Complications of Acute M.I.

Douglas Burtt, M.D.

Complications of MI
Arrhythmias
Heart Block Bradyarrhythmia Tachyarrhythmia
Supraventricular Ventricular

Hemodynamic disruption
Congestive Heart failure Hypotension / Shock

Complications of MI
Mechanical Complications
Papillary muscle rupture Free Wall Rupture Acute VSD LV apical aneurysm

Pericarditis Thromboembolism

Anatomic consequences of 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

THE ISCHEMIC CASCADE

Chest pressure, etc. Diastolic dysfunction

ACUTE M.I.

Acute MI
Ischemic EKG changes

Release of CPK

Localized systolic dysfunction

THE ISCHEMIC CASCADE

ACUTE M.I.

1. 2. 3. 4. 5.

Diastolic dysfunction Localized systolic dysfunction Ischemic EKG changes Chest pressure, etc. Release of CPK

Time course of cell death

20 - 30 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 twothirds 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: 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

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

Acute ______ MI

Acute Inferior MI

What is the rhythm???

Cherchez la P

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 anterior MI

Hemodynamic Consequences of MI
Congestive Heart Failure
Diastolic dysfunction Systolic dysfunction Increased LVEDP pulmonary congestion

Hypotension / Shock
May be due to low preload May be due to decreased stroke volume
i.e. Cardiogenic Shock

Congestive Heart Failure

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
6 5 4 3 2 1 0

Cardiac Output

L.V.E.D.P.

3 2.5 Cardiac 2 Index (L/min/m2) 1.5 1 0.5 0

L.V.E.D.P.

Hemodynamic Subsets

3 2.5 Cardiac 2 Index (L/min/m2) 1.5 1 0.5 0

Patients in Quadrant 1 Best Prognosis Quadrants 2 + 3 Intermediate Prognosis Quadrant 4 Cardiogenic Shock WORST PROGNOSIS

10

20

30

L.V.E.D.P.

Cardiogenic Shock
Early reperfusion strategy Supportive measures
Inotropic drugs Intra-aortic balloon pump Left ventricular assist device

Look for correctable causes

RV infarct Mechanical complications

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

Gated MRI of Acute M.R. due to papillary muscle dysfunction

AnGa cine 3CH MR.mov

Acute M.R. due to papillary muscle dysfunction

Development of giant V waves

Development of giant V waves

P. A. pressure P.C. Wedge 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 leftto-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 M.I. Acute Ventricular Septal Defect

Oxygen saturation step-up

IV C sat SV C sat RA sat RV sat PA sat 70% 65% 68% 88% 88%

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

Cardiac Tamponade
Equalization of diastolic pressures Hypotension J.V.D. Clear lung fields Pulsus paradoxus

Pseudoaneurysm
Enlarged cardiac silhouette Echocardiographic diagnosis

ACUTE M.I. Apical Aneurysm

Associated with large, transmural anteroapical 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

ACUTE M.I. Apical Aneurysm

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

3 2.5 Cardiac 2 Index (L/min/m2) 1.5 1 0.5 0

L.V.E.D.P.

Where is the patient with RV infarct?

ACUTE M.I. Pericarditis

Related to acute inflammatory process

Pleuritic chest pain Radiation to the trapezius ridge Fever Pericardial friction rub

ACUTE M.I. CARDIOGENIC SHOCK (recap)

Usually due to a large area of myocardial necrosis

Aim for rapid reperfusion strategy e.g. Stent Exclude easily correctable causes -- i.e. hypovolemia or R.V. infarct Consider mechanical complications Employ supportive measures with:
I.A.B.P. inotropic drugs LV assist device

Summary for RCA (or circumflex) infarct

Right coronary artery Right ventricular infarct S-A nodal infarct A-V nodal infarct Bradyarrhythmias 1st degree A-V block Mobitz I 2nd degree block A-V dissociation Postero-medial papillary muscle infarct Acute mitral regurgitation (with or without papillary muscle rupture)

Hypotension due to decreased L.V. filling

Summary for LAD infarct

Left anterior descending artery 40% of LV myocardium Cardiogenic shock due loss of large amount of to myocardium Intraventricular septum (upper two-thirds) Antero-apical wall His-Purkinje system Advanced Heart Block (LBBB, 3rd degree A-V block and Mobitz II 2nd degree)

Acute ventricular septal defect

Apical L.V. aneurysm Apical thrombus formation Arterial embolism originating in the L.V.

Ventricular arrhythmias

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

THE END