CHAPTER 7: CARDIOVASCULAR THE HEART
C. 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 rheumatic fever are exactly the same. They are both immunologic dz’s. Late manifestation of Jones’ criteria is abnormal movements – called Syndham’s chorea. Example: pt with acute rheumatic fever (grade 3, pansystolic, apex, rales, S3 and S4, nodules, erythema marginatum) - 6 weeks later have Syndham’s chorea. ASO titer is imp, too – b/c it’s a group A strep infection and its elevated. Aschoff nodules – reactive histiocytes in the myocardium; only find with bx on death. Summary: immunologic dz, will not culture out group A strep in the blood, Jones criteria (polyarthritis, MC carditis, subcutaneous nodules, erythema marginatum, Syndham’s chorea.
Ie mitral stenosis, looking from left atrium, down to the ventricle – looks like a fishmouth (fishmouth appearance).
Example: what is the most posteriorly located chamber of you heart? Left atrium. Seen best on transesophageal ultrasound. B/c it is posteriorly located, and enlarged when dilated, it can press on the esophagus, leading to dsyphagia with solids (not liquids). Also, it can stretch the left recurrent laryngeal nerve and cause hoarseness. This is called Orner’s syndrome.
Example: if they have an irregular irregular pulse, what does that mean? Atrial fibrillation. Does it surprise you that they get thrombus in the left atrium? No. B/c there is a lot of stasis b/c blood is having trouble getting through, leading to stasis and thromboses. So, have to anticoagulate the pts, which is a bad combo.
Atrial fib + thrombus = bad combo. When you picture A fib, its like a vibrator and lil chips can come off and embolize – this is very common in patients with MITRAL STENOSIS.
MVP – valve is being prolapsed into atrium, b/c it is so redundant, and, chordae tendinae will rupture, leading to acute mitral insufficiency. This is not common in MVP – most of the time it is asymptomatic. MC symptomatic thing = palpitations.
2 genetic dz’s with MVP assoc: Marfan’s and Ehler Danlos syndrome. Marfan pt and pt died suddenly, why? NOT dissecting aortic aneurysm (do not die immediately with dissections – get
pain, radiation and cardiac tamponade) – answer is MVP and conduction defects. So, pt with marfan and dies suddenly, this is due to MVP and conduction defects (not dissecting aortic aneurysm).
Tricuspid regurg – know about IVDA with infective endocarditis.
Carcinoid syndrome – in order to have carcinoid syndrome, must have metassis to liver of carcinoid tumor. Serotonin and the tumor nodules gets into hepatic vein tributaries and gets into the venous blood and bathes the right side of the heart, and serotonin produces a fibrous tissue response of the valves. So, will get tricuspid insuff and pulmonic stenosis. These are the 2 valvular lesions assoc with carcinoid syndrome. (TIPS)
IX. Infective endocarditis
Mitral valve with vegetations and rupture chordae tendinae; vegetations are big and bulky and destroying the valve (hence, infective).
What is MCC? Strep viridians; 2nd MCC = Staph
While brushing teeth, have a transient strep viridians infection. If you have an underlying cardiac dz, then you run the risk of developing a bacterial endocarditis b/c just brushing your teeth can cause it to get into the bloodstream; with damaged valves, it can seed into it and produce vegetations.
Staph aureus can affect a NORMAL valve OR a damaged valve.
MC valve involved in infective endocarditis = mitral valve; 2nd MC valve = aortic valve
If you are an IVDA (who inject into veins), MC valve involved = Tricuspid valve, 2nd MC is aortic Tricuspid involved = Murmur of tricuspid regurg, pansystolic, increased on inspiration
Aortic valve involved: aortic regurg, high pitched diastolic after S2 Staph is #1 (MCC) for IVDA
If you have colon cancer/ulcerative colitis (any type of ulceration of the colonic mucosa), there is a unique type of infective endocarditis – this is strep bovis = group D strep – commonly involved with dz’s that produce ulceration of the colonic mucosa – ie UC or colon cancer.
