Cardio valvular disease Flashcards
right side
tricuspid
pulmonary
left side
mitral
aortic
3 leaflets
tricuspid
aortic
pulmonary
2 leaflets
mitral
what is prolapse
different version of regurgitation
-valve will open, but don’t close in the proper plane
right sided failure
- increased RV pressure
- increased RA pressure
- increased CVP
- increased JVD
- hepatomegaly
- ascites
- edema (peripheral)
left sided failure
- increased LV pressure
- increased LA pressure
- increased PA pressure
- shortness of breathe (congestion)
- CHF
- decreased EF
- decreased systemic perfusion
go to test for valvular disease
Echo
- TTE
- TEE
what is a CXR good for looking at?
chamber size
aortic dilation
pulmonary edema
cardiac cath is good for looking at?
mainly a pre-op tool for coronary artery evaluation
swan ganz catheter is goof for looking at
different pressures of the chambers in the heart
treatment
observation
medical
precutaneous
surgery
causes for tricuspid stenosis
*Rheumatic
congenital
*carcinoid
rheumatic
seen in combination with mitral rheumatic disease
- usually results in regurgitation with varaible stenosis
- rare cases are pure stenosis
- chordal thickening and mild fusion
- calcification absent
hallmark of rheumatic disease
commissural fusion
carcinoid
secondary to serotonin production from liver mets
- carcinoid syndrome
- cicatricial deformity in TV and PV
- fibrous plague forms on leaflets
- commissure fusion, leaflets thicken and shorten, chordae become thick and fused
- combined stenosis and regurgitation.
symptoms of tricuspid stenosis
- excessive fatigue
- dyspnea
- forward failure: decreased preload LV, decreased SV, salt and water retention via renin-aldosterone-angiotensin system
- backward failure: hepatic congestion and peripheral edema
physical exam for tricuspid stenosis
- mid diastolic murmur over left lower sternal border
- murmur increases on INSPIRATION
- liver enlarged but not pulsatile
- peripheral edema-> if stay in sinus rhythm, unlikely, if in atrial fib-> more likely
imaging on tricuspid stenosis
- CXR: increased RA, lack of pulmonary artery enlargement and clear lung flields
- ECG: prominent p waves unless atrial fib present
- Echo: RA enlargement, leaflet thickening, measure gradients across RA to RV, look for associated lesions
Cath- identify gradient (rarely needed, unless surgery)
tricuspid regurgitation cases
- Rheumatic
- Endocarditis (like in Lupus, Libmann’s Sack disease)
- Trauma
- Carcinoid
- Myxoma: atrial myxoma, grow near valve structure and brush up against leaflet
- Diffuse collagen disorders
- Fibroelastosis
- Functional: MV disease
- Congenital: Ebstein’s Anomaly
tricuspid regurgitation
Pansystolic murmur, maximal over lower sternal border -murmur increases with INSPIRATION -enlarged liver shows systolic pulsations, tender JVD hepato-jugular reflux present edema ascites anasarca
symptoms for tricuspid regurgitation
- dyspnea, orthopnea
- prone to having atrial fibrillation
what do you see one echo with regurgitations
- echo-quantitates degree of insufficiency/annular size, see associated lesions and vegetations
- how much flow is going backward
treatment options for tricuspid disease
- observation: mild to moderate disease
- medical- most time treating left sided valve lesions for functional disease, diuretics, afterload reduciton
- valvuloplasty repiar, tricuspid valve ring
- commissurotomy
- tricuspid valve replacement
when to do tricuspid valve replacement
infective endocarditis
carcinoid
tricuspid stenosis
when to do valvuloplasty repair, or tricuspid valve ring
- For symptomatic severe disease of functional MR
- Moderate-severe MR when preforming other concominant valve or coronary procedures
what valve is least likely to be repaired?
