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Myocardial Infarction

Title               

Ñ    Myocardial Infarction (MI)    

Definition

Ñ    Ischaemic necrosis of a segment of myocardium

Ñ    Result of an abrupt reduction in coronary blood flow

Pathogenesis

Causes

Ñ    Partially stenosing coronary atheroma undergoes plaque change with superadded thrombosis

·          Precipitating factors thought to be vasospasm or haemodynamic stress

·          Plaque change is a collective term for the following:

Erosion, ulceration, fissuring, rupture, haemorrhagic expansion

Ñ    Arterial embolisation from mitral stenosis, aortic stenosis, infective endocarditis, marantic endocarditis:

Rare

Ñ    Coronary spasm:

·          For example in cocaine users:

Rare

Effects

Ñ    Transmural infarction involves the whole thickness of the myocardium

·          It is characterised by abnormal Q waves on ECG

Ñ    Subendocardial infarction involves the inner 1/3 of the myocardium where wall tension is greatest and myocardial blood flow is most vulnerable

·          This results in ST segment and T wave changes

Pathological Process

Ñ    Within 1 hour

Death of fibres and intercellular oedema

Ñ    12 to 72 hours:

Coagulative necrosis of myocytes

Neutrophil infiltration of necrotic tissue

Ñ    3 to 7 days

Dead myocytes begin to disintegrate

Resorbed by macrophages and enzymatic proteolysis

Ñ    7-10 days

Granulation tissue forms

Necrotic tissue replaced by a fibrous scar

Clinical Features

History

Ñ    Silent myocardial infarction:

Diabetics

Elderly patients

CVS

Ñ    Pain:

·          Usually deep, retrosternal

·          Radiation to back, jaw, left arm

·          Described as an ache, pressure, tightening, crushing

RS

Ñ    Dyspnoea

GIT

Ñ    Nausea and vomiting

IS

Ñ    Sweating

CNS

Ñ    Apprehension

Ñ    Sense of impending doom

Examination

E&M

Ñ    Fever (38°C)

IS

Ñ    Pale, cold, sweaty skin

Ñ    Cyanosis

CVS

Ñ    Tachycardia, pulse thready

Ñ    Blood pressure variable

Ñ    JVP elevated

Ñ    Heart sounds distant

Ñ    Fourth heart sound

Ñ    Soft blowing systolic murmur at apex:

Papillary muscle dysfunction

RS

Ñ    Normal

Ñ    Bibasal crepitations

Ñ    Pleural effusion

Complications

CVS

Ñ    Sinus arrhythmias:

Sinus bradycardia

Sinus tachycardia

Ñ    Atrial arrhythmias:

Atrial ectopics

Atrial fibrillation

Atrial flutter

Ñ    Atrioventricular block

Ñ    Ventricular arrhythmias:

Ventricular ectopics

Ventricular tachycardia

Ventricular fibrillation

Ñ    Heart failure:

·          Classification (Killip class):

I No heart failure

II Mild LVF

III Pulmonary oedema

IV Cardiogenic shock

Ñ    Right ventricular infarction:

Hypotension

Distended jugular veins

Clear lung fields

ST elevation of 1 mm in V₄ R

Ñ    Hypoxia:

Due to increased left atrial pressure, altered pulmonary ventilation / perfusion, pulmonary oedema, alveolar collapse

Ñ    Hypotension:

Hypovolaemia

Right ventricular infarction

Ñ    Cardiogenic shock:

Usually associated with anterior infarction

Ñ    Recurrent ischaemia

Ñ    Papillary muscle dysfunction

Ñ    Myomalacia cordis (weakness of cardiac muscle due to disintegration of dead myocytes):

Rupture of weakened cardiac muscle may result in:

·          Mitral regurgitation:

Apical thrill, systolic murmur and pulmonary oedema

·          Ventricular septal defect:

Left sternal edge thrill, murmur, hypotension

·          External rupture:

Cardiac tamponade

Ñ    Pseudoaneurysm:

Free wall rupture with clot and pericardium forming an aneurysmal wall thereby preventing tamponade and exsanguination

Ñ    Ventricular aneurysm:

·          May develop in days, weeks, months

·          Presents with ventricular arrhythmias and decreased cardiac output

·          Causes paradoxical praecordial movement

·          Persistent ST elevation on ECG

·          Bulge of the cardiac shadow on chest X-ray 

Ñ    Ventricular asynergy:

Causes:

·          Reduced ventricular function

·          Mural thrombosis

Ñ    Pericarditis:

Occurs 24- 96 hours after MI

Ñ    Post Myocardial infarction syndrome (Dressler’s syndrome):

·          Days, weeks or months after acute MI

·          Fever, pericarditis, pericardial effusion, pleurisy, pleural effusions, pulmonary infiltrates, joint pains

·          Cardiac enzymes do not rise significantly

Investigations

Fluids

Blood

Haematology

Ñ    WBC:

Elevated (moderately) with left shift

Ñ    ESR:

Elevated

Biochemistry

Ñ    CK-MB:

