MODULE 17 Dr. dr. K. Rina, Sp PD, Sp JP
AIMS:
Describe to diagnose and manage Ischaemic Heart Disease IHD and Acute Coronary Syndromes ACS
LEARNING OUTCOME: 1. Can describe to diagnose and manage Ischaemic Heart Disease IHD
2. Can describe to diagnose and manage Acute Coronary Syndromes ACS
CURRICULUM CONTENS:
1. Pathogenesis of 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, hyperlipidaemia, family history,
hypertension and diabetes mellitus. Atherosclerosis is a chronic process initiated by lipid deposition and vascular wall
injury that causes increased endothelial permeability, inflammation and recruitment of monocytes and leucocytes. These cells accumulate oxidized lipids to form macrophages
and foam cells, and lead to the formation of ‘fatty streak’ and then ‘atheroma’. Eventually, all these process becomes ‘atherosclerotic plaque’.
Chronic stable angina is caused by atheroma obstructing coronary artery lumen by more than 70. Acute coronary syndromes ACS = unstable angina and myocardial
infarction arise when atherosclerotic plaque becomes unstable and either ruptures or are eroded. The complicated plaque is a nidus for thrombus formation and may lead to vessel
occlusion.
Stable coronary artery disease is generally characterized by episodes of reversible myocardial 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
divided into four categories: location, character, duration and relationship to exertion and other exacerbating or relieving factors. The discomfort caused by myocardial ischaemia is
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usually located in the chest, near the sternum, but may be felt anywhere from the epigastrium to the lower jaw or teeth, between the shoulder blades or in either arm to the
wrist and fingers. The discomfort is often described as pressure, tightness or heaviness; sometimes strangling, constricting or burning. The duration of the discomfort is brief—no
more than 10 min in the majority of cases and more commonly even minutes or less— but chest pain lasting for seconds is unlikely to be due to angina. An important characteristic is
the relationship to exercise, specific activities or emotional stress. Symptoms classically appear or become more severe with increased levels of exertion and rapidly disappear
within a few minutes when these causal factors abate.
Basic first-line testing in patients with suspected SCAD includes standard laboratory biochemical testing, a resting ECG, possibly ambulatoryECGmonitoring if there
is clinical suspicion that symptoms may be associated with a paroxysmal arrhythmia, resting echocardiography and, in selected patients, a chest X-ray CXR. Such testing can
be done on an outpatient basis. The aim of the management of SCAD is to reduce symptoms and improve prognosis. The management of CAD patients encompasses
lifestyle modification, control of CAD risk factors, evidence-based pharmacological therapy and patient education.
The acute coronary syndromes encompass a spectrum of unstable coronary artery disease that includes unstable angina and myocardial infarction ST segment elevation
myocardial infarction and non-ST segment elevation myocardial infarction. The history, electrocardiogram, and cardiac markers determine the presence and the type of ACS.
Patients with an acute coronary syndrome usually present with prolonged anginal sympoms that occur at rest. Patients with persistent chest pain lasting more than 20
minutes should seek urgent medical attention because of the likelihood of myocardial amage an dinfarction. The electrocardiogram will often show evidence of ischaemia that
classically takes the form of ST segment shifts, T-wave inversion, and new bundle branch block. Cardiac enzymes and markers are the principal determinans that define the
category of the acute coronary syndrome. Patients should be given analgesia, oxygen and transferred to intensive coronary care unit. Treatments consist of aspirin, clopidogrel, low-
molecular weight heparin, beta-blockers and intravenous nitrate infusion. Where available, percutaneous coronary intervention PCI is the treatment of choice. Thrombolytic therapy
is an effective alternative.
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: CASE:
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A 70-year old male, came to Emergency Room due to chest pain and shortness of breath. The pain was felt retro-sternally since 10-hours prior to admission, it was dull pain of 8 of
10 pain scale, not relieved by resting, accompanied by shortness of breath since 5 hours PTA that is relieved by sitting position. He is suffered from uncontrolled DM and
Hypertension since 10 years ago. He appeared severely ill and dyspnea. The blood pressure was 80palp mmHg; pulse rate was 120 beats per-minute, regular. There was
rales on both lung fields and cold extremity. ECG revealed sinus tachycardia 120 beats per-minute. Elevated ST-segment of ECG was noted at the precordial leads.
LEARNING TASK :
1. What is the most likely diagnosis? 2. What the next procedure do you plan?
3. What is your initial treatment? 4. What is the role of inotropic support in this case?
5. What is the definitive therapy for this case?
SELF-ASSESSMENT :
1. Please explain the risk factors of ischaemic heart 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 bys-pass
graft grafting?
MODULE
MODULE 18 dr Wayan Winarti, SpPA
Prof dr. I Gusti Made Aman, SpFK
AIMS:
1. Describe the pathogenesis of atherosclerosis related to Ischemic Heart Disease IHD
2. Describe drug used in Angina Pectoris
LEARNING OUTCOME:
1. Able to explain the pathogenesis of 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
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Day 18
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
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
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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.
