Myocardial Ischemia and Acute M.I.

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Complications of Acute M.I.
Douglas Burtt, M.D.
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Coronary atherosclerosis
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Schematic of an Unstable Plaque
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Cross section of acomplicated plaque
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Journey down a coronary
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Frank Netter View of the Heart
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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

1. Diastolic dysfunction
2. Localized systolic dysfunction
3. Ischemic EKG changes
4. Chest pressure, etc.
5. Release of CPK

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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

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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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ACUTE M.I.Arrhythmias

• Sinus bradycardia
• Sinus tachycardia
• Atrial fibrillation
• PVCs / ventricular tachycardia /ventricular
  fibrillation
• Heart block

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ArrhythmiasInferior 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

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ArrhythmiasAnterior 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

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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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Cardiac Index (L/min/m2)
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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 RuptureLeading to
Acute M.R.
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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

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Flail Mitral Leaflet
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Echo/Color Doppler of Acute M.R.
LV
LA
RA
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Development of giant V waves
P.C. Wedge pressure
P. A. pressure
V-wave
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Acute Mitral RegurgitationTreatment

• 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 TamponadeEqualization of diastolic
  pressuresHypotensionJ.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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Cardiac Index (L/min/m2)
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L.V.E.D.P.
Hemodynamic Subsets
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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!!!
• LAD vs. RCA

• Think hemodynamic subsets!!!

Watch for mechanical complications
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THE END