Valvular Heart Dz Flashcards
(149 cards