History of colon cancer and have infective endo – organism is strep bovis (not staph).
Aortic valve – close relationship of membranous portion of the septum with the aortic valve. So, why did pt get vegetations of the aortic valve? B/c they got VSD that was not picked up. If you have congenital heart dz, you have an increased risk for infective endocarditis. VSD that someone did not pick up caused aortic valve to get infective and cause aortic regurg. Therefore, on the test, will be mitral valve infective endo, or aortic infective endo with a VSD.
Splinter hemorrhages; Painful = osler’s nodes; painless = janeway lesion; in eye – Roth spot (red with white center – just like Koplik spots in measles, which are red with a white center). This is why it is called the Koplik spot of the eye. What do they all have in common (aside from the fact that they are seen in infective endocarditis)? Splinter hemorrhages, Osler’s nodes, janeway lesions, Roth spots, and glomerulonephritis? All are type III HPY. All these lesions are immune complex
vasculitis.
Vegetations all over surface of the valve and pt has a “+” serum ANA – dx? Libman sacs endocarditis – pt has Lupus (Libman sacs is not the MC lesion of the heart with Lupus – pericarditis is); Libman sacs is the 2nd MCC, which is fibrinoid necrosis like rheumatic fever.
Marantic vegetations in mucous secreting colon cancer = Paraneoplastic syndrome (it is marantic endocarditis in a pt with colon cancer). Acute rheumatic fever looks like it.
X. Myocarditis vs. Pericarditis
On the test, if you have an infection question, it is Coxsackie virus.
MCC of myocarditis and pericarditis;
MCC viral meningitis = Coxsackie virus.
Cause of hand, foot and mouth dz? Coxsackie virus Herpangina is due to Coxsackie’s virus.
Example: Pt with heart failure did an endomyocardial bx and it had lymphocytic infiltrate in there, and it was due to Coxsackie’s myocarditis. To dx, need to do a bx of subendocardial tissue, and will see lymphocytic infiltrate (as expected with ANY virus). Therefore, ie, pt in heart failure, bx of myocardium has lymphocytes = Coxsackie’s virus myocarditis
Chest x-ray – see water bottle config – this pt as muffled heart sounds (cannot hear anything), when the pt breaths in, neck veins distend (shouldn’t happen b/c when you breath in and increase neg intrathoracic pressure, the neck veins should collapse on inspiration), radial pulse is decreased on inspiration, when you take BP there is a drop of 10mmHg during inspiration. Dx? Pericardial effusion
What the name of the triad? Beck’s triad. What is the name of the sign? Kussmaul’s sign. What is the drop of 10 mm Hb on inspiration? Pulsus paradoxus. How does all this occur? B/c there is an effusion of the pericardial sac, meaning that that heart cannot fill up (b/c there is fluid around it) – leading to muffled heart sounds. So, when you breath in and blood is supposed to get into the right side of your heart, it cannot expand. So, the neck veins distend instead of collapse, which is called Kussmaul’s sign. What ever happens to right side of the heart affects the left side of the heart b/c the left side receive blood from the right side. So, there is no blood going into the right heart, and therefore, no blood is going out of the left heart, either. So, on inspiration, blood cannot get out of left side (b/c blood is not coming out of the right heart), leading to a drop in pulse – hence pulsus paradoxus. Always see these things together: neck vein distension, drop in pulse magnitude, and drop in BP, Kussmaul’s sign, pulsus paradoxus = pericardial effusion. However, this is not what they will ask you – they will ask what is first step in management? Echocardiogram – shows that they have fluid (proves it – b/c need to call surgeon to do pericardiocentesis).
What is it MC due to? Pericarditis. What is the MCC pericarditis? Coxsackie.
What if woman has this and a “+” serum ANA? Lupus.
Any young woman that has an unexplained pericardial or pleural effusion is lupus until proven otherwise. Why? Serositis = inflame serosal membranes – its gonna leak fluid, leading to effusions.
And is a feature of Lupus.