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Flashcards in Regurgitations Deck (50):

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

-false; can coexist


4 differences (general concepts) between stenosis and regurgitation

-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


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

-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



-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


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

-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


5 components of mitral anatomy and function

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


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

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


Functional classification of Mitral Regurgitation (Capentier Classification)

-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)


Degenerative MR: capentier type II

-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)


Functional mitral regurgitation

-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


Endocarditis capentier and potential issues

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


Rheumatic disease capentier and isses

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


What is unique about MVR endocarditis?

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


2 meanings for ischemia MR

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


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

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


Absolute volume of MR depends on what 3 things?

-size of regurgitant orifice surface

-pressure gradient from LV to LA (drives flow)

-LV systolic ejection time and time orifice is regurgitant


Theoretical possibility of lowering SVR in MR may allow....

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


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

-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


Compensatory mechanisms in acute MR

-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)


Acute MR symptoms

-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


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

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


Compensatory changes in chronic MR

-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


Chronic compensated MR

-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


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


3 things the LA V wave depends on

-volume of regurgitant blood

-relative position of LA on PV curve

-acute vs chronic pressure volume curves (LA compliance)


Does LA compliance increase or decrease in chronic MR?



Chronic decompensated MR

-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


Are MR severity and survival correlated?

-yes, worse MR = worse prognosis


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

-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


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

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

-if EF was below normal, you do worse


Impact of LV performance on outcomes as measured by LVESD

-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!!


How to manage pts with sxs of severe MR

-if sxs: surgery

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


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



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

-the same

-since regurgitation occurs in diastole not systole

-decreased effective flow since V of blood is regurgitated back during systole


5 causes of AR

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)


Bicuspid aortic valve (BAV)

-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


Rheumatic dz and AR

-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


AR pathophysiology

-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



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

-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!


Volume of AR regurgitation depends on

-P gradient from aorta to LV

-regurgitant orifice area

-duration of diastole


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

-reduces diastole and therefore time for regurgitation


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

-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


Acute severe AR

-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


Acute severe hemodynamics in AR

-severely increases LVEDP and severely decreasing aortic diastolic P


Chronic AR

-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


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

-NO! they need shortened diastole!


Ischemia in aortic regurgitation

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


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


Indications for surgery in AR

-sxs patient

-LVESD >55 mm *smaller in women

-fall in EF 55% is abnormal!!!

-LVEDD >70 associated with sudden death--ischemia arrythmias


MR murmur

1. MVP: only during late systole and preceded by a click

2. many other types is holosystolic: occurs from S1 all through S2