS medical rehabilitation and its rehabilitations References: 1. Mann, DL et all. Braunwald’s Heart Disease, 10 th ed. Philadelphia, Elsevier Saunders, 2015. 2. Montalescot G. Et al. 2013 ESC Guidelines on The Management of Stable Coronary Artery Disease. Eur H J. 2013:34,2949-3003 SCENARIO 1: Udayana University Faculty of Medicine, DME 52 CASE Acute Coronary syndrome: A 56-year old male, came to Emergency Room due to severe chest pain. The pain was felt since 6-hours prior to admission,it was heavy sensation and radiating to left arm and jaw, not relieved by resting, accompanied by shortness of breathsince 5 hours PTA that is relieved by sitting position. He is suffered from uncontrolled DM and Hypertension since 7 years ago. He appeared severely ill and dyspnea. The blood pressure was 17090 mmHg; pulse rate was 110 beats per-minute, regular. There was rales on both lung fields ECG showed : LEARNING TASK : 1. What is the most likely diagnosis? 2. What the next procedure do you plan? 3. What is your initial treatment? 4. What is the definitive therapy for this case? 5. What is the could be complication for this case? SELF-ASSESSMENT : 1. Please explain the risk factors of ischaemic heart disease 2. What are the complications of acute myocardial infarction 3. What is the treatment of choice in ST-elevation myocardial infarction? 4. Please describe the indication and the benefit of CABG coronary artery by-pass graft? SCENARIO 2: CASE ischemic Heart Disease : A 60-year old female, came to policlinic.She complaint of chest discomfort since 2 month ago. The discomfort is usually described as tightness. Symptoms deteriorate during walking up an incline and rapidly disappear within few minutes. She has history of dyslipidemia and hypertension since 3 year ago. The blood pressure was 15090 mmHg; pulse rate was 90 beats per-minute, regular. Normal physical examination, ECG Normal sinus Rhythm. LEARNING TASK : 1. What the next procedure do you plan? 2. What is your initial treatment? 3. What is the differential diagnosis for this case? Udayana University Faculty of Medicine, DME 53 SELF-ASSESSMENT : 1. Please explain the risk factors of ischemic heart disease 2. Please describe laboratory recommendation for assessment stable angina? 3. What is the non invasive and invasive recommendation for assessment stable angina? 4. What is the treatment of choice for Stable angina pectoris? 5. Please describe the indication and the benefit of revascularization? MODULE MODULE 18 dr. Ni Putu Ekawati, SpPA Prof dr. I Gusti Made Aman, SpFK AIMS: 1. Describe the pathogenesis of atherosclerosis related to Ischemic Heart Disease IHD 2. Describe drug used in Angina Pectoris LEARNING OUTCOME: 1. Able to explain the pathogenesis of atherosclerosis 2. Able to describe the morphology of atherosclerosis 3. Able to explain the pathogenesis of IHD 4. Able to describe the morphology of myocardial infarction MI 5. Able to describe drug used in Angina Pectoris CURRICULUM CONTENT 1. Pathogenesis of atherosclerosis 2. Morphology of atherosclerosis 3. Pathogenesis of IHD 4. Morphology of MI 5. Drug used in Angina Pectoris ABSTRACT I: Angina pectoris s characteristically describes as a retrosternal chest discomfort constricting, pressing or tight that has a close relation to physical or emotional stress, and is rapidly relieved with rest or nitrates. It is commonly, the consequence of obstructive atheromatous coronary artery disease. The retrosternal discomfort in angina pectoris is caused by myocardial ischemia. The myocardial ischemia is due to an imbalance between myocardial oxygen supply and demand. Decreased myocardial oxygen supply can result from the presence of flow- limiting chronic stenoses in atherosclerotic coronary arteries, or can occur acutely as a result of vasospasm or thrombosis. The increased in myocardial oxygen demand may arise as a result of physical exertion or emotional stress, the two common precipitating factors for angina. Myocardial oxygen demand is principally determined by heart rate, ventricular contractility, and by myocardial wall tension, the latter in turn is influenced by cardiac Udayana University Faculty of Medicine, DME 54 Day 18 preload ventricular filling pressure, ventricular volume, contractility and afterload. Drugs that ameliorate or prevent angina either decrease myocardial demand by slowing heart rate, decreasing ventricular contractility, preload and afterload or increase myocardial blood supply by inducing epicardial coronary artery vasodilatation or preventing epicardial coronary artery vasoconstriction. Three classes of drugs are used in the treatment of angina : nitrates, betablockers and calcium channel blockers. ABSTRACT II: Ischemic Heart Disease IHD is the generic designation for a group of pathophysiologically related syndromes resulting from myocardial ischemia. In more than 90 of cases, the cause of myocardial ischemia is reduced blood flow due to obstructive atherosclerotic lesions in the coronary arteries. Atherosclerosis is characterized by intimal lesions called atheromas also called atheromatous or atherosclerotic plaques that protrude into vessel lumens. Besides mechanically obstructing blood flow, atherosclerotic plaques can rupture, leading to catastrophic vessel thrombosis; plaques also weaken the underlying media and thereby lead to aneurysm formation. Historically, there have been two dominant hypotheses of atherogenesis: one emphasizes intimal cellular proliferation, while the other focuses on the repetitive formation and organization of thrombi. The contemporary view of atherogenesis incorporates elements of both theories and also integrates the risk factors constitutional risk factors, modifiable risk factors and additional risk factors. The key processes in atherosclerosis are intimal thickening and lipid accumulation. Atheromatous plaques impinge on the lumen of the artery and grossly appear white to yellow; superimposed thrombus over ulcerated plaques is red-brown. Plaques vary from 0.3 to 1.5 cm in diameter but can coalesce to form larger masses. Atherosclerotic plaques have three principal components: 1 cells, including smooth muscle cells, macrophages, and T cells; 2 ECM, including collagen, elastic fibers, and proteoglycans; and 3 intracellular and extracellular lipid. Chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries, and variable degrees of superimposed acute plaque change, thrombosis, and vasospasm will lead to vary clinical coronary syndromes such as angina, myocardial infarction MI, and even sudden death. Some also fall into chronic ischemic heart disease state. The distribution of myocardial necrosis correlates with the location of the decreased perfusion. Most myocardial infarcts are transmural, in which the ischemic necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery. In contrast, a subendocardial nontransmural infarct constitutes an area of ischemic necrosis limited to the inner one third to one half of the ventricular wall. The gross and microscopic appearance of an infarct depends on the duration of survival of the patient following the MI. Areas of damage undergo a progressive sequence of morphologic changes that consist of typical ischemic coagulative necrosis the predominant mechanism of cell death in MI, although apoptosis may also occur, followed by inflammation and repair that closely parallels tissue responses to injury at other sites. Standard References : 1. McPhee SJ, Papadakis MA. Current Medical Diagnosis Treatment. 47 th ed. New York: Lange Mecical Book`sThe McGraw-Hill Companies, 2008.p. 300-324. 2. Kumar V, Cotran R S, Robbins SL: Robbin’s Basic Pathology, 7 th ed. Philadelphia, Saunders, 2003. p. 328 – 338; 363 – 372. Udayana University Faculty of Medicine, DME 55 3. Trevor AJ, Katzung BG, Masters SB: Katzung Trevor’s Pharmacology, 7 th ed. New York, McGraw-HillLange., 2005. p 105-113 SELF DIRECTING LEARNING 1. Pathogenesis of atherosclerosis 2. Morphology of atherosclerosis macroscopy and microscopy 3. Relation between atherosclerosis and IHD 4. Morphology of MI macroscopy and microscopy 5. Principles of anti angina pectoris therapy. 6. Classification of anti angina pectoris drugs 7. Important pharmacokinetic properties of anti angina pectoris drugs. 8. Mechanism of actions of anti angina pectoris drugs. 9. Important adverse effects of anti angina pectoris drugs. SCENARIO: CASE I: A 55 year old male experiences crushing substernal chest pain on arriving at work in the morning. Over the next few hours the pain persists and begins to radiate to his left arm. He becomes diaphoretic and short of breath. He goes to emergency unit immediately. Laboratory and ECG findings are consistent with myocardial infarction. LEARNING TASK I: 1. Important adverse effects of anti angina pectoris drugs 2. Describe the morphology gross and microscopy of MI 3. Explain the morphologic differences between angina and MI 4. Explain the correlation between atherosclerosis and IHD 5. Explain about the pathogenesis of atherosclerosis Mention it risk factors 6. Describe the morphology gross and microscopy of fatty streak and atherosclerotic plaque LEARNING TASK II: 1. Describe the principles of anti angina pectoris therapy. 