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Valvular Heart Disease.docx

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University of Calgary
NURS 203

Valvular Heart Disease Mitral Valve Prolapse – MC mitral valve lesion – more common in women; too much valve and looks like a parachute (air goes under a parachute and fills it up – same with blood) – blood will prolapse into left atrium, and when it stops, it causes a click. Prolapse means that something is coming out – ie rectal prolapse. So, with mitral valve prolapse, it is extending into the left atrium. When it stops, and cannot go in anymore, it stops and causes a click, and it followed by a short mitral regurg murmur. So, it goes “click murmur, click murmur” (not “snap murmur” – opening snaps occur in mitral and tricuspid stenosis). What is the pathology? Myxomatous degeneration. What GAG makes up the valve? Dermatan sulfate, therefore its an excess of dermatan sulfate in the mitral valve, and it becomes redundant (too much of it), blood goes under it and causes a click and murmur. Is it closer to S1 or S2? It deals with preload. If we increased vol of blood in the left ventricle, then the click and murmur will come closer to S2 b/c it takes longer for all the events to get blood out. If we decrease the amount of blood coming into the left ventricle (decrease preload), the click and murmur come closer to S1. So, when standing and have MVP, what is preload vs. lying down? It is less. Less preload = less blood in the ventricle = click and murmur closer to S1. Now, let’s say pt lies down – click and murmur closer to S2 b/c increasing preload. They will ask: what will happen to click and murmur with anxiety? What will happen to heart rate with anxiety? Increase. Therefore, will have less time to fill ventricles, therefore will come closer to S1. Aortic Stenosis MC valvular cause of syncope with exercise MCC angina with exercise. MCC microangiopathic hemolytic anemia This will an ejection murmur, right 2 ICS, radiation into the neck, systolic, increases in intensity on expiration. Intensity of murmur with different positions: what will increase the intensity of the murmur (what will make it worse and therefore louder)? Increasing preload in the ventricle. With decreased blood in the ventricle, it will decrease the intensity of the ejection murmur b/c it has to go out the stenotic valve. If you are putting more blood into the LV and need to get it out, it will increase the intensity - this is imp b/c it differentiates it from hypertrophic cardiomyopathy. Why do they get angina with exercise? Pulse is diminished and therefore the stroke volume will decrease. So, when do the coronary arteries fill up? Diastole. With less blood there (b/c couldn’t get it out and had to get it through the valve), there is thickened muscle and less blood going to the heart, leading to angina. So, this is the MC valvular lesion leading to angina. Also, with syncope with exercise, b/c you have decreased cardiac output, you will faint. Mitral stenosis Slide: Thrombi, left atrium is dilated; murmur in diastole (stenosis prob in opening and this valve opens in diastole, leading to snap and rumble), heard at apex and increases in intensity on expiration. MCC mitral stenosis – rheumatic fever (acute). Rheumatic fever -vegetations; due to group A beta hemolytic streptococcal infection. Usually occurs as post-pharyngitis. As opposed to post streptococcal glomerulonephritis, this can be pharyngitis or a skin infection. Most of time rheumatic fever is from a previous tonsillitis. When you culture blood in pts with rheumatic fever, it will be negative. Will not be able to grow the organisms b/c its not an infective endocarditis. It is an immunologic mechanism. With strep, M protein is the pathogenic factor for group A strep. Certain strains have Ag’s similar to the heart and joints. So, when we make Ab’s against the group A strep, we are also making Ag’s against the heart (our own tissue) – therefore we attack our own heart, joints, basal ganglia and elsewhere. This is called mimicry b/c we are developing Ab’s against our own tissue, b/c there are similar Ag’s in the M protein of the bacteria, so its is all immunologic! MC valve involved is the mitral valve. The vegetations are sterile and line along the closure of the valve. The vegetations usually do not embolize. Know Jones criteria for dx of acute rheumatic fever – ie young person, few weeks ago had an exudative tonsillitis, now presents with joint pain and swelling and dyspnea, rales in the lung, pansystolic murmur, apex, and increases in intensity on expiration, S3 and S4 heart sound – due to acute rheumatic fever. Dx is rheumatic fever. MC symptom is polyarthritis. They like this question b/c in children, there is a limited d/d for polyarthritis – it includes juvenile rheumatic arthritis, Henoch Schonlein purpura, rubella, acute rheumatic fever. However, none of these have symptoms of heart failure and mitral insufficiency except for acute rheumatic fever. So, if they ask you the MC valvular lesion in acute rheumatic fever, it is NOT mitral stenosis. It takes 10 years to have a stenotic valve (mitral stenosis). So, the murmur that you hear is mitral REGURG, b/c all parts of the heart are inflamed, leading to friction rub, myocarditis (inflamed myocardium), and endocarditis (these are the valves with the vegetations). So, will get mitral regurg murmur with acute rheumatic fever. Other features of Jones criteria: joints, cardiac abnormalities, erythema marginatum (skin zit), subcutaneous nodules (like rheumatic nodules on the extensor surfaces – they are exactly the same). Rh nodules and nodules associated with acute rheum
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