Valvular Heart Disease Flashcards
doppler effect
as the police siren travels towards you, the frequency of the wave (pitch) appears to be higher than if it was stationary; as the siren travels away, the pitch appears to be lower.
change in pitch coming off the red cells
aliasing effect
when the velocity gets higher than the maximum velocity of blood flow away
seen as yellow
aliasing is an effect that causes different signals to become indistinguishable (or aliases of one another) when sampled
two most common valvular dzs
aortic stenosis and mitral regurg are the two most common valve disease
what should you be weary of in a pt with a bicuspid aorta
strong correlation between bicuspid valve and marfans syndrome which results in an aneurysm and rupture
if you hear that there is a bicupid valve in the aorta it is essential to do an echo to look for aneurysm
congenital types of aortic stenosis
” Bicuspid AS: MC of these (usually aortic valve is TRIcuspid)
“ Membranous subvalvar
“ Fused leaflets w/ doming
acquired degenerative types of aortic stenosis
Calcific AS: MC type you will see (RF: smoking, HTN, hyperlipidemia, DM - same RF as CAD)
Thickening & calcification develops @ 40-60yo
Hypertrophic subaortic: need an echocardiogram to distinguish
Rheumatic heart dz - caused by AS but affects mitral valve more than aortic
what % of the population has aortic stenosis
1% of population w/ M>W;
what is th epathophysiology of AS
aortic leaflets do not oppen and pressure in the LV increases in order to compensate with increased
results in muscle hyeprtrophy
early phase of aortic stenosis is seen as
diastolic dysfunction - heart stiffens/can’t relax, smaller chamber, reducing amnt of blood it can receive
late phased of AS
” Late Phase: systolic de-compensation - muscles can’t keep up w/ pressure
reduced EF
What type of pulse pressures do we see at the end stage of AS
b/c fall of ejection fraction; drop in amount of blood w/ each beat (difference in systol/diast pressures narrows) –> HYPOTENSION
classic triad of AS
Angina - d/t supply/demand mismatch when O2 demand of hypertrophied LV (& CAD) exceeds supply –>5yr survival AVR
CHF (diastolic & systolic) - bad if present –> 2yrs
Stokes-Adams attacks - exertional (pre-syncope + syncope); from reduced stroke volume & inadequate cerebral perfusion —>3yr AVR
why do we see angina in AS
NO obstruction in the coronary artery
the muscle needs a certain amt of oxygen and the coronary flow can not keep up
the result of this is exertion angina
most common presentation of AS
diastolic HF
LA pressure rises in order to fill LVE and backup leads to the lungs
Stokes-Adams attacks
(pre-syncope + syncope); from reduced stroke volume & inadequate cerebral perfusion –>3yr AVR
classically seen on the end of exertion when the peripheral vasculature is still dialated
person slows done and sympathetic tone falls
dip in blood pressure followed by a loss of consciousness
murmur we hear with AS
SYSTOLIC (harsh) ejection murmur
thrill (palpable murmur), over aortic area radiating to carotids; high enough energy sound can be felt
when do you hear the murmur with AS and what does it sound like
” Mid-systolic crescendo decrescendo mumur
which peaks later in systole w/ worsening severity
if you can feel the artery filling through your finger tips which could happen with AS what is this indicative of
Delayed arterial upstroke - reduction in stroke volume (hypertrophy = small chamber)
felt as a quick tap
pulse pressure with AS
” Narrow pulse pressure - brisk, weakened, delayed = pulsus parvis
what heart sounds do we hear with AS (describe S2)
” Soft S2 - leaflets snapping, S4 present if LVH
prognosis of AS
Long interval of compensation as stenosis develops; once sxs occur (angina, CHF, syncope) –> Pt is DOOMED!
When HF starts to occur í RAPID deterioration w/ poor prognosis at the point of decompensating, especially if patient is symptomatic
very
1 diagnostic test used for diagnosing AS
red cells have to really speed up and you can measure this velocity with an echocardiogram
o ↑ leaflet thickness (don’t open well) & echodensity w/ ↓ excursion on structural views
o ↑ systolic velocity of blood flow w/ reduced valve area on Doppler measured
o Aortic valve calcif
Echo aortic valve area and continuity equation
Echo aortic valve area: flow rate is constant regardless of where it’s measured.