2. Describe the classification of anti angina pectoris drugs 3. Describe the important pharmacokinetic properties of anti angina pectoris drugs. 4. Describe the mechanism of actions of anti angina pectoris drugs. SELF ASSESSMENT: 1. Describe the morphology of 3 days old MI 2. Mention risk factors of IHD 3. Mention the main component of atherosclerotic plaque 4. Describe the principles of anti angina pectoris therapy. 5. Describe the classification of anti angina pectoris drugs 6. Describe the mechanism of actions and the important pharmacokinetic properties of anti angina pectoris drugs Udayana University Faculty of Medicine, DME 56 Day 19 MODULE 19 dr. I Made Putra Swi Antara, SpJP, FIHA Prof dr. I Gusti Made Aman, SpFK AIMS: Able to diagnose and manage Arrhythmias LEARNING OUTCOME: 1. Can describe to diagnose Arrhythmias 2. Can describe manage Arrhythmias CURRICULUM CONTENS: 1. Etiology and pathophysiology of Arrhythmias 2. Clinical approach of Arrhythmias 3. Treatment of Arrhythmias 4. Prognosis of Arrhythmias ABSTRACT I: An arrhythmia or dysrhythmia is a disturbance of the electrical rhythm of the heart. Most arrhythmias are benign and are only troublesome because of the symptoms they cause. However, some arrhythmias are dangerous and require treatment to prevent haemodynamic compromise or cardiac arrest, and it is important to recognize these. In the management of clinical arrhythmias, the physician must evaluate and treat the whole patient, not just the rhythm disturbance. Some arrhythmias are hazardous to the patient, regardless of the clinical setting e.g., ventricular fibrillation, VF, whereas others are hazardous because of the clinical setting e.g., rapidly conducted atrial fibrillation in a patient with severe coronary artery stenoses. Patients with cardiac rhythm disturbances can present with various complaints, but symptoms such as palpitations, syncope, presyncope, or congestive heart failure commonly cause them to seek a physician’s help. Their awareness of palpitations and of a regular or irregular cardiac rhythm varies greatly. A careful drug and dietary history should also be sought; some nasal decongestants can provoke tachycardia episodes, whereas betaadrenergic blocking eye drops for treatment of glaucoma can drain into tear ducts, be absorbed systemically, and precipitate syncope caused by bradycardia. Examination of the patient during a symptomatic episode can be revealing. Clearly, heart rate and blood pressure are key measurements to make. Assessment of the jugular venous pressure and waveform can disclose the rapid oscillations of atrial flutter or “cannon” A waves indicative of contraction of the right atrium against a closed tricuspid valve in patients with AV dissociation in disorders such as complete heart block or VT. Variations in the intensity of the first heart sound and systolic blood pressure have the same implications. The ECG is the primary tool in arrhythmia analysis; an EPS, in which intracardiac catheters are used to record activity from several regions of the heart at one time, is more definitive. Initially, a 12-lead ECG is recorded. In addition, a long continuous recording with use of the lead that shows distinct P waves is often helpful for closer analysis; most commonly, this is one of the inferior leads 2, 3, aVF, V1, or aVR. The ECG obtained during an episode of arrhythmia may be diagnostic by itself, obviating the need for further diagnostic testing The following additional tests can be used to evaluate patients who have cardiac arrhythmias. The physician’s choice of which test to use depends on the clinical circumstances. For example, a patient with multiple daily episodes of presyncope Udayana University Faculty of Medicine, DME 57 is likely to have an event recorded on a 24-hour ambulatory electrocardiographic Holter monitor, whereas in a patient who complains of infrequent anxiety- or exercise-induced palpitations, exercise stress testing may be more likely to provide a diagnosis. Normal sinus rhythm is arbitrarily limited to impulse formation beginning in the sinus node at rates between 60 and 100 beatsmin. Infants and children generally have faster heart rates than adults do, both at rest and during exercise. Rates below 50 beatsmin are considered to be bradycardia, and rates above 100 beatsmin are considered to be tachycardia. Tachyarrhythmias are broadly characterized as supraventricular tachycardia SVT, defined as a tachycardia in which the driving circuit or focus originates, at least in part, in tissue above the level of the ventricle i.e., sinus node, atria, AV node, or His bundle, and ventricular tachycardia VT, defined as a tachycardia in which the driving circuit or focus solely originates in ventricular tissue or Purkinje fibers. Because of differences in prognosis and management, the distinction between SVT and VT is critical early in the acute management of a tachyarrhythmia. In general with the exception of idiopathic VT, VT often carries a much graver prognosis, usually implies the presence of significant heart disease, results in more profound hemodynamic compromise, and therefore requires immediate attention and measures to revert to sinus rhythm. On the other hand, SVT is usually not lethal and often does not result in hemodynamic collapse; therefore, more conservative measures can be applied initially to convert to sinus rhythm. Supraventricular tachycardia SVTs are almost benign. Initial management of SVT comprises the Valsalva manuver, carotid sinus pressure or administration of intra venous adenosine. Beta-blocker and verapamil reduce symptoms significantly in two-thirds of patients with recurrent SVT. Radio frequency ablation should be considered for all patients with frequent SVT Tachycardia in an adult is defined as a rate of 100 beatsmin. During sinus tachycardia, the sinus node exhibits a discharge frequency between 100 and 180 beatsmin, 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 beatsmin at 20 years to less than 140 beatsmin at 80 years. Premature complexes are among the most common causes of an irregular pulse. They can originate from any area in the heart—most frequently from the ventricles, less often from the atria and the AV junctional area, and rarely from the sinus node. Although premature complexes arise commonly in normal hearts, they are more often associated with structural heart disease and increase in frequency with age. The diagnosis of premature atrial complexes PACs is made on the ECG by the presence of a premature P wave with a PR interval of 120 milliseconds except in Wolff- Parkinson-White syndrome, in which case the PR interval is usually shorter than 120 milliseconds. Although the contour of a premature P wave can resemble that of a normal sinus P wave, it generally differs. Atrial fibrillation AF is a supraventricular arrhythmia characterized electrocardiographically by low-amplitude baseline oscillations fibrillatory or f waves and an irregularly irregular ventricular rhythm. AF is the most common arrhythmia treated in clinical practice and the most common arrhythmia for which patients are hospitalized; approximately 33 of arrhythmia-related hospitalizations are for AF. The symptoms of AF 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 beatsmin, although it is occasionally slower, particularly when the patient is treated with antiarrhythmic drugs, which can reduce the rate to about 200 beatsmin. In typical atrial flutter, the ECG reveals identically recurring, regular, sawtooth flutter waves and evidence of continual electrical activity lack of an isoelectric interval between flutter waves, often best visualized in leads II, III, aVF, or V1. Management of atrial fibrillation and flutter is the rate control strategy. It is directed at limiting the ventricular response to atrial fibrillation by using AV node blocking drugs, Udayana University Faculty of Medicine, DME 58 such as digoxin, beta-blockers and verapamil. Cardioversion and anti-arrhythmic drugs are used to restore and maintain sinus rhythm. Anti-coagulation with warfarin should be considered for patients with atrial fibrillation and risk factors for stroke. The prevalence of premature ventricular complexes increases with age; they are associated with male gender and a reduced serum potassium concentration. Symptoms of palpitations or discomfort in the neck or chest can result because of the greater than normal contractile force of the postextrasystolic beat or the feeling that the heart has stopped during the long pause after the premature complex. A PVC is characterized by the premature occurrence of a QRS complex that is abnormal in shape and has a duration usually exceeding the dominant QRS complex, generally longer than 120 milliseconds. In most patients, PVCs occurring as single PVCs, bigeminy, or trigeminy but excluding nonsustained VT do not need to be treated and treatment is usually dictated by the presence of symptoms attributable to the PVCs. In general, the specific type, prognosis, and management