Lecture 36: Valvular Regurgitation I & II Flashcards Preview

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Flashcards in Lecture 36: Valvular Regurgitation I & II Deck (62):

What is regurgitant volume?

The volume of fluid that flows back into a chamber
The severity of valvular regurgitation can be expressed as regurgitant volume (or regurgitant fraction)
Leads to volume overload


What is the difference between valvular regurgitation and stenosis?

Two chambers are affected by volume load
Can be acute or chronic
-stenosis can only be chronic
Regurgitant volume and regurgitant fraction expresses severity of lesion better than simply regurgitant orifice area
Better able to increase SV and CO


What are the characteristics of LV hypertrophy?

It is a CHRONIC adaptive response to volume and pressure overload
Attempts to normalize LV wall stress and optimize mO2 consumption
Increase in myocyte mass but no increase in number


What is the etiology of LV hypertrophy?

According to LaPlace’s Law
In order to keep wall tension constant, chamber radius increases as well as wall thickness
Increase wall thickness = myofibril addition in series
There is no change in relative wall thickness (see equation below)


What is relative wall thickness?

-LVID = left ventricular interior diameter
Normal = 0.34


What is the effect of chordae and papillary muscles?

Papillary muscles contract to keep the valve from prolapsing into the upstream chamber
posterior papillary muscle is more likely to become ischemic


What are the different types of chordae tendinae?

1. primary chordae
2. secondary chordae
3. tertiary chordae


What is the zone of coaptation?

The space between the leaflets that needs to be closed in order to prevent regurgitation


What is the effect of ACUTE regurg on LV?

Not enough time to hypertrophy so LV is largely normal


What is the effect of CHRONIC regurg on LV?

Eccentric hypertrophy


What are the two types of etiologies of MR?

1. Functional
2. Anatomic


What are the three types of leaflet motions (anatomic etiologies of MR)?

1. type I (normal)
2. type II (increased leaflet motion goes into upstream chamber
3. type III (decreased leaflet motion, doesn’t close all the way)


What are the types of anatomic etiologies of MR?

1. Myxomatous Degeneration that leads to MVP or flail leaflet
2. Endocarditis with leaflet destruction
3. Dilation of mitral annulus due to atrial remodeling
4. Functional MR due to LV dilation/remodeling
5. Ischemic MR due to LV remodeling in setting of prior MI
6. Rheumatic disease


What are the key characteristics of myxomatous degeneration leading to mitral valve disease?

One etiology of MR
MVP or flail leaflet because chords rupture
Can be referred to as degenerative disease
Two types: classic vs non-classic
Classic = abnormal leaflets
MR will be eccentric (away from leaflet that prolapses
Chordal rupture can result in flail segment and sudden increase in MR (so disease can change)


What is the difference between MVP and flail?

MVP means chordae is still attached
Flail = chord has broken


Whats the difference between myxomatous and Barlow’s valves?

1. Myxomatous is a systemic disease with poor connective tissue everywhere
2. Barlow’s valves just means theres a dysfunction with the valve itself (either the chordae or with the annulus)


What are the key characteristics of MR due to LV remodeling?

Occurs when papillary muscle moves towards apex and laterally
Leaflets are normal, but are getting pulled farther apart, so coaptation is dysfunctional
Annular dilation can also happen
Remodeling thus can be due to
i. ventricular remodeling
ii. annular dilation
iii. reduced ejection fraction (ejection fraction is the force that closes the mitral valve)


What are the key characteristics of MR caused by endocarditis?

Normal valve movement
Vegetations interfere with coaptation
Leaflet perforation due to infection


What are the key characteristics of MR caused by endocarditis?

Valve movement is decreased (Carpentier Type III)
Thickened leaflet tips prevents coaptations
Shortened or ruptured chords due to rheumatic process
Often coexists with MStenosis as well
Mixed disease


What are the key characteristics of MR caused by ischemia?

Occurs because remodeling of infarcted segments lead to focal dilation/wall displacement
-can be due to annular dilation as well
Transient MR that occurs during ischemia
-posteromedial papillary muscle more vulnerable to ischemia (single blood supply)
MR can also occur if previous MI caused restriction of posterior leaflet in
FOCAL remodelingd


What is RV?

Regurgitant volume
One of the things you need to consider for MR
Volume of fluid that is being pumped into
“upstream” chamber


What is FSV?

Forward stroke volume (ml/beat)
Volume of fluid being pumped into
“downstream” chamber or aorta


What is TSV?

