11/9 Valvular Disease - Ghosh Flashcards
classification of cardiac murmurs
-
systolic murmurs
- holosystolic (pansystolic) murmurs: S1→S2
- midsystolic (systolic ejection) murmurs: peaks between S1, S2
- early systolic murmurs
- mid to late systolic murmurs
-
diastolic murmurs
- early diastolic murmurs
- middiastolic murmurs
- presystolic murmurs
- continuous murmurs
*
systolic murmurs
holosystolic/pansystolic
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
crescendo-decrescendo
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:
- migratory arthritis (large joints)
- dartisis/valvulitis
- Sydenham chorea
- erythema marginatum
- subcutaneous nodules
other causes: congenital, LA myxoma, calcific, endocarditis
pathology
- 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:
- LA enlargement
- atrial fibrillation
- thrombus formation → stroke
- pulmo HTN
mitral stenosis
presentation
physical exam
imaging
treatment
early/mid
- 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
late/severe
- 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
imaging
- LA enlargement
- pulmo vascular congestion
- RV enlargement
treatment
- 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
causes:
- mitral valve prolapse
- rheumatic heart disease
- CAD
- mitral annular calcification
- systolic anterior motion
- infective endocarditis
- collagen vascular disease
- ruptured chrodae tendinae or papillary muscle
pathophys
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:
- size of mitral orifice during regurg
- systolic pressure gradient between LV and LA
- systemic vascular resistance
- LA compliance
- duration of regurg
acute severe MR
vs
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:
- MV repair
- best option; preserves native valve
- avoids risk of chronic anticoag and prosthetic valve failure
- MV replacement w/ preservation of part or all of mitral apparatus
- 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
pathophysiology
- valve narrows → incr LV pressure required → LV concentric hypertrophy/decr compliance
- LA also hypertrophies so as to fill the noncompliant LV!
symptoms
- 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)
treatment
- surgical replacement of valve
TAVR
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
pathophysiology
- 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
symptoms
- 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)
treatment
- 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
vs
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
symptoms/exam
- 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
