Valvular Regurgitation Flashcards
Generally compared to stenosis, how well are hearts with a regurgitant valve able to increase CO?
Hearts with a regurgitant valve are better able to increase CO.
What is regurgitant volume?
The extra volume that the upstream chamber receives through the regurgitant valve.
What’s the best way to express the severity of regurgitation?
Regurgitant volume and regurgitant fraction.
What’s the regurgitant fraction?
correction: this is just for mitral regurgitation
The fraction of total stroke volume (TSV = EDV - ESV) that enters the upstream chamber.
What’s the regurgitant fraction?
The fraction of total stroke volume (TSV = EDV - ESV) that enters the upstream chamber.
What is the “mission statement” of eccentric hypertrophy?
To minimize the increases in wall stress associated with increases in wall pressure.
Do the mitral valve leaflets normally overlap?
Yes. If the valve annulus gets stretched, they might overlap less, and have more risk of regurgitation.
What are the 3 Carpenter types of valve motion perturbation in mitral regurgitation (MR)? (conditions that cause these)
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)
3 causes of reduced leaflet motion in type III MR?
Dilated cardiac myopathy.
Remodeling in response to ischemia (MI).
Rheumatic disease.
Two types of myxomatous degneration MR?
Fibroelastic deficiency (isolated flail segment) Barlow's disease (prolapse)
How can ischemia cause transient MR?
The posteromedial papillary muscle has a single blood supply, and can have reduced function that resolves when the ischemia does.
How can ischemia cause chronic MR?
Post-MI remodeling of the ventricle can change the angles by which papillary muscles pull on the leaflets, causing MR.
How does mitral valve prolapse (MVP) sound different from other MR regurgitation?
MVP often occurs in late systole, preceded by a click.
Other MR murmurs are holosystolic (present all the way from S1 to S2).
What’s the forward stroke volume (FSV)?
The portion of the stroke volume that moves into the downstream chamber.
3-4 variables effecting the regurgitant volume?
Pressure gradient from LV to LA.
Size of mitral regurgitant orifice.
LV systolic ejection time, and time that orifice is regurgitant.
How does SVR affect the regurgitant fraction?
The lower the SVR, the greater the proportion of blood flow that enters systemic circulation.
What happens in acute MR? (to the LA, LV, CO, LVEF)
LA pressure increases (pulmonary edema if severe)
CO is reduced, though preload does increase.
Ejection fraction increases, but much of it isn’t useful.
Compensatory mechanisms that occur during acute MR?
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)
Bad consequences of severe acute MR?
Treatment?
Rise in LA pressure transmitted to pulmonary veins -> acute pulmonary edema. (acute congestive HF).
Treatment = O2, diuresis, vasodilators, and immediate valve repair/replacement.
What does the LA pressure waveform look like in acute MR?
The V waves are high due to augmented diastolic filling.
How does the LV change in chronic MR?
How doe the LA change?
Eccentric hypertophy - allowing increased LVEDV at lower LVEDP.
The LA becomes more compliant.
How is CO in chronic compensated MR?
It’s actually pretty close to normal.
Why does decompensation of chronic MR occur?
Loss of contractile function -> reduced EF, FSF, and increased RF.
3 reasons that make you think it’s time to replace/repair the valve in MR?
Symptoms of HF (acute or decompensated chronic).
Reduced LV contractility.
Significant LV remodeling.
Should you worry if someone in MR has a normal EF?
Yes. Their EF should be hypernormal. Normal EF will probably be producing inadequate FSV and CO.
Does a good repair beat valve replacement?
Yup.
Major problem with mechanical valves?
With bioprosthetic valves?
With both?
Mechanical valves require lifelong warfarin.
Bioprosthetic valves wear out relatively quickly.
Both are quite susceptible to endocarditis.
In aortic regurgitation (AR), how does the FSV compare to TSV?
FSV = TSV, because regurgitation occurs in diastole.
How is the regurgitant fraction defined in AR?
Regurgitant stroke volume / TSV.
5 causes of AR?
Aortoannular ectasia (dilation). Dissection (esp. in Marfan's). Congenitally abnormal aortic valve. Fixed leaflets w/ mixed stenosis/regurg (rheumatic or calcific). Endocarditis.
What’s the association between a bicuspid aortic valve and aortic enlargement?
Both are products of abnormal development.
What do aortic valves affected by rheumatic disease look like?
Fixed orifices due to fused commissures. Will have both stenosis and regurg.
How does LV wall stress in AR compare to that in MR? What effect does that have?
LV wall stress is greater in AR, leading to a higher degree of eccentric hypertrophy.
Why does exercise actually help some aspects of AR?
SVR drops, so more blood flows forward.
Diastole is shortened, so there’s less time for regurgitation.
What do systolic / diastolic BP do in severe AR?
Systolic increases with increased FSV.
Diastolic drops due to rapid regurgitation back into LV (you can see a pressure like 170/50).
Consequences of acute severe AR?
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.
Review: Which pressure gradient drives coronary perfusion?
Aortic diastolic pressure - LVEDP
How can AR cause angina despite absence of CAD?
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.
4 indications for surgical in AR?
Symptoms
LV end systolic dimension too big.
Fall in EF to normal range.
LV end diastolic dimension too big.
