Murmurs and Valvular Disease Flashcards
Etiology of mitral stenosis
Most commonly rheumatic, although hx of acute rheumatic fever is now uncommon
[rare causes include congenital MS, calcification of the mitral annulus with extension onto leaflets]
With mitral stenosis, sx most commonly begin in ____ decade, but MS causes severe disability at earlier ages in developing nations
4th
Principle symptoms of mitral stenosis
Dyspnea and pulmonary edema precipitated by exertion, excitement, fever, anemia, tachycardia, pregnancy, sexual intercourse, etc.
Complications of mitral stenosis
Hemoptysis, PE, pulmonary infxn, systemic embolization
Note that systemic endocarditis is uncommon in pure MS
Lab ECG findings with mitral stenosis
Atrial fibrillation or left atrial enlargement when sinus rhythm is resent
Right axis deviation and RV hypertrophy in presence of pulmonary HTN
CXR findings with mitral stenosis
LA and RV enlargement with Kerley B lines
Echocardiogram is most useful noninvasive test for mitral stenosis. What are the typical findings?
Shows reduced separation, calcification, and thickening of valve leaflets and subvalvular apparatus, and LA enlargement
Doppler flow recordings provide estimation of transvalvular gradient, mitral valve area, and degree of pulmonary HTN
Treatment for mitral stenosis
At-risk pts should receive prophylaxis for recurrent rheumatic fever (penicillin V 250-500 mg PO BID or benzathine penicillin G 1-2 M units IM monthly).
In the presence of dyspnea, sodium restriction and oral diuretic therapy; beta blockers, rate-limiting calcium channel blockers (i.e., verapamil or diltiazem), or digoxin to slow ventricular rate in afib. Warfarin (with target INR of 2-3) for pts with afib or hx of thromboembolism. For afib of recent onset, consider conversion (chemical or electrical) to sinus rhythm, ideally after > 3 weeks AC therapy.
Mitral valvotomy in the presence of symptoms and mitral orific < 1.5cm. In uncomplicated MS, percutaneous balloon valvuloplasty is the procedure of choice; if not feasible, then open surgical valvotomy.
Etiology of mitral regurg
Mitral valve prolapse, rheumatic heart disease, ischemic heart disease with papillary muscle dysfunction, LV dilation of any cause, mitral annular calcification, hypertrophic cardiomyopathy, IE, congenital
Echocardiogram findings with mitral regurg
Enlarged LA, hyperdynamic LV, identifies mechanism of MR; Doppler analysis helpful in dx and assessment of severity & degree of pulmonary HTN
Treatment for mitral regurg
For severe/decompensated MR, treat as for heart failure. IV vasodilators (e.g., nitroprusside) are beneficial for acute, severe MR. AC is indicated in the presence of afib.
For chronic pulmonary MR, surgical tx — either valve repair or replacement — is appropriate if pt has symptoms or evidence of progressive LV dysfunction (e.g., LV ejection fraction [LVEF] < 60% or end-systolic LV diameter by echo > 40 mm). Operation should be carried out before development of chronic heart failure symptoms. Pts with functional ischemic MR may require coronary artery revascularization along with valve repair.
Functional nonischemic MR d/t LV enlargement with impaired contractile function should be treated with aggressive heart failure therapies and consideration of cardiac resynchronization therapy.
Etiology of MVP
Most commonly idiopathic
May accompany Marfan or EDS
Pathology associated with MVP
Redundant mitral valve tissue with myxedematous degeneration and elongated chordae tendinae
Most imporant complication of MVP
Progressive MR; rarely, systemic emboli from platelet-fibrin deposits on valve
Sudden death is very rare outcome
Treatment for MVP
Asymptomatic pts should be reassurd
Beta blockers may lessen chest discomfort and palpitations
Prophylaxis for infective endocarditis is indicated only if prior hx of endocarditis
Valve repair or replacement for pts with severe mitral regurg; ASA or AC therapy for pts with hx of TIA or embolization
PE findings with mitral stenosis
Right ventricular lift; palpable S1; opening snap (OS) follows A2 by 0.06=0.12 seconds; OS-A2 interval inversely proportional to severity of obstruction
Diastolic rumbling murmur with presystolic accentuation when in sinus rhythm, best heard in left lateral decubitus position
Duration of murmur correlates with severity of obstruction
Other: may see malar rash or blue facies
Clinical manifestations with mitral regurg (including sx and PE findings)
Sx: Fatigue, weakness, and exertional dyspnea
Physical exam:
Sharp low-volume upstroke of carotid arterial pulse, LV lift, S1 diminished: wide splitting of S2; S3 common; loud holosystolic murmur at apex (less than holosystolic in acute severe MR) and often a brief early-mid-diastolic murmur d/t increased transvalvular flow
Clinical manifestations with mitral valve prolapse (including sx and PE findings)
More common in females; Most pts are asymptomatic and remain that way
Potential symptoms include vague chest pain and supraventricular and ventricular arrhythmias.
PE:
Mid or late systolic click(s) followed by late systolic murmur at apex; exaggeration by valvsalva maneuver, reduced by squatting and isometric exercise
3 most common etiologies of aortic stenosis
Degeneration calcification of a congenitally bicuspid aortic valve
Chronic deterioration and calcification of a trileaflet valve
Rheumatic heart disease (almost always associated with rheumatic MITRAL dz)
Symptoms associated with aortic stenosis
Exertional dyspnea, angina, and syncope are cardinal sx; they occur late, after years of obstruction and aortic valve area <1 cm
PE findings with aortic stenosis
Weak and delayed (parvus et tardus) arterial pulses with carotid thrill
A2 soft or absent; S4 common. Crescendo-decrescendo systolic murmur, often with systolic thrill. Murmur is typically loudest at second right intercostal space, with radiation to carotids and sometimes at apex (Gallavardin effect)
ECG and echo findings with aortic stenosis
ECG: often shows LV hypertrophy, but not useful for predicting gradient
Echo:
Shows LV hypertrophy, calcification and thickening of aortic valve cusps with reduced systolic opening. Dilation and reduced contraction of LV indicate poor prognosis. Doppler quantitates systolic gradient and allows calculation of valve area.
Treatment for aortic stenosis
Avoid strenuous activity in severe AS, even in asymptomatic phase.
Treat heart failure in standard fashion, but use vasodilators with caution in pts with advanced disease.
Valve replacement is indicated in adults with symptoms resulting from AS and hemodynamic evidence of severe obstruction. Transcatheter aortic valve implantation (TAVI) is an alternative approach for pts at excessive or prohibitive surgical risk.
2 major etiologies of aortic regurg
Valvular: rheumatic (especially if mitral disease is present), biscuspid valve, endocarditis
Dilated aortic root: dilation d/t cystic medial necrosis, aortic dissection, ankylosing spondyliitis, syphilis
