In rheumatic fever, an autoimmune disease of the heart triggered by the "strep throat" bacterium's molecular mimicry, little masses of fibrin accumulate on the lines of closure of some or all of the cardiac valves. These may eventually stick together and heal with fusion of cusps ("stenosis"), and/or scar and contract, rendering the cusps incapable of full closure ("insufficiency" / "regurgitation").
Rose had an episode of rheumatic fever as a child, after which "murmurs" were detected. Dyspnea grew more severe during her adult life, and by age 52 she was housebound and had constant atrial fibrillation. At age 61, she underwent mitral valvuloplasty (one of the first people in the world to have this done), and resumed a normal life. At age 63, she survived a "small" posterolateral myocardial infarct. At age 72, she attended the International Cardiology Foundation in Switzerland and was described as "the life of the party".
At age 75, she was noted to have cardiac enlargement to the anterior axillary line, a wide-split S2, a "machinery" murmur at the apex, grade iii in systole and grade ii and rumbling in diastole, and another continuous grade ii murmur to the right of the xyphoid. EKG showed atrial fibrillation with a ventricular rate of 100. Digitalis was given with improvement in her exercise tolerance.
At age 82, Rose returned to the hospital because of marked dyspnea, and swelling of the ankles. The murmur at the apex was the same, but the continuous murmur had disappeared. Jugular venous pressure was 20 mm H20. She died a few days later.
A left-to-right shunt sends a greatly-excessive amount of blood recirculating through the lungs. Eventually this damages the pulmonary arterioles, making them more narrow. This means, of course, increased resistance to flow through the lungs, and hence a need for ever-increasing pressure. A vicious cycle develops, ending only when the pulmonary arterial resistance exceeds systemic resistance. Unless a transplant is available, death soon follows.
You will see these pictures (25-1976) in class:
What sounds make up S1? S2?
How does the splitting of a healthy person's S2 vary with respiration? HINT: Breathing-in makes A2 happen a bit earlier, and P2 happen a bit later. Why?
Why would a continuous flow of blood from the left atrium to the right atrium cause S2 to be much more widely split? HINT: A2 comes much earlier (why?) and P2 comes much later (why?)
What produces murmurs? What makes a murmur loud or soft, high-pitched or low-pitched? What determines its location?
What would the murmur of mitral stenosis sound like? When would it occur?
What would the murmur of mitral regurgitation sound like? When would it occur?
What is atrial fibrillation? Why do you think that a massively-stretched left atrium might cause it?
What determines heart rate during atrial fibrillation?
What would the murmur of atrial septal defect sound like?
What effect would the reopening of the atrial septum have on the splintting of the second heart sound, and its variation with respiration?
Why is an enlarged left atrium likely to produce a cough? Think about the anatomy!
What percent of people have a slightly-patent foramen ovale?
What is a more common cause of a "machinery" murmur? Explain.
Why do you think she had an elevated jugular venous pressure at the end?
What is edema? What kinds of things produce edema of the legs?
Rather than simply accepting that "rheumatic fever ruins valves", let's think... What is "fibrin", anyway? Can you guess what it might be doing on the lines of closure of the mitral valve in an autoimmune attack on the endocardium?
How can a good primary care physician prevent rheumatic fever? Go a little deeper than "just give penicillin."
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