Valvular Regurgitation Flashcards

0
Q

Generally compared to stenosis, how well are hearts with a regurgitant valve able to increase CO?

A

Hearts with a regurgitant valve are better able to increase CO.

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1
Q

What is regurgitant volume?

A

The extra volume that the upstream chamber receives through the regurgitant valve.

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2
Q

What’s the best way to express the severity of regurgitation?

A

Regurgitant volume and regurgitant fraction.

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3
Q

What’s the regurgitant fraction?

correction: this is just for mitral regurgitation

A

The fraction of total stroke volume (TSV = EDV - ESV) that enters the upstream chamber.

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4
Q

What’s the regurgitant fraction?

A

The fraction of total stroke volume (TSV = EDV - ESV) that enters the upstream chamber.

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5
Q

What is the “mission statement” of eccentric hypertrophy?

A

To minimize the increases in wall stress associated with increases in wall pressure.

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6
Q

Do the mitral valve leaflets normally overlap?

A

Yes. If the valve annulus gets stretched, they might overlap less, and have more risk of regurgitation.

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7
Q

What are the 3 Carpenter types of valve motion perturbation in mitral regurgitation (MR)? (conditions that cause these)

A

Type I: normal leaflet motion (e.g. perforation, annular dilation)
Type II: increased motion (e.g. snapped chordae, myxomatous degen.)
Type III: decreased motion (IIIa is due to rheumatic disease, IIIb is due to things like dilated cardiac myopathy)

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8
Q

3 causes of reduced leaflet motion in type III MR?

A

Dilated cardiac myopathy.
Remodeling in response to ischemia (MI).
Rheumatic disease.

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9
Q

Two types of myxomatous degneration MR?

A
Fibroelastic deficiency (isolated flail segment)
Barlow's disease (prolapse)
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10
Q

How can ischemia cause transient MR?

A

The posteromedial papillary muscle has a single blood supply, and can have reduced function that resolves when the ischemia does.

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12
Q

How can ischemia cause chronic MR?

A

Post-MI remodeling of the ventricle can change the angles by which papillary muscles pull on the leaflets, causing MR.

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13
Q

How does mitral valve prolapse (MVP) sound different from other MR regurgitation?

A

MVP often occurs in late systole, preceded by a click.

Other MR murmurs are holosystolic (present all the way from S1 to S2).

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14
Q

What’s the forward stroke volume (FSV)?

A

The portion of the stroke volume that moves into the downstream chamber.

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15
Q

3-4 variables effecting the regurgitant volume?

A

Pressure gradient from LV to LA.
Size of mitral regurgitant orifice.
LV systolic ejection time, and time that orifice is regurgitant.

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16
Q

How does SVR affect the regurgitant fraction?

A

The lower the SVR, the greater the proportion of blood flow that enters systemic circulation.

17
Q

What happens in acute MR? (to the LA, LV, CO, LVEF)

A

LA pressure increases (pulmonary edema if severe)
CO is reduced, though preload does increase.
Ejection fraction increases, but much of it isn’t useful.

18
Q

Compensatory mechanisms that occur during acute MR?

A
LV dilation (sarcomere stretching) due to increased volume.
Adrenergic circulatory reflexes: increased HR, contractility, and vasoconstriction to maintain BP/perfusion (but overall SVR does drop)
19
Q

Bad consequences of severe acute MR?

Treatment?

A

Rise in LA pressure transmitted to pulmonary veins -> acute pulmonary edema. (acute congestive HF).
Treatment = O2, diuresis, vasodilators, and immediate valve repair/replacement.

20
Q

What does the LA pressure waveform look like in acute MR?

A

The V waves are high due to augmented diastolic filling.

21
Q

How does the LV change in chronic MR?

How doe the LA change?

A

Eccentric hypertophy - allowing increased LVEDV at lower LVEDP.
The LA becomes more compliant.

22
Q

How is CO in chronic compensated MR?

A

It’s actually pretty close to normal.

23
Q

Why does decompensation of chronic MR occur?

A

Loss of contractile function -> reduced EF, FSF, and increased RF.

24
Q

3 reasons that make you think it’s time to replace/repair the valve in MR?

A

Symptoms of HF (acute or decompensated chronic).
Reduced LV contractility.
Significant LV remodeling.

25
Q

Should you worry if someone in MR has a normal EF?

A

Yes. Their EF should be hypernormal. Normal EF will probably be producing inadequate FSV and CO.

26
Q

Does a good repair beat valve replacement?

A

Yup.

27
Q

Major problem with mechanical valves?
With bioprosthetic valves?
With both?

A

Mechanical valves require lifelong warfarin.
Bioprosthetic valves wear out relatively quickly.
Both are quite susceptible to endocarditis.

28
Q

In aortic regurgitation (AR), how does the FSV compare to TSV?

A

FSV = TSV, because regurgitation occurs in diastole.

29
Q

How is the regurgitant fraction defined in AR?

A

Regurgitant stroke volume / TSV.

30
Q

5 causes of AR?

A
Aortoannular ectasia (dilation).
Dissection (esp. in Marfan's).
Congenitally abnormal aortic valve.
Fixed leaflets w/ mixed stenosis/regurg (rheumatic or calcific).
Endocarditis.
31
Q

What’s the association between a bicuspid aortic valve and aortic enlargement?

A

Both are products of abnormal development.

32
Q

What do aortic valves affected by rheumatic disease look like?

A

Fixed orifices due to fused commissures. Will have both stenosis and regurg.

33
Q

How does LV wall stress in AR compare to that in MR? What effect does that have?

A

LV wall stress is greater in AR, leading to a higher degree of eccentric hypertrophy.

34
Q

Why does exercise actually help some aspects of AR?

A

SVR drops, so more blood flows forward.

Diastole is shortened, so there’s less time for regurgitation.

35
Q

What do systolic / diastolic BP do in severe AR?

A

Systolic increases with increased FSV.

Diastolic drops due to rapid regurgitation back into LV (you can see a pressure like 170/50).

36
Q

Consequences of acute severe AR?

A

LVEDP and LA pressure rise dramatically -> CHF.
Sympathetic responses kick in, but the tachycardia and increased contractility aren’t enough to get CO up.
Low CO -> cardiogenic shock.

37
Q

Review: Which pressure gradient drives coronary perfusion?

A

Aortic diastolic pressure - LVEDP

38
Q

How can AR cause angina despite absence of CAD?

A

Impaired coronary perfusion: Aortic diastolic pressure is low, and the LVEDP is high. Also increased HR -> shorter diastole. (and high endocardial pressures impair subendocardial perfusion)
Increased metabolic demands of heart due to increased HR and wall stress.

39
Q

4 indications for surgical in AR?

A

Symptoms
LV end systolic dimension too big.
Fall in EF to normal range.
LV end diastolic dimension too big.