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Flashcards in 3: Valvular Disease Deck (60)

causes of mitral regurgitation

-rheumatic disease
-dystrophic/degenerative valves
-ischemic (secondary to CAD, MI)
-infective endocarditis - bacterial > fungal
-cardiomyopathies (dilated/distorted LV)
-CT disease
-myxomatous/Barlows disease
-papillary mm. rupture/dysfunction/displacement
-LV aneurysm
-atrial myxoma
-effects on annulus, leaflets, chordae, papillary, wall, chamber size


type of murmur seen in mitral regurgitation

loud pansystolic murmur transmitted to axilla


where do you get increased pressure with mitral regurgitation?

increased LA pressure, PCWP, pulmonary vein pressure


what symptoms will a patient with mitral regurgitation get?

-decreased exercise tolerance
-palpitations/a fib


what happens to the size of the LA in mitral regurgitation? in gradual onset vs acute onset?

increased size - if gradual can accommodate the extra load without pressure rise until late and then becomes symptomatic

acute: (ex: ruptured papillary muscle post MI) then the normal/small LA cannot accommodate with resultant acute pulmonary edema and possible extremis status


what pathologic changes occur in right sided heart failure?

increased RA and RV pressure
increased CVP
increased JVD


what pathologic changes occur in left sided heart failure?

increased LA and LV pressure
increased PA pressure
CHF + pulmonary edema
decreased EF
decreased systemic perfusion


what is important when evaluating a potential valvular disease patient?

-CXR - chamber size, aortic dilatation, pulmonary edema
***ECHO - TTE, then TEE (this is go-to test for valve disease)
-Cardiac cath - mainly for pre-op coronary artery eval
-Swan ganz cath - pressures/waveforms
-CT/gated MRA - myxoma, aorta size evaluation


general possibilities for valvular disease

-medical: diuresis, afterload reduction
-percutaneous: balloon valvuloplasty, TAVR (valve w/i valve)
-surgery: repair (mitral mostly, some tricuspid/aortic), replacement (bioprosthetic, mechanical, autograft/homograft)


causes of tricuspid stenosis

-rheumatic disease
-carcinoid disease
-congenital (Ebstein's anomaly, tricuspid atresia)


describe tricuspid stenosis in rheumatic heart disease

-usually associated with acute rheumatic disease
-not usually an isolated lesion (mitral too)
-regurgitation w/ variable stenosis
**commissural fusion
-choral thickening, mild fusion
-NO calcification


describe tricuspid stenosis in carcinoid disease

-secondary to serotonin production from liver mets
-sx: flushing, diarrhea, palpitations
-cicatricial deformity in TV, PV (ice-like frozen sheet)
-fibrous plaques on leaflets and onto endocardium
-commissure fusion
-leaflets thicken and shorten
-chordae thick and fused
-combined stenosis and regurgitation


symptoms of tricuspid stenosis

-excessive fatigue
-dyspnea (can be from associated L sided lesions)
-forward failure (decreased preload LV, SV; salt and water retention from RAA)
-backward failure (hepatic congestion, peripheral edema)


physical findings with tricuspid stenosis

-mid-diastolic murmur over lower LSB
-murmur increases with inspiration
-liver large but NOT pulsatile
-peripheral edema (if a fib present, rate with NSR)


test findings with tricuspid stenosis: CXR

CXR: increased RA, normal pulmonary artery size, clear lung fields (this triad***)

EKG: prominent p waves unless a fib present

echo: RA enlargement, leaflet thickening, measure gradient, look for associated lesions

cath: identify gradient/CAD eval pre-op


causes of tricuspid regurgitation

-rheumatic disease
-endocarditis (infective - IV drug abuse; non - LSE)
-trauma (penetrating, blunt, pacemakers)
-diffuse collagen disorders
-congenital: Ebstein's anomaly
-due to MV disease mainly (MR) - functional disease


physical findings in tricuspid regurgitation

-pansystolic murmur maximal over LSB
-increases with inspiration
-enlarged liver + systolic pulsations, tender
-hepato-jugular reflex present
-anasarca (extreme generalized edema)


which murmurs increase with inspiration? which increase with expiration?