aortic
-usually replace
when is commissurotomy done
congenital lesions
rheumatic disease
pulmonary valve
mainly congenital lesions: Tetralogy Fallot, pulmonary atresia
-mainly are children
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
Mitral stenosis
- decreased flow of blood to LV
- decreased cardiac output-> b/c decreased SV (fatigue, muscle wasting, weakness)
- LA hypertrophy-> b/c back flow and resistance of mitral valve (atrial fib, mural thrombi, systemic emboli)
- pulmonary hypertension
- increased pulmonary vascular resistance
- pulmonary edema (if mean LA pressure exceeds oncotic pressure of plasma)
mitral valve anatomy
- leaflets: anterior and posterior
- annulus: attachment point of leaflets
- chordae tendineae
- papillary muscle: attached to ventricle
portion of annulus that enlarges in Mitral stenosis
posterior part
what is important when operating for mitral stenosis
keep chordae tendineae and papillary muscle as attached as possible
mitral stenosis means
stiffening of the mitral leaflets
right sided lesions mainly
deal with back up into the body
left sided lesions mainly
back up into the lungs
clots on the right side can go to
lungs
clots on the left side
can cause stroke (go to brain)
or go to other parts of body-> like arm and cause ischemia of arm
symptoms of MS
- pulmonary congestion
- cough
- hemoptysis (coughing up blood)
- orthopnea
- PND
- pulmondary edema
- dyspnea on exertion
- cardiac cachexia: thin, frail, patients
classic symptom of MS
dyspnea on exertion
-patients learn to avoid exertion
imaging on mitral stenosis
- heart size usually normal or small
- auscultatory Triad
- CXR: increased LA, normal cardiac size, straight left heart border
- MV can be calcified (seen on CXR, echo, cath)
- Kerley’s lines
auscultatory Triad in MS
apical diastolic rumble
increased 1st heart sound
opening snap
why do you see a straight cardiac border on CXR in MS?
increased LA and PA obliterates the normal concavity between Aortic and LV
exclusive cause of MS
- rheumatic disease*
- some small cases of congenital lesions, extra-valvular causes like myxoma, severe senile calcific disease
- 2/3 are usually female (same as tricuspid)
what does progressive disease result in for MS
fibrosis of leaflets, commissures, subvalvular apparatus and calcifies
what can calcium cause if it grows in conduction system
heart block
what is the worst part to get calcifications
annulus (mitral valve)
what are Kerley’s lines (seen with MS)?
seen with severe MS
-engorged pulmonary lymphatics
imaging seen with MS
Echo-> LA enlargement, leaflet thickness, vegetations, valve area, EF, associated lesions, thrombus, calcifications, see leaflet “doming” secondary to restrictive opening of stenotic valve
Cath-> mainly check coronaries prior to surgery
treatment of MS
- Observation/medical: asymptomatic patients looking for LA thrombus, mitral valve area (MVA), valve gradient, PA pressures
- anticoagulant for thrombus, emboli, atrial fib, - Precutaneous balloon commissurotomy
- mitral valve commissurotomy or MV replacement
- rheumatic MS more difficult to treat and not routinely done
- pulmonary hypertension usually reverses post op
- left atrial appendage is obliterated if thrombus present
when do you preform precutaneous balloon commissurotomy
symptomatic patients with MVA less than/equal to 1.5, minimal calcium and favorable anatomy in absence LA thrombus and moderately-severe MR
-fractures fibrotic lesions and calcium
when is a mitral valve commissurotomy or MV replacement performed?
severe MS with severe symptoms
-MVA less/equal 1.5
Mitral regurgitation causes
- Rheumatic
- Dystrophic/degenerative
- ischemic-> secondary to coronary disease, MI
- infective endocarditis bacterial fungi
- cardiomyopathies-> from dilated /distorted LV
- connective tissue disease-> Marfan, Ehlers Danlos, Oteogenis imperfecta
- Prolapse
- Myxomatous/Barlows disease
- trauma
- papillary muscle rupture/dysfunction/displacement
- LV aneurysm
- atrial mxyoma
- annulus, leaflets, chordae, papillary muscle, ventricular wall/chamber size effects
- loud pansystolic murmur trans
murmur for MR
Loud pansystolic murmur transmitted to axilla
MR characteristics
- increased LA pressure/PCWP/pulmonary vein pressure
- can decrease CO
papillary muscle most effect my ischemia?