of ventricular tachycardia VT depend on whether underlying structural heart disease is present. The electrocardiographic diagnosis of VT is suggested by the occurrence of a series of three or more consecutive, abnormally shaped PVCs whose duration exceeds 120 milliseconds, with the ST-T vector pointing opposite the major QRS deflection. Symptoms occurring during VT depend on the ventricular rate, duration of tachycardia, and presence and extent of the underlying heart disease and peripheral vascular disease. VT can occur in several forms: short, asymptomatic, nonsustained episodes; sustained, hemodynamically stable events, generally occurring at slower rates or in otherwise normal hearts; or unstable runs, often degenerating into VF. The dramatic changes in the management of VT and aborted sudden death during the past decade have been fueled by several large clinical trials and development of the ICD. Management decisions can be stratified into those involved in acute management or termination and those involved in long-term therapy or prevention of recurrence or sudden death. Ventricular fibrillation VF occurs in various clinical situations but most commonly in association with coronary artery disease and as a terminal event. Ventricular flutter or VF results in faintness, followed by loss of consciousness, seizures, apnea, and eventually, if the rhythm continues untreated, death. The blood pressure is unobtainable, and heart sounds are usually absent. These arrhythmias represent severe derangements of the heartbeat that usually terminate fatally within 3 to 5 minutes unless corrective measures are undertaken promptly. Ventricular flutter is manifested as a sine wave in appearance—regular large oscillations occurring at a rate of 150 to 300 beatsmin usually about 200. The distinction between rapid VT and ventricular flutter can be difficult and is usually of academic interest only. Hemodynamic collapse is present with both. VF is recognized by the presence of irregular undulations of varying contour and amplitude. Distinct QRS complexes, ST segments, and T waves are absent. Fine-amplitude fibrillatory waves 0.2 mV are present with prolonged VF. These fine waves identify patients with worse survival rates and are sometimes confused with asystole. Management should follow basic life support and advanced cardiac life support guidelines. Bradyarrhythmias are arbitrarily defined as a heart rate below 60 beatsmin. In some cases, bradyarrhythmias are physiologic, as in well-conditioned athletes with low resting heart rates or type I AV block during sleep, and in other cases are pathologic. Like tachyarrhythmias, bradyarrhythmias can be categorized on the basis of the level of disturbance in the hierarchy of the normal impulse generation and conduction system from sinus node to AV node to His-Purkinje system. Sinus bradycardia exists in an adult when the sinus node discharges at a rate slower than 60 beatsmin. P waves have a normal contour and occur before each QRS complex, usually with a constant PR interval longer than 120 milliseconds. Sinus arrhythmia often coexists. Heart block is a disturbance of impulse conduction that can be permanent or transient, depending on the anatomic or functional impairment. It must be distinguished from interference, a normal phenomenon that is a disturbance of impulse conduction caused by physiologic refractoriness resulting from inexcitability caused by a preceding Udayana University Faculty of Medicine, DME 59 impulse. Interference or block can occur at any site where impulses are conducted, but they are recognized most commonly between the sinus node and atrium SA block, between the atria and ventricles AV block, within the atria intra-atrial block, or within the ventricles intraventricular block. An AV block exists when the atrial impulse is conducted with delay or is not conducted at all to the ventricle when the AV junction is not physiologically refractory. In some cases of bundle branch block, the impulse may only be delayed and not completely blocked in the bundle branch, yet the resulting QRS complex may be indistinguishable from a QRS complex generated by a complete bundle branch block. . Standard References : 1. Mann, DL et all. Braunwald’s Heart Disease, 10 th ed. Philadelphia, Elsevier Saunders, 2015. p. 687-837 SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Etiology of Arrhythmias 2. Pathophysiology of Arrhythmias 3. Clinical approach of Arrhythmias 4. Treatment of Arrhythmias 5. Prognosis of Arrhythmias ABSTRACT II: ANTI ARRHYTHMIC DRUGS Many factors can precipitate or exacerbate arrhythmias: ischemia, hypoxia, acidosis or alkalosis, electrolyte abnormalities, excessive catecholamine exposure, autonomic influences, drug toxicity eg, digitalis or antiarrhythmic drugs, overstretching of cardiac fibers, and the presence of scarred or otherwise diseased tissue. However, all arrhythmias result from 1 disturbances in impulse formation, 2 disturbances in impulse conduction, or 3 both. Arrhythmias may require treatment because rhythms that are too rapid, too slow, or asynchronous can reduce cardiac output. Some arrhythmias can precipitate more serious or even lethal rhythm disturbances. In such patients, antiarrhythmic drugs may be lifesaving.Arrhythmias can be treated with the drugs and with nonpharmacologic therapies such as pacemakers,cardioversion, catheter ablation, and surgery. The aim of therapy of the arrhythmias is to reduce ectopic pacemaker activity and modify conduction or refractoriness in reentry circuits to disable circus movement. Antiarrhythmic drugs decrease the automaticity of ectopic pacemakers more than that of the sinoatrial node The major mechanisms currently available for accomplishing these goals are 1 sodium channel blockade, 2 blockade of sympathetic autonomic effects in the heart, 3 prolongation of the effective refractory period, and 4 calcium channel blockade.Antiarrhythmic drugs and in particular the fact that they can precipitate lethal arrhythmias in some patients has led to a reevaluation of their relative risks and benefits. In general, treatment of asymptomatic or minimally symptomatic arrhythmias should be avoided for this reason. Standard References : Udayana University Faculty of Medicine, DME 60 1. Trevor AJ, Katzung BG, Masters SB: Katzung Trevor’s Pharmacology, 7 th ed. New York, McGraw-HillLange., 2005. p 124-136 SELF-DIRECTED LEARNING 1. Principles of arrhythmias therapy. 2. Classification of Antiarrhythmic drugs. 3. Important pharmacokinetic properties of Antiarrhythmic drugs. 4. Mechanism of actions of Antiarrhythmic drugs. 5. Important adverse effects of Antiarrhythmic drugs.. SCENARIO CASE 1 : A 45-year old gentleman presented with irregular heart beat and dizzy. On physical examination, the blood pressure was 11575 mmHg; heart rate was 148 beats per-minute, irregular and pulse rate was 102 beats per-minute, irregular. S 1 and S 2 were single, grade 36 rumbling diastolic murmur was heard at apex cordis. LEARNING TASK I : 1. What is the most likely arrhythmia found in this patient? 2. What is the terminology of differentiation between irregular higher heart rate and irregular lower pulse rate? CASE 2 : A 45-year-old man is noted to have dilated cardiomyopathy with atrial fibrillation and a rapid ventricular rate. A drug is used to control theventricular rate, but the cardiac contractility is also affected, placing him in pulmonary edema. Discuss in your group the following issues. LEARNING TASK II: A 65-year-old man is noted to have atrial fibrillation. He also have hospitalized 1 year ago because of heart failure. A drug is used to control the symptom. After 1 week he come back to the doctor complain about discoloration of his skin, the colour of his skin become gray-blue especially in the area exposed to the sun and sometimes it is itchy. Discuss in your group the following issues. 1. Which antiarrhythmic drug likely is used to the patient? 2. To what class of antiarrhythmic does the drug belong? 3. What is the drug’s mechanism of action? 4. Which antiarrhythmic drug should be given to the patient to avoid such event? 5. What is the drug’s mechanism of action? 