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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

  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
  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
  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%)
  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