posterior medial papillary muscle
- comes from RCA or Posterior circumflex (depends on dominance)
- only has a single blood supply
symptoms of MR
-fatigue, dyspnea, decreased exercise tolerance, palpitations/atrial fib.
imaging for MR
- increased LA size
- if gradual can accommodate the extra load without pressure rise till late and then will become symptomatic
CXR-> enlarged LA and eventually LV, various degrees of pulmonary congestion
acute MR
ruptured papillary muscle post MI->normal or small LA cannot accommodate with resultant acute pulmonary edema and possible in extremis status
- they flood lungs and don’t get enough blood to rest of body
- blood goes in two different directions
anterior papillary muscle supplied by
LAD and lateral circumflex
-dual blood supply
in MR, mitral annulus dilates
posteriorly
LV function in MR
LV function (chronic forms of MR) usually remains adequate for a long period of time even with severe MR, but eventually decompensates with LV dilatations and decreased EF
what do patients with MR have increased risk for?
bacterial endocarditis
treatment of MR
observation
medical treamtent
surgery
which patients should be observed?
mild disease, serial echo exams to look for evidence of LV decompensation, LA thrombus, degree of regurgitation
which patients should get medical treatment
diuresis, afterload reduction, rhythm control/possible anticoagulation, possible beta-blockers
which patients should receive surgery as a treatment?
MV repair/MV annuloplasty ring is procedure of choice for symptomatic patients with severe MR
- asymptomatic patients with severe MR, LVESD greater than/equal to 40mm and EF less than 60
- MV repair/annuloplasty ring for asymptomatic moderate MR and undergoing a concomminant cardiac valve/coronary procedure
- MV replacement indicated if unable to perform adequate repair
- MV replacement then posterior leaflet chords are preserved to preserve LV geometry and funciton
- Acute MR usually deteriorates quickly and needs urgent/emergent surgery
Aortic stenosis causes
- Degenerative/calcific, senile calcific
- greater in males
- may affect conduction system if Ca extends to conduction system - congenital-> Bicuspid most common, (age 30-60)
- Rheumatic (usually associated with MV)
most common cause of aortic stenosis
- Degenerative/calcific, senile calcific
pathology of AS
- increased afterload with secondary impaired LV emptying in systole
- concentric LV hypertrophy
- as LV gets less compliant, then atrial systole becomes more important for LV filling and maintaining CO
- atrial fib can worsen symptoms
- LVH may eventually lead to LV failure chronically
- hypertrophy of LV with increased muscle mass and increased O2 demands, along with decreased subendocardial flow in diastole creates mismatch of supply and demand whereby angina can occur in face of normal coronary arteries
- resultant microinfarcts occur with resultant myocardial scarring/muscle loss and decreased ventricular function
classic symptoms of AS
angina
syncope
CHF (exertional dyspnea)
sudden death (ventricular arrhythmias) (20% present with symptoms)
most common fatal valve lesion
Aortic stenosis
what do most untreated patients with AS die from?
CHF (congestive heart failure)
natural progression of AS
- asymptomatic for years prior to symptoms
- once clinical symptoms occur the clinical course is malignant
- average survivial post onset of symptoms
CHF: 2 years
Syncope: 3 years
Angina: 5 years
murmur for AS
systolic ejection murmur in right 2nd ICS that radiates to carotids
AS diagnosis
- murmur
- carotid pulse has diminished upstroke
- ECG: LVH, IVC delays like right/left BBB, AV nodal block or atrial fib
- CXR: calcifications of aortic valve/aorta, LVH, post-stenotic aorta enlargement
- echo: measure AVA (.8 or less severe), look for associated lesions, EF, wall motion, chamber size, leaflet motion, aortic size
- cath: assess coronaries for patients going to surgery, measure gradients, aorta assessment, look for AI
- CTA chest with 3D reconstruction: to assess aortic dilation/aneurysm/root
AS treatment: observation
mild to moderate disease
AS treatment: medical treatment
control hypertension (careful in severe end stage disease)
control arrhythmias
cautious use of diuretics
AS treatment: surgery for symptomatic patients
Symptomatic patients with severe AS
- .8 AVA
- mean gradient 40mmHG or greater
- aortic velocity 4.0m/sec or greater
AS treatment: surgery for asymptomatic patients
asymptomatic with severe AS
- EF 50% or less
- undergoing cardiac surgery for another reason
types of surgery for AS
AVR (aortic valve replacement)
-if patients at acceptable surgical risk
TAVR (transcatheter aortic valve replacement)
-performed when surgical risk too high and patient has a life expectancy greater than 1 year.
