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Chapter 20.docx

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University of Calgary
NURS 203

Chapter 20: Major risk factors for coronary artery Age is the most imp risk factor (cannot control) -45 for males; 55 for women – why? Higher estrogen levels, which affect HDL levels. Risk factor for CAD is not LDL, its HDL. HDL visits fatty streaks, sucks LDL out, takes it to the liver to be metabolized. 55 in women b/c that is the age of menopause; not taking estrogens and that is the age when estrogens go down; HDL levels go down and risk goes up. Family history of premature artery dz, cig smoking, HP, HDL<35, diabetes, LDL (cholesterol is not a risk factor, LDL is) b/c all therapeutic decisions are based on LDL levels, not cholesterol levels. HDL is a negative risk factor: if your HDL is greater than 60, you can subtract one from your major risk factor - ie 58 y/o, but HDL is above 60, can subtract the age risk factor and will have no risk factors. VII. Ischemic Heart Disease: 4 types: Angina, Myocardial Infarct, Sudden Cardiac Death Syndrome, Chronic Ischemic Heart Disease Sudden cardiac death syndrome = death within the last hr – what will you see at autopsy? Will NOT see a coronary thrombus, will see severe coronary artery atherosclerosis. So, usually these pts do not have a thrombus, but do have severe coronary artery dz, leading to ischemia, PVC’s, ventricular fibrillation (die of ventricular arrhythmia just like in MI); die so fast that there are no changes in the heart (ie pallor/Coagulation necrosis); see severe coronary artery dz and dx sudden cardiac death. Very high risk in smokers. Chronic ischemia heart dz –It’s a lot of our parents, uncles and aunts who have coronary artery dz with little infarcts, or had a small heart attack, basically talking about subendocardial infarctions. What happens is that the muscle gets replaced by fibrous tissue and eventually the poor LV is all fibrous tissue, with no muscle therefore the ejection fraction is very low. Its 0.2 instead of the normal 0.66 and they die from heart failure. Fibrous tissue does not have contractility; this dz is the 2 MC indication for a heart transplant. Angina (MC type of heart dz) 3 types – exertional, prinzmetal, unstable (resting) angina 1. Exertional – chest pain on exertion, goes away within 5-10 minutes of resting; ST depression on EKG (1-2 mm depression) – therefore a candidate for coronary angiogram to see what’s going on. 2. Prinzmetal’s – seen in women, occurs in morning; due to vasospasm of the coronary arteries, NOT atherosclerosis. In some people, TxA2 is implicated for the vasospasm. ST depression means subendocardial ischemia. Coronary arteries penetrate the outside of the heart and go in, so the subendocardial tissue get screwed b/c its furtherest from the blood supply. Therefore, with coronary artery atherosclerosis, and decreased blood flow, who gets screwed? Subendocardium and it reacts to it with pain and ST depression. With vasospasm of coronary artery, get transmural ischemia – therefore there is ischemia throughout the entire thickness of the muscle – this produces ST elevation. So, Prinzmetal’s angina has ST elevation b/c transmural ischemia. 3. Unstable – aka pre-infarction angina – get angina on resting. Classic hx: initially had stable angina, now pt just get it when they are sitting. This means that they will need angioplasty and put into the hospital. Do not put on treadmill, they will die. What veins do they use? Saphenous vein – over 10 years will become arterialized (it will look exactly like an artery). If you take a vein, and put arterial pressures into it, it will change its histology and look exactly like an artery. They have a high tendency for fibrosing off after 10 years b/c they are veins. Internal mammary is an artery, therefore won’t have the same problem b/c it is used to those pressures. They will remain patent, but cannot do four vessel bypass with one internal mammary artery. So, they use the saphenous vein, which has the tendency to undergo fibrosis over time b/c they are arterialized under pressure. They can also use the internal mammary. Acute MI Thrombus composed of group of platelet cells bound together with fibrin. TPA doesn’t have a problem with this b/c it just breaks the fibrin bonds to destroy the clot. It has a much bigger problem with the breakdown of a venous clot b/c those have more fibrin. The thromboses/clots in the heart do not have that much fibrin. Another factor to deal with is reperfusion injury – O2’d blood goes into injured tissue, superoxide free radicals form, Ca form, and a few of the injured myocardial cells will die. Once those die, it will still improve longevity. Complications of MI: a) LAD coronary artery is MC vessel thrombosed, and supplies entire anterior part of your heart and the anterior 2/3’s of the interventricular septum. So, there will be paleness, with the ant 2/3’s knocked off. Where are most of the conduction bundles? Anterior 2/3’s. So, if you have complete heart block that requires ectopic pacemaker, what is the most likely vessel thrombosed? LAD. When you have LAD occlusion, you have classical signs – pain radiating the jaw, pain down the left arm, substernal chest pain. nd b) RCA = 2 MC thrombosed artery – which supplies the entire posterior part of the heart and the posterior 1/3 of the ventricular septum and the entire right ventricle. So, it supplies the post heart, post 1/3 of the septum and the entire right ventricle. The mitral valve has two valves with papillary muscles – posteromedial papillary muscle and posteromedio papillary muscle. So, what supplies the posterior? RCA. Also have the SA node and AV node. The SA node has an equal distribution between left and right. However, the AV node has a 95% supply from the branches of the RCA – this brings up interesting complications. Example: pt with mitral regurg murmur, which is related to posteromedial papillary muscle dysfunction, or may break – what is the problem? Thrombosis of the RCA b/c the RCA supplies that papillary muscle. So, mitral regurg murmur that occurs during MI would be due to RCA. If you knock off the AV node, this is sinus bradycardia, and atypical chest pain. The RCA is dangerous b/c sometimes pt will get epigastric pain, which is an atypical pain. This simulates GERD; ie pt sent home with pepto bismol, and ends up dying
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