Valves 2 Flashcards
mitral regurgitation - defined
*a backflow of blood from the left ventricle into the left atrium, resulting from imperfect closure of the mitral valve
*mitral valve has become “leaky”; aka mitral valve insufficiency
*during SYSTOLE, a jet of blood is able to go from the LV to the left atrium
acute etiologies of mitral regurgitation
*endocarditis
*papillary muscle rupture
*chordae tendinae rupture
chronic etiologies of mitral regurgitation
*mitral valve prolapse
*mitral annular calcification
*LV dilation
*myxomatous degeneration
*HOCM (hypertrophic obstructive cardiomyopathy)
*rheumatic disease
mitral regurgitation due to LV dilation
*as the LV dilates, it starts to pull and dilate the mitral annulus → mitral valve leaflets may be unable to close properly
mitral regurgitation due to papillary muscle rupture
*occurs 5-14 days after an acute inferior ST segment elevation myocardial infarction which was not revascularized
*usually the posterior-medial papillary muscle, b/c it is only supplied by one artery (posterior descending artery)
mitral regurgitation due to myxomatous degeneration
*myxomatous degeneration represents a breakdown of connective tissue
*the degeneration occurs in conjunction with accumulation of dermatan sulfate, a glycosaminoglycan, within the connective tissue matrix of the valve
*can be seen in individuals with connective tissue disorders, such as MARFAN’S SYNDROME or EHLERS-DANLOS SYNDROME
mitral regurgitation due to hypertrophic obstructive cardiomyopathy (HOCM)
*HOCM leads to distortion of the mitral valve by sucking the anterior leaflet of the mitral valve into the LV outflow tract
mitral regurgitation due to mitral annular calcification
*mitral annular calcifications leads to MR by making the bases of the valve leaflet less mobile and more fixed
mitral regurgitation due to mitral valve prolapse (MVP)
*MVP is a common, usually asymptomatic billowing of the mitral leaflets back into the left atrium
*usually inherited as an autosomal dominant disorder with variable penetrance
*can be seen individuals with Marfan’s and Ehlers-Danlos
*associated with MID-SYTOLIC CLICK
note - for mitral valve prolapse, you may have non-holosystolic MR (more late-systolic)
where to auscultate for mitral regurgitation
*left 5th intercostal space, midclavicular line (LV apex)
mitral regurgitation - auscultation findings
*holosystolic, high-pitched “blowing” murmur
*loudest at apex, radiates toward axilla
note - mitral regurgitation significantly increases the left atrial pressure
*the pressure difference is high between the LV and LA throughout systole, which is why it is holosystolic (heard throughout the entirety of systole)
note - for mitral valve prolapse, you may have non-holosystolic MR (more late-systolic)
mitral regurgitation - Wigger’s Diagram
*significant increase in LA pressure during systole
acute mitral regurgitation - pressure volume loop
*increased EDV (increased preload)
*increased stroke volume
note - although the stroke volume is increased on the loop, the EFFECTIVE stroke volume is decreased
chronic mitral regurgitation - pressure-volume loop
*chronic mitral regurgitation is able to adapt by dilating, and as such, is able to buffer itself from a drop in afterload
*eventually, it does develop an increase in afterload, and the contractility starts to go down in spite of a normal LV ejection fraction
assessing mitral regurgitation severity
*one way to estimate the severity of MR is the Regurgitant Fraction = regurgitant volume divided by LV stroke volume
*mild: regurg fraction < 30%
*moderate: regurg fraction 30-50%
*severe: regurg fraction > 50%
mitral regurgitation and contractility
*because of the stroke volume goes to the left atrium, it makes the LV EF appear better than it really is
*as such, you can start to have significant remodeling and damage and still have a normal LV EF
*in comparison, in aortic regurgitation, because AR increases afterload, it makes the LV EF look worse than it really is
LV compensation to mitral regurgitation
- decreased forward flow (acute > chronic; having to compete with lower pressure in left atrium) → decreased afterload → unchanged wall thickness
- increased filling of LV chamber during diastole b/c of regurgitant flow having to come into LV → increased preload → increased LV dilation (eccentric left ventricular hypertrophy)
treatment for mitral regurgitation
*treat when symptoms develop (CHF, cardiogenic shock) or when LV function starts to decline (LV EF < 60%)
note - in almost all cases, the cutoff for LV EF is < 50%, but in mitral regurgitation, the cutoff is < 60% because MR hides it well
mitral stenosis - defined
*a heart valve disease characterized by the narrowing of the mitral valve orifice, which leads to obstruction of blood flow from the left atrium to the left ventricle
*leads to increased left atrial pressure
*as time progresses, can lead to pulmonary HTN and RV failure
etiologies of mitral stenosis
*rheumatic heart disease!!!