Elevated

6-48 hours

Ñ    Troponin T, Troponin I:

Elevated

2 hours – 7 days

Ñ    AST:

Non-specific

Ñ    LDH:

Non-specific

May remain elevated for up to 10 days

Electrophysiology

ECG

Ñ    Transmural Infarction

Progression of changes:

·          T waves become tall and upright in a few minutes

·          ST segment elevation occurs shortly after this

·          T inversion few hours later

·          R wave voltage decreases

·          Q waves appear:

Pathological Q waves are broad (> 1 mm) and deep (> 2 mm or 25% of the following R wave)

Resolution of changes:

·          ST segment returns to normal after a few days

·          T waves may return to upright in weeks or months

·          Q waves remain

Ñ    Subendocardial infarction:

ST depression, T inversion

Ñ    Location:

·          Anterior infarction:

Small (septal):

V₃-V₄

Extensive:

V₂-V₅

·          Anteroseptal infarction:

V₁-V₃

·          Anterolateral infarction:

I, AVL, V₄-V₆

·          Lateral infarction:

I, aVL

·          Inferior infarction:

II, III, AVF

·          Right ventricular infarction:

V₄R

·          True posterior infarction:

Reciprocal changes in V₁, V₂

Tall R, ST depression, upright T

Ñ    New onset of left bundle branch block:

Compatible with coronary occlusion requiring reperfusion therapy

Imaging

Echocardiogram

Ñ    Useful in evaluating wall motion, ventricular function, presence of ventricular thrombus, papillary muscle rupture, ventricular septal rupture

Physiological studies

Right heart catheterisation

Ñ    Management of complications

Management

Control

Drugs

Ñ    Aspirin

Ñ    Thrombolysis:

Streptokinase, tissue plasminogen activator, reteplase, tenecteplase

Ñ    Pain relief:

Morphine, diamorphine

Ñ    Nitrates

Ñ    Beta blockers:

If no contraindication

Ñ    Oxygen:

·          Oxygen saturation:

94-98% < 70 years

92-98% > 70 years

Ñ    Glycoprotein IIb/IIIa inhibitor:

If primary percutaneous coronary intervention is available

Contraindications to thrombolysis

Absolute

HS

Ñ    Active internal haemorrhage or uncontrollable external haemorrhage

CVS

Ñ    Aortic dissection:

Suspected

Ñ    Uncontrolled hypertension:

> 200/120 mm of Hg

CNS

Ñ    Recent head trauma:

< 2 weeks

Ñ    Intracranial neoplasm

Ñ    Stroke:

< 2 months

RAG

Ñ    Pregnancy

Relative

CVS

Ñ    Prolonged, traumatic cardiopulmonary resuscitation

Ñ    Probable intracardiac thrombus

HS

Ñ    Bleeding disorders

Ñ    Anticoagulation INR > 1.8

E&M

Ñ    Diabetic haemorrhagic retinopathy:

Active

Surgery

Ñ    Percutaneous Coronary Intervention (PCI):

·          Primary angioplasty:

Percutaneous transluminal angioplasty and stenting may be offered as primary treatment

Staffing

Ñ    Expert nursing and physiotherapy for early mobilisation

Equipment

Ñ    ECG monitoring

Residence

Ñ    Coronary care unit

Support

Management of complications:

Ñ    Sinus bradycardia:

Usually not treated

Rate < 50 /min atropine, rarely pacing

Ñ    Atrial ectopics:

Beta-blockers, verapamil

Ñ    Atrial fibrillation:

Heparin, beta-blockers, digoxin        

Ñ    Atrioventricular block:

Temporary pacing

Ñ    Ventricular arrhythmias:

·          Treat underlying cause

Hypoxia, hypokalaemia, low magnesium

·          Ventricular tachycardia

Lignocaine, amiodarone, DC cardioversion

·          Ventricular fibrillation

Defibrillation, lignocaine

Ñ    Heart failure:

Diuretics

Vasodilators

Venodilators

Ñ    RV infarction:

Volume loading

Inotropic support

Ñ    Cardiogenic shock:

Inotropic support

Intra-aortic balloon pump

Ñ    Emergency surgical intervention:

Aneurysm, mitral regurgitation, ventricular septal perforation

Ñ    Pericarditis

Aspirin, paracetamol

Ñ    Dressler’s syndrome:

Aspirin

Corticosteroids

Ñ    Left ventricular aneurysm:

Anticoagulation, antiarrythmics drugs, ACE inhibitors, surgery

Prevention

Drugs

Ñ    Aspirin

Ñ    Statins

Ñ    Beta blockers

Ñ    ACE inhibitors

Ñ    Nitrates for angina

Surgery

Ñ    Angioplasty

Ñ    Stents

Ñ    Coronary artery bypass grafting

Lifestyle Adjustments

Ñ    Diet

Ñ    Exercise

Ñ    Stop smoking

Prognosis

Ñ    2-year mortality 10%

Ñ    5-year mortality approaching 20%

Ñ    < 50 years <3%

Ñ    > 70 years >15%

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