Myocardial Infarction

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1. Acute Myocardial Infarction

Obstruction> Thrombosis> Occlusion

Ischemic injury prolonged> Irreversible injury

2. Location and Size

Location and severity of obstruction

Size of vascular bed

O₂ needs of myocardium

Collateral development

Coronary artery spasm

Tissue factors

Thrombotic and thrombolytic substances

3. Types of Infarction

Transmural

Acute coronary thrombosis

Localized zone of distribution

Subendothelial (non-transmural)

Coronaries narrowed but patent

Thrombotic occlusion> thrombolysis

Increased oxygen demand and/or decreased oxygen delivery

Pulmonary embolism

Hypotension

Hypertension

Aortic stenosis

Anemia

Operative procedures

Cerebrovascular accident

4. Sites of Involvement

Most involve LV and interventricular septum

Up to 65% or IMI involve RV

Isolated RV in 3-5%

COPD

RVH

5. Pathology

Gross Changes
Time	Changes
< 6 hours	No change
> 6 hours	Pale, bluish, edematous
18-36 hours	Tan, reddish purple
>48 hours	Gray, yellow lines at periphery
8-10 days	decreased wall thickness, coagulation necrosis
2-3 months	Thin, form scar

6. Coronary Artery Thrombosis

Coronary atherosclerosis

Vasospasm

Plaque rupture

Platelet actuation

7. Coronary Atherosclerosis

Acute occlusion =Rapidity of development/Collateral circulation

Transmural

Subendocardial

None

Vasospasm

Increased Thromboxane A₂

Plaque rupture

Ulceration

Fissure formation

Platelet activation

Adhesion> aggregates> increase Thromboxane A₂

Decreased Fibrinolytic activity

Decreased tissue plasminogen activator

8. Collateral Circulation

Coronary occlusive disease

Chronic hypoxia

COPD

Anemia

Cyanotic CHF

LVH

9. Pathophysiology

Systolic Function

Infarcted area

Dyssynchrony

Hypokinesis

Akenisis

Dyskinesis

Non-infarcted areas

Hyperkinesis

Manifestations

Decreased diastolic compliance

Decreased ejection fraction (>15%)

CHF (>25)

Cardiogenic shock (>40%)

10. Infarct Size Limitation

O₂ supply (coronary perfusion pressure)

O₂ demand (ventricular wall tension)
Oxygen Supply and Demand

11. Complications

Hypotension

Arrhythmias

Congestive heart failure

Hypoxemia

Anemia

Infections

Hypertension

Cardiogenic shock

Pharmacologic

Mechanical

Surgical VSD, MR, Ventricular rupture

12. Reperfusion of infarction

Increased systolic function

Increased diastolic function

Decreased mortality

13. Treatment

Coronary thrombolysis

Angioplasty

Coronary Atery Bypass

14. Coronary Thrombolysis

Agents

Streptokinase

Plasminogen streptokinase activation complex (APSAC)

Tissue-type plasminogen activator (tPA)

Indications

Impending or evolving MI

3 hours of symptom onset

Heparin (bolus ==>infusion)

ASA

Duration of Coronary Occlusion
Time from Onset of Sypmtoms

15. Contraindications

Recent trauma

Major surgery (6 weeks)

GI bleeding (3 months)

Bleeding diathesis

Chronic liver disease

Allergy to thrombolytics

Stroke with residual

TIA (6 months)

Cerebral hemorrhage

Pregnancy

16. Angioplasty

Indications

Thrombolytic contraindicated

Thrombolytic unsuccessful

Extensive ischemia

17. Summary

Atherosclerotic coronary artery disease

Stenosis

Thrombosis

Vasoconstriction

Plaque disruption

Segmental disease

Endocardium> epicardium

Irreversible injury >15-20 minutes occlusion

Maximal damage 4-6 hours

Best salvage 1-2

Size depends on collateral

Morbidity and mortality

O₂ supply/O₂demand

RV infarct with inferior MI