*mitral annular calcification
acute rheumatic fever - overview
*consequence of upper respiratory tract infection from group A strep (Streptococcus pyogenes)
*formation of an antibody (anti-streptolysin O) against the M protein of S. pyogenes, which mimics collagen and its associated proteins, so ASO Ab can attack the heart valves (and other places)
*involves heart, skin, brain, and connective tissue
acute rheumatic fever - acute carditis
*in the acute manifestation of carditis, all 3 layers of the heart (pericardium, myocardium, and endocardium) are affected
*acutely, Aschoff bodies are present (a focal area of fibrinoid necrosis surrounded by inflammation - see image); these later resolve to form scar tissue
*most devastating sequelae result from involvement of valvular endocardium, but usually sx manifest 10-30 years later
acute rheumatic fever - Jones Criteria
*requires 2 major criteria OR 1 major plus 2 minor criteria for dx:
- major criteria:
-carditis (CHF/murmur)
-polyarthritis
-chorea
-erythema marginatum
-subcutaneous nodules - minor criteria:
-clinical: fever, arthralgia
-labs: elevated erythrocyte sedimentation rate (ESR), C-reactive protein
-EKG: PR prolongation
evidence of streptococcal infection within the past 45 days (for acute rheumatic fever)
- elevated anti-streptolysin O (ASO) or other strep antibodies
- positive throat culture
- rapid antigen test for group A strep
acute rheumatic fever - anti-streptolysin O antibodies (ASO Ab)
*antigen mimics collagen & its associated proteins, so ASO Abs can attack heart valves
*presence of these antibodies indicates exposure to these bacteria
valve disease in acute rheumatic fever
*about 40% will have MITRAL VALVE INVOLEMENT (mitral stenosis most common)
*additional 25% will have both aortic + mitral involvement
*a small subset will have involvement of the tricuspid valve
acute rheumatic fever - secondary prevention
*prevention of recurrent episodes of group A strep pharyngitis is the most effective method to prevent the development of severe rheumatic heart disease
*a GAS infection need not be symptomatic to trigger a recurrence
*recurrence can occur even when a symptomatic infection is treated optimally
*prevention (secondary prophylaxis) requires continuous antimicrobial prophylaxis rather than recognition of new infection = PENICILLIN
mitral stenosis due to mitral annular calcification
*increased calcium deposits at the base of the mitral valve leaflet cause the valve to become more stiff
*mostly encountered in those who are advanced in years
where to auscultate for mitral stenosis
*left 5th intercostal space, midclavicular line (LV apex)
mitral stenosis - auscultation findings
*diastolic murmur which starts with an OPENING SNAP and decreases in intensity throughout diastole
*note - opening snap is only heard in rheumatic disease MS
*the more severe the stenosis, the earlier the opening snap will be
mitral stenosis - Wiggers Diagram
*significant increase in LA pressure during diastole
mitral stenosis - pressure-volume loops
*severe MS: decreased preload due to difficulty filling the left ventricle → decreased stroke volume
*lungs and RV bear the brunt of mitral stenosis
treatment of mitral stenosis
*if symptomatic, can offer balloon valvuloplasty to those with moderate MS
*if not a candidate for balloon valvuloplasty, can have a mitral valve replacement
*goal = intervene while pulmonary HTN is reversible (if present)
*prone to developing clots with atrial fibrillation, so need to anticoagulate
tricuspid regurgitation - defined