things don’t pile up
place of cardiac catheterization
Cardiac catheterization primarily to evaluate coronaries b/c CAD frequently
can be used to measure the gradient across the valve
first measuring the pressure in the LV
210 in the LV
130 in the aorta
that is the gradient
you can calculate the valve area and the restriction
Tx of aortic stenosis in a pt with sxs of diastolic dysfunction
CHF from diastolic dysfunction: Diuretics
Tx of aortic stenosis in pt
For classical triad of angina, CHF (systolic dysfxn), Stokes-Adam attack, mechanical intervention: valve replacement or balloon valvuloplasty
increase the valve a little bit but you see restenosis in a good portion of this pt
conventional surgical valve replacement : advantages and disadvantages of mechanical
mechanical: indefinite durability advantage but requires chronic anticoagulation
conventional surgical valve replacement : advantages and disadvantages of Heterograft (tissue)
good for AS at young age; anticoag NOT necessary in absence of Afib; durability finite but w/ the modern ways of treating the tissue before the valve is put in durability is longer
often times pt die before the end of the valve
what is the most common surgical tx of AS
heterograft from bovines
human valve replacement
what is it called and what are the advantages and disadvantages
Homograft - at one time more durable; rarely used
TAVR
Transcatheter Aortic Valve Replace
tissue valve is sewn into a metallic stent
balloon is inserted in the femoral artery, threaded up to the heart and placed in the aortic valve
where would we find the PMI in a pt with AS
” Medially displaced PMI (should be at 5th intercostal space, mid-clavicularly)
where is the murmur of AS best heard
” Systolic “ejection” crescendo-decrescendo @ RUSB
other than cardio findings what would we see in the PE of a pt with AS
” Rales & other CHF signs
pulsus parvis et tardus
slow-rising pulse and anacrotic pulse, is a sign where, upon palpation, the pulse is weak/small (parvus), and late (tardus) relative to its expected characteristics. It is seen in aortic valve stenosis.
chronic I causes of Aortic Regurgitation
HTN (& other root dilation)
Atherosclerosis
Aortic Stenosis:
so stiff that they don’t come together well
Prosthesis (leaflet vs. perivalvular)
in a mechanical leaflet if not on anticoagulants you can have soft tissue growth into the valve region or leaflet develops a tear
Endocarditis: causes both leaflet and perivalvular
CT Dz - Marfan’s (dilation of aortic root)
Inflamm dz - Lupus, RA
Chronic II causes of aortic regurg
Congenital dz (Bicuspid, vent septal defect)
Sinus of valsalva Aneurysm
most common rupture is the one adjacent to the right side of the heart
Aortitis
Rheumatic: doesn’t affect the aortic valves but can stiffen leaflets
3˚ Syphilis
potential etiologies of acute aortic regurgitation
rapid brkdown: aortic dissection (MC reason - infection chews through valve & leaflet ruptures),
endocarditis trauma rheumatic fever valve prosthesis rupture of sinus of Valsalva aneurysm
pathophysiology of aortic rugurg
Opposite problem of AS. No restriction of opening í instead, leaflets do NOT come together in diastole í so blood regurgitates from aorta back to LV d/t dilation of aorta í MC d/t HTN
Blood regurg into LV in diastole 2˚ widening/aneurysmal ∆ of aortic annulus
LV dilates and increase stroke volume to maintain CO
acute decompensation of aortic regurg causes
diastolic pressure rises so high
pulmonary congestion
chronic decompensation of aortic regurg causes
LV systolic failure
what type of pulse pressure would we see with aortic regurg
diastolic pressure falls and systolic pressure increases resulting in a wide pulse pressue
Common presentation with aortic regurg
” CHF - dyspnea on exertion, orthopnea, fatigue
“ Palpitation - awareness of heartbeat
í increased SV + arrhythmia (↑HR)
water hammer pulse refers to
” LRG Stroke Volume (bounding pulse):
Rapid upstroke
what type of heart sounds would you hear with aortic regurg
Systolic flow murmur louder than diastolic
you really need to play close attention for the diastolic murmur
Diastolic decrescendo (blowing) murmur after S2, radiating to LSB & apex - high pitch!
” Severe AR is heard as what heart sound
AUSTIN FLINT Murmur/ mitral valve rumble
why is the diagnosis of aortic regurg so difficult to make?
decomposition is severe
severe SOB w/in 30min
CXR is white
severe pulm edema
but you see a NORMAL HEART SIZE
most people with congestive heart failure you would see enlargement of at least one chamber of the heart
(pulmonary problem= right side enlargement)
Inaudible murmur (low output, wide open valve, noisy respiration)
diastolic pressure may not be low
you should be able to hear the first heart sound in someone BUT the mitral leaflets are already touching each other and don’t hit each other
S1 is MISSING because the mitral valves are closed due to high pressure
why do you not hear a murmur with Acute severe AR
sudden severe rupture of a leaflet and you need turbulence for a murmur but if it is wide open there is no turbulent flow
why is the diastolic pressure normal with acute severe AR
left ventricle is so small that it can’t accept much flow
back flow causes pressure to rise
periphery is clamped down with low CO
diastolic pressure doesn’t drop very much
diagnostic of AR
” ECHO-Doppler - 1st Tx of Choice
REGURGITATION WITH DOPPLER
” Regurgitation by Doppler
“ Abnormal structures - vegetation, dialted root
“ LV size and Function
indications of cardiac cath for diagnosis of AR?