Total stroke volume (ml/beat)
Total amount of fluid being pumped out of chamber (but in this case there are two fluid volumes you have to measure since you have two open holes)


What is RF?

Regurgitant fraction
Percent of fluid being pumped into the “upstream” chamber (the chamber you don’t want
Smaller the RF, the better patient is doing


What are the two parameters you need to consider for MR?

1. RV (regurgitant volume)
2. RF (regurgitant fraction)


What determines the volume of MR?

1. pressure gradient from LV to LA
2. size of mitral regurgitant orifice
3. LV systolic ejection time and time orifice is open
4. the extent of SVR (but only in theory because SVR is always much higher than LA)


What is the hemodynamic response to acute MR?

Normal LA size and compliance (doesn’t hypertrophy yet)
Acute rise in LA pressure leading to pulmonary edema
Decreased effective CO
-because LV stroke volume divided between FSV and RV
Volume overload in both LA and LV


What happens to TSV in acute MR?

Increased in total stroke volume because you have less afterload (since LA pressure is lower)


What happens to preload in acute MR?

Increased preload due to return of RV, increased SV (Frank Starling) and increased LVEDP as the consequence
That’s why you have volume overload at diastole


Why is there a lower afterload in acute MR?

Because left atrium offers another avenue for blood to flow, thereby reducing overall afterload (because it can go through two valves)
Afterload decreases even if you have peripheral vasoconstriction


What are the compensatory mechanisms in acute MR?

1. LV dilation (increase sarcomere length) due to increased LV volume
-preserves FSV
2. Activate circulatory reflexes adrenergically
-increased HR
-increased LV contractility with rise LVEF
-vasoconstriction to maintain BP/organ perfusion


What are the acute MR symptoms?

1. acute pulmonary edema (due to pressure rise in LA)
2. No eccentric hypertrophy yet
3. Acute CHF because patient unable to meet CO demand


What is the therapy for acute MR?

1. diuresis
2. supportive care
3. vasodilator therapy (to decrease SVR)
4. surgery


What happens to the v wave in acute MR?

It becomes a lot bigger because LA because of RegurgVolume from ventricular systole
V wave > a wave


How do you get chronic MR?

Slow progression of MR or management of acute MR into chronic phase


What are the compensatory changes for CHRONIC compensated MR?

1. LV dilation increases EDV and total stroke volume
2. LV eccentric hypertrophy occurs to allow
i. increased LVEDV at lower LVEDP
ii. increased LV compliance
iii. serves to normalize wall stress as stated in LaPlace’s law
3. Increased LA compliance


What does eccentric hypertrophy do for the ventricle?

Chronic compensated MR
1. Reduced diastolic wall stress
2. Normalizes afterload
3. Increased FSV (and thus greater CO)
3. Greater Regurg Volume (because of hypertrophy)
Regrugitant fraction remains the same even though there is a greater regurgitant volume
Bigger cavity = more compliant ventricle and atrium
Patient gets more fluid moving towards BOTH upstream chamber and downstream chamber


Why are the sarcomeres less stretched out in chronic compensated MR?

Because they are used to eccentric hypertrophy
In acute setting, doesn’t have time to adjust


What is the difference between acute and chronic COMPENSATED MR?

Chronic = normal CO; Acute = decreased CO
LVEDP is greater in acute because compensation hasn’t kicked in
LV size is greater in chronic because of compensatory mechanisms
LVEF is greater than normal for both acute and chronic
-greater in acute because of decreased afterload from LA pathway
-greater in chronic because of increased preload


What causes chronic Decompensated MR?

Occurs when you have loss of contractile function
-not known why contractile function is lost


What is the hemodynamic response to Decompensated MR?

1. Reduced FSV
2. Reduced Cardiac output
3. Reduced EF
4. Reduced RF (see how its only 85 cc compared to 95 cc in compensated chronic)
5. Increased EDV and ESV


What are the differences between chronic compensated and chronic decompensated MR?

Decompensated MR has no contractile function so has lower CO, lower EF and lower RV and lower RF
Decompensated MR also has greater EDV and ESV
LA pressure is higher in decomp (25 vs 15)


What happens to the LA after MR?

Increased compliance
Acute patients increases pressure and compliance faster than chronic patients


Why are V waves big when measuring pulmonary wedge pressure for MR?

Because of the regurgitant volume going into the LA during ventricular systole


How does one know when its time to fix MR?