aortic regurgitation causes
- mixed AS/AR
- degenerative calcific AV disease
- rheumatic
- congenital-> usually bicuspid
- annuloaortic ectasia: abnormal dilatation of annulous and aortic root, or ascending aorta. leaflets can’t touch eachother
- marfans
- myxoid degeneration aortic leaflets
- aortic dissection
- bacterial endocarditis: perforation leaflets, annular destruction, vegetations with obstruction
- rheumatic arthritis
- ankylosing spondylitis
- blunt/penetrating trauma
- (rare, see in congenital patients) VSD: supracristal defect, from prolapse of leaflet/cusp into defect
- atrial myxomas
most common valvular lesion in blunt chest trauma
Aortic regurgitation
AR pathology
- AR results in volume overload of LV
- increased LVEDP/LV diastolic volume/wall stress
- leads to progressive LV dilatations
- eccentric hypertrophy of LV-> increased chamber size and increased wall thickness
- massive dilatations of LV-Cor Bovinum
- progressive LV dilatation and failure-> fall in contractility and EF until forward CO cannot be maintained and patient expires from progressive CHF
- subendocardial ischemia from decreased diastolic coronary blood flow, increased diastolic ventricular pressure, LVH and increased workload
- may get angina
difference between with AS and AR
- in AR, get eccentric hypertrophy and increased LV chamber size
- AS-> concentric hypertrophy
- both have increased wall thickness, but in AS don’t see increased chamber size (till failure long term)
symptoms of AR
dyspnea
orthopnea
PND
angina
syncope
can be asymptomatic: herald LV dysfunction with frank CHF coming several years later
widen pulse pressure (increased systolic and decreased diastolic pressure
murmur/special things in AR
- diastolic blowing murmur
- austin flint murmur
- water hammer pulse
- De musset’s sign
- quincke’s pulse
- Duroziez’s sign
- Traube’s sign
austin flint murmur is from
regurgitation jet hits anterior leaflet of mitral valve and tends to close it and causes a murmur at apex
water hammer pulse
bounding and forceful peripheral pulse
- Corrigans: carotid artery
- Waston’s-> limb pulse
De musset’s sign
bobbing of head with cardiac cycle
quincke’s pulse
pulsating nail beds
Duroziez’s sign
systolic/diastolic murmur over femoral arteries
Traube’s sign
pistol shot sounds over large arteries
imaging for AR
-lateral displacement of LV apical pulse
-CXR: LV enlargement, enlarged ascending aorta, pulmonary edema, increased LA
-ECG: LVH
-Echo: regurgitant jet, EF, chamber sizes
cath: view coronaries if going to surgery, evaluate aorta/root
CT: evaluate aorta
AR treatment: observation
mild to moderate, serial echo exams
AR treatment: medical
afterload reduction, diuretics, treat hypertension
AR surgery as treatment
AVR (aortic valvular replacement)
occasionally can repair
may need to replace ascending aorta
who gets an AVR
- patients with severe regurgitation in symptomatic patients
- asymptomatic disease with EF of 50% or less, severe LV dilatation (greater than 50mmHg)
who tends to recover better, AS or AR patients?
AS patients ventricular wall mass, volumes and function recover better overall after surgery compared to AR patients post op