6. List some of the important adverse effects of some important drugs from each class of antiarrhythmic drug. SELF ASSESSMENT 1. The following adverse effects are associated with amiodarone: a. Visual disturbances b. Hyperthyroidism c. Hypothyroidism d. Pulmonary fibrosis Udayana University Faculty of Medicine, DME 61 e. Photosensitivity 2. Sotalol: a. Is effective in supraventricular and ventricular arrhythmias b. Is not effective when given by mounth c. The dose should be reduced in renal impairment d. May cause torsades de pointes e. Is a less potent negative inotropes tha amiodarone 3. Lidocaine a. Is a class Ib agent that block cardiac Na+ channels, reducing the rate of rise of the cardiac action potential and increasing the effective refractory period b. Is epileptogenic c. Is a positive inotrope d. Is usually administered as an intravenous bolus followed by infusion e. Is the drug of first choice for supraventricular tachycardia 4. Digoxin: a. Reduces the ventricular rate in atrial fibrilation b. Is contraindicated in second degree heart block c. Has narrow theraupetic index d. Induced arrhytmias may be terminated by magnesium e. 80 of adminestered digoxin is excreted unchanged in the bile MODULE 20 dr. A.A. Ayu Dwi Adelia Yasmin, SpJP, FIHA AIMS: Describe to diagnose and manage Hypertension and Vascular disease LEARNING OUTCOME: 1. Can describe to diagnose and manage the Hypertension 2. Can describe diagnose and manage the Vascular disease CURRICULUM CONTENS: 1. Etiology and pathophysiology of Hypertension and Vascular disease 2. Clinical criteria of Hypertension and Vascular disease 3. Diagnostic approach of Hypertension and Vascular disease 4. Management and prognosis of Hypertension and Vascular diseases ABSTRACT I : Hypertension is one of the most common worldwide diseases afflicting humans and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. Despite extensive research over the past several decades, the etiology of most cases of adult hypertension is still unknown, and control of blood pressure is Udayana University Faculty of Medicine, DME 62 Day 20 suboptimal in the general population. Approximately 75 million adults in the United States are affected by hypertension. Hypertension is the most important modifiable risk factor for coronary heart disease the leading cause of death in North America, stroke the third leading cause, congestive heart failure, end-stage renal disease, and peripheral vascular disease. Defining abnormally high blood pressure BP is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high BP must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or therapeutic interventions. Based on recommendations of the JNC 7, the classification of BP expressed in mm Hg for adults aged 18 years or older is as follows [3] :  Normal: systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg  Prehypertension: systolic 120-139 mm Hg, diastolic 80-89 mm Hg  Stage 1: systolic 140-159 mm Hg, diastolic 90-99 mm Hg  Stage 2: systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater Cardiovascular morbidity and mortality rises proportionately with increases in systolic blood pressure. In 95 of cases, the etiology of hypertension is idiopathic or essential hypertension. Secondary hypertension ~ 5 of cases should be identified and treated. Hypertension is an asymptomatic condition unless associated with hypertensive crises, and is often an incidental finding on routine examination. Patients with hypertension should undergo initial basic screening for the secondary causes of hypertension, and should be assessed for evidence of end-organ damage. All patients should have urinalysis, serum biochemistry electrolytes, glucose, urea and creatinin concentrations and thyroid function tests and ECG electrocardiogram for looking signs of left ventricular hypertrophy or ischaemic heart disease. Treatment of hypertension is associated with primary and secondary preventive benefits. Selection of anti hypertensive drugs is dependent upon patient choice, side effects, risk factors profile and co-morbidity. Standard References : 1. McPhee SJ, Papadakis MA. Current Medical Diagnosis Treatment. 47 th ed. New York: Lange Mecical Book`sThe McGraw-Hill Companies, 2008.p.370-397. 2. Chobanian A. et al. Seventh Report Of The Joint National Committee On Prevention, Detection, Evaluation, And Treatment Of High Blood Pressure. Hypertension. 2003;42:1206–1252 SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Etiology of Hypertension and Vascular disease 2. Pathophysiology of Hypertension and Vascular disease 3. Clinical criteria of Hypertension and Vascular disease 4. Diagnostic approach of Hypertension and Vascular disease 5. Management and prognosis of Hypertension and Vascular diseases SCENARIO CASE: Udayana University Faculty of Medicine, DME 63 A 65-year old female, came to Emergency Room due to weakness of the left side of the body, accompanied by confusion and slurred speech since 6 hours PTA when she was wake up in the morning. She had history of high blood pressure since 5 years PTA and not took the medicine regularly. The blood pressure at presentation was 230140 mmHg, pulse rate 98 beats per minute, regular. The ECG revealed sinus rhythm 98 bpm with LV High Voltage and LV strain. LEARNING TASK : 1. What is the diagnosis of the patient? 2. How will you manage the blood pressure of this patient? 3. What is the treatment of choice for this patient? SELF-ASSESSMENT : 1. What are the complications of hypertension? 2. Please explain the pathogenesis of peripheral arterial disease 3. What are the side effects of hydro-chlorothiazide? 4. Please mention 3 examples of secondary hypertension MODULE 21 dr. I Kadek Susila Surya Darma, SpJP AIMS: Describe to pathophysiology, diagnosis, diagnostic test and treatment Heart Failure LEARNING OUTCOME: 1. Can describe pathophysiology of Heart Failure 2. Can describe diagnosis of Heart Failure 3. Can describe diagnostic test of Heart Failure 4. Can describe treatment of Heart Failure CURRICULUM CONTENS: 1. Etiology and pathophysiology of Heart Failure 2. Clinical and diagnostic approach of Heart Failure 3. Pharmacologic treatment of Heart Failure 4. Prognosis of Heart Failure ABSTRACT I : Heart failure HF can be defined as an abnormality of cardiac structureor function leading to failure of the heart to deliver oxygen at a rate commensurate with the requirements of the metabolizing tissues, despite normal filling pressures or only at the Udayana University Faculty of Medicine, DME 64 Day 21 expense of increased filling pressures.HF is defined, clinically, as a syndrome in which patients have typical symptoms e.g. breathlessness, ankle swelling, and fatigue and signs e.g. elevated jugular venous pressure, pulmonary crackles, and displaced apex beat resulting from an abnormality of cardiac structure or function. Approximately 1–2 of the adult population in developed countrieshas HF, with the prevalence rising to ≥10 among persons 70 years of age or older.There are many causes of HF, and these vary in different parts of the world. At least half of patients with HF have a low ejection fraction EF. Coronary artery disease CAD is the cause of approximately two-thirds of cases of systolic HF, although hypertension and diabetes are probable contributing factors in many cases. There are many other causes of systolic HF, which include previous viral infection recognized or unrecognized, alcohol abuse, chemotherapy e.g. doxorubicin or trastuzumab, and ‘idiopathic’ dilated cardiomyopathy although the cause is thought to be unknown, some of these cases may have a genetic basis. Two key neurohumoral systems activated in HF are the renin–angiotensin– aldosterone system and sympathetic nervous system. In addition to causing further myocardial injury, these systemicresponses have detrimental effects on the blood vessels, kidneys, muscles, bone marrow, lungs, and liver, and create a pathophysiological ‘vicious cycle’, accounting for many of the clinical features of the HF syndrome, including myocardial electrical instability. Interruption of these two key processes is the basis of much of the effective treatment of HF. The diagnosis of HF can be difficult, especially in the early stages.Although symptoms bring patients to medical attention, many of the symptoms of HF are non- specific and do not, therefore,help discriminate between HF and other problems. Symptoms that are more specific i.e. orthopnoea and paroxysmal nocturnal dyspnoea are less common, especially in patients with milder symptoms, and are, therefore, insensitive.Many of the signs of HF result from sodium and water retention, and are, therefore, also not specific. Peripheral oedema has other causes as well, and is particularly non-specific. Signs resulting from sodium and water retention e.g. peripheral oedema resolve quickly with diuretic therapy i.e. may be absent in patients receiving such treatment, making it more difficult to assess patients already treated in this way. More specific signs, such as elevated jugular venous pressure and displacement of the apical impulse, are harder to detect and, therefore, less reproducible i.e. agreement between different doctors examining the same patient maybe poor. Symptoms and signs may be particularly difficult to identify andinterpret in obese individuals, in the elderly, and in patients with chronic lung disease.The patient’s medical history is also important. HF is unusual in an individual with no relevant medical history e.g. a potential cause of cardiac damage, whereas certain features, particularly previous myocardial infarction, greatly increase the likelihood of HF in apatient with appropriate symptoms and signs.These points highlight the need to obtain objective evidence of a structural or functional cardiac abnormality that is thought to account for the patient’s symptoms and signs, to secure the diagnosis of HF. Once the diagnosis of HF has been made, it is important to establish the cause, particularly specific correctable causes. Symptoms and signs are important in