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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

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slide1

Complications of Acute M.I.

Douglas Burtt, M.D.

slide2

Left Anterior Descending Occlusion

Occlusion of the

left anterior descending

coronary artery

experimental data
Experimental Data
  • Canine studies – transient artery clamping or ligation
  • Balloon angioplasty studies
    • Time dependent series of events
    • Chest Pain as a late event
slide4

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
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
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
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 anatomically1
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

ACUTE M.I.Anatomical correlates

LAD occlusion causes extensive infarction associated with:

  • LV failure
  • High grade heart block
  • Apical aneurysm formation
  • Thrombo-embolic complications
slide13

ACUTE M.I.Anatomical correlates

RCA occlusion causes moderate infarction associated with:

  • RV failure
  • Bradyarrhythmias
  • Occasional mechanical complications
acute m i arrhythmias
ACUTE M.I.Arrhythmias
  • Sinus bradycardia
  • Sinus tachycardia
  • Atrial fibrillation
  • PVCs / ventricular tachycardia /ventricular fibrillation
  • Heart block
arrhythmias inferior m i
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
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
ACUTE M.I.Hypotension
  • Identify hemodynamic subset
  • Distinguish decreased preload from decreased cardiac output
  • Think about hemodynamic monitoring
hemodynamic subsets
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.

slide19

1

3

Cardiac

Index

(L/min/m2)

2

4

L.V.E.D.P.

Hemodynamic Subsets

acute m i 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 r1
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
development of giant v waves
Development of giant “V waves”

P.C. Wedge pressure

P. A. pressure

V-wave

acute mitral regurgitation treatment
Acute Mitral Regurgitation:Treatment
  • Rapid diagnosis
  • Afterload reduction
  • Inotropic support
  • Intra-aortic balloon pump
  • Surgical valve replacement
acute m i acute ventricular septal defect
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 defect1
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
Acute V.S.D.:Treatment
  • Rapid diagnosis
  • Afterload reduction
  • Inotropic support
  • Intra-aortic balloon pump
  • Surgical repair of ruptured septum
intra aortic balloon pump
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
free wall rupture
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
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 aneurysm1
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
slide37

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
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
slide39

1

3

Cardiac

Index

(L/min/m2)

2

4

L.V.E.D.P.

Hemodynamic Subsets

acute m i pericarditis
ACUTE M.I.Pericarditis
  • Pleuritic chest pain
  • Radiation to the trapezius ridge
  • Fever
  • Pericardial friction rub
acute m i cardiogenic shock
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!!!

LAD vs. RCA

Think hemodynamic subsets!!!

Summary

Watch for mechanical complications