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Stenotic Atrioventricular Valve Disease Mitral Stenosis (MS)
Clinical Presentation: (symptoms of L sided, then later R sided, heart failure)
depends on degree of stenosis (mild=less stenosis/larger valve opening; severe=more stenosis/smaller valve opening)
early symptoms: dyspnea, reduced exercise capacity
mild MS: may lack dyspnea at rest; can develop it with exertion (or fever, anemia, hyperthyroid, pregnancy, etc.)
severe MS: dyspnea at rest, fatigue, signs of pulmonary congestion (i.e. orthopnea, paroxysmal nocturnal dyspnea)
advanced MS & pulmonary hypertension: progression to signs of right heart failure (JVD, hepatomegaly, ascites, peripheral edema), can compress recurrent laryngeal nerve w/ enlarged pulmonary artery or left atrium to cause hoarseness
complications: atrial fibrillation, thromboembolism, infective endocarditis, hemoptysis
precordial palpation: right ventricular “tap”
auscultation: loud S1 in almost all cases, high-pitched “opening snap” (OS) after S2 – interval btw S2 and OS relates inversely to severity of the MS, OS followed by low-frequency decrescendo murmur (diastolic “rumble”) of which the duration relates to the MS severity
note that other valvular murmurs are often found in conjunction with MS (i.e. mitral regurgitation)
MS almost always a sequela of rheumatic fever (50% cases); if a consequence of acute rheumatic fever (ARF), occurs on average 20 years post ARF.
Also see rare cases of congenital mitral stenosis, calcifications of the mitral valve in elderly patients, or endocarditis with large vegetations that obstruct the valve orifice.
Typical path features of rheumatic MS come from acute and recurrent inflammation – get fibrous thickening, calcification of valve leaflets, fusion of commissures of valves, and thickening and shortening of the chordae tendineae.
In MS, have obstruction to blood flow across the mitral valve – emptying of the LA is impeded and there’s an abnormal pressure gradient between the LA and LV.
Get high LA pressure, normal LV pressure…sometimes reduced LV stroke volume and cardiac output.
High LA pressure can be transmitted to the pulmonary circulation – can cause transudation of plasma into the lung interstitium and alveoli (causing the dyspnea) and can sometimes cause rupture of a bronchial vein into lung parenchyma, giving hemoptysis (coughing of blood).
60% of MS patients get passive pulmonary hypertension: an obligatory increase in pulmonary artery pressure that develops to preserve forward flow in the setting of increased left atrial and pulmonary venous pressures.
40% of MS patients get reactive pulmonary hypertension: medial hypertrophy and intimal fibrosis of the pulmonary arterioles – this causes decreased blood flow through the pulmonary vasculature, which results in increased right-side heart pressures and eventually right heart hypertrophy and failure.
High LA pressure leads to LA enlargement, which stretches the atrial conduction fibers and may disrupt the cardiac conduction system…resulting in Atrial Fibrillation, and can predispose the patient for thrombus formation in the LA.
Turbulent blood flow across the obstructed mitral valve can predispose patient to infective endocarditis – though not likely with MS.