*a backflow of blood from the right ventricle into the right atrium
*tricuspid valve is “leaky”
*during systole, a jet of blood is able to go from the right ventricle to the right atrium
primary etiologies of tricuspid regurgitation
*endocarditis
*Ebstein’s Anomaly
*chordae tendinae rupture
secondary etiologies of tricuspid regurgitation
*tricuspid valve prolapse
*RV dilation
*myxomatous degeneration
*rheumatic heart disease
*carcinoid heart disease
*pacemaker lead
where to auscultate for tricuspid regurgitation
*LLSB: left 4th intercostal space, beside the sternal border
tricuspid regurgitation - auscultation findings
*holosystolic, high-pitched blowing murmur
*loudest at tricuspid area
*worsened by inspiration and softens with expiration because of changes in volume in the right heart with the respiratory cycle
tricuspid regurgitation due to Ebstein’s Anomaly
*congenital defect in the septal and posterior leaflets of the tricuspid valve are displaced towards the RV apex
*50% have some type of accessory pathway (i.e. Wolff-Parkinson-White)
tricuspid regurgitation due to carcinoid heart disease
*tricuspid leaflets are fixed by fibrosis induced by serotonin, which is produced by the carcinoid tumor
*this results in torrential tricuspid regurgitation
tricuspid stenosis - defined
*a narrowing of the opening of the tricuspid valve
*fixed leaflet tips leading to stenosis due to antibodies against streptolysin O (rheumatic heart disease)
tricuspid valve surgery
*operating on the tricuspid valve is not common (not as important as mitral valve; frequently its problems are function rather than structural)
*tricuspid valve annuloplasty
-cinch it up with a ring to minimize regurgitation
-NOT A STAND-ALONE PROCEDURE
pulmonic stenosis - defined
*a narrowing of the pulmonic valve opening
etiologies of pulmonic stenosis
*congenital pulmonic stenosis
*Noonan Syndrome
*part of Tetralogy of Fallot
Noonan Syndrome - overview
*a genetic disorder that may present with mildly unusual facial features, short height, congenital heart disease, bleeding problems, and skeletal malformations
*a type of RASopathy, the underlying mechanism for which involves over-activation within RAS-MAPK cell signaling pathway
*autosomal dominant
where to auscultate for pulmonic stenosis
*left 2nd intercostal space, upper sternal border (LUSB)
pulmonic stenosis - auscultation findings
*systolic crescendo-decrescendo murmur
*worsened by inspiration and softens with expiration because of changes in volume in the right heart with the respiratory cycle
ancillary findings in pulmonic stenosis
*in some instances, questions about pulmonic stenosis may purposefully leave the murmur itself out
*when that’s the case, look for some of the following indicators:
-right ventricular heave
-exaggerated physiologic splitting of S2
velocity of blood flow across pulmonic valve
*normal: 3-4 cm
*severe pulmonic stenosis: peak velocity > 4 m/sec
pulmonic stenosis therapy
*balloon valvuloplasty:
-tear it open with a balloon
-unlike aortic stenosis, this works well because pulmonary pressures are much less than systemic pressures (resulting pulmonic regurgitation is not as big of a problem as causing aortic regurgitation)
pulmonary regurgitation - defined
*pulmonic valve has become leaky
*during diastole, a jet of blood is able to go from the pulmonary artery to the right ventricle
etiologies of pulmonic regurgitation
*acute = endocarditis
*chronic:
-bicuspid pulmonic valve
-pulmonary HTN (most common)
-repair of Tetralogy of Fallot
-rheumatic heart disease
-carcinoid heart disease
