Valve Dz 2 Flashcards
mc cause of mitral stenosis
rheumatic fever
followed by denegeration of valve apparatus
2/3 of people are female
pathophys of mitral stenosis (6)
- decreased emptying of LA causes increased LA pressure
- LA pressure causes pulmonary venous congestion
- vasoconstriction and hypertrophy of pulmonary arteries
- remodeling and pulmonary HTN
- increased RV pressure leads to RV hypertrophy
- RV failure
** LV remains preserved until MS becomes so severe diastolic filling declines
symptoms of MS
YOUNG (30-40)
- dyspnea/orthopnea
- AFib and other dysrhythmia, atrial thombus/emboli
- chest pain, palpitations, fatigue, weakness and peripheral edema, blood tinged sputum (pulmonary edema)
signs of mitral stenosis (murmur)
Opening snap
low, rumbling diastolic murmur @ LV apex (5-6th ICS)
evaluation of MS
echo (okay for right side, might find it)
cardiac (L heart cath, femoral artery and thru LV to LA)
elements of MS treatment (6)
- diuretics
- dietary sodium reduction and nitrates
- rate control (esp. in AF w/CCB or BB)
- consider anticoagulation
- Statins (anti inflammatory, slows progression)
- avoid after load reduction
surgical MS treatment (3)
given to patients with severe symptoms and moderate to severe stenosis
percutaneous valvuloplasty
open mitral valve commissurotomy
open mitral valve replacement
critical MS value
< 1.5
percutaneous balloon valuloplasty
abrupt inflation of balloon across mitral valve
results in separation of fused cusps
PREFERRED if test is available
open mitral valve comissurotomy or replacement
2 dif surgeries
commissurotomy - debridement and separation of fused cusps
replacement - mechanical or tissue valve entirely replaced
blood ejects into aorta as well as left atrium during systole
mitral regurgitation
functional etiologies of mitral regurg
valve apparatus degeneration or deformation
i.e. CAD, dilated CM, papillary muscle dysfunction
organic etiologies of mitral regurge (3)
- myxedematous degeneration of mitral valve, associated with MVP
- Infectious endocarditis valve leaflet/chordae destruction
- Rheumatic disease
pathophysiology of MR (6)
- Atria dilate
- LV dilation – pre load + regurgitated volume (some hypertrophy)
- Pulmonary congestion
- Pulmonary HTN (due to vasoconstriction and hypertrophy of pulmonary arteries)Pulmonary veins engorged
- RV hypertrophy
- RV fails—losing systolic function, can’t squeeze
symptoms of MR
Asymptomatic gradually develop increasing pulmonary HTN
symptoms start at exercise
HF secondary to reduced CO and pulmonary congestion (DOE, fatigue, AF)
MR signs
holosystolic murmur (high pitched, blowing)
could be: wide split, S3, hyper dynamic LV, brisk upstroke
MR diagnostics
ECHO
can do cardiac cath
MR monitoring
followed annually
surgery done before LV remodeling can occur
pharm tx of MR
decreased after load (equalized pressure b/t systemic and LA)
via ACEI, nitrates, anti-HTN and diuretics
surgical MR tx
pulmonary HTN and AF indicated earlier surgery
procedure of choice is REPAIR rather than replacement
true replacement indicated if valve is too damaged, papillary muscle dysfunction, or IE
why do we repair instead of replace valve in MR
- less need for IE prophylaxis
- permanent fix
- decreased need for anti-coagulation
Acute MR due to
ischemia or infarction of chordae, papillary muscles, or IE
acutely ill due to less time to compensate and make hemodynamic changes(RV) and decreased preload (LV)
Symptoms of acute AR
Acute LV Failure
Acute RV Failure
Rapid pulmonary congestion/Pulmonary edema
HoTN/shock
acute AR tx
after load reduction
nitroprusside and urgent valve replacement
MVP etiologies
pevelance greater in women
- genetic (marfan’s, connective tissue dz)
- myxedematous deteriorated leaflets = large floppy leaflet
symptoms of MVP
asymptomatic
minor amounts have palpitations, anxiety, dizziness, CP
may be associated with MR but not always
murmur MVP
mid systolic click
late systolic murmur
diagnostics of MVP
2D echo (determines if there, and if MR as well)
serial echo 1-2 yrs to document lack of progression
MVP treatment
stimulant avoidance (cocaine, caffeine, tobacco, chocolate)
propranolol if palpitations
tricuspid stenosis etiologies
rheumatic heart disease
typically concomitant mitral or aortic valve disease
female predominance
Tricuspide stenosis symptoms
signs of RV failure
peripheral edema
ascites
hepatic congestion (pain in RUQ)
tricuspid stenosis signs
opening snap at LSB
palpable pre-systolic pulsation over liver
tricuspid stenosis treatment
medical and surgical treatment to treat other valvular disease
may do a valve replacement
pathophys Tricuspid regurge
RV dilation secondary to pulmonary HTN and RV failure
caused by: COPD, Pulmonary emboli, HF
symptoms of TR
initially tolerated
pulmonary HTN –> symptomatic
systemic back up = peripheral edema, hepatic congestion
TR signs
pan systolic, high pitched murmur
best heart at sternal border, augmented by increased venous return
TR treatment
treating underlying cause of pulmonary HTN or RV failure
may need valve replacement
pulmonic stenosis
congenital
doesn’t req. tx until adulthood
can treat with balloon valvuloplasty
pulmonic regurgitation
occurs when valve annals dilates secondary to pulmonary HTN
tx directed at cause of pulmonary HTN or RV failure
bioprosthetic valves pros and cons
only need anticoagulation for a few months BUT degeneration sooner (10 yrs)
mechanical valves pros and cons
req. anticoagulation for life
lasts longer than bioprosthetic (20yrs)
when is greatest risk of clot following valve replacement?
first three months
ONLY give warfarin
aortic valve mechanical replacement no risk factors
anticoagulation with VKA (warfarin) to INR 2.5 + ASA
aortic mechanical valve replacement and risk factors
VKA(warfarin) to INR 3 + ASA
AF, prior thrombus, LV dysfunction, hyper coagulable conditions
mitral valve replacement
VKA (warfarin) target INR of 3 + ASA
bioprosthetic valve replacement guidelines
3-6 months, 2.5 INR + ASA
TAVR anticoagulation
low bleeding risk = anticoagulate 3+ months for INR 2.5 + ASA
MAYBE clopidogril for 6 mo.
