Yr 2 CVS- Acute Coronary Syndrome Flashcards
Describe how the pathophysiology differ in stable and unstable angina?
Stable/Chronic: This is when you have greater than or equal to 70% stenosis (blocked by plaque). These patients experience chest pain on exertion as the heart cannot meet the oxygen demands of the myocardium (ie during exercise or stress). Pain will go away with rest. Usually, the angina is caused by atherosclerosis, hypertrophic, cardiomyopathy (thickening of the heart wall- genetic) or pumping against high pressure (ie Hypertension/aortic stenosis). Usually will have subendocardial ischaemia (may stimulate the release of adenosine and bradykinin causing pain)
Unstable: (0% or greater blockage of the coronary vessel. These patients experience pain/symptoms during exercise and stress but also at rest. Causes sub-endocardial ischaemia and should be treated as an emergency as there is ahigh risk of myocardial infarction- pain on threshold l. Rupture of the plaque
Describe how the pathophysiology differ in ST elevation and non-ST elevation MI?
If there is a pattern known as ST-elevation on the ECG, this is called a STEMI, short for ST elevation myocardial infarction. If there is elevation of the blood markers suggesting heart damage, but no ST elevation seen on the ECG tracing, this is known as a NSTEMI.
Myocardial ischemia results from decreased myocardial oxygen supply and/or increased demand. In the majority of cases, NSTEMI is due to a sudden decrease in blood supply via partial occlusion of the affected vessel.Unstabel angina can lead to nstemi- rbc and platelets get activated. Sudden pain is due to the plaque gets swollen up and sudden occlusion
STEMI is complete occulsion
Why is the myocardial hypoxia limited to the subendocardial area of the myocardium in non-ST elevation MI?
Coronary arteries run on the surfaceof the heart and oenertrares into the muscular layer almost perpendicular. Thus the deeper (close to the endocardium) we go the narrower the vessels. Deeper the go the narrower they get so if there is an occlusion it was limit the supply even more to the muscles. The muscles on the inside are gonna get hypoxic first. Purkinji fibres run sub endocardially so inside to the outside. So the depolaristation and contraction of the myocardium moves from inside out. Area inside is what contracts first so that’s what should get the blood most. SO blood reaching the inside is a lot less anyway which makes it more prone to hypoxia
- What causes the pain in myocardial ischemia? Based on the biochemistry how quickly would you expect ischemia-related chest pain to develop?
Anaerobic resp- leading to Lactic acid. Muscles cells don’t get oxygen so they starve and they cant contracts
The body makes lactic acid when it is low in the oxygen it needs to convert glucose into energy. Lactic acid buildup can result in muscle pain, cramps, and muscular fatigue.
6-8hours
Describe the biological role of troponin I and T.?
Functionally, troponin T serves to bind the troponin complex to the tropomyosin strand of the actin thin filament. Troponin I functions to inhibit the activity of actinomycin ATPase. Troponin C serves to bind four calcium ions and regulates contraction.
Troponin I and T. How is the measurement of these biomarkers used in the assessment of acute coronary syndrome?
An elevated troponin T or I level is helpful in identifying patients at increased risk for death or the development of acute myocardial infarction. 16 Increased risk is related quantitatively to the serum troponin level. The troponins also can help identify low-risk patients who may be sent home with close follow-up
Unstable angina have no elevation in these. Normal 0-0.4 ngml troponin levels .Peaks to about 6-12 hours
Does elvated tropinin levels suggest the damage in heart?
No
What is the effect of heparin on the coagulation cascade?
Heparin is an injectable anticoagulant that activates antithrombin III, which inhibits thrombin and factor Xa (warfarin) , factors necessary in the final stages of blood clotting cascade
