Complications of Acute M.I.

1. Complications of Acute M.I. Douglas Burtt, M.D.

2. Left Anterior Descending Occlusion Occlusion of the left anterior descending coronary artery

3. Experimental Data • Canine studies – transient artery clamping or ligation • Balloon angioplasty studies • Time dependent series of events • Chest Pain as a late event

4. ACUTE M.I.THE “ISCHEMIC CASCADE” Diastolic dysfunction Chest pressure, etc. Acute MI Release of CPK Ischemic EKG changes Localized systolic dysfunction

5. ACUTE M.I.THE “ISCHEMIC CASCADE” • Diastolic dysfunction • Localized systolic dysfunction • Ischemic EKG changes • Chest pressure, etc. • Release of CPK

6. Time course of cell death • 20 - 40 minutes to irreversible cell injury • ~ 24 hours to coagulation necrosis • 5 - 7 days to “yellow softening” • 1 - 4 weeks: ventricular “remodeling” • 6 - 8 weeks: fibrosis completed

7. Think Anatomically!! • Left main coronary artery supplies two-thirds of the myocardium • LAD supplies ~ 40% of the L.V., including apex, septum and anterior wall • RCA supplies less L.V. myocardium, but all of the R.V. myocardium

8. Blood supply of the septum

9. Think Anatomically!!! • LAD supplies most of the conduction system below the A-V node(i.e. the His-Purkinje system) • RCA supplies most of the conduction system at or above the A-V node(i.e. the A-V node and, usually, the S-A node)

10. Conduction System of the Heart

11. Conduction System: detail

12. ACUTE M.I.Anatomical correlates LAD occlusion causes extensive infarction associated with: • LV failure • High grade heart block • Apical aneurysm formation • Thrombo-embolic complications

13. ACUTE M.I.Anatomical correlates RCA occlusion causes moderate infarction associated with: • RV failure • Bradyarrhythmias • Occasional mechanical complications

14. ACUTE M.I.Arrhythmias • Sinus bradycardia • Sinus tachycardia • Atrial fibrillation • PVCs / ventricular tachycardia /ventricular fibrillation • Heart block

15. Arrhythmias:Inferior M.I. • Sinus bradycardia -- S.A. nodal artery and increased vagal tone • Heart block -- A-V nodal artery1st degree A-V blockWenckebach 2nd degree A-V blockA-V dissociation • Atrial fibrillation -- L.A. stretch • Ventricular tachycardia / fibrillation -- via “re-entry” or increased automaticity

16. Arrhythmias:Anterior M.I. • Sinus tachycardia -- low stroke volume • Heart block -- His-Purkinje systemLeft or Right Bundle branch blockComplete Heart Block • Ventricular tachycardia / fibrillation due to “re-entry” or increased automaticity

17. ACUTE M.I.Hypotension • Identify hemodynamic subset • Distinguish decreased preload from decreased cardiac output • Think about hemodynamic monitoring

18. Hemodynamic subsets • Starling curves to plot “preload” versus cardiac output • Identification of high risk subgroups • Definition of cardiogenic shock Cardiac Output L.V.E.D.P.

19. 1 3 Cardiac Index (L/min/m2) 2 4 L.V.E.D.P. Hemodynamic Subsets

20. Acute M.I.Mechanical Complications • Rupture of free wall Tamponade Pseudoaneurysm • Rupture of papillary muscle Acute Mitral regurgitation • Rupture of intraventricular septum Acute V.S.D.

21. ACUTE M.I.Papillary Muscle RuptureLeading to Acute M.R.

22. ACUTE M.I.Papillary Muscle RuptureLeading to Acute M.R. • Systolic murmur • Giant V - waves on PC Wedge tracing • Echo/Doppler confirmation • RX with Afterload reduction • Intra-aortic balloon pump

23. “Flail” Mitral Leaflet

24. Echo/Color Doppler of Acute M.R. LV RA LA

25. Development of giant “V waves” P.C. Wedge pressure P. A. pressure V-wave

26. Acute Mitral Regurgitation:Treatment • Rapid diagnosis • Afterload reduction • Inotropic support • Intra-aortic balloon pump • Surgical valve replacement

27. ACUTE M.I.Acute Ventricular Septal Defect • Can occur with either anterior or inferior MI • Peak incidence on days 3-7 • Causes an abrupt left-to-right “shunt”

28. ACUTE M.I.Acute Ventricular Septal Defect • Abrupt onset of a harsh systolic murmur, often with a “thrill” • Detected by an oxygen saturation “step-up”

29. Oxygen saturation “step-up”

30. Acute V.S.D.:Treatment • Rapid diagnosis • Afterload reduction • Inotropic support • Intra-aortic balloon pump • Surgical repair of ruptured septum

31. Intra-Aortic Balloon Pump • Augments coronary blood flow during diastole • Decreases afterload during systole by deflating at the onset of systole • Reduces myocardial ischemia by both mechanisms

32. Intra aortic balloon pump

33. Intra-aortic balloon pump

34. Cardiac TamponadeEqualization of diastolic pressuresHypotensionJ.V.D.Clear lung fields Pulsus paradoxus Pseudoaneurysm Enlarged cardiac silhouette Echocardiographic diagnosis Free Wall Rupture

35. ACUTE M.I.Apical Aneurysm • Associated with large, transmural antero-apical MI • Can lead to LV apical thrombus • Is associated with ventricular arrhythmias

36. ACUTE M.I.Apical Aneurysm • Causes “dyskinesis” of the apex • Can be detected by cardiac echo • Can lead to systemic emboli • Anticoagulants may prevent embolization

37. Right Heart Failure • Very commonly a sequela of Left Heart Failure • LVEDP • PCW • PA pressure • Right heart pressure overload • Cardiac causes • Pulmonic valve stenosis • RV infarction • Parenchymal pulmonary causes • COPD • ILD • Pulmonary vascular disease • Pulmonary embolism • Primary Pulmonary hypertension

38. ACUTE M.I.Right Ventricular Infarction • Jugular venous distention with clear lungs • Equalization of right atrial and PCW pressures • ST elevation in right precordial leads • Therapy with fluids

39. 1 3 Cardiac Index (L/min/m2) 2 4 L.V.E.D.P. Hemodynamic Subsets

40. ACUTE M.I.Pericarditis • Pleuritic chest pain • Radiation to the trapezius ridge • Fever • Pericardial friction rub

41. ACUTE M.I.CARDIOGENIC SHOCK • Large area of myocardial necrosis • Consider mechanical complications • Exclude correctable causes -- i.e. hypovolemia or R.V. infarct • I.A.B.P. C.A.B.G. OR P.T.C.A.

44. Think anatomically!!! LAD vs. RCA Think hemodynamic subsets!!! Summary Watch for mechanical complications

45. THE END