Bio-Med 350 Complications of Acute M.I. Douglas Burtt, M.D.

Bio-Med 350 Coronary atherosclerosis

Bio-Med 350 Schematic of an Unstable Plaque

Bio-Med 350 Cross section of a complicated plaque

Bio-Med 350 Journey down a coronary…

Bio-Med 350 Frank Netter: View of the Heart

Bio-Med 350 Left Anterior Descending Occlusion Occlusion of the left anterior descending coronary artery

Bio-Med 350 Experimental Data Canine studies – transient artery clamping or ligation Balloon angioplasty studies Time dependent series of events Chest Pain as a late event

Bio-Med 350 ACUTE M.I. THE “ISCHEMIC CASCADE” Chest pressure, etc. Localized systolic dysfunction Diastolic dysfunction Release of CPK Ischemic EKG changes Acute MI

Bio-Med 350 ACUTE M.I. THE “ISCHEMIC CASCADE” 1. Diastolic dysfunction 2. Localized systolic dysfunction 3. Ischemic EKG changes 4. Chest pressure, etc. 5. Release of CPK

Bio-Med 350 Time course of cell death minutes to irreversible cell injury ~ 24 hours to coagulation necrosis days to “yellow softening” weeks: ventricular “remodeling” weeks: fibrosis completed

Bio-Med 350 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

Bio-Med 350 Blood supply of the septum

Bio-Med 350 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)

Bio-Med 350 Conduction System of the Heart

Bio-Med 350 Conduction System: detail

Bio-Med 350 ACUTE M.I. Anatomical correlates LAD occlusion causes extensive infarction associated with: LV failure High grade heart block Apical aneurysm formation Thrombo-embolic complications

Bio-Med 350 ACUTE M.I. Anatomical correlates RCA occlusion causes moderate infarction associated with: RV failure Bradyarrhythmias Occasional mechanical complications

Bio-Med 350 ACUTE M.I. Arrhythmias Sinus bradycardia Sinus tachycardia Atrial fibrillation PVCs / ventricular tachycardia /ventricular fibrillation Heart block

Bio-Med 350 Arrhythmias: Inferior M.I. Sinus bradycardia -- S.A. nodal artery and increased vagal tone Heart block -- A-V nodal artery 1st degree A-V block Wenckebach 2nd degree A-V block A-V dissociation Atrial fibrillation -- L.A. stretch Ventricular tachycardia / fibrillation -- via “re-entry” or increased automaticity

Bio-Med 350 Arrhythmias: Anterior M.I. Sinus tachycardia -- low stroke volume Heart block -- His-Purkinje system Left or Right Bundle branch block Complete Heart Block Ventricular tachycardia / fibrillation due to “re-entry” or increased automaticity

Bio-Med 350 ACUTE M.I. Hypotension Identify hemodynamic subset Distinguish decreased preload from decreased cardiac output Think about hemodynamic monitoring

Bio-Med 350 Hemodynamic subsets Starling curves to plot “preload” versus cardiac output Identification of high risk subgroups Definition of cardiogenic shock L.V.E.D.P. Cardiac Output

Bio-Med 350 L.V.E.D.P. Cardiac Index (L/min/m2) Hemodynamic Subsets

Bio-Med 350 Acute M.I. Mechanical Complications ª Rupture of free wall Tamponade Pseudoaneurysm ª Rupture of papillary muscle Acute Mitral regurgitation ª Rupture of intraventricular septum Acute V.S.D.

Bio-Med 350 ACUTE M.I. Papillary Muscle Rupture Leading to Acute M.R.

Bio-Med 350 ACUTE M.I. Papillary Muscle Rupture Leading to Acute M.R. Systolic murmur Giant V - waves on PC Wedge tracing Echo/Doppler confirmation RX with Afterload reduction Intra-aortic balloon pump

Bio-Med 350 “Flail” Mitral Leaflet

Bio-Med 350 Echo/Color Doppler of Acute M.R. LA LV RA

Bio-Med 350 Development of giant “V waves” P. A. pressure V-wave P.C. Wedge pressure

Bio-Med 350 Acute Mitral Regurgitation: Treatment Rapid diagnosis Afterload reduction Inotropic support Intra-aortic balloon pump Surgical valve replacement

Bio-Med 350 ACUTE M.I. Acute Ventricular Septal Defect Can occur with either anterior or inferior MICan occur with either anterior or inferior MI Peak incidence on days 3-7Peak incidence on days 3-7 Causes an abrupt left- to-right “shunt”Causes an abrupt left- to-right “shunt”

Bio-Med 350 ACUTE M.I. Acute Ventricular Septal Defect Abrupt onset of a harsh systolic murmur, often with a “thrill”Abrupt onset of a harsh systolic murmur, often with a “thrill” Detected by an oxygen saturation “step-up”Detected by an oxygen saturation “step-up”

Bio-Med 350 Oxygen saturation “step-up”

Bio-Med 350 Acute V.S.D.: Treatment Rapid diagnosis Afterload reduction Inotropic support Intra-aortic balloon pump Surgical repair of ruptured septum

Bio-Med 350 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

Bio-Med 350 Intra aortic balloon pump

Bio-Med 350 Intra-aortic balloon pump

Bio-Med 350 Free Wall Rupture Cardiac Tamponade Equalization of diastolic pressures Hypotension J.V.D. Clear lung fields Pulsus paradoxus Pseudoaneurysm Enlarged cardiac silhouette Echocardiographic diagnosis

Bio-Med 350 ACUTE M.I. Apical Aneurysm Associated with large, transmural antero-apical MI Can lead to LV apical thrombus Is associated with ventricular arrhythmias

Bio-Med 350 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

Bio-Med 350 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

Bio-Med 350 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

Bio-Med 350 L.V.E.D.P. Cardiac Index (L/min/m2) Hemodynamic Subsets

Bio-Med 350 ACUTE M.I. Pericarditis Pleuritic chest pain Radiation to the trapezius ridge Fever Pericardial friction rub

Bio-Med 350 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.

Bio-Med 350

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

Bio-Med 350 THE END