Regurgitations

Question 1

T/F: A valve can be regurgitant or stenotic, but not both.

Answer 1

-false; can coexist

Question 2

4 differences (general concepts) between stenosis and regurgitation

Answer 2

-unlike stenosis, regurgitation is: 1. better able to increase forward stroke volume and CO 2. can be acute or chronic 3. 2 chambers affected by volume load 4. regurgitant volume and regurgitant fraction better express severity of lesion than simply regurgitant orifice area

Question 3

Consider the mitral valve as part of the ______ and the aortic valve as part of the _______ when thinking of regurgitation.

Answer 3

-LV: normal LV size and shape is integral to normal MV function -Aorta: enlargement of the aorta can lead to AR in addition to disease of leaflets

Question 4

LVH

Answer 4

-CHRONIC adaptive response to volume and/or pressure overload as an attempt to reduce or normalize LV wall stress and optimize myocardial O2 consumption -increase in myocyte MASS not NUMBER

Question 5

Eccentric hypertrophy occurs due to _______ overload. Explain this using LaPlace

Answer 5

-volume overload= increase in wall stress associated with increase in diastolic volume and pressure -add myofibrils in series -Wall stress is increased by an increase in chamber radius, so increase in wall thickness helps reduce this -end result: increase LV wall thickness, increase LV mass, no change in RWT

Question 6

5 components of mitral anatomy and function

Answer 6

-annulus (saddle shaped) -leaflets: overlap=redundancy -chords: primary, secondary, tertiary -papillary muscles -ventricular function and geometry

Question 7

T/F: Chordae and papillary muscles are responsible for closing the valve.

Answer 7

-false; P closes it, pap muscles keep it closed!

Question 8

Functional classification of Mitral Regurgitation (Capentier Classification)

Answer 8

-type 1: normal leaflet motion; endocarditis hole is ex -type 2: increased leaflet motion (prolapse in systole) -type 3: decreased leaflet motion (3a is rheumatic dz, 3b is ventricular issue)

Question 9

Degenerative MR: capentier type II

Answer 9

-myomatous degeneration aka degenerative disease; GENETIC and progressive -prolapse, flail, floppy, billowing -2 commonly occurring but very different diseases: fibroelastic deficiency (ruptures chord in 1 segment) and Barlow’s disease (abnormal leaflets, elongates chordae)

Question 10

Functional mitral regurgitation

Answer 10

-leaflets normal -LV modeling moves pap muscles towards apex and laterally–gets worse with LVH -also component of mitral annular dilation -decreased closing forces from decreased LVEF -class 3b

Question 11

Endocarditis capentier and potential issues

Answer 11

-Type 1 MR -vegetations interfere with coaptation -leaflet perforation due to infection

Question 12

Rheumatic disease capentier and isses

Answer 12

-type III -thickened leaflet tips prevents coaptation -shortened or ruptured chords due to rheumatic process -often coexists with MS as well

Question 13

What is unique about MVR endocarditis?

Answer 13

-it can happen acutely! as opposed to myxomatous degeneration or rheumatic disease

Question 14

2 meanings for ischemia MR

Answer 14

1. can be used to refer to transient MR which occurs during ischemic episodes– posteromedial papillary muscle more vulnerable to ischemia (single blood supply) 2. more typically used as description of mechanism of MR with prior MI which results in FOCAL LV remodeling and distortion -mostly inferior infarctions cause restriction of posterior leaflet motion

Question 15

Regurgitant V, forward stroke V, total stroke V, regurgitant fraction, LVEF definitions in MR

Answer 15

1. regurg volime (ml/beat):RV 2. FSV: ml/beat 3. TSV: FSV+RV 4. regurg fraction: RV/TSV 5. EF: TSV/EDV

Question 16

Absolute volume of MR depends on what 3 things?

Answer 16

• size of regurgitant orifice surface
• pressure gradient from LV to LA (drives flow)
• LV systolic ejection time and time orifice is regurgitant

Question 17

Theoretical possibility of lowering SVR in MR may allow….