R sided problems - increase with inspiration
"it's right to inspire"

L sided problems - increase with expiration


symptoms of tricuspid regurgitation

-depend on etiology
-may have dyspnea, or orthopnea
-majority get a fib
-echo: quantitates degree of insufficiency/annular size, see associated lesions and vegetations


tricuspid valve treatment: observation and medical

observation: mild/moderate asymptomatic disease

-depends on etiology
-generally treat left sided valve lesion for functional disease
-possible afterload reduction


tricuspid valve treatment: surgery options (3)

ring valvuloplasty/repair:
-for symptomatic severe disease of functional MR
-for moderate-severe MR when performing other concominant valve or coronary procedures

-for some rheumatic disease, congenital
-knife to leaflet at commissure, cut apart fusions

-for infective endocarditis
-for carcinoid
-for tricuspid stenosis


causes of pulmonary valve disease

-mainly congenital: tetralogy of Fallot, pulmonary atresia


what is the Ross procedure?

remove pulmonary valve to use as an autograft to replace aortic valve
-valve can grow with child as child grows
-can be done in adults occasionally


pathologic findings in mitral stenosis

-decreased flow of blood to LV
-decreased CO (fatigue, muscle wasting, weakness)
-LA hypertrophy (a fib, mural thrombi, systemic emboli)
-pulmonary HTN
-increased pulm vasculature resistance
-pulmonary edema + alveolar hemorrhage
-LA hypertrophy and dilation can compress esophagus - dysphagia for solid foods


symptoms of mitral stenosis

-pulmonary congestion
-pulmonary edema
-dyspnea on exertion (classic symptom)***
-cardiac cachexia


physical findings in mitral stenosis

-heart size (LV) normal or small
-ausculatory triad: apical diastolic rumble, increased S1, opening snap*****


test findings in mitral stenosis: CXR, other, echo, cath

CXR: increased LA, normal cardiac size, straight left heart border (increased LA and PA obliterates normal concavity between Ao and LV)

often MV is calcified - see on CXR, echo, cath, CT

Kerley's lines with severe MS (engorged pulmonary lymphatics)

echo: LA enlargement, leaflet thickness, vegetations, valve area, EF, associated lesions, thrombus, calcification, leaflet 'doming' secondary to restrictive opening of stenotic valve

cath: mainly for CAD eval pre-op


causes of mitral stenosis

**rheumatic disease is nearly the exclusive cause of mitral stenosis**

exceptions: rare congenital lesions, extra-valvular causes like myxoma and severe senile calcific disease (this is increasing though)


mitral stenosis treatment: observation and medical

observation: centered around following echo exams on asymptomatic patients looking for:
-LA thrombus
-mitral valve area (MVA)
-valve gradient
-PA pressures

-anticoagulation for thrombus, emboli, a fib
-medical tx of a fib and HR control


mitral stenosis treatment: surgery options

percutaneous balloon commissurotomy:
-symptomatic patients w/ MVA less than/= to 1.5, minimal calcium, and favorable anatomy in absence of LA thrombus and mod-severe MR

commissurotomy or replacement:
-severe MS (MVA less than 1.5) w/ severe sx or if undergoing other concominant cardiac surgery

-rheumatic MS more difficult, but not routinely done secondary to significant fibrosis
-obliterate left atrial appendage if thrombus present


what happens to the mitral annulus in mitral regurgitation?

dilates posteriorly (posterior 2/3 dilates up)


what happens to LV function in mitral regurgitation?

in chronic forms of MR, usually remains adequate for a long period of time even with severe MR, but eventually decompensates with LV dilatation and decreased EF


what are patients with MR more susceptible to?

bacterial endocarditis



enlarged LA and eventually LV
various degrees of pulmonary congestion


MR treatment: observation and medical

-mild disease
-serial echos to look for LV decompensation, LA thrombus, degree of regurgitation

-afterload reduction
-rhythm control/possible anticoagulation
-possible B blockers


MR treatment: surgery options

MV repair/annuloplasty ring:
-for symptomatic patients with severe MR
-for asymptomatic patients with severe MR
-for LVESD greater than/equal to 40 mm and EF below 60
-for asymptomatic moderate MR with concomitant cardiac valve/coronary artery procedure

-if unable to perform adequate repair
-posterior leaflet chords preserved to preserve LV geometry and function****


treatment for acute MR

usually deteriorates quickly and needs urgent/emergent surgery


causes of aortic stenosis

-degenerative/calcific - senile calcific most common*, more in males, may affect conduction system
-congenital: bicuspid most common*, occurs at earlier age (30-60y/o)
-rheumatic - usually has associated MV disease


AS pathology

-increased afterload + secondary impaired LV emptying
-concentric LV hypertrophy- increased mm mass + increased O2 demands + decreased subendocardial flow in diastole = mismatch (angina)
-LVH may eventually lead to LV failure chronically
-resultant microinfarcts occur with resultant myocardial scarring/muscle loss and decreased ventricular function


what happens to the maintenance of CO as LV gets more compliant in AS?

atrial systole becomes more important for LV filling and maintaining CO - therefore, if a fib develops, can suddenly worsen clinical symptoms


AS symptoms

classic: angina, syncope, CHF (exertional dyspnea)
-sudden death (ventricular arrhythmias)


what is the most common 'fatal' valve lesion?

