ST elevation MI, non - ST elevation MI, Acute Coronary Syndrome Flashcards
What does ACS encompass
STEMI
NSTEMI
Unstable angina
All have reduction of coronary blood supply/ complete occlusion
What does myocardial infarction mean?
Cell death (necrosis) of heart muscle as a result to severe lack of oxygen (ischaemia)
What are NSTEMI and unstable angina caused by? How does this appear on an ECG?
Incomplete occlusion of a coronary artery ( no ST elevation, associated with ST depression or T wave changes (flat/ depressed))
How do you test for NSTEMI
Seem troponin increase in the absence of ST elevation
What is a STEMI
ST elevation with complete occlusion of coronary arteries
What makes unstable angina different to NSTEMI?
No infarction is present, however it can progress to NSTEMI
Describe NSTEMI pathophysiology
In NSTEMI there is significant occlusion of the artery due to a rupture plaque and subsequently thrombosis leading to poor blood supply.
However, the vessel is not fully occluded, the significant reduction of oxygen blood supply to the muscle wall causes infarction distally and the ischaemia proximally to the artery, causing elevation of cardiac enzymes (troponin).
The infarcted area is called subendocardial infarction, however endocardium is not fully infarcted as getting blood from LV.
NSTEMI can progress to STEMI (transmural myocardial injury) with complete occlusion of artery. No blood supply to myocardium = infarction distally (increase in cardiac enzymes) to where the vessel supplies if not treated ASAP.
What are some STEMI changes?
Up to 12 hrs following MI : hyper acute (peaked) T waves that are more evident in chest leads and ST changes. Reciprocal ST depression is an indicator of acute MI.
12-24 hrs : transmural infarction has occurred. Site is now damaged and inflamed. Gross ST changes with tombstone like R waves and loss of ST-T wave angle. May already have Q waves and inverted T waves
First week following MI : pathological Q waves and inverted T waves showing permanent signs of infarction.
STEMI treatment
Immediate PCI (primary percutaneous coronary intervention) -> an angiogram is performed to evaluate which and how many vessels are damaged, if PCI or bypass is necessary
When PCI is possible, a catheter is inserted throwing wrist or groin to coronary artery and a balloon is used to dilate the vessel. A stent ( wire mesh tube) can be inserted to keep the artery open. This procedure does not destroy the plaque, only prevents the vessel from getting occluded.
Medication is prescribed to prevent further ischaemic events:
- ACE inhibitors to relax the vessels and lower blood pressure (ramipiril)
- Anti platelets (aspirin/ clopidogrel) to reduce blood clots forming
- BB to reduce heart rate
- Nitrates to dilate vessels (isosorbide/ glyceryl trinitrate)
- Anti ischaemic agents (ranolazine/ ivabradine)
- Ca channel blockers to reduce workload on the heart (amlopdipine)
What happens if immediate treatment is not possible?
- occlusion untreated, infarction progresses to transmural (all across myocardium)
- irreversible myocardium necrosis occurs which can cause damage and rupture of heart muscles and/or valves
How can you confirm necrosis/ infarction of cardiac muscle? What is this protein?
Troponin helps cardiac muscle to contract. When a muscle cell dies, troponin is released into circulation, leading to increased troponin levels in blood. This way it is possible to confirm necrosis has occurred through a blood test, depending on time between onset of chest pain and blood test.
Troponin levels rise very rapidly within first few hours and peaks about day 2 after onset of chest pain. Can be elevated until day 7!
Other causes of ST elevation
LBBB - ST elevation with upright T waves
High take off - isolated upsloping in right sided chest leads
LVH - St elevation in precordial leads
Prinzmetal’s angina - caused by coronary vasospasm, ST elevation only with pain
Brugada syndrome - RBBB and ST elevation in right precordial leads. Familial and mostly in young men
Benign early repolarisation - precordial leads, mostly V4 (young adults and African/ Asian descent) with ST elevation of J point above isoelectric line and tall T waves
Pericarditis - No reciprocal change, ST elevation is not localised so present in all the leads and PR depression and absence of Q waves helps distinguish this from MI