Answer 17

-greater direct proportion of blood flow into systemic circulation (mostly when acute)

Question 18

Explain why pulmonary edema occurs in AR. Describe what happens to effective CO and how this is dealt with.

Answer 18

• RV results in acute LA P transmitted back to lungs=pulmonary edema
• LV stroke volume is now divided between FSV and RV which decreases effective CO. TSV increases due to more complete emptying (lower afterload due to dec SVR in acute MR); increased preload due to RV= increased SV and EF
• AMR: higher preload, lower afterload, normal contractile function, higher EF than normal

Question 19

Compensatory mechanisms in acute MR

Answer 19

• LV dilation (increased preload) due to increased LV volume helps to preserve FSV
• reduced afterload (acute) allows emptying down to smaller ESV
• activate reflexes (adrenergic activation) to increase HR and CO; increase contractility of LV with rise LVEF, vasoconstriction to maintain BP/organ perfusion (despite this, still an acute decrease in afterload)

Question 20

Acute MR symptoms

Answer 20

• with a too large of an addition of RV: rapid and sudden increase in LAP= acute pulmonary edema
• dont have time to develop eccentric hypertrophy!!
• despite normal contractile function, pt suffers acute CHF
• therapy= supportive (o2), diuresis, vasodilator therapy, and immediate surgery to repair/replace valve

Question 21

What is uniquely seen on acute MR hemodynamic LA LV pressure waveforms?

Answer 21

-quick, large V waves due to regurgitation to LA during systole

Question 22

Compensatory changes in chronic MR

Answer 22

• slow increment in MR or management of acute MR into chronic phase
• initial LV dilation increases EDV and TSV
• LV eccentric hypertrophy occurs to allow increased LVEDV at lower LVEDP: increased compliance, serves to normalize wall stress (laplace)
• increased LA compliance

Question 23

Chronic compensated MR

Answer 23

• eccentric hypertrophy reduced diastolic wall stress, normalizes afterload, increases FSV to almost normal
• regurg fraction remains the same with a greater regurgitant volume
• decrease preload, increased afterload, normal contractile function, decreased EF, same RF, increase FSV vs AMR

Question 24

Acute vs Chronic MR in CO (FSV), LVEDP, LV size, LVEF

Answer 24

Question 25

3 things the LA V wave depends on

Answer 25

- volume of regurgitant blood - relative position of LA on PV curve - acute vs chronic pressure volume curves (LA compliance)

Question 26

Does LA compliance increase or decrease in chronic MR?

Answer 26

-increase!

Question 27

Chronic decompensated MR

Answer 27

- occurs as a result of loss of contractile function (catecholamine excess, loss of contractile elements, abnormal Ca handling, fibrosis) - reduced LVEF to a normal level, reduced FSV, increase in RF

Question 28

Are MR severity and survival correlated?

Answer 28

-yes, worse MR = worse prognosis

Question 29

How do you know when your chronic MR patient is decompensating? and its time to fix MR

Answer 29

- when LVEF returns to normal!!!! (reduced contractile function) - sxs of CHF: acute MR that cannot be stabilized or chronic MR decompensating) - significant levels of LV remodeling (eccentric hypertrophy) - prophylactiv surgery IF high probability of repair

Question 30

Effect of sxs on survival post MVR; effect of LVEF on survival post MVR

Answer 30

- regardless of EF, if you have sxs, you do worse! - if EF was below normal, you do worse

Question 31

Impact of LV performance on outcomes as measured by LVESD

Answer 31

- once LVESD is greater than 45 mm (indicating advanced remodeling and beginning of contractile dysfunction) the chance of a poor outcome dramatically increases!! - risk of CHF is lower if surgery is done earlier!!

Question 32

How to manage pts with sxs of severe MR

Answer 32

- if sxs: surgery - if no sxs and EF\>6-. ESD \<40-45 and normal pulm AP then echo and follow up

Question 33

T/F: MR has functional and anatomic classification while AR only has anatomic classifications

Answer 33

-true

Question 34

Unlike, MR FSV and TSV are the _____ in AR. Why?