monitoring a patient’s response to treatment and stability over time. Persistence of symptoms despite treatment usually indicates the need for additional therapy, and worsening of symptoms is a serious development placing the patient at risk of urgent hospital admission and death and merits prompt medical attention. The echocardiogram and electrocardiogram ECG are the mostuseful tests in patients with suspected HF. The echocardiogram provides immediate information on chamber volumes, ventricular systolic and diastolic function, wall thickness, and valve function. This information is crucial in determining appropriate treatment e.g. an ACE inhibitor and beta-blocker for systolic dysfunction or surgery for aortic stenosis. The ECG shows the heart rhythm and electrical conduction, i.e. whether there is sinoatrialdisease, atrioventricular AV block, or abnormal intraventricular conduction. These findings are Udayana University Faculty of Medicine, DME 65 also important for decisions about treatment e.g. rate control and anticoagulation for AF, pacing for bradycardia, or CRT if the patient has LBBB. The ECG may also show evidence of LV hypertrophy or Q waves indicating loss of viable myocardium, giving a possible clue to the aetiology of HF. HF is very unlikely likelihood ,2 in patients presenting acutely and with a completely normal ECG.The information provided by these two tests will permit an initial working diagnosis and treatment plan in the majority of patients. Routine biochemical and haematological investigations are also important, partly to determine whether renin–angiotensin– aldosterone blockade can be initiated safely renal function and potassium and to exclude anaemia which can mimic or aggravate HF and because they provide other, useful information. Because the signs and symptoms of HF are so non-specific, many patients with suspected HF referred for echocardiography are not found to have an important cardiac abnormality. Where the availability of echocardiography is limited, an alternative approach to diagnosis is to measure the blood concentration of a natriuretic peptide, a family of hormones secreted in increased amounts when the heart is diseased or the load on any chamber is increased e.g. by AF, pulmonary embolism, and some non-cardiovascular conditions, including renal failure.A chest X-ray is of limited use in the diagnostic work-up of patientswith suspected HF. It is probably most useful in identifying an alternative,pulmonary explanation for a patient’s symptoms and signs. It may,however, show pulmonary venous congestion or oedema in a patientwith HF. It is important to note that significant LV systolic dysfunction may be present without cardiomegaly on the chest X-ray. Many variables provide prognostic information, althoughmost of this can be obtained from readily available datasuch as age, aetiology, NYHA class, EF, key co- morbidities renaldysfunction, diabetes, anaemia, hyperuricaemia, and plasma natriuretic peptide concentration.Clearly these variables change over time, as does prognosis. Assessment of prognosis is particularly important when counselling patients about devices and surgery including transplantation and in planning end-of-life care with patients, their family, and caregivers. The goals of treatment in patients with established HF are torelieve symptoms and signs e.g. oedema, prevent hospital admission, and improve survival. Although the focus of clinical trials was previously mortality, it is now recognized that preventing HF hospitalization is important for patients and healthcare systems.Reductions in mortality and hospital admission rates both reflect the ability of effective treatments to slow or prevent progressive worsening of HF. This is often accompanied by reverse LV remodeling and a reduction in circulating natriuretic peptide concentrations.The relief of symptoms, improvement in quality of life, and increasein functional capacity are also of the utmost importanceto patients, but they have not been the primary outcome in most trials.Three neurohumoral antagonists— an ACE inhibitor [or angiotensin receptor blocker ARB], a beta-blocker, and an MRA—are fundamentally important in modifying the course of systolic HF and should at least be considered in every patient. They are commonly used in conjunction with a diuretic given to relieve the symptoms and signs of congestion. Standard References: 1. Mann, DL et all. Braunwald’s Heart Disease, 10 th ed. Philadelphia, Elsevier Saunders, 2015. p. 429-615 2. McMurray et al. ESC Guidelines For The Diagnosis and Treatment of Acute and Chronic Heart Failure. European Heart Journal. 2012;33.1787-1847 SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Etiology of Heart Failure Udayana University Faculty of Medicine, DME 66 2. Pathophysiology of Heart Failure 3. Clinical and diagnostic approach of Heart Failure 4. Pharmacologic treatment of Heart Failure 5. Prognosis of 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 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 180110 mmHg and heart rate is 120min 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 lung. No heart murmur are 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 farmacological 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 is 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 heart failure? 7. Please explain farmacological treatment for patients with chronic heart failure 8. What are the precipitans and causes of acute heart failure? 9. Please explain farmacological treatment for patients with acute heart failure Udayana University Faculty of Medicine, DME 67 Day 22 MODULE 22 Prof dr. I Gusti Made Aman, SpFK AIMS: 1. Describe the anti hypertensive drugs 2. Describe the heart failure drugs LEARNING OUTCOME: 1. Can describe the anti hypertensive drugs 2. Can describe the heart failure drugs CURRICULUM CONTENS: 1. Principles and classification of anti hypertensive drugs 2. Important pharmacokinetic properties of anti hypertensive drugs. 3. Mechanism of actions of anti anti hypertensive drugs. 4. Important adverse effects of anti hypertensive drugs 5. Principles and classification of heart failure drugs 6. Important pharmacokinetic properties of heart failure drugs. 7. Mechanism of actions of heart failure drugs. 8. Important adverse effects of heart failure drugs ABSTRACT I : ANTI HYPERTENSIVE DRUGS Hypertension is important because elevated blood pressure BP confers a greater risk of stroke, heart failure, coronary artery disease including angina, myocard infarction, and sudden death, renal disease and peripheral vascular disease. There is a continuous, direct relationship between elevation in blood pressure and increases the risk. JNC 7, 2003 classification of blood pressure in adults is as follows: normal, prehypertension, stage I hypertension and stage 2 hypertension. In general, the higher the blood pressure and the greater the number of risk factors, indicate higher urgency and stringency in treating hypertension. Lowering blood pressure is just one way to prevent complications; attention must also be paid to the presence and reversal of other cardiovascular risk factors such as cigarette smoking, hyperlipidemia and especially in diabetes mellitus. Drugs used in lowering blood pressure will decrease peripheral vascular resistance orand 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. ABSTRACT II: Heart failure occurs when the heart is unable to pump blood at a rate sufficient to meet the metabolic requirements of the tissues. Heart failure is frequently, but not always, caused by a defect in myocardial contraction that may result from a primary abnormality Udayana University Faculty of Medicine, DME 68 in heart muscle, as occurs in the cardiomyopathies or in viral myocarditis. Heart failure also result from coronary atherosclerosis, which interferes with cardiac contraction by causing myocardial infarction. Heart failure may also occur in congenital, valvular and hypertensive heart disease in which myocardium is damaged by the long standing hemodynamic overload. Drugs used in heart failure include diuretics, vasodilators, nitrate, angiotensin antagonist, beta blockers and positive inotropes. Positive inotropes increase the myocardial contractility. They improves the symptoms of heart failure but at the cost of increasing mortality. They induce arrhythmias, increase myocardial oxygen consumption and reduced myocardial perfusion reduction blood flow. They are several classes of positive inotropes such as beta1 agonis e.g. dopamine, dobutamine, phosphodiesterase inhibitors eg amrinone, milrinone, and digitalis e.g. digoxin. Beta 1 agonists and phosphodiesterase inhibitors are not used in chronic heart failure. Standard References: 1. Trevor AJ, Katzung BG, Masters SB: Katzung Trevor’s Pharmacology, 7 th ed. New York, McGraw-HillLange., 2005. p 66-93, 95-104 and p. 114-123. SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Principles of anti hypertensive therapy. 2. Classification of anti hypertensive drugs 3. Important pharmacokinetic properties of anti hypertensive drugs. 