ChristieTWong- Comp Lication of Acute MI Notes

7/29/2019 ChristieTWong- Comp Lication of Acute MI Notes

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Complications of Acute M.I.

Douglas Burtt, M.D.


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Complications of MI

Arrhythmias

Heart Block

Bradyarrhythmia

Tachyarrhythmia Supraventricular

Ventricular

Hemodynamic disruption

Congestive Heart failure

Hypotension / Shock


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Complications of MI

Mechanical Complications

Papillary muscle rupture

Free Wall Rupture

Acute VSD

LV apical aneurysm

Pericarditis

Thromboembolism


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Anatomic consequences ofLeft Anterior Descending Occlusion

Occlusion oftheleft anteriordescending

coronaryartery


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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

Chest pressure, etc.

Localized systolic dysfunction

Diastolic dysfunction

Release of CPK

Ischemic EKG changes

Acute MI


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ACUTE M.I.THE ISCHEMIC CASCADE

1. Diastolic dysfunction

2. Localized systolic dysfunction3. Ischemic EKG changes

4. Chest pressure, etc.

5. Release of CPK


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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


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Think Anatomically!!

Left main coronary artery supplies two-

thirds of the myocardium

LAD supplies ~ 40% of the L.V., includingapex, septum and anterior wall

RCA supplies less L.V.

myocardium, but all ofthe 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: 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 tachycardiaAtrial fibrillation

PVCs / ventricular tachycardia /ventricular

fibrillationHeart block


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Arrhythmias:

Inferior M.I.

Sinus bradycardia -- S.A. nodal artery and increasedvagal tone

Heart block -- A-V nodal artery1st degree A-V block

Wenckebach 2nd degree A-V blockA-V dissociation

Atrial fibrillation -- L.A. stretch

Ventricular tachycardia / fibrillation --

via

re-entry

or increasedautomaticity


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Acute ______ MI


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Acute Inferior MI

What is the rhythm???


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Cherchez la P


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Arrhythmias:

Anterior M.I.

Sinus tachycardia -- low stroke volume

Heart block -- His-Purkinje system

Left or Right Bundle branch blockComplete Heart Block

Ventricular tachycardia / fibrillation

due to re-entry or increased

automaticity


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Acute anterior MI


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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


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Congestive Heart Failure


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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

0

1

2

3

4

5

6

L.V.E.D.P.

CardiacOutput


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0

0.51

1.5

2

2.5

3

L.V.E.D.P.

Cardiac

Index

(L/min/m2)

4

31

2

Hemodynamic Subsets


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0

0.51

1.5

2

2.5

3

Cardiac

Index

(L/min/m2)

L.V.E.D.P.

4

31

2

Patients in

Quadrant 1Best Prognosis

Quadrants 2 + 3

Intermediate

Prognosis

Quadrant 4

Cardiogenic

ShockWORST

PROGNOSIS

10 20 30


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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


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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 Rupture

Leading to Acute M.R.

Systolic murmur

Giant V - waves on PC Wedge tracing

Echo/Doppler confirmation

RX with Afterload reduction



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Flail Mitral Leaflet


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Echo/Color Doppler of Acute M.R.

LA

LV

RA


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Gated MRI of Acute M.R. due to

papillary muscle dysfunction

AnGa cine 3CH MR.mov


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Acute M.R. due to

papillary muscle dysfunction


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Development of giant V waves


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Development of giant V waves

P. A. pressure

V-wave

P.C. Wedge pressure


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Acute Mitral Regurgitation:

Treatment

Rapid diagnosis

Afterload reduction Inotropic support


Surgical valve replacement


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ACUTE M.I.

Acute Ventricular Septal Defect

Can occur with eitheranterior or inferior MIPeak incidence ondays 3-7

Causes an abrupt left-to-right shunt


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ACUTE M.I.

Acute Ventricular Septal Defect

Abrupt onset of aharsh systolic murmur,often with a thrillDetected by an

oxygen saturationstep-up


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ACUTE M.I.Acute Ventricular Septal Defect


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Oxygen saturation step-up

IV C sat

7 0 %

SV C sat

6 5 %

RA sat

6 8 %

RV sat

8 8 %

PA sat

8 8 %


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Acute V.S.D.:

Treatment

Rapid diagnosis

Afterload reduction Inotropic support


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 theonset of systole

Reduces myocardial ischemia

by both mechanisms


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Intra aortic balloon pump


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Free Wall Rupture

Cardiac Tamponade

Equalization of diastolic

pressures

Hypotension

J.V.D.

Clear lung fields

Pulsus paradoxus

Pseudoaneurysm

Enlarged cardiac

silhouette

Echocardiographic

diagnosis


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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

ventriculararrhythmias


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ACUTE M.I.

Apical Aneurysm Causes dyskinesis of

the apex

Can be detected bycardiac echo

Can lead to systemicemboli

Anticoagulants mayprevent embolization


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ACUTE M.I.

Apical Aneurysm


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Right Heart Failure

Very commonly asequela of LeftHeart Failure

LVEDP

PCW

PA pressure

Right heart pressure

overload

Cardiac causes Pulmonic valve stenosis

RV infarction

Parenchymal pulmonarycauses COPD

ILD

Pulmonary vascular

disease Pulmonary embolism

Primary Pulmonary

hypertension

ACUTE M I


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ACUTE M.I.

Right Ventricular Infarction

Jugular venous distention with clear lungs

Equalization of right atrial and PCWpressures

ST elevation in right precordial leads

Therapy with fluids


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0

0.5

1

1.5

2

2.5

3

L.V.E.D.P.

Cardiac

Index

(L/min/m2)4

31

2

Where is the patient with RV infarct?

ACUTE M I


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ACUTE M.I.

Pericarditis

Pleuritic chest painRadiation to the trapezius ridge

Fever

Pericardial friction rub

Related to acute inflammatory process

ACUTE M I


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ACUTE M.I.

CARDIOGENIC SHOCK (recap)

Usually due to a large area ofmyocardial 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


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Summary for RCA (orSummary for RCA (or

circumflex) infarctcircumflex) infarct

Hypotension due todecreased L.V. filling

Right ventricular infarct

Bradyarrhythmias1st degree A-V block

Mobitz I 2nd degree blockA-V dissociation

S-A nodal infarctA-V nodal infarct

Acute mitral regurgitation(with or without

papillary muscle rupture)

Postero-medial papillarymuscle infarct

Right coronary artery


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Summar for LAD infarctSummary for LAD infarct

Cardiogenic shock dueloss of large amount of

myocardium

Acute ventricular septal defect

Intraventricular septum(upper two-thirds)

Ventriculararrhythmias

Arterial embolismoriginating in the L.V.

Apical thrombusformation

Apical L.V. aneurysm

Antero-apical wall

40% of LV myocardium

Advanced Heart Block(LBBB, 3rd degree A-V bloc

and Mobitz II 2nd degree)

His-Purkinje system

Left anterior descending artery

Summary


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Summary

Think anatomically!!!

LAD vs. RCA

Think hemodynamic

subsets!!!

Watch formechanicalcomplications


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THE END

Documents

ChristieTWong- Comp Lication of Acute MI Notes