Complications Of Acute Mi

Front 1

Discuss the Complications of MI:

Back 1

*Arrhythmias
-Heart Block
-Bradyarrhythmia
-Tachyarrhythmia: Supraventricular or Ventricular

*Hemodynamic disruption
-Congestive Heart failure
-Hypotension / Shock

*Mechanical Complications
-Papillary muscle rupture
-Free Wall Rupture
-Acute VSD
-LV apical aneurysm

*Pericarditis
*Thromboembolism

Front 2

What are the Anatomic consequences of Left Anterior Descending Occlusion:

Back 2

*Occlusion of the left anterior descending coronary artery.

Front 3

Experimental Data--how long does it take to develop necrosis?

Back 3

*We've done Canine studies – transient artery clamping or ligation -- to see how long it takes.
*Balloon angioplasty studies have shown this, too.

*Time dependent series of events.
*Chest Pain is a LATE event

Front 4

Discuss THE “ISCHEMIC CASCADE” in acute MI: 5

Back 4

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

Front 5

What is the Time course of cell death:

Back 5

* 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

Front 6

What happens in real life when you have a MI:
What's the worst artery to have an occlusion in?

Back 6

1) Left main coronary artery supplies two-thirds of the myocardium--worst outcome.
2) LAD supplies ~ 40% of the L.V., including apex, septum and anterior wall. BAD.
3) RCA supplies less L.V. myocardium, but all of the R.V. myocardium. Less bad...

Front 7

Discuss Blood supply of the septum:

Back 7

LAD feeds anterior 2/3 of septum.

Front 8

Discuss Blood supply of conduction system:

Back 8

*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)

Front 9

Discuss the Conduction System anatomy:

Back 9

Front 10

Discuss Left side ACUTE M.I. Anatomical correlates: 4

Back 10

*LAD occlusion causes extensive infarction associated with:

-LV failure
-High grade heart block (lack of His/purkinje blood flow)
-Apical aneurysm formation
-Thrombo-embolic complications

Front 11

Discuss right side ACUTE M.I. Anatomical correlates: 3

Back 11

*RCA occlusion causes moderate infarction associated with:

*RV failure
*Bradyarrhythmias
*Occasional mechanical complications

*"Best" MI to have.

Front 12

Discuss ACUTE M.I. Arrhythmias:

Back 12

-Sinus bradycardia
-Sinus tachycardia
-Atrial fibrillation from LA enlargement.
-PVCs from re-entry / ventricular tachycardia / ventricular fibrillation (convertible in 90% of people...uncorrected, it will kill you).
-Heart block.

Front 13

Discuss Arrhythmias in Inferior M.I.:

Back 13

*From occlusion of RCA.

*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 -- from L.A. stretch

*Ventricular tachycardia / fibrillation -- via “re-entry” or increased autmaticity.

Front 14

Back 14

Acute inferior MI with ST elevation.

Front 15

Discuss Arrhythmias in Anterior M.I.:

Back 15

*LAD occlusion.

*Sinus tachycardia -- low stroke volume.

*Heart block -- His-Purkinje system (BAD!!!):
-Left or Right Bundle branch block.
-Complete Heart Block.
*Requires pacemaker for permanent correction.

*VT/VF due to “re-entry” or increased automaticity.

Front 16

Back 16

*Acute anterior MI with STE
*"tombstone" STEs are signs of anterior MI.

Front 17

Discuss the Hemodynamic Consequences of MI:

Back 17

*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.” (worst prognosis)

Front 18

Back 18

Congestive Heart Failure--curve shift right and LVEDP must increase to maintain CO.

Front 19

ACUTE M.I.Hypotension

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Back 19

Identify hemodynamic subset
Distinguish decreased preload from decreased cardiac output
Think about hemodynamic monitoring

Front 20

Discuss Hemodynamic subsets in MI patients.:

Back 20

*We use Starling curves to plot “preload” versus cardiac output
*Identification of high risk subgroups
*Definition of cardiogenic shock

Front 21

Discuss the "quadrants" of Frank-Starling curves to ID prognosis of HF patients:

Back 21

*Quadrant 1 is best--low LVEDP, normal cardiac index.
*Quadrant 2 has low BP, decreased organ perfusion, decreased mentation, but not CHF...LVEDP isn't high.
*3 has high cardiac index, but high LVEDP! --> pulmonary edema, but normal blood pressure.
*Sweet spot is in quadrant 1.
*Quadrant 4 is worst prognosis!

