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Complications of Acute Complications of Acute M.I.M.I.

Douglas Burtt, M.D.

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Left Anterior Descending OcclusionLeft Anterior Descending Occlusion

Occlusion of theleft anterior descendingcoronary artery

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Experimental DataExperimental Data

Canine studies – transient artery clamping or ligation

Balloon angioplasty studiesTime dependent series of eventsChest Pain as a late event

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ACUTE M.I.ACUTE M.I.THE “ISCHEMIC CASCADE”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.ACUTE M.I.THE “ISCHEMIC CASCADE”THE “ISCHEMIC CASCADE”

1. Diastolic dysfunction2. Localized systolic dysfunction3. Ischemic EKG changes4. Chest pressure, etc.5. Release of CPK

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Time course of cell deathTime 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!!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 Blood supply of the septumseptum

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Think Anatomically!!!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 Conduction System of the HeartHeart

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Conduction System: detailConduction System: detail

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ACUTE M.I.ACUTE M.I.Anatomical correlatesAnatomical 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.ACUTE M.I.Anatomical correlatesAnatomical correlates

RCA occlusion causes moderate infarction

associated with: RV failure

Bradyarrhythmias Occasional mechanical

complications

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ACUTE M.I.ACUTE M.I.ArrhythmiasArrhythmias

Sinus bradycardia Sinus tachycardia Atrial fibrillation

PVCs / ventricular tachycardia /ventricular

fibrillation Heart block

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Arrhythmias:Arrhythmias:Inferior M.I.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

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Arrhythmias:Arrhythmias:Anterior M.I.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

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ACUTE M.I.ACUTE M.I.HypotensionHypotension

Identify hemodynamic subset Distinguish decreased preload

from decreased cardiac output Think about hemodynamic

monitoring

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Hemodynamic subsetsHemodynamic subsets

0123456

Starling curves to plot “preload” versus cardiac output

Identification of high risk subgroups

Definition of cardiogenic shock

L.V.E.D.P.

CardiacOutput

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00.5

11.5

22.5

3

L.V.E.D.P.

CardiacIndex

(L/min/m2)4

31

2

Hemodynamic Subsets

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Acute M.I.Acute M.I.Mechanical ComplicationsMechanical 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.ACUTE M.I.Papillary Muscle RupturePapillary Muscle Rupture

Leading to Acute M.R.Leading to Acute M.R.

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ACUTE M.I.ACUTE M.I.Papillary Muscle RupturePapillary Muscle Rupture

Leading to Acute M.R.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

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““Flail” Mitral LeafletFlail” Mitral Leaflet

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Echo/Color Doppler of Acute M.R.Echo/Color Doppler of Acute M.R.

LA

LV

RA

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Development of giant “V Development of giant “V waves”waves”

P. A. pressureV-wave

P.C. Wedge pressure

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Acute Mitral Regurgitation:Acute Mitral Regurgitation:TreatmentTreatment

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

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ACUTE M.I.ACUTE M.I.Acute Ventricular Septal Acute Ventricular Septal

DefectDefect

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

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ACUTE M.I.ACUTE M.I.Acute Ventricular Septal Acute Ventricular Septal

DefectDefect

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

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Oxygen saturation “step-Oxygen saturation “step-up”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.:Acute V.S.D.:TreatmentTreatment

Rapid diagnosis Afterload reduction Inotropic support Intra-aortic balloon pump Surgical repair of ruptured septum

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Intra-Aortic Balloon PumpIntra-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 pumpIntra aortic balloon pump

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Intra-aortic balloon pumpIntra-aortic balloon pump

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Free Wall RuptureFree 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.ACUTE M.I.Apical AneurysmApical 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.ACUTE M.I.Apical AneurysmApical 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 FailureRight Heart Failure

Very commonly a sequela of Left Heart Failure LVEDP PCW PA pressureRight 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.ACUTE M.I.Right Ventricular InfarctionRight 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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00.5

11.5

22.5

3

L.V.E.D.P.

CardiacIndex

(L/min/m2)4

31

2

Hemodynamic Subsets

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ACUTE M.I.ACUTE M.I.PericarditisPericarditis

Pleuritic chest pain Radiation to the trapezius ridge

Fever Pericardial friction rub

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ACUTE M.I.ACUTE M.I.CARDIOGENIC SHOCKCARDIOGENIC 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 for RCA (orSummary for RCA (orcircumflex) infarctcircumflex) infarct

H ypotension due todecreased L.V. filling

R ight ventricular infarct

Bradyarrhythm ias1st degree A-V block

M obitz I 2nd degree blockA-V dissociation

S-A nodal infarctA-V nodal infarct

Acute m itral regurgitation(w ith or w ithout

papillary m uscle rupture)

Postero-m edial papillarym uscle infarct

R ight coronary artery

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Summary for LAD infarct Summary for LAD infarct

Cardiogenic shock due to loss of large amount of

myocardium

Acute ventricular septal defect

Intraventricular septum (upper two-thirds)

Ventricular arrhythmias

Arterial embolism originating in the L.V.

Apical thrombus formation

Apical L.V. aneurysm

Antero-apical wall

40% of LV myocardium

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

and Mobitz II 2nd degree)

His-Purkinje system

Left anterior descending artery

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SummarySummary

Think anatomically!!!

LAD vs. RCA

Think hemodynamic subsets!!!

Watch for mechanical complications

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THE ENDTHE END