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Explore the anatomical correlates, arrhythmias, mechanical complications, and treatment options for patients experiencing an acute MI, including factors related to acute ventricular septal defects and papillary muscle ruptures. Understand the physiological cascades and time course of cell death to enhance clinical management.
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Complications of Acute M.I. Douglas Burtt, M.D.
Left Anterior Descending Occlusion Occlusion of the left anterior descending coronary artery
Experimental Data • Canine studies – transient artery clamping or ligation • Balloon angioplasty studies • Time dependent series of events • Chest Pain as a late event
ACUTE M.I.THE “ISCHEMIC CASCADE” Diastolic dysfunction Chest pressure, etc. Acute MI Release of CPK Ischemic EKG changes Localized systolic dysfunction
ACUTE M.I.THE “ISCHEMIC CASCADE” • Diastolic dysfunction • Localized systolic dysfunction • Ischemic EKG changes • Chest pressure, etc. • Release of CPK
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
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
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)
ACUTE M.I.Anatomical correlates LAD occlusion causes extensive infarction associated with: • LV failure • High grade heart block • Apical aneurysm formation • Thrombo-embolic complications
ACUTE M.I.Anatomical correlates RCA occlusion causes moderate infarction associated with: • RV failure • Bradyarrhythmias • Occasional mechanical complications
ACUTE M.I.Arrhythmias • Sinus bradycardia • Sinus tachycardia • Atrial fibrillation • PVCs / ventricular tachycardia /ventricular fibrillation • Heart block
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
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
ACUTE M.I.Hypotension • Identify hemodynamic subset • Distinguish decreased preload from decreased cardiac output • Think about hemodynamic monitoring
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.
1 3 Cardiac Index (L/min/m2) 2 4 L.V.E.D.P. Hemodynamic Subsets
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.
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
Echo/Color Doppler of Acute M.R. LV RA LA
Development of giant “V waves” P.C. Wedge pressure P. A. pressure V-wave
Acute Mitral Regurgitation:Treatment • Rapid diagnosis • Afterload reduction • Inotropic support • Intra-aortic balloon pump • Surgical valve replacement
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”
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”
Acute V.S.D.:Treatment • Rapid diagnosis • Afterload reduction • Inotropic support • Intra-aortic balloon pump • Surgical repair of ruptured septum
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
Cardiac TamponadeEqualization of diastolic pressuresHypotensionJ.V.D.Clear lung fields Pulsus paradoxus Pseudoaneurysm Enlarged cardiac silhouette Echocardiographic diagnosis Free Wall Rupture
ACUTE M.I.Apical Aneurysm • Associated with large, transmural antero-apical MI • Can lead to LV apical thrombus • Is associated with ventricular arrhythmias
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
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
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
1 3 Cardiac Index (L/min/m2) 2 4 L.V.E.D.P. Hemodynamic Subsets
ACUTE M.I.Pericarditis • Pleuritic chest pain • Radiation to the trapezius ridge • Fever • Pericardial friction rub
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.
Think anatomically!!! LAD vs. RCA Think hemodynamic subsets!!! Summary Watch for mechanical complications