Myocardial Infarction (MI)
Due to occlusive thrombus at site of rupture of atheromatous plaque in coronary artery necrosis and death of myocardium. Thrombosis dissolves over a few days, but irreversible damage occurs first.
Most take around 8 hours to develop
25-50% fatal within a few minutes
Older age; male; dyslipidaemia; hypertension; smoking; diabetes mellitus; lack of exercise; genetic factors play a role; stress
Cardinal symptom is pain – same as angina pain, but more severe and prolonged; a tightness, heaviness and/or constriction in chest.
Also commonly get breathlessness, vomiting and syncope (due to hypotension).
Anxiety is common from fear.
Have signs of sympathetic activation (pallor, sweating, tachycardia); signs of vagal activation (vomiting, bradycardia); cardiac function is impaired hypotension, cold extremities, narrowed pulse pressure, third heart sound, quiet first heart sound
Investigations – ECG (ST elevation, prominent Q wave, symmetric T-wave inversion); plasma enzymes (creatine kinase, cardiac isoenzyme, aspartate transminase, lactate dehydrogenase), chest x-ray, cardiac ultrasound.
Mitral regurgitation; pericarditis; cardiac failure; arrhythmias (commonly ventricular fibrillation); embolism; shock; hypertension; DVT
Early – defibrillation if needed, 24hr bed rest, aspirin, high flow oxygen, no smoking, IV analgesia (opiates) and antiemetic, thrombolysis (eg stretokinase), anticoagulants (heparin), beta-adrenoceptor antagonist, glycerol trinitrate, ECG monitor, monitor cardiac enzymes, monitor for complications – may also do immediate angioplasty
Late/prevention of reinfarct – stratify as to risk modify and mange risk factors (smoking, dyslipidaemia etc); routine pharmacological management (aspirin, beta-adrenoceptor, ACE inhibitor); psychosocial management
Surgical – angioplasty