AS - most untreated AS patients die of CHF


AS natural history

-asymptomatic for years prior to symptoms
-once clinical symptoms occur, the clinical course is malignant
-average survival post onset of symptoms:
CHF 2 years
syncope 3 years
angina 5 years


diagnosis of AS: murmur, pulses, EKG, CXR, echo, cath, CTA

-systolic ejection murmur in 2nd ICS that radiates to carotids
-carotid pulse with diminished upstroke
-EKG: LVH, may see IVC delays like R/LBBB, AV nodal block, or a fib
-CXR: calcification or aortic valve/aorta, LVH, post-stenotic aorta enlargement
-echo: measure AVA (0.8 or less is severe), look for associated lesions, EF, wall motion, chamber size, leaflet motion, aorta size
-cath: assess CAD/Ao, measure gradients, look for AI
-CTA: chest w/ 3D reconstruction to assess aortic dilation/aneurysm/root


AS Treatment: observation and medical

-mild to moderate disease

-control HTN (be careful in severe end stage disease)
-control arrhythmias
-cautious use of diuretics


AS treatment: surgery for who?

-symptomatic patients with severe AS: 0.8 AVA, mean gradient 40 mmHg or greater, aortic velocity 4.0m/s or greater
-asymptomatic patients with severe AS: + EF 50% or less or undergoing cardiac surgery for another reason


AS treatment: what surgery?

AVR (replacement) if patient is an acceptable surgical risk

TAVR (transcatheter AV replacement) is performed when surgical risks are too high and patient has a life expectancy greater than 1year


AR causes

-mixed AS/AR
-degenerative calcific AV disease
-rheumatic disease
-congenital- usually bicuspid
-annuloaortic ectasia (abnormal dilatation of annulus, root)
-myxoid degeneration aortic leaflets
-aortic dissection
-bacterial endocarditis
-rheumatoid arthritis
-ankylosing spondylitis
-blunt/penetrating trauma
-VSD - supracristal defects, from prolapse of leaflet/cusp
-atrial myxomas


most common valvular lesion in blunt chest trauma



AR pathology

-volume overload of LV
-increased LVEDP/LV diastolic volume/ wall stress
-leads to progressive LV dilatation
-eccentric hypertrophy of LV
-may get massive dilatation of LV - cor bovinum
-subendocardial ischemia from decreased diastolic coronary blood flow, increased diastolic ventricular pressure, LVH, and increased workload
-may get angina in face of normal coronaries


describe the progressive LV dilatation and failure in AR

fall in contractility and EF until forward CO cannot be maintained and patient expires from progressive CHF


AR symptoms

-dyspnea, orthopnea, PND, angina (less than 50%), syncope (rare)
-may be asymptomatic for years with moderate to severe AR, but when symptoms begin they herald LV dysfunction with frank CHF coming usually several years later


what is an Austin Flint murmur?

when regurgitant jet hits anterior leaflet of mitral valve, it tends to close and causes murmur at apex


what is water hammer pulse?

bounding and forceful peripheral pulse:
-Corrigans = carotid artery
-Watsons = limb pulse


physical findings in AR (many, many)

-widened pulse pressure (increased SBP + decreased DBP)
-diastolic blowing murmur
-Austin Flint murmur
-water hammer pulse
-DeMusset's sign (bobbing of head with cardiac cycle)
-Quincke's pulse (pulsating nail beds)
-Duroziez's sign (systolic/diastolic murmur over femoral aa)
-Traube's sign (pistol shot sounds over large arteries)
-lateral displacement of LV apical pulse


AR tests: CXR, EKG, echo, cath, CT

-CXR: LV enlargement, enlarged ascending aorta, pulmonary edema, increased LA
-Echo: regurgitant jet, EF, chamber sizes, also helps define etiology
-Cath: CAD eval pre-op, evaluate aorta/root
-CT: evaluate aorta


AR treatment: observation and medical

-mild to moderate
-serial echo exams

-afterload reduction
-treat HTN


AR treatment: surgery

-usually AVR
-occasionally repair/re-suspend valve/commissures
-may need to replace ascending aorta dependent on etiology of AR and size of aorta


when to use AVR for AR

-severe regurgitation in symptomatic patients
-severe asymptomatic disease with EF 50% or less, or severe LV dilatation (LVESD greater than 50mm)
-moderate to severe disease and undergoing another cardiac or aortic surgery


describe AVR recovery AS vs. AR

AS patients ventricular wall mass, volumes, and function recover better overall post-op than AR