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

Blood supply of the septum

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)

Conduction System of the Heart

Conduction System: detail

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

PVCs / ventricular tachycardia /ventricular fibrillation 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 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

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

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 Rupture Leading to Acute M.R.

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

“Flail” Mitral Leaflet

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”

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

Intra aortic balloon pump

Intra-aortic balloon pump

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

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

Radiation to the trapezius ridge Pericardial friction rub 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.

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

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