Myocardial Infarction - Definition

Myocardial Infarction Definition Blockage of a vessel for more than 20 minutes Types • • Subendocardial (NSTEMI) - Only subendocardial affected - Decreased blood flow -> blood does not go through the entire depth of the myocardium -> subendocardial is the first layer to be affected -> less ATP -> K+ channels open -> K+ leaks out -> K+ accumulate outside of the cell -> early depolarisation -> spreads out to the tissue that is not meant to be doing anything -> early depolarisation -> isoelectric line starts higher -> ST wave depression and T wave inversion Transmural - Affects entire depth of the wall - Increase K+ leakage -> depolarisation -> away from lead -> isoelectric line begins depressed (lower than usual) -> ST elevation Aetiology • • • • Same causes as atherosclerosis Coronary artery vasospasm Coronary artery embolism Myocarditis Pathophysiology Cause/ risk factor present -> damage epithelial cells lining the arteries -> promote atherosclerosis -> lack of blood flow for 20 min or more -> unable to supply heart region -> necrosis Signs and Symptoms • • • • • • • • • • • Fatigue, because of the lack of oxygen supply Sweating (diaphoresis) , due to SNS activation Shortness of breath, again due to low oxygen supply Dull squeezing pressure/tightness Pallor Dizziness, light headedness, syncope Nausea and vomiting Tachycardia Blood not meeting the demands of the heart -> adenosine and bradykinin release -> stimulate nerve fibres -> nerve irritation -> dull squeezing or tightness chest pain 4th heart sound, may also find a murmur being present With inferior wall infarction, one may find: - Epigastric pain: may be mistaken with reflux oesophagus - Bradycardia Hypotension Elevated jugular venous pressure (due to fluid back up) Diagnosis • • • • • ECG: - Pathological Q waves ✓ Infarct location indication: ➢ V1 and V2 -> septal ➢ V3 and V4 -> anterior wall ➢ V3 -V6, leads 1 and aVL -> anterolateral wall ➢ If none are present, this could mean that the infarct is still conducting electricity, so this is a subendocardial infarction - ST segment shifts - T wave inversion Lab tests: - Troponin I and T ✓ Elevated in blood after 2 hours ✓ Peak at 48 hours ✓ Remains elevated for 7 -10 days - CK-MB creatin kinase M + B ✓ Rise 2-4 hours ✓ Peak at 24 hours at peak ✓ Back to normal after 48 hours - Inflammatory markers: WBC, neutrophils Coronary angiography Patho-histology: - Elongated cells (fibroblasts) replace the dead cardiomyocytes - Evidence of the process of granulation - Sprouting capillaries - Inflammatory cells; lymphocytes, macrophages etc. - May be able to see tissue eosinophilia from acidosis - Haemorrhagic infarct margin: ✓ After 24 hours inflammatory cells migrate from the blood vessels into the tissue and begin to clear the necrotic tissue. Because capillaries are better perfused, this margin of the necrosis appears dark red on microscope - May be able to see nuclear degradation - May be able to see signs of thrombosis, which may be the actual cause of this disease - White, grey lines or regions -> scar tissue as a result of cardiomyocyte death - Within the scar one may be able to see wavy collagen fibres X-ray - Herat size - Fluid in lungs Treatment • • • Medications: - Anti-platelet meds - Beta blockers - Cholesterol meds - Nitroglycerin for chest pain - Thrombolytics to dissolve blood clots Surgical treatment: - Coronary angioplasty and stenting - Coronary artery bypass Others - Pacemaker - Oxygen therapy/supply - Life style modifications Complications • • • • 0-24 hours: - Damage disturbs the cell’s electrical conductivity -> arrythmias - Heart tissue damage -> decrease ability to pump blood 1-3 days: - Tissue around infected area -> invaded by neutrophils -> inflammation -> pericarditis 3-14 days - Macrophages invade tissue -> healing process -> granulation tissue -> granulation tissue is most at risk of rupture due to its’ weakness ad softness -> myocardial rupture - May also experience papillary muscle rupture After 2 weeks - Cardiac tissue sacring ends -> scar tissue does not help with pumping blood -> reaming heart muscle either grows or modifies its’ shape to compensate -> heart pumps harder but fails -> heart failure