Download Free Medical Complications of Acute M I PowerPoint Presentation

Complications of Acute M I PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Complications of Acute M.I.".

This medical PowerPoint presentation talks about complications of acute MI. Acute myocardial infarction (MI), also known as a heart attack, is a medical emergency that occurs when blood flow to the heart muscle is blocked, leading to damage or death of heart muscle cells. The complications of acute MI can range from mild to severe and can affect various organs and systems in the body.

Some of the common complications of acute MI include Arrhythmias, Heart failure, Cardiogenic shock, Pericarditis, Thromboembolism, Ventricular aneurysm, and Sudden cardiac arrest.

Tags : Acute M.I., Acute myocardial infarction, heart attack, Arrhythmias, Heart failure, Cardiogenic shock, Pericarditis, Thromboembolism, Ventricular aneurysm, Sudden cardiac arrest, cardiology, cardiology PowerPoint presentation

Published on : Mar 17, 2023 | Views : 1118 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Complications of Acute M.I. Douglas Burtt, M.D.
Slide 2-

Coronary atherosclerosis
Slide 3-

Schematic of an Unstable Plaque
Slide 4-

Cross section of acomplicated plaque
Slide 5-

Journey down a coronary…
Slide 6-

Frank Netter: View of the Heart
Slide 7-

Left Anterior Descending Occlusion Occlusion of the left anterior descending coronary artery
Slide 8-

Experimental Data Canine studies – transient artery clamping or ligation Balloon angioplasty studies Time dependent series of events Chest Pain as a late event
Slide 9-

ACUTE M.I.THE “ISCHEMIC CASCADE” Chest pressure, etc. Localized systolic dysfunction Diastolic dysfunction Release of CPK Ischemic EKG changes Acute MI
Slide 10-

ACUTE M.I.THE “ISCHEMIC CASCADE” Diastolic dysfunction Localized systolic dysfunction Ischemic EKG changes Chest pressure, etc. Release of CPK
Slide 11-

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
Slide 12-

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
Slide 13-

Blood supply of the septum
Slide 14-

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)
Slide 15-

Conduction System of the Heart
Slide 16-

Conduction System: detail
Slide 17-

ACUTE M.I.Anatomical correlates LAD occlusion causes extensive infarction associated with: LV failure High grade heart block Apical aneurysm formation Thrombo-embolic complications
Slide 18-

ACUTE M.I.Anatomical correlates RCA occlusion causes moderate infarction associated with: RV failure Bradyarrhythmias Occasional mechanical complications
Slide 19-

ACUTE M.I.Arrhythmias Sinus bradycardia Sinus tachycardia Atrial fibrillation PVCs / ventricular tachycardia /ventricular fibrillation Heart block
Slide 20-

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
Slide 21-

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
Slide 22-

ACUTE M.I.Hypotension Identify hemodynamic subset Distinguish decreased preload from decreased cardiac output Think about hemodynamic monitoring
Slide 23-

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
Slide 24-

L.V.E.D.P. Cardiac Index (L/min/m2) 4 3 1 2 Hemodynamic Subsets
Slide 25-

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.
Slide 26-

ACUTE M.I.Papillary Muscle RuptureLeading to Acute M.R.
Slide 27-

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
Slide 28-

“Flail” Mitral Leaflet
Slide 29-

Echo/Color Doppler of Acute M.R. LA LV RA
Slide 30-

Development of giant “V waves” P. A. pressure V-wave P.C. Wedge pressure
Slide 31-

Acute Mitral Regurgitation:Treatment Rapid diagnosis Afterload reduction Inotropic support Intra-aortic balloon pump Surgical valve replacement
Slide 32-

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”
Slide 33-

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”
Slide 34-

Oxygen saturation “step-up”
Slide 35-

Acute V.S.D.:Treatment Rapid diagnosis Afterload reduction Inotropic support Intra-aortic balloon pump Surgical repair of ruptured septum
Slide 36-

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
Slide 37-

Intra aortic balloon pump
Slide 38-

Intra-aortic balloon pump
Slide 39-

Free Wall Rupture Cardiac TamponadeEqualization of diastolic pressuresHypotensionJ.V.D.Clear lung fields Pulsus paradoxus Pseudoaneurysm Enlarged cardiac silhouette Echocardiographic diagnosis
Slide 40-

ACUTE M.I.Apical Aneurysm Associated with large, transmural antero-apical MI Can lead to LV apical thrombus Is associated with ventricular arrhythmias
Slide 41-

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
Slide 42-

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
Slide 43-

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
Slide 44-

L.V.E.D.P. Cardiac Index (L/min/m2) 4 3 1 2 Hemodynamic Subsets
Slide 45-

ACUTE M.I.Pericarditis Pleuritic chest pain Radiation to the trapezius ridge Fever Pericardial friction rub
Slide 46-

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.
Slide 47-

ppt slide no 47 content not found
Slide 48-

ppt slide no 48 content not found
Slide 49-

Summary Think anatomically!!! LAD vs. RCA Think hemodynamic subsets!!! Watch for mechanical complications
Slide 50-

THE END