Front 22

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Back 22

Patients in Quadrant 1 
Best Prognosis

Quadrants 2 + 3 
Intermediate Prognosis

Quadrant 4 
“Cardiogenic Shock”
WORST PROGNOSIS

Front 23

HOW DO WE TREAT Cardiogenic Shock?

Back 23

*Early reperfusion strategy. Reduces mortality to 30-50% (from 60-80%).

*Supportive measures:
-Inotropic drugs.
-Intra-aortic balloon pump.
-Left ventricular assist device (a temporary bridge to heart transplant).

*Look for correctable causes:
-RV infarct.
-Mechanical complications.

Front 24

What are the Acute M.I. Mechanical Complications? 3

Back 24

*Occur during yellow softening phase-- heart muscle is vulnerable to tear and rupture.
*Acute MR from flail MV.

Front 25

ACUTE M.I.--discuss Papillary Muscle Rupture Leading to Acute M.R. :

Back 25

*It's usually a posterior papillary muscle tear...chordae are totally flail.
*Systolic murmur
*Giant V - waves on PC Wedge tracing
*Echo/Doppler confirmation
*RX with Afterload reduction
*Intra-aortic balloon pump

Front 26

Back 26

*“Flail” Mitral Leaflet (sickle shaped) post MI.

Front 27

Back 27

*Echo/Color Doppler of Acute M.R.
*LV at top; LA at bottom.
*Blue flow is MR thru a flail mitral leaflet.

Front 28

Back 28

Acute M.R. due to papillary muscle dysfunction post MI.

Front 29

Back 29

Development of giant “V waves” on wedge tracing.

Front 30

Development of giant “V waves”

Back 30

*Occurs with acute MR. Pathognomonic for acute MR.

Front 31

Discuss treatment of Acute Mitral Regurgitation:

Back 31

Rapid diagnosis
Afterload reduction
Inotropic support
Intra-aortic balloon pump
Surgical valve replacement!!!!!

Front 32

Back 32

*ACUTE M.I. resulting in Acute Ventricular Septal Defect. Muscle looks like softened ground beef around the VSD.

*Can occur with either anterior or inferior MI
*Peak incidence on days 3-7
*Causes an abrupt left-to-right “shunt”

*Abrupt onset of a harsh systolic murmur, often with a “thrill”-- grade IV.
*Detected by an oxygen saturation “step-up.”

Front 33

Discuss Oxygen saturation “step-up”:

Back 33

*RA saturation normally 75%.
*In VSD, RA saturation will be ~70%.
*RV will be much higher...this saturation shows that there is a shunt.
*SVC will be lower than IVC in oxygen content...brain sucks up a lot of blood. Kidney just filters...doesn't use as much blood. That's a way to think about the ∆.

Front 34

Discuss Acute V.S.D. Treatment:

Back 34

Rapid diagnosis
Afterload reduction
Inotropic support
Intra-aortic balloon pump (a bridge before surgery)
Surgical repair of ruptured septum!!!!!

Front 35

Back 35

*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.
*Timed to cardiac cycle; inflates and deflates to assist blood flow.

Front 36

Back 36

Intra aortic balloon pump

Front 37

Back 37

Intra-aortic balloon pump

Front 38

Discuss complications of Free Wall Rupture: 9

Back 38

Front 39

Back 39

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

Front 40

Complications of apical aneurysm:

Back 40

ACUTE M.I.-- Apical Aneurysm.

*Causes “dyskinesis” (expansion) of the apex.
*Can be detected by cardiac echo.
*Can lead to systemic emboli.
*Anticoagulants may prevent embolization.

Front 41

Discuss Right Heart Failure:

Back 41

Front 42

ACUTE M.I.--Right Ventricular Infarction:
findings--
treatment--

Back 42

*Jugular venous distention with clear lungs
*Equalization of right atrial and PCW pressures
*ST elevation in right precordial leads
*Therapy with FLUIDS.

Front 43

Back 43

Front 44

ACUTE M.I.Pericarditis
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Back 44

Related to acute inflammatory process

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

Front 45

ACUTE M.I.CARDIOGENIC SHOCK (recap):

Back 45

*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:
1) I.A.B.P.
2) inotropic drugs.
3) LV assist device.

Front 46

Summary for RCA or circumflex infarct:

Back 46

Front 47

Summary for LAD infarct:
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Back 47