4. Mechanism of actions of anti anti hypertensive drugs. 5. Important adverse effects of anti hypertensive drugs 6. Principles of heart failure therapy. 7. Classification of heart failure drugs 8. Important pharmacokinetic properties of heart failure drugs. 9. Mechanism of actions of heart failure drugs. 10. Important adverse effects of heart failure drugs. CASE 1: A 60-year-old man was brought to your private practice, and said that he was suffering from headache since 2 days before. He had gone to many doctors. He brought his ECG, urine and blood examination results which were appeared normal. He took with him antihypertensive drugs captopril and hydrochlorthiazide, but they were not taken for the last 6 days because he had no headache. Aside from his BP 17095, results of physical examination appeared normal. LEARNING TASK I: 1. Compare the mechanism of action of antihypertensive drugs. 2. Describe the compensatory responses, if any, to each types of antihypertensive drugs 3. List the major sites of action of sympathoplegic drugs and give examples of drugs that act on each site 4. List the 4 mechanism of action of vasodilator drugs and describe their effects 5. Describe the difference between 2 types of angiotensin antagonists 6. List the major side effects of the prototype antihypertensive drugs 7. Compare the indication and contraindication of antihypertensive drugs 8. Explain the interaction between angiotensin antagonist with potassium sparing diuretics Udayana University Faculty of Medicine, DME 69 CASE 2 : A 45-year-old woman was admitted to the hospital with shortness of breath when he walked about 2 meters, for about 6 months on and off , but became worst since 2 days ago. She also suffered from ankle swelling and fatigue. Her symptoms were improved when she took the prescribed drugs. She had a history of high blood pressure. On admission her blood pressure was 13080, heart rate 100min, regular, raised jugular venous pressure, dilatation of the heart to the right and left, hepatomegaly, ankle edema, basal lung rales on the right and left, no murmur. She was diagnosed chronic heart failure. Digoxin, captopril and furosemide was given to her. LEARNING TASK II : 1. Compare the mechanism of action and clinical uses of positive inotropes.. 2. Describe toxic action of digitalis on the heart 3. Describe the effect of electrolyte imbalance on digitalis effect 4. Describe the interaction between digitalis and diuretic and quinidine Explain either the statement is True or False 1. Severe bradycardia may occur after clonidine overdose 2. Captopril decreases sodium and increases potassium in the urine 3. Hemolytic anemia caused by antihypertensive drug clonidine 4. Postural hypotension is a common adverse effect of alfa blocker 5. Losartan most likely causes cough 6. Nitroprusside must be given by intravenous infusion 7. Minoxidil causes vasodilatation by opening potassium channels MODULE 23 Dr I Nyoman Wiryawan, SpJP, FIHA AIMS: Describe to diagnose and manage Cor Pulmonale Pulmonary Heart Disease. LEARNING OUTCOME: 1. Can describe to diagnose and manage Acute Cor Pulmonale. 2. Can describe to diagnose and manage Chronic Cor Pulmonale. CURRICULUM CONTENS: 1. Etiology of Acute and Chronic Cor Pulmonale. 2. Pathogenesis of Pulmonary Hypertension. 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 andor impaired function of the right ventricle that results from pulmonary hypertension that is associated with diseases of Udayana University Faculty of Medicine, DME 70 Day 23 the lung eg, chronic obstructive pulmonary disease, vasculature eg, idiopathic lumonary arterial hypertension, upper airway eg, obstructive sleep apnea, or chest wall eg, kyphoscoliosis. Right sided heart disease due to left sided heart disease is not considered cor pulmonale. Pulmonary hypertension PH is defined as PA Pressure .20 mmHg and is placed in the heterogeneous group of PH associated with disorders of the respiratory system andor hypoxaemia. The reason for setting such a threshold is that in healthy subjects PA Pressure is always 20 mmHg at rest and, as stated above, a PA Pressure 20 mmHg is associated with increased morbidity and mortality. However, in some recent studies PH was defined by PA Pressure 25 mmHg. Cor pulmonale tends to be chronic and slowly progressive, but it can be acute. Acute cor pulmonale occurs when the right ventricle cannot adapt to an increase in the pulmonary arterial pressure. The increased pulmonary artery pressure may be consequence of a new acute process, such as pulmonary embolism, or progression of the chronic disease. The diagnostic evaluation of cor pulmonale is inseparable from the evaluation for pulmonary hypertension. Cor pulmonale could be diagnosed based on the clinical manifestation and using chest x-ray, electrocardiography, and echocardiography as well as magnetic resonance imaging, pulmonary function testing, and right heart catheterization. Symptoms attributable to cor pulmonale include dyspnea on exertion, fatigue, lethargy, exertional syncope, and exertional angina. Patients with cor pulmonale have physical findings related to both pulmonary hypertension and righ-sided heart disease. All patients with cor pulmonale should have the underlying cause of the cor pulmonale and pulmonary hypertension treated. The treatment of cor pulmonale can be conceptualized as having three major physiological gols: reduction of right ventricular afterload eg, pulmonary artery pressure, decrease of right ventricular pressure, and improvement of right ventricular contractility. In the cor pulmonale condition that leads into heart failure, diuretics and nitrates may be needed to improve the condition of the patient. Oxygen supplementation is often required to resolve the shortness of breath. Treatments of PAH have shown a dramatic change in the past few years. Synthetic prostacyclin epoprostenol, prostacyclin analogues, endothelin-1 receptor antagonists and phosphodiesterase-5 inhibitors were tested in randomised controlled trials, leading to the approval of several drugs in each class. SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Etiology of Acute and Chronic Cor Pulmonale. 2. Pathogenesis of Pulmonary Hypertension. 3. Clinical Manifestation of Cor Pulmonale. 4. Physical Findings of Cor Pulmonale. 5. Diagnostic techniques for Cor Pulmonale. 6. Prevention and Treatment of Cor Pulmonale. SCENARIO: CASE 1: A 70-year old male, came to Emergency Room due to swelling on abdomen and both legs. The complaints were suffered since 1 month ago and become worsen. He also complains of shortness of breath and cough, that was experienced since years and usually could be resolved by nebulizer. He used to be a heavy smoker for 30 years, with 1-2 packs cigarette per day. The blood pressure was 12080 mmHg; pulse rate was 110 beats per-minute, regular. There were wheezing at both lung field, ascites on abdomen, and pitting edema on both legs, and increased of jugular venous pressure. ECG revealed Udayana University Faculty of Medicine, DME 71 sinus tachycardia 110 beats per-minute with P pulmonale on lead II, III and aVF. The urinary production is good. LEARNING TASK : 1. What is the most likely diagnosis? 2. What the next procedure do you plan? 3. What is your initial treatment? CASE 2: A 65-year-old man with a history of radiation therapy to thechest for lymphoma presents with worsening exertionaldyspnea. On physical examination the heart rate is 120beatsmin, blood pressure 9055 mm Hg, with pulsus paradoxusof 15 mm Hg. The jugular venous pressure is 10 cmH2O with a prominent x descent. He is found by echocardiographyto have a large pericardial effusion, which isdrained by pericardiocentesis. After the procedure in thecardiac catheterization laboratory the intrapericardial pressurenormalizes but the initially elevated right atrial pressurefails to decline and displays a prominent y descent. This scenario is most consistent with A. Persistence of pericardial tamponade B. Cor pulmonale C. Effusive-constrictive pericarditis D. Restrictive cardiomyopathy E. Uremic pericarditis LEARNING TASK : 1. What is the most likely diagnosis? 2. What the next procedure do you plan? 3. What is your initial treatment? SELF-ASSESSMENT : 1. Please explain the risk factors of cor pulmonale. 2. What are the complications of pulmonary hypertension? 3. What is the treatment of choice in acute and chronic cor pulmonale? Udayana University Faculty of Medicine, DME 72 Day 24 MODULE 24 dr. I B Rangga Wibhuti, M.Biomed, SpJP, FIHA dr. LuhKamiati, SpRM AIMS: 1. Able to diagnose and manage Valvular Heart Disease VHD 2. Able to diagnose and manage Pericardial disease and Endocardial disease 3. Able todo cardiac rehabilitation on patient with Cardiovascular Disease LEARNING OUTCOME: 1. Able to combine history taking, physical examination, and supportive examinations to make initialworking diagnosis of VHD patients, and able to suggest further examinations needed to diagnose VHD 2. Able to manage VHD patients in short term and long term management. 