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
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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
MODULE 19 dr. Bajra Nadha, SpJP
dr. I G Md Gd Surya Candra Trapika, MSc
AIMS:
Able to diagnose and manage Arrhythmias
LEARNING OUTCOME:
1. Can describe to diagnose 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.
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Day 19
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 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
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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,
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
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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
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: ANTIARRHYTHMIC DRUGS
Many factors can precipitate or exacerbate arrhythmias: ischemia, hypoxia, acidosis or alkalosis, electrolyte abnormalities, excessive catecholamine exposure,
autonomic influences, drug toxicity eg, digitalis or antiarrhythmic drugs, overstretching of cardiac fibers, and the presence of scarred or otherwise diseased tissue. However, all
arrhythmias result from 1 disturbances in impulse formation, 2 disturbances in impulse conduction, or 3 both. Arrhythmias may require treatment because rhythms that are too
rapid, too slow, or asynchronous can reduce cardiac output. Some arrhythmias can precipitate more serious or even lethal rhythm disturbances. In such patients,
antiarrhythmic drugs may be lifesaving.Arrhythmias can be treated with the drugs and with nonpharmacologic therapies such as pacemakers,cardioversion, catheter ablation, and
surgery.
The aim of therapy of the arrhythmias is to reduce ectopic pacemaker activity and modify conduction or refractoriness in reentry circuits to disable circus movement.
Antiarrhythmic drugs decrease the automaticity of ectopic pacemakers more than that of the sinoatrial node The major mechanisms currently available for accomplishing these
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goals are 1 sodium channel blockade, 2 blockade of sympathetic autonomic effects in the heart, 3 prolongation of the effective refractory period, and 4
calcium channel blockade.Antiarrhythmic drugs and in particular the fact that they can precipitate lethal arrhythmias in some patients has led to a reevaluation of their relative
risks and benefits. In general, treatment of asymptomatic or minimally symptomatic arrhythmias should be avoided for this reason.
Standard References :
1. Trevor AJ, Katzung BG, Masters SB: Katzung Trevor’s Pharmacology, 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
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1. The following adverse effects are associated with amiodarone:
a.
Visual disturbances
b.
Hyperthyroidism
c.
Hypothyroidism
d.
Pulmonary fibrosis
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. Susila Surya Darma, SpJP
AIMS:
Describe to diagnose and manage Hypertension and Vascular disease
LEARNING OUTCOME:
1. Can describe to diagnose and manage the Hypertension 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
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Day 20
ABSTRACT I :
Hypertension is one of the most common worldwide diseases afflicting humans and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic
kidney disease. Despite extensive research over the past several decades, the etiology of most cases of adult hypertension is still unknown, and control of blood pressure is
suboptimal in the general population. Approximately 75 million adults in the United States are affected by hypertension. Hypertension is the most important modifiable risk factor for
coronary heart disease the leading cause of death in North America, stroke the third leading cause, congestive heart failure, end-stage renal disease, and peripheral vascular
disease.
Defining abnormally high blood pressure BP is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to
be quantitative rather than qualitative. A level for high BP must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation
and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about
aggressiveness of treatment or therapeutic interventions. Based on recommendations of the JNC 7, the classification of BP expressed in mm Hg
for adults aged 18 years or older is as follows
[3]
:
Normal: systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg
Prehypertension: systolic 120-139 mm Hg, diastolic 80-89 mm Hg
Stage 1: systolic 140-159 mm Hg, diastolic 90-99 mm Hg
Stage 2: systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater Cardiovascular morbidity and mortality rises proportionately with increases in
systolic blood pressure. In 95 of cases, the etiology of hypertension is idiopathic or essential hypertension. Secondary hypertension ~ 5 of cases should be identified and
treated. Hypertension is an asymptomatic condition unless associated with hypertensive crises, and is often an incidental finding on routine examination.
Patients with hypertension should undergo initial basic screening for the secondary causes of hypertension, and should be assessed for evidence of end-organ damage. All
patients should have urinalysis, serum biochemistry electrolytes, glucose, urea and creatinin concentrations and thyroid function tests and ECG electrocardiogram for
looking signs of left ventricular hypertrophy or ischaemic heart disease. Treatment of hypertension is associated with primary and secondary preventive
benefits. Selection of anti hypertensive drugs is dependent upon patient choice, side effects, risk factors profile and co-morbidity.
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
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5. Management and prognosis of Hypertension and Vascular diseases
SCENARIO CASE:
A 65-year old female, came to Emergency Room due to weakness of the left side of the body, accompanied by confusion and slurred speech since 6 hours PTA when she was
wake up in the morning. She had history of high blood pressure since 5 years PTA and not took the medicine regularly. The blood pressure at presentation was 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. Made Junior Rina Artha, Sp JP
AIMS:
Describe to diagnose and manage Heart Failure
LEARNING OUTCOME:
1. Can describe to diagnose the Heart Failure 2. Can describe manage the 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. Rehabilitation and prognosis of Heart Failure
ABSTRACT I : Heart failure HF is a complex clinical syndrome resulting from structural and functional
impairment of ventricular filling or ejection of blood. Although the clinical syndrome of HF may arise as consequence of abnormalities or disorder involving all aspects of cardiac
structure and function, most patients have impairment of myocardial performance, with findings ranging from normal ventricular size and function to marked dilatation and
reduced function.
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Day 21
Heart failure is defined, clinically, as a syndrome in which patients have typical symptoms breathlessness, ankle swelling, and fatigue and sign elevated jugular venous
pressure, pulmonary crackles and displaced apex beat resulting from abnormality of cardiac structure and function. Its about 1-2 of the adult population in developed country
has HF, with the prevalence rising to more than 10 among persons 70 years of age or older. Coronary artery disease CAD is the cause of approximately two-third of cases of
systolic HF, although hypertension and diabetes are probable contributing factors in many cases. There are many other causes of systolic HF, which include previous viral infection
recognized or unrecognized, alcohol abuse, chemotherapy and idiopathic.
Approximately half of the patients with HF have normal left ventricular function, that is, HF with preserved ejection fraction HFpEF, and another half is HF with reduced
ejection fraction HFrEF. HFpEF generally is defined as a left ventricular ejection fraction of 50 or grated, whereas HFrEF is defined as an ejection fraction below 40. These
distinction are crucial because treatment strategies for treating HF is different between these two entity.
The diagnosis of HF can be difficult, especially in the early stages. Although symptoms bring patients to medical attention, many of the symptoms of HF are non
specific and do not, therefore, help discriminate between HF and other problems. Symptoms that are more specific orthopnea and paroxysmal nocturnal dyspnea are less
common, especially in patiens with milder disease. Many of the signs of HF results from sodium and water retention, and are, therefore, also no specific. Elevated jugular venous
pressure, displacement of the apical impuls, are more specific.
A patient who has never exhibited the typical signs or symptoms of HF is described as having asymptomatic LV systolic dysfunction or whatever the underlying cardiac
abnormality is. Patients who have had HF for some time are often said to have ‘chronic HF’. A treated patient with symptoms and signs, which have remained generally
unchanged for at least a month, is said to be ‘stable’. If chronic stable HF deteriorates, the patient may be described as ‘decompensated’ and this may happen suddenly, i.e.
‘acutely’, usually leading to hospital admission, an event of considerable prognostic importance. New ‘de novo’ HF may present acutely, for example as a consequence of
acute myocardial infarction or in a subacute gradual fashion, for example in a patient who has had asymptomatic cardiac dysfunction, often for an indeterminate period, and
may persist or resolve patients may become ‘compensated’.
When HF is suspected, the goal of the clinical assessments are to determine whether HF is present, define the underlying cause, assess severity of the disease and
the patients prognosis and identify comorbid condition. When the diagnosis of HF has already been established, the goal are similar, with a particular focus on optimal
therapeutic intervention. The goals of treatment in patients with established HF are to
relieve symptoms and signs e.g. oedema, prevent hospital admission, and improve survival. The relief of symptoms, improvement in quality of life, and increase
in functional capacity are also of the utmost importance to patients. Effective pharmacological therapies and CRT improve these outcomes, as well as mortality and
hospitalization. Three neurohumoral antagonists—an ACE inhibitor [or angiotensin receptor blocker ARB], a beta-blocker, and an MRA—are fundamentally important in
modifying the course of systolic HF and should at least be considered in every patient. They are commonly used in conjunction with a diuretic given to relieve the symptoms and
signs of congestion.
Standard References: 1.Mann, DL et all. Braunwald’s Heart Disease, 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
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SELF DIRECTING LEARNING
Basic knowledge that must be known: 1. Etiology of Heart Failure
2. Pathophysiology of Heart Failure 3. Clinical and diagnostic approach of Heart Failure
4. Pharmacologic treatment of Heart Failure 5. Rehabilitation and prognosis of Heart Failure
SCENARIO : CASE:
A 28-year old female, came to Emergency Room due to shortness of breath since 1 week PTA, and getting worse since 1 day PTA. The shortness of breath was aggravated by
supine position and alleviated by sitting position. She had history of taking Benzathine Penicillin intramuscular every month for 2 years due to Rheumatic Heart Disease. The
blood pressure at presentation was 10070 mmHg, pulse rate 130 beats per minute, irregular. The physical examination revealed irregular heartbeat, diastolic rumbling
murmur at apex, rales on both lung fields. The ECG revealed atrial fibrillation 130 bpm with Right axis deviation and right ventricular hyperthropy.
LEARNING TASK :
1. What is the most likely diagnosis of the patient? 2. What is the treatment of choice for this patient?
3. What is the parameters that you should monitor for evaluating the response to therapy in this patient?
SELF ASSESSMENT:
1. Please describe the Framingham score of heart failure
2. What are the treatment of chronic heart failure?
3. In heart failure, the heart usually increase doe to hypertrophy and dilatation.
Explain about morphology of concentric and eccentric hypertrophy 4.
Please describe the classification of primary cardiomyopathy
5. A 50 year old man complain from fatigue, short of breath, left chest pain when