MI Flashcards
Definiton
ACS= unstable angina, NSTEMI, STEMI
NSTEMI- ECG may show STD, T inversion or nothing.
Aetiology
Plaque rupture
Thrombosis
Inflammation
Rarely- emboli, coronary spasm, vasculitis.
Symptoms
Acute central crushing CP over 20 mins, radiates neck, arm, jaw. Nausea sweaty Dizzy Dyspnoea Palpitations Syncope Pulmonary oedema Epigastric pain Confusion Stroke
Signs
Distress Pallor Sweaty, clammy Pulse change either way Arrhythmia Low BP S4 HF signs eg JVP, S3, basal creps Pansystolic murmur Low fever Late- pericardial rub, peripheral oedema. Xanthelasma, carotid bruit, aortic aneurysm.
Diagnosis
-STEMI ECG- due to transmural injury from total occlusion. Extends to subepicardium.
Early- hyperacute T, STE (more than 2 leads facing same area, 1mm in limb leads, 2mm in chest leads) or new LBBB
Hours to days- T inversion, pathological Q (over 1SS wide, over 25% QRS deep)
Weeks- T recovery
-NSTEMI- STD, T inversion or normal.
-CXR- cardiomegaly, pulmonary oedema, aortic rupture.
-Trop T+I (not in unstable angina)- increase in 3-12 hour, peak 24-48 hours, then fall slowly.
creatine kinase MB- increase in 3-12 hour, peak 24 hours, then fall faster.
Differentials
Angina Pericarditis Myocarditis Aortic dissection PE Pneumothorax Cardiomyopathy Oesophageal reflux or spasm.
Management
Aspirin
GTN
Morphine IV
Oxygen if sats under 94%
STEMI- angioplasty or thrombolysis, BB, ACEi, clopidogrel.
NSTEMI- BB, LMWH, aspirin, clopidogrel, angiography.
LT- warfarin, aspirin, BB, ACEi, statin, lifestyle.
Complications
Sudden cardiac death-VF or asystole.
Arryhtmia- sinus tachyc, sinus bradyc.
HB- AVN ischaemia. May need pm.
VT/VF- ventricular iaschaemia causing re entry loops or increased automaticity.
AF
HF- loss myocardium, decreased contractility.
Cardiogenic shock- when over 40% myocardium infarcted, severe reduced CO, SBP under 90.
Stroke
Aortic aneurysm
Claudication
Renal A stenosis
ECG localisation of MI
- inferior RCA- leads II, III, aVF
- antero septal LAD- V1-2
- antero apical distal LAD- V3-4
- antero lateral L circumlfex- I, aVL, V5-6
- extensive anterior proximal LCA- I, aVL, V2-6
- true posterior RCA- tall R in V1
Atherosclerosis process
Endothelial damage Fatty streak intima Macs, oxidised LDL, sm cells. Foam cells form core of lipis, then fibrous cap Thrombosis on rupture
Explanation
- MI is when a vessel supplying your heart muscle with oxygen and nutrients gets blocked so that part of heart muscle dies. This stops the heart pumping properly.
- it often occurs because there is a build of fat in the vessels called a plaque. This plaque grows and can rupture. This causes a blood clot to form over the plaque, blocking the vessel.
- lifestyle- diet, exercise, smoking, alcohol.
- tx- initially trying to clear the artery by giving drug to expand it and then putting in a stent to hold it open. Long term treatment will include aspirin and warfarin to stop blood clotting so easily in the future. Statin to reduce fat in the blood. Some drugs to reduce the workload of the heart.