Emergency - Acute coronary syndromes Flashcards
Describe the pathophysiology of coronary artery disease.
- Atherosclerotic plaque formation narrows the coronary artery. The atherosclerotic plaque may rupture and lead to thrombus formation, further narrowing the coronary artery.
- This reduces blood flow and hence the delivery of oxygen and glucose to the myocardium, resulting in ischaemia.
- Depending on the extent of narrowing, the ischaemia may:
- only be present when there is an increased demand for oxygen and glucose during exertion (stable angina)
- or may be present at rest (acute coronary syndrome)
- If the narrowing is severe enough, ischaemia can result in necrosis and the myocardium undergoes infarction.
- Partial occlusion of the artery (NSTEMI)
- Complete occlusion of the artery (STEMI)

Describe the formation of an atherosclerotic plaque.
- Chronic endothelial injury - raised LDL, toxins, hypertension
- Endothelial dysfunction with platelet adhesion and monocyte acccummulation, causing release of growth factors and cytokines
- Smooth muscle emigration from tunica media to tunica intima
- Macrophages and smooth muscle cells engulf lipid to form foam cells
- Smooth muscle proliferation, collagen and matrix deposition, extracellular lipid deposition and neovascularisation

What is meant by the stability of an atherosclerotic plaque?
An unstable atherosclerotic plaque is more likely to rupture and lead to thrombus formation.
- Rupture of the plaque allows blood to enter the plaque
- This causes smooth muscle constriction which narrows the artery
- Thrombus formation can occlude the artery completely

Which clinical syndromes are classed as acute coronary syndromes?
Unstable angina
Non-ST-elevation myocardial infarction
ST-elevation myocardial infarction
How can unstable angina present?
- Angina on exertion with increasing frequency over a few days, provoked by less exertion (crescendo angina)
or - Angina occurring recurrently and unpredictably - not specific to exercise
or - Unprovoked and prolonged episode of chest pain
ECG and Troponin in unstable angina?
- Non-specific ECG change OR commonly, a normal ECG
- T wave inversion
- ST segment depression suggests high risk of progressing to MI
- No troponin release
ECG and Troponin in NSTEMI?
- Non-specific ECG abnormalities (usually these are present, though ECG can be normal)
- ST segment depression
- T wave inversion
- Troponin release

What differentiates unstable angina and NSTEMI?
Unstable angina - no troponin release (no myocardial cell death)
NSTEMI - TROPONIN RELEASE (MYOCARDIAL CELL DEATH)
Does a STEMI require troponin to confirm diagnosis?
NO
Does an NSTEMI require troponin to confirm diagnosis?
YES
What are the typical features of an acute MI?
- prolonged chest, throat or arm pain
- usually lasts for 20 mins or longer
- SOB
- clammy
- nauseous
Is the immediate management of an NSTEMI and STEMI the same?
NO
ECG and Troponin in STEMI?
- ECG - Acute ST-segment elevation / new LBBB
- Q waves likely to develop
- Troponin release
(ECG shows STEMI in lateral limb leads and anterior chest leads, the anterior chest leads show pathological q waves)

What do pathological q waves represent?
myocardial necrosis
What is the difference between the immediate management of an NSTEMI and STEMI?
STEMI - immediate reperfusion therapy