: not needed for dx - but can evaluate if pt has other valvular lesions or check for CAD
Transesophageal can be used to see what with AR
abscess vegetation, aortic dissection
prognosis of pt with chronic AR
” Long period of compensation w/o sxs
“ Gradual LV ENLARGEMENT w/ norm systolic fxn
Sxs and/or LV dysfxn assoc w/ RAPID deterioration
LV systolic dysfxn w/o sxs = RARE!
if the person has sxsx you usually see reduced EF
Tx of aortic regurgitation
Tx of Choice: Afterload reduction (vasodilators) to encourage forward flw
Abx prophylaxis pre-procedure
CHF treatment: diuretics
when is surgical tx of AR indicated for acute?
when is indicated for chronic?
Surgical Valve Replacement
o Acute, severe AR is emergency
oChronic AR: sxs, sys dysfxn, progressive LV dilation (>55cm)
AVR w/ endocarditis is often successful
Mitral Regurgitation common chronic causes
" MCC coronary dz (papillary muscle malfunction) " LV dilatation, any cause " Endocarditis " Myxomatous degeneration/prolapse " Rheumatic " Other CT dz " Congenital - lupus, Marfans
common causes of acute mitral regurg
Acute:
“ Chordal rupture: myxomatous, endocard, trauma
“ Papillary rupture: infarction, trauma
“ Acute papillary ischemia (usually circumflex - REVERSIBLE!)
“ Valve perforation: endocarditis
Dilation = regurgitation
what myocardial changes will we see in MR
” Blood regurg into LA in SYSTOLE –> LVH comps by enlarging
Chronic MR: LV systolic failure, LV becomes weak
- Regurg unloads LV in systole reducing LVES volume
what do we see as the result of acute MR
Acute MR: congestion, can cause pulmonary edema
what type of HF do we see with MR
” 1st L then 2nd R CHF
murmur seen with MR
Mid-systolic click and late systolic murmur (usually from S1-S2)
–>
Typically holosystolic murmur
- Papillary dysfxn
- Prolapse after click
PMI in MR
LV enlargement if chronic (PMI)
displaced
sxs of chronic MR decompensation
” Typical CHF signs - dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue
EKF of MR
non-specific findings, tell you nothing abt etiology
“ LVH
“ LAA - left atrial abnorm
“ A-Fib
CXR finding with MR
” LA enlargement - splaying of bronchi
“ LV enlargement
“ CHF
MR echocardiogram how to diagnose (2 ways)
Semi-quantitative MR estimation
(depth/width of jet, vol of LA filled)
Quantitative (orifice area, analogous to aortic
can see moicardial infarction hx
Lv function an ot
indications of cardiac cath for MR
Cardiac catheterization
“ Etiology &/or other dz (CAD)
“ Large V wave in pulmonary wedge pressure, LV size & contractility confirmed
Hemodynamic effects: output & RH pressures
TX for MR
Medical:
Analogous to AR; vasodilator (afterload reduction - ACE-I) so less backflow
- Tx underlying dz
- Endocarditis prophylaxis
- Pther tx for CHF & arrhythmias PRN
when is surgery indicated for MR
Timing was hardest issue, easy now b/c adv tech
- Perform when symptomatic despite Rx
- Before LV deteriorates: post-op afterload is higher
if the EF if abnormal before mitral valve replacement it would be worse than before
surgical tx for MR
Valve repair is INCREASINGLY COMMON
- Shorten or reattach chords
- Tuck leaflets
- Reduce annular diameter w/ ring
Catheter based
Repeat w/ clips and/or annular rings (mitraclip approved) Replace valve (valves that are delivered on a cather are developing)
causes of Tricuspid regurgitation
anything that causes failure to the right ventricle
dilation of the tricuspid ring can be caused by pulmonary HTN
RV failure or dilatation - not structural abnormality:
“ Pulm HTN–> RV dilation + tricuspid regurg d/t:
o Primary = RARE
o 2ndary: COPD, intracardiac shunts, LV failure, mitral dz, Eisenmenger synd (End stage vol overload: atrial/ventricular septal defect)
Endocarditis: IVDU -tricuspid is the valve of choice for this population
Rheumatic: very rare as primary lesion
what fo we see in the neck tricuspid regurgitation
” Large V waves in jugular veins (JVD)
venus pulsations
murmur heard with tricuspid regurg
no murmur because of the low pressure
sxs of tricuspid regurg
” peripheral edema
“ ascities
“ ↓exercise tolerance
tx of tricuspid regurg
Medical TX of CHOICE: diuretics (usually all you need)
–>Tx underlying condition
surgical tx for tricuspid regurg
Surgical:
MUST Tx primary lesion (ex: mitral) - sometimes that is enough
Tricuspid annuloplasty w/ ring
Valve Replacement = UNCOMMON!
