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Ischaemic Heart Disease (STEMI (Non pharmacological mangement: (Diet: low…
Ischaemic Heart Disease
STEMI
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Investigations:
ECG:
- Acute: ST elevation, ST depression, tall T waves, new LBBB.
- Late changes: T wave inversion, Q waves (appear hours to days after)
Troponins: raised, repeat at 8 hours, peak at 24-48 hours
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Long term medications
B-blocker: Atenolol or metoprolol - start immediately after event, life long therapy is not an indication in all patients, cease after 12 months in low risk patients i.e. no left ventricular dysfunction
Antiplatelet therapy: Aspirin +/- clopidegrol based on risk, for approximately 12 months
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Statins: Atorvastatin, continue for life. MOA: decreases LDL, increases HDL and has pleitropic effects of anti-inflammation in the plaque.
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NSTEMI/Unstable angina
Definition:
On the same spectrum , distinguished by time of ischaemia (< 20mins: unstable, >20mins leads to irreversible injury i.e. sub endocardial infarction --> NSTEMI)
Investigations:
Troponins: Rise in NSTEMI, not unstable angina
ECG findings: ST depression, T wave inversion
Management
Immediate management same for NSTEMI and unstable angina, see previous coggle
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Stable angina
Long term medications:
Prevention: Statin, aspirin
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Pathophysiology: Very thick fibrous cap, therefore less likely to rupture
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Definition of ACS:
Life threatening conditions that can occur at any time in a pt with coronary artery disease, ranging from unstable angina to a MI
Pathophysiology:
Plaque is vulnerable
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Erosions expose the thrombogenic endothelium --> platelet aggregation and clot formation at the site
Artherosclerotic plaque formation (dysfunctional endothelium, inflammatory sub endothelium where foam cells (macrophages and smooth muscle) aggregate and form a lipid core with a fibrous cap)
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