Valves 2 Flashcards

1
Q

mitral regurgitation - defined

A

*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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

acute etiologies of mitral regurgitation

A

*endocarditis
*papillary muscle rupture
*chordae tendinae rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

chronic etiologies of mitral regurgitation

A

*mitral valve prolapse
*mitral annular calcification
*LV dilation
*myxomatous degeneration
*HOCM (hypertrophic obstructive cardiomyopathy)
*rheumatic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

mitral regurgitation due to LV dilation

A

*as the LV dilates, it starts to pull and dilate the mitral annulus → mitral valve leaflets may be unable to close properly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

mitral regurgitation due to papillary muscle rupture

A

*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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

mitral regurgitation due to myxomatous degeneration

A

*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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

mitral regurgitation due to hypertrophic obstructive cardiomyopathy (HOCM)

A

*HOCM leads to distortion of the mitral valve by sucking the anterior leaflet of the mitral valve into the LV outflow tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

mitral regurgitation due to mitral annular calcification

A

*mitral annular calcifications leads to MR by making the bases of the valve leaflet less mobile and more fixed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

mitral regurgitation due to mitral valve prolapse (MVP)

A

*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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

where to auscultate for mitral regurgitation

A

*left 5th intercostal space, midclavicular line (LV apex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

mitral regurgitation - auscultation findings

A

*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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

mitral regurgitation - Wigger’s Diagram

A

*significant increase in LA pressure during systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

acute mitral regurgitation - pressure volume loop

A

*increased EDV (increased preload)
*increased stroke volume

note - although the stroke volume is increased on the loop, the EFFECTIVE stroke volume is decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

chronic mitral regurgitation - pressure-volume loop

A

*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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

assessing mitral regurgitation severity

A

*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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

mitral regurgitation and contractility

A

*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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

LV compensation to mitral regurgitation

A
  1. decreased forward flow (acute > chronic; having to compete with lower pressure in left atrium) → decreased afterload → unchanged wall thickness
  2. 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

treatment for mitral regurgitation

A

*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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

mitral stenosis - defined

A

*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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

etiologies of mitral stenosis

A

*rheumatic heart disease!!!
*mitral annular calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

acute rheumatic fever - overview

A

*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

22
Q

acute rheumatic fever - acute carditis

A

*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

23
Q

acute rheumatic fever - Jones Criteria

A

*requires 2 major criteria OR 1 major plus 2 minor criteria for dx:

  1. major criteria:
    -carditis (CHF/murmur)
    -polyarthritis
    -chorea
    -erythema marginatum
    -subcutaneous nodules
  2. minor criteria:
    -clinical: fever, arthralgia
    -labs: elevated erythrocyte sedimentation rate (ESR), C-reactive protein
    -EKG: PR prolongation
24
Q

evidence of streptococcal infection within the past 45 days (for acute rheumatic fever)

A
  1. elevated anti-streptolysin O (ASO) or other strep antibodies
  2. positive throat culture
  3. rapid antigen test for group A strep
25
Q

acute rheumatic fever - anti-streptolysin O antibodies (ASO Ab)

A

*antigen mimics collagen & its associated proteins, so ASO Abs can attack heart valves
*presence of these antibodies indicates exposure to these bacteria

26
Q

valve disease in acute rheumatic fever

A

*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

27
Q

acute rheumatic fever - secondary prevention

A

*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

28
Q

mitral stenosis due to mitral annular calcification

A

*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

29
Q

where to auscultate for mitral stenosis

A

*left 5th intercostal space, midclavicular line (LV apex)

30
Q

mitral stenosis - auscultation findings

A

*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

31
Q

mitral stenosis - Wiggers Diagram

A

*significant increase in LA pressure during diastole

32
Q

mitral stenosis - pressure-volume loops

A

*severe MS: decreased preload due to difficulty filling the left ventricle → decreased stroke volume
*lungs and RV bear the brunt of mitral stenosis

33
Q

treatment of mitral stenosis

A

*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

34
Q

tricuspid regurgitation - defined

A

*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

35
Q

primary etiologies of tricuspid regurgitation

A

*endocarditis
*Ebstein’s Anomaly
*chordae tendinae rupture

36
Q

secondary etiologies of tricuspid regurgitation

A

*tricuspid valve prolapse
*RV dilation
*myxomatous degeneration
*rheumatic heart disease
*carcinoid heart disease
*pacemaker lead

37
Q

where to auscultate for tricuspid regurgitation

A

*LLSB: left 4th intercostal space, beside the sternal border

38
Q

tricuspid regurgitation - auscultation findings

A

*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

39
Q

tricuspid regurgitation due to Ebstein’s Anomaly

A

*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)

40
Q

tricuspid regurgitation due to carcinoid heart disease

A

*tricuspid leaflets are fixed by fibrosis induced by serotonin, which is produced by the carcinoid tumor
*this results in torrential tricuspid regurgitation

41
Q

tricuspid stenosis - defined

A

*a narrowing of the opening of the tricuspid valve
*fixed leaflet tips leading to stenosis due to antibodies against streptolysin O (rheumatic heart disease)

42
Q

tricuspid valve surgery

A

*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

43
Q

pulmonic stenosis - defined

A

*a narrowing of the pulmonic valve opening

44
Q

etiologies of pulmonic stenosis

A

*congenital pulmonic stenosis
*Noonan Syndrome
*part of Tetralogy of Fallot

45
Q

Noonan Syndrome - overview

A

*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

46
Q

where to auscultate for pulmonic stenosis

A

*left 2nd intercostal space, upper sternal border (LUSB)

47
Q

pulmonic stenosis - auscultation findings

A

*systolic crescendo-decrescendo murmur
*worsened by inspiration and softens with expiration because of changes in volume in the right heart with the respiratory cycle

48
Q

ancillary findings in pulmonic stenosis

A

*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

49
Q

velocity of blood flow across pulmonic valve

A

*normal: 3-4 cm
*severe pulmonic stenosis: peak velocity > 4 m/sec

50
Q

pulmonic stenosis therapy

A

*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)

51
Q

pulmonary regurgitation - defined

A

*pulmonic valve has become leaky
*during diastole, a jet of blood is able to go from the pulmonary artery to the right ventricle

52
Q

etiologies of pulmonic regurgitation

A

*acute = endocarditis
*chronic:
-bicuspid pulmonic valve
-pulmonary HTN (most common)
-repair of Tetralogy of Fallot
-rheumatic heart disease
-carcinoid heart disease