Answer 34

- the same - since regurgitation occurs in diastole not systole - decreased effective flow since V of blood is regurgitated back during systole

Question 35

5 causes of AR

Answer 35

1. aortoannular ectasia: dilated root due to HTN most common!!; aging= central malcoaptation 2. dissection: marfan syndrome 3. bicuspid or congenitally abnormal aortic valve 4. fixed aortic valve leaflets with mixed stenosis/regurgitation: rheumatic disease, calcific degenerative disease 5. endocarditis (acute)

Question 36

Bicuspid aortic valve (BAV)

Answer 36

- most common congenital abnormality - most BAV are at least mildly regurgitant - not only calcify prematurely, but also AR progresses more rapidly than anatomically normal valves with AR - also associated with aortic enlargement

Question 37

Rheumatic dz and AR

Answer 37

- fusion of commissures leads to simultaneous development of stenosis and regurgitation - severe rheumatic disease results in a fixed orifice throughout cardiac cycle--AS will predominate at this point

Question 38

AR pathophysiology

Answer 38

-V load to LV fills retrograde from aorta in addition to normal diastolic inflow from LA; must be ejected to a higher P chamber therefore, higher wall stress than MR= greater degree of eccentric hypertrophy

Question 39

Would you expect greater eccentric hypertrophy in AR or MR? Why?

Answer 39

- AR: it fills more during diastole (RV and LA flow) and this blood ALL needs to be moved upward and out the aorta to achieve CO - also get some concentric hypertrophy too!

Question 40

Volume of AR regurgitation depends on

Answer 40

- P gradient from aorta to LV - regurgitant orifice area - duration of diastole

Question 41

Why might raising the heart rate of someone with AR be helpful?

Answer 41

-reduces diastole and therefore time for regurgitation

Question 42

Difference between mild and severe AR when analyzing LVDP and aortic systolic P

Answer 42

- steep decline in aortic diastolic pressure and steep incline in LVDP due to regurg - increase pulse pressure due to systolic HTN due to increased FSV and then rapid runoff back into LV during diastole decreasing diastolic blood pressure rapidly

Question 43

Acute severe AR

Answer 43

- sudden addition of large regurgitant volume to naive ventricle - causes abrupt, severe increase in EDV, operates on steep portion of FS curve (more preload) - LVEDP and LAPs rise dramatically=pulmonary edema - similar sympathetic compensation as in MR: tachycardia and hypercontractile LV function, but these are often inadequate - cardiogenic shock and CHF develops

Question 44

Acute severe hemodynamics in AR

Answer 44

-severely increases LVEDP and severely decreasing aortic diastolic P

Question 45

Chronic AR

Answer 45

- LV adaptation= eccentric hypertrophy - massive LV enlargement, large FSV delivered into aorta=systolic HTN with low diastolic P (rapid runoff) = widened pulse pressure - preserved effort tolerance!!! decrease SVR, inc contractility, and increase HR to dec diastolic time and regurg time

Question 46

Does it make sense to give someone with chronic AR a beta blocker?

Answer 46

-NO! they need shortened diastole!

Question 47

Ischemia in aortic regurgitation

Answer 47

increases O2 demand of myocardium (acutely due to inc HR and wall stress; chronically lower mag increase due to chronic compensation) - impaired O2 supply: due to reduced coronary perfusion gradient (low diastolic pressure gradient), inc HR with decreased filling time (when CBF occurs), impaired subendocardial perfusion due to high endocardial pressures - net result: ischemia in absence of atherosclerotic CAD

Question 48

Acute vs Chronic Compensated AR: CO, LVEDP, LV size, LVEF

Answer 48

Question 49

Indications for surgery in AR

Answer 49

- sxs patient - LVESD \>55 mm \*smaller in women - fall in EF 55% is abnormal!!! - LVEDD \>70 associated with sudden death--ischemia arrythmias

Question 50

MR murmur

Answer 50

1. MVP: only during late systole and preceded by a click 2. many other types is holosystolic: occurs from S1 all through S2