3. Able to combine history taking, physical examination, and supportive examinations to make initialworking diagnosis of pericardial diseaseand endocardial disease patients, and able to suggest further examinations needed to diagnose pericardial disease and endocardial disease. 4. Able to manage pericardial disease and endocardial disease patients in short term and long term management. 5. Able to describe cardiac rehabilitation in patient with cardiovascular disease CURRICULUM CONTENS: 1. Etiology, pathophysiology, and clinical spectrum of VHD 2. Indication and interpretationof supportive examinationsfor VHD 3. Management of VHD patients 4. Cardiac rehabilitation in patients with cardiovascular disease 5. Etiology, pathophysiology, and clinical spectrum of pericardial and endocardial disease 6. Indication and interpretation of supportive examinations forpericardial and endocardial diseases 7. Management of patient with pericardial and endocardial disease 8. Cardiac rehabilitation in patient with cardiovascular disease ABSTRACT I: Valvular heart disease is characterized by damage to or a defect in one of the four heart valves: the mitral, aortic, tricuspid or pulmonary. The mitral and tricuspid valves control the flow of blood between the atria and the ventricles the upper and lower chambers of the heart. The pulmonary valve controls the flow of blood from the heart to the lungs, and the aortic valvegoverns blood flow between the heart and the aorta, and thereby the blood vessels to the rest of the body. The mitral and aortic valves are the ones most frequently affected by valvular heart disease. Normally functioning valves ensure that blood flows with proper force in the proper direction at the proper time. In valvular heart disease, the valves become too narrow and hardened stenotic to open fully, or are unable to close completely incompetent. A stenotic valve forces blood to back up in the adjacent heart chamber, while an incompetent valve allows blood to leak back into the chamber it previously exited. To compensate for poor pumping action, the heart muscle enlarges and thickens, thereby losing elasticity and efficiency. In addition, in Udayana University Faculty of Medicine, DME 73 some cases, blood pooling in the chambers of the heart has a greater tendency to clot, increasing the risk of stroke or pulmonary embolism. The severity of valvular heart disease varies. In mild cases there may be no symptoms, while in advanced cases, valvular heart disease may lead to congestive heart failure and other complications. Valvular heart disease accounts for 10 to 20 of all cardiac surgical procedure. The primary causes of valve disease are age-associated calcific valve changes and inherited or congenital conditions. The prevalence of rheumatic valve disease now is very low in the United States and Europe because of primary prevention of rheumatic fever, although rheumatic valve disease remains prevalent in the developing world.In addition to patients with severe valve disease that eventually requires mechanical intervention, there is a larger group of patients with mild to moderate disease who need accurate diagnosis and appropriate medical management. The most prevalent valvular heart disease is the following: 1 mitral valve disease, 2 aortic valve disease, and 3 tricuspid and pulmonary valve disease. Most valvular abnormalities can be managed with medical therapy, percutaneous intervention, or surgical intervention. Standard References: 1. Mann, DL et all. Braunwald’s Heart Disease, 10 th ed. Philadelphia, Elsevier Saunders, 2015. ABSTRACT II: Pericardium is composed of two layers, the visceral pericaradium, a monolayer of mesothelial cells and collagenand elastin fibers that is adherent to the epicardial surface of the heart and the fibrous parietal layer, which is approximately 2mm thick in normal humans and surrounds most of the heart. The pericardial space or sac is contained within these two layers and normally has up to 50ml of serous fluid. Pericardium serves as barrier to infection, as well as lubrication between the visceral and parietal layers. The best characterized mechanical function of the pericardium is its restraining effect on cardiac volume. The spectrum of pericardial diseas comprises congenital defects, pericarditis dry, effusive, effusive-constrictive, constrictive, neoplasm, and cysts. Congenital defect of the pericardium occure 1 in 10.000 autopsies. It comprises partial left 70, right 17 or total bilateral extremely rare pericardial absence. The diagnosis is confirmed by echocardiography and CTMRI. Acute pericarditis is either dry, fibrinous or effusive, independent from its aetiology. A prodrome of fever, malaise, and myalgia is common, but elderly patients may not be febrile. Major symptoms are retrosternal or left precordial chest pain radiates to the trapezius ridge, can be pleuritic or stimulate ischemia, and varies with posture, non-productive cough, and shortness of breath. Pericardial friction rub and pleural effusion may be present. Diagnosis can be made by history taking, physical examination, laboratory and imaging. Management include hospitalization, finding the etiology, observe for tamponade and start anti-inflammatory and symptomatic treatment. Endocardium is innermost layer of the heart. Its atrial component is thicker than ventricular, where purkinje fibers are distributed throughout the ventricular subendocardium. Primary endocardial diseases are not common, usually non inflammatory in nature. Endocardialfibroelastosis is familial disease which involve progressive edema of endocardium, fibroblast proliferation and increased amount of collagen withing endocardium lead to restrictive cardiomyopathy and interfere cardiac output. Secondary cause of endocardial disease usually from infection. Infective endocarditis IE incidence range from 3-10 episodes100.000 person-years, male to female ratio is 2:1. Neither the incidence nor the mortality of the disease have decreased in the past 30 years, this disease still carries poor prognosis and high mortality. IE should be suspected in some clinical situations, such as fever, new heart murmur, anemia and Udayana University Faculty of Medicine, DME 74 embolic events. Up to 90 patient with fever, often associated with systemic symptoms of chills, poor appetite and weight loss. Transthoracic echocardiography must be performed rapidly as soos as IE is suspected. Diagnosis of IE based on modified Duke criteria that composed with mayor and minor criteria. Treatment include supportive therapy based on sign and symptoms and combination with antibiotic which can be start soon despite waiting for blood culture result. Standard References: 1. Mann, DL et all. Braunwald’s Heart Disease, 10 th ed. Philadelphia, Elsevier Saunders, 2015. p. 1391-1550 2. Habib, Gilbert et al. Guidelines on The Prevention, Diagnosis, and Treatment of Infective Endocarditis. European Heart Journal. 2009;30.2369-2413 3. Maisch, Bernhard et al. Guidelines on The Diagnosis and Management of Pericardial Disease. European Heart Journal. 2004; 1-28 Additional reading: 1.Constant, Jules. Essential of Bedside Cardiology, 2 nd ed. New Jersey, Humana Press Inc. 2003 ABSTRACT III: Cardiac rehabilitation is multidisciplinary program of education and exercise established to assist individual with heart disease in achieving optimal physical, psychological and functional status within thw limits of the diseased. The basic goal of cardiac rehabitation are to restore and improve cardiac function, reduce disability, identify and cardiac risk factors, increased cardiac conditioning. Cardiac rehabilitation programs consist primary prevention education, behavior modification, secondary prevention, and exercise program. Cardiac rehabilitation outcomes that can be expected decreased length of hospital stay, more ripid, more complete resumption of ususal activities, self confident, less pshychological distress, and fewer readmissions. Standard References : 1. McPhee SJ, Papadakis MA. Current Medical Diagnosis Treatment. 47 th ed. New York: Lange Mecical Book`sThe McGraw-Hill Companies, 2008.p. 287-299, 351-358; 398-416, 360-363; 1241-1246 2. Garrison SJ: Hand Book of Physical Medicine and Rehabilitation, 2 nd ed, 2003, p. 86 3. Bartels MN: Cardiac Rehabilitation in Grant Cooper: Essential Physical Medicine and Rehabilitation, 2006, p. 119. SCENARIO: CASE I: A 30 year old woman complained of progressive exertional shortness of breath in the past one year. Physical examination revealed a loud first heart sound, an opening snap and a mid diastolic rumbling murmur with an irregularly irregular pulse. LEARNING TASK: 1. What diagnosis do these findings suggest? Udayana University Faculty of Medicine, DME 75 2. What is the underlying etiology? 3. What investigation is useful and describe the findings that is consistent with the initialworking diagnosis? 4. What pharmacological treatment does she need? Describe the mechanism of action for the medicines and why she need itthem? 