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