1. Symptoms of heart failure
2. acute MR cannot be stabilized
3. Chronic compensated that becomes decompensated
4. reduced LV contractile function
5. Significant levels of LV remodeling (eccentric hypertrophy)
Important to consider that artificial valve has own risks so may not be best for patients


When does regurg happen in AR?

During diastole rather than systole (blood from aorta comes back to aorta)


What is the difference between AR and MR?

Forward stroke volume and total stroke volume are the SAME for AR because regurg occurs in diastole
Decreased effective flow since volume of blood is regurgitated


What are the etiologies of AR?

1. aortoannular ectasia
-dilated root due to hypertension most common cause
2. Dissection
-Marfan Syndrome
3. Bicuspid/congenitally abnormal aortic valve
4. Fixed aortic valve leaflets with mixed stenosis/regurg
5. rheumatic disease
6. calcific degenerated disease
7. Endocarditis


What are the key characteristics of AR caused by bicuspid aortic valve?

Most common congenital abnormality
Can be associated with both stenosis and regurg
Calcification progresses more rapidly
Aortic valve and aorta come from same tissue so they can both be dysfunctional (ie aorta is expanded)
Aortic enlargement


What are the characteristics of AR caused by rheumatic disease?

Fusion of commissures leads to simultaneous development of stenosis and regurg
Severe rheumatic disease leads to fixed orifice throughout cardiac cycle and stenotic symptoms will predominate


What is the pathophysiology of AR?

Pathologic Volume load because of retrograde flow from aorta into LV during diastole
Must overcome higher afterload
Leads to eccentric hypertrophy and higher LVEDP


What does volume of regurg depend on?

Pressure gradient from aorta to LV
Regurg orifice area
Duration of diastole


What are the hemodynamic consequences of AR?

1. Lower diastolic pressure (because blood in elastic arteries are going back to LV instead of towards systemic vasculature)
2. Higher systolic pressure because LV is contracting harder
3. Thus, higher pulse pressure (more difference between SBP and DBP
4. Higher LVEDP (due to regurg volume)
Leads to more wall stress


What is acute severe AR?

When there is a sudden addition of large regurg volume in naïve ventricle


What happens hemodynamically during ACUTE severe AR?

1. abrupt severe increase in EDV, operates on steep portion of FS curve
2. LVEDP and LA pressure rises dramatically (because mitral valve is open now and pressure in LV and LA equilibrate
3. Compensatory = increase HR and contractility by SNS
-compensation often inadequate
4. cardiogenic shock and CHF can develop


What is chronic AR?

When there is a progression in symptoms of AR


What happens hemodynamically during CHRONIC AR?

1. Eccentric hypertrophy (cow hearts!)
2. Widened pulse pressure (because increased systolic pressure but low diastole due to regurg volume)
3. Preserved exercise tolerance (because patient is better able to handle AR


Why is exercise beneficial for CHRONIC AR patients?

1. fall in SVR
2. increase HR (diastolic time decreases so less AR regurg)
3. Increased contractility
Thus you get less diastolic BP drop
Also you get greater CO


How does ischemia develop in AR patients?

1. Increased oxygen demand due to increased wall stress (in both acute and chronic)
2. Decreased supply due to low diastolic pressure (blood not getting to coronaries through aortic leaflets
-increased HR decreases diastolic filling time for CBF
-impaired subendocardial perfusion due to high endocardial pressures

What is the difference in risk of CAD in AR, AS and HTN?
Patients with AR are at greater risk of ischemia because of lack of supply


What is the difference of between acute and chronic compensated regurg?

Same differences between acute and chronic MR
Acute = less CO; chronic = almost normal CO
Acute = greatly increased LVEDP because can only mildly increase LV size
Chronic = mildly incrased LVEDP because of eccentric hypertrophy (being able to increase LV size to a greater extent)
Bigger LVEF for both acute and chronic due to bigger preload


What is the difference in risk of CAD in AR, AS and HTN?

Patients with AR are at greater risk of ischemia because of lack of supply
-lack of supply is unique because diastolic pressure in AR is much LOWER due to regurgitation going through aortic valve
-ischemia leads to angina
AS and HTN are much more likely to get ischemia due to increase in DEMAND rather than lacking supply
-because AS and HTN sees an increase in both SBP and DBP, unlike AR


What are the indications for surgery for AR?

An LVEF of 55% is abnormal!
Symptomatic patients
End-systolic LV diameter > 55mm