5. What other treatment does she might need? Please describe the indication, procedure, and complication that might occur. CASE 2: A 23-year old man visited the hospital due to chest pain. The chest pain was sharp in nature. The pain scale was 7 of 10, it was becoming severe when he took a deep breath and radiating to the neck. He suffered from ‘flu-like syndromes’ since the last 1 week. LEARNING TASK: 1. What is the most likely diagnosis? 2. What is the treatment do you plan? 3. What is the common etiology of this situation? CASE 3: 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 3. Mention the contraindication exercise therapy 4. Explain the benefit effect of exercise therapy 5. Explain stages of cardiovascular rehabilitation MI 6. Mention effect of exercise to CHF SELF DIRECTING LEARNING and SELF-ASSESSMENT 1. Describe the etiology and clinical sign and symptoms foreach valvular heart disease aortic valve regurgitationstenosis, mitral valve regurgitationstenosis, tricuspid valve regurgitationstenosis, pulmonic valve regurgitationstenosis 2. Please explain the complication of mitral stenosis 3. Please describe the ECG findings in aortic stenosis 4. What is the Austin-Flint murmur? 5. Please explain the indication of mitral valve replacement procedure? 6. What is the treatment of constrictive pericarditis? 7. How to diagnose pericardial effusion from clinical signs and symptoms? 8. What is the management of pericardial effusion? 9. What is the most accurate diagnostic tool of pericardial effusion? 10. Mention definition of cardiovascular rehabilitation 11. Explain the objective of cardiovascular rehabilitation Udayana University Faculty of Medicine, DME 76 12. Mention the contraindication exercise therapy 13. Explain the benefit effect of exercise therapy 14. Explain stages of cardiovascular rehabilitation MI 15. Mention effect of exercise to CHF MODULE 25 dr. I Nyoman Semadi, SpB, SpBTKV SURGERY IN CARDIAC DISEASES AIMS: Describe the basic principles of surgery in cardiac diseases LEARNING OUTCOME: 1. Can describe the basic principles of cardiac surgery 2. Can describe the basic aspect in cardiac surgery 3. Can describe the cardiac diseases who need surgery CURRICULUM CONTENTS: 1. Surgery of the congenital heart 2. Surgery of the acquired heart diseases ABSTRACT: Atrial septal defects ASD and ventricular septal defect VSD and others are the congenital cardiac anomaly. The intracardiac defects makes the shunt and blood flows through the shunt from right-to-left or reverse of the heart. Atrial septal defects ASD are most common in the vicinity of the fossa ovalis. Septum secundum defects, the typical patent foramen ovale, account for 10-15 of all cardiac anomalies. Normal left atrial pressure is slightly greater than right atrial pressure, a left-to-right shunt occur through an open ASD, oxygenated blood from the left side of the heart is shunted to the right side, thus not associated with cyanosis. An ASD is usually compatible with normal life, except at an extreme exercise, cardiac disease, or pulmonary disease alter chamber pressures, a right-to-left shunt will produce cyanosis. Ventricular septal defect VSD is usually happened at the upper membranous portion that composed of connective tissue continuous with the annulus fibrosus. A small VSD may result in an inconsequential left-to-right shunt. In the presence of pulmonary stenosis, a VSD produces a right-to-left shunt with cyanosis and the blue-baby syndrome. A large VSD is a principal factor in Tetralogy of Fallot. Patent ductus arteriosus PDA is a persistence of the fetal connection ductus arteriosus between the aorta and pulmonary artery after birth, resulting in a left-to-right shunt. Symptoms may include failure to thrive, poor feeding, tachycardia and tachypneu due to lung infection. Udayana University Faculty of Medicine, DME 77 Day 25 Others cardiac diseases are more common as a coronary arterial diseases CAD, Acquierd Valve diaseses of rheumatic heart disease and congenital valve anomaly Standard References: 1. Stuart W. Jamieson and Norman E Shumway: Cardiac Surgery in Rob Smith’s Operative Surgery, 4th edition. Butterworths London, 2004 SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Cardiac surgery in principles SCENARIO: CASE 1; This baby aged 4 months has been known to have a cardiac murmur since birth. He was born 8 weeks prematurely and developed respiratory distress requiring high oxygen concentration for the first week. Since then he has feed satisfactorily but height and weight growth have been poor even allowing for prematurity. The diagnosis after examination and investigations: Patent Ductus Arteriosus PDA. LEARNING TASK I 1. How to prepare if the patient have surgery 2. What is cardic surgery category for PDA closure 3. PDA commonly concomittent with congenital anomaly. Is it every PDA have surgery to close the shunt 4. After an operation to close the PDA, why is there a risk of the patient becoming hoarse? CASE 2 : This 13 year old girl was recently found to have a cardiac murmur. She has been generally healthy with good growth, but on questioning her mother admitted she has noticed that girl tends to tire easily with exercise. The diagnosis after examination and investigations: Atrial Septal Defect A.S.D. LEARNING TASK II: 1. What is cardic surgery category for ASD closure 2. What the different between close and open cardiac surgery 3. After ASD was closured, why the patient getting good growing of the body 4. And why is the patient after ASD closure getting arrythmia CASE 3 : A 2 year old boy was admitted to the hospital for evaluation of a heart murmur previously detect at birth. He was less active than other children his age, but although over-exertion was followed frequently by cyanosis of the lips and nails, there was no history of unconsciousness. Initial examination revealed a thin, physically retarded, cyanotic child with no respiratory difficulty. There was moderate clubbing of the fingers. A harsh systolic murmur was maximal over the mid-precardial area. The first heart sound was normal while the second was single, distinct and loud.The lungs were clear. X-ray showed a normal sized heart dominated by a boot-shaped right ventricular outflow tract. Diagnosis of Tetralogy of Fallot. LEARNING TASK III: 1. The cardiac anomaly are PS, VSD, Overriding aorta and RVH. How do repair it Udayana University Faculty of Medicine, DME 78 2. Why the patient becoming worse after the surgery repair of the defect SELF-ASSESSMENT : 1. Describe the principle cardiac surgery 2. Describe the principle coronary heart surgery 3. Describe the principle of Valve surgery TREATMENT FOR AORTA AND ARTERIAL DISEASES AIMS: Describe the basic principles of surgery in aorta and arteries LEARNING OUTCOME: 1. Can describe the basic principles of aorta and arteries 2. Can describe the basic aspect in aorta arteries 3. Can describe the aorta and arteries diseases who need surgery CURRICULUM CONTENTS: 1. Surgery of the aneurysm of aorta 2. Surgery of the peripheral artery diseases ABSTRACT: Atherosclerosis is the usual cause of vascular diseases. The aneurysm of aorta is dilated of aorta lumen over one and half size of normal lumen of aorta. The aorta can enlargement, elongated and tortous with or without thrombus in the lumen of aorta. It can be found on thoracic region or abdominal region or both. The patient got pain of the chest or abdominal pain depend the aneurysm posotion. If you found the abdominal aortic aneurysm triple A, the large pulsatil tumor was found on central topographic of abdomen. The patient become dengerous if aortic aneurysm ruptured and the patient getting haemorhagic shock. Atherosclerosis can cause the peripheral artery diseases. The artery become aneurysm, stenosis and occluded. If the artery got occlusion on midle size of that, the distal part of organ will ischemic and become death of the tissue that call ganggrene. Standard References: 1. Allan D. Callow, Calvin B. Erust. : Vascular surgery, Theory and Practice, Prentice- Hall International Inc.London , 1995 SELF DIRECTING LEARNING Basic knowledge that must be known: 1. Vascular surgery in principles SCENARIO: CASE 1; Old man, he was pain on abdomen and the tumor was found on abdomen palpation. The tumor was pulsatil and 7 cm in diameter and fixed. The blood pressure of the patient got high. The diagnose of the disease is triple A with stable hemodinamically LEARNING TASK I: 1. How to diagnose the patient 2. How to prepare if the patient have surgery Udayana University Faculty of Medicine, DME 79 3. How to do to enlargement of aorta 4. Any complication to surgery of aorta CASE 2 : This 43 year old man was recently found to have cold of feet. He has been generally healthy with pain on both leg if he walking for while, he was heavy smoking from teeneger. The diagnosis after phisical examination that conclude: peripheral artery diseases of both popliteal artery LEARNING TASK II: 1. What will you do to investigate the patient for difinitive diagnosis 2. What will you do to improve the blood flow to the distal end of feet 3. How the prognosis and reccurent rate SELF-ASSESSMENT : 1. Describe the principle of vascular surgery 2. Describe the principle arterial repair 3. Describe the principle of care after vascular surgery

8. REFERENCES