11/9 Valvular Disease - Ghosh Flashcards Preview

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Flashcards in 11/9 Valvular Disease - Ghosh Deck (22):

classification of cardiac murmurs

  1. systolic murmurs
    • holosystolic (pansystolic) murmurs: S1→S2
    • midsystolic (systolic ejection) murmurs: peaks between S1, S2
    • early systolic murmurs
    • mid to late systolic murmurs
  2. diastolic murmurs
    • early diastolic murmurs
    • middiastolic murmurs
    • presystolic murmurs
  3. continuous murmurs


systolic murmurs



generated when there's flow between champbers that have widely diff pressures throughout systole

pressure gradient (and resulting regurg) begins early in contraction and lasts until relaxation is complete


ex. mitral regurg, tricuspid regurg, ventricular septal defect


systolic murmurs


midsystolic/systolic ejection


generated when blood is ejected across aortic or pulmonic outflow tracts

starts after S1, when ventricular pressure rises enough to open the valve

  • ejection increasing → murmur is louder
  • ejection decreasing → murmur is diminished



ex. aortic stenosis, pulmonic stenosis, elevated CO, innocent murmurs, supra/subvalvular stenosis


systolic murmurs


early systolic murmurs

begins with S1, ends in midsystole

  • often due to tricuspid regurg occuring in absence of pulmo HTN
  • also occurs in pt with acute mitral regurg


systolic murmurs


mid to late systolic murmurs

high pitched murmur at LV apex

start after S1, ends in before or at S2

  • often due to tethering and malcoaptation of mitral leaflets (MVP)


diastolic murmurs


early diastolic murmurs

usually high pitched, decrescendo

begin with S2 (when ventricular pressure drops below aorta, pulmo a pressure)


ex. aortic insufficiency, pulmonary insufficiency


diastolic murmurs


mid diastolic murmurs

occur early (during ventricular filling)

due to relative disprop between valve orifice size and diastolic blood flow volume


usually originate from mitral and tricuspid valves

ex. mitral stenosis, tricuspid stenosis


diastolic murmurs


late diastolic (/presystolic) murmurs

begin during period of ventricular filling that follows atrial contraction

occur only in sinus rhythm


usually due to mitral and tricuspid stenosis

can also be due to left or right atrial myxoma


continuous murmurs

begin in systole, peak near S2, continue into all or part of diastole

many causes:

  • venous hum
  • mammary souffle
  • PDA
  • AV fistulas

uncommon in pt with valvular HD


mitral stenosis

most common cause: rheumatic fever (chills, fever, fatigue, migratory arthritis)

  • Jones criteria:
  1. migratory arthritis (large joints)
  2. dartisis/valvulitis
  3. Sydenham chorea
  4. erythema marginatum
  5. subcutaneous nodules

other causes: congenital, LA myxoma, calcific, endocarditis



  • acute and recurrent infl → leaflet thickening and calcification
  • commissural fusion
  • chordal fusion
  • end result? funnel shaped mitral apparatus in which the orific of mitral opening is decr in size
    • ​narrow valve → decreased emptying of LA to LV...
    • incr LA pressure
    • decr filling (and CO) of LV
    • high LA pressure is transmitted to pulmonary circ → pulmo HTN over time

common findings:

  1. LA enlargement
  2. atrial fibrillation
  3. thrombus formation → stroke
  4. pulmo HTN

A image thumb

mitral stenosis



physical exam




  • dyspnea
  • sx brought on by factors taht decrease diastolic filling time (exercise, emotional stress, infection, etc)
  • as obstruction across MV incrases, decreasing effort tolerance occurs


  • CO becomes subnormal at rest, fails to incr during exercise
  • dyspnea at rest
  • fatigure
  • pulmo congestion


physical exam

  • loud S1 (MV closure) early
  • soft S1 late in disease
  • opening snap following S2 (interval inversely related to severity)
  • low pitched middiastolic rumble (decrescendo)
  • presystolic accentuation murmur


  • LA enlargement
  • pulmo vascular congestion
  • RV enlargement


  • diuretics: congestion and edema
  • medication to slow HR, incr diastolic filling time
    • Ca channel blockers
    • beta blockers
    • digoxin
  • antiarrhythmics to prevent afib
  • anticoag if pt has thrombus or afib


mitral regurgitation


  • mitral valve prolapse
  • rheumatic heart disease
  • CAD
  • mitral annular calcification
  • systolic anterior motion
  • infective endocarditis
  • collagen vascular disease
  • ruptured chrodae tendinae or papillary muscle


portion of LV stroke volume is ejected back into LA →

  • incr LA volume and pressure
  • decr CO
  • incr volume load in LV (normal venous return + regurgitant fraction that keeps coming back)

overall: LV volume inc → myofiber stretch, which ultimately leads to decr SV (past optimal stretch on Starling curve)



severity is determined by:

  1. size of mitral orifice during regurg
  2. systolic pressure gradient between LV and LA
  3. systemic vascular resistance
  4. LA compliance
  5. duration of regurg

A image thumb

acute severe MR


chronic MR

acute severe MR

  • hemodynamic changes not tolerated, resulting in acute decompensation
  • increase in ventricular preload → decreased stroke volume and pulmo congestion
  • presentation
    • pulmonary edema
  • physical exam
    • murmur has decrescendo quality due to rapid equilibration between LV and LA pressure
  • treatment
    • diuretics to relieve pulmo edema
    • vasodilators to reduce SVR, augment CO

chronic MR

  • compensated phase can last many years
    • incr preload, decr afterload of LV (due to regurg)
    • LV and LA dilate
    • total stroke volume increases
    • EF maintained
  • physical exam
    • apical holosystolic murmur radiating to axilla
    • murmur intensifies with maneuvers that increase SVR (fist clenching)
    • S3 due to LV volume overload
    • apical impulse displaced to axilla because of LV enlargement
  • treatment
    • diuretics
    • vasodilators are not so useful (dont allow delay of surgery)


mitral valve surgery

three types:

1. MV repair

  • best option; preserves native valve
  • avoids risk of chronic anticoag and prosthetic valve failure

2. MV replacement w/ preservation of part or all of mitral apparatus

3. MV replacement with removal of mitral apparatus


mitral valve prolapse

systolic billowing of one or both mitral leaflets into LA with or without MR

can be familial (auto dom) or not 


symptoms: usually asymptomatic. can have chest pain/palpitation

physical exam

  • mid systolic click (tensing of chordae tendonae mm)
  • late systolic murmur at apex
  • murmur and click occur later with incr venous return, sooner with decr venous return


aortic stenosis

  • in adults, most commonly due to calcification of normal or congenitally deformed valve
    • calcification progresses from base of cusp to leaflets →→ reduction in leaflet motion and effective valve area
  • rheumatic AS: due to fusion of commissures with scarring and eventual calcification of cusps
  • congenital malformation is more common in YAs



  • valve narrows → incr LV pressure required → LV concentric hypertrophy/decr compliance
    • LA also hypertrophies so as to fill the noncompliant LV!


  • angina: demand increased due to incr muscle mass, wall stress; supply reduced due to high diastolic filling pressure
  • CHF: ventricle cant increase CO
  • syncope

physical exam

  • coarse, systolic ejection murmur. late peaking = more severe
  • weakened and delayed carotid pulse: "pulsus parvus et tardus"
  • S4 sound (stiff LV)
  • reduced intensity or absent aortic component of S2 (diminished A2)


  • surgical replacement of valve



transcatheter aortic valve replacement


  • minimally invasive
  • valve inside a stent deployed in area of old valve
  • moderate-high risk patients


aortic regurgitation

50% due to aortic root dilation (annuloaortic ectasia_

  • idiopathic
  • aging
  • syphilitic aortitis
  • osteogenesis imperfecta
  • aortic dissection
  • systemic HTN

15% bicuspid aortic valves

15% retraction of cusps as part of postinfl processes of endocarditis, rheumatic fever, collagen vascular disorders



  • blood regurgs from aorta into LV in diastole
  • LV must pump normal pulmo renous return PLUS regurg volume
  • increased myofiber stretch due to incr volume → initial boost to contractility and CO, eventual increase to point of inefficiency


  • dyspnea on exertion
  • fatigue
  • decreased exercise tolerance
  • sensation of forceful heartbeat

physical exam

  • bounding pulse; hyperdynamic LV pulse
  • blowing murmur in early diastole at left sternal border
  • Austin Flint murmur: low freq mid diastolic rumble (due to flow across mitral valve)


  • slowly progressive disease, so you can just monitor mostly
  • afterload reduction: Ca channel blockers, ACE inhibitors
  • surgery if...sx, or LV dysfx (high mortality rate once you have sx)


acute AR


chronic AR

acute AR

  • LV is normal size and noncompliant
  • regurg volume → LV diastolic pressure increase! → transmitted to LA and pulmocirc
    • dyspnea and pulmo edema

chronic AR

  • LV dilates and hypertrophies over time
  • compliance increases → LV can accomodate larger regurg volumes
  • aortic and systemic diastolic pressures drop → widened pulse pressure, decr coronary artery perfusion
  • over long time: systolic dysfx, decreased CO, HF


tricuspid valve stenosis/regurg

tricuspid stenosis

  • most commonly rheumatic in origin


  • murmur: opening snap, diastolic rumble, incr on inspiration
  • large a wave on neck veins
  • similar sx to mitral stenosis

tx: valvuloplasty or valve replacement


tricuspid regurg

  • usually functional origin (elevation of RV pressure, RB cavity enlargement,  tricuspid annular dilatation)
  • structural usually due to rheumatic valvulitis or carcinoid syndrome

physical exam

  • prominent v waves
  • holosystolic murmur that increases with inspiration
  • pulsatile liver


pulmonic valve stenosis/regurg

pulmonic stenosis

  • rare, usually congenital
  • valvuloplasty for pt with moderate to severe stenosis

pulmonic regurgitation

  • usually due to severe pulmo HTN
  • high pitched decrescendo murmur along left sternal border