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Acute Coronary Syndrome (ACS), Medicine

Medicine posting includes definition, etiologies, pathogenesis, clinical features, investigations, complications, managements, and prognosis of acute coronary syndrome

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Acute Coronary Syndrome (ACS), Medicine

  1. 1. ACUTE CORONARY SYNDROME MARYAM JAMILAH BINTI ABDUL HAMID 082013100002 IMS BANGALORE
  2. 2. LEARNING OUTCOME •Definition •Etiology •Pathogenesis •Clinical features •Investigation •Management •Prognosis
  3. 3. INTRODUCTION Acute coronary syndrome: Encompasses both unstable angina and myocardial infarction (MI) Unstable angina: Characterized by new-onset or rapidly worsening angina (crescendo angina), angina on minimal exertion or angina at rest in the absence of myocardial damage MI: Symptoms occur at rest and there is evidence of myocardial necrosis, as demonstrated by an elevation in cardiac troponin or CK- MB isoenzyme
  4. 4. ETIOLOGY • Atherosclerosis • Arteritis • Coronary dissection • Embolism • Coronary mural thickening • Causes of coronary luminal narrowing • Congenital coronary artery disease
  5. 5. PATHOGENESIS
  6. 6. UNSTABLE ANGINA • Pattern of pain that is progressive with increasing frequency • Precipitated by less effort • Often occurs at rest. Tends to be long duration. • Induced by disruption of atherosclerotic plaques, with superadded thrombosis, embolization & vasospasm. • Pre Infarction Angina
  7. 7. MYOCARDIAL INFARCTION TYPES •TRANSMURAL •SUBENDOCARDIAL
  8. 8. LOCATION OF INFARCT •LAD  Anterior & Apical LV & 2/3 IV Septum [40--50%] •RCA  Post & Basal LV & Post 1/3 of IV Septum [30--40%] •LCA  Lateral wall of LV [15 - 20% ]
  9. 9. CLINICAL FEATURES SYMPTOMS • Prolonged cardiac pain: chest, throat, arms, epigastrium or back • Anxiety and fear of impending death • Nausea & vomiting • Breathlessness • Collapse/syncope
  10. 10. PHYSICAL SIGNS • Signs of sympathetic activation: pallor, sweating, tachycardia • Signs of vagal activation: vomiting, bradycardia • Signs of impaired myocardial function Hypotension, oliguria, cold peripheries Narrow pulse pressure Raised JVP S3 S1 –quiet Apical impulse: diffuse Lung crepitation • Signs of tissue damage: fever • Signs of complications: mitral regurgitation, pericarditis
  11. 11. Condition Duration Quality Location Associated features Unstable angina 10-20 min Pressure, tightness, heaviness, burning Retrosternal, often with radiation to or isolated discomfort in neck, jaw, sholders, or arms- freq. left Precipitated by low exertion, at rest, exposure to cold, psychologic stress S4 gallop or mitral regurgitation murmur during pain Acute MI Variable; often >30 min Unrelieved with nitroglycerin May be associated with heart failure or arrhythmia
  12. 12. KILLIP CLASS • 1967, Acute myocardial infarction • Focus on physical examination & development of heart failure to predict risk • Class I: No evidence of heart failure (mortality 6%) • Class II: Mild to moderate heart failure (S3 gallop, rales < half-way up lung fields or elevated JVP) • Class III: Pulmonary edema (mortality 38%) • Class IV: Cardiogenic shock defined as SBP <90 mmHg, signs of hypoperfusion; oligouria, cyanosis, swelling (mortality 67%)
  13. 13. RISK STRATIFICATION
  14. 14. INVESTIGATION • Electrocardiography • Plasma cardiac biomarkers • Other blood tests • Chest X-Ray • Echocardiography
  15. 15. ECG • Confirming diagnosis • To be repeated • Limitation: difficult to interpret if bundle branch block (BBB) or previous MI present • Best seen in the leads ‘face’ ischaemic or infected area
  16. 16. • Anteroseptal infarction: V1 to V4 • Anterolateral infarction: V4 to V6, aVL, lead I • Inferior infarction: lead II, lead III, aVF, ‘reciprocal’ changes of ST depression on lead I, aVL and anterior chest lead if involve RV– need additional leads on right pericardium • Posterior wall infarction: no ST elevation or Q waves in standard leads, ‘reciprocal’ changes (ST-segment depress), tall R wave V1-V4
  17. 17. Transmural MI 1. Proximal occlusion of a major coronary artery; ST-segment elevation (or new BBB) 2. Diminution size of R wave 3. Transmural  develop Q wave 4. T wave inverted; change in ventricular repolarisation
  18. 18. Subendocardial MI • Non ST-segment elevation • Partial occlusion of a major vessel or complete occlusion of a minor vessel • Unstable angina, subendothelial MI • T wave inversion • Loss of R wave • Absence of Q wave
  19. 19. MARKER ONSET PEAK DURATION NORMAL VALUE CK-MB 3-6 hours 18-24 hours 36-72 hours 0-5.5 ng/ml Troponins 4-10 hours 18-24 hours 8-14 days 0-0.1 ng/ml Myoglobin 1-4 hours 6-7 hours 24 hours 10-95 ng/ml (M) 10-65 ng/ml (F) LDH 6-12 hours 24-72 hours 6-8 days 125-220 U/L AST 24-36 hours 4-5 days 10-12 days 10-45 U/L
  20. 20. IMMEDIATE MANAGEMENT- FIRST 12 HOURS •Analgesia •Antithrombotic therapy •Anti-angina therapy •Reperfusion therapy
  21. 21. COMPLICATIONS OF ACUTE CORONARY SYNDROME • Arrhythmias • Ischemia • Acute circulatory failure • Pericarditis • Mechanical complication • Embolism • Impaired ventricular function, remodeling and ventricular aneurysm
  22. 22. LATE MANAGEMENT IN MI •Risk stratification and further investigation •Lifestyle modification •Secondary prevention drug therapy •Rehabilitation •Device
  23. 23. PROGNOSIS • ¼ cases, death within few minutes without medical care • ½ death within 24 hours of onset • 40% affected patients die within first month • Reach hospital & receive medication; 28-day survival >85% • Worse prognosis with anterior and inferior infarction • Who survive acute attack; >80% live a further year 75% for 5 years 50% for 10 years 25% for 20 years
  24. 24. CONCLUSION
  25. 25. REFERENCES • BRIAN R. WALKER, NICKI R. COLLEDGE, STUART H. RALSTON, IAN D. PENMAN, Davidson’s Principles & Practice of Medicine, 22nd Edition • MICHAEL GLYNN, WILLIAM DRAKE, Hutchinson’s Clinical Methods, 23rd Edition
  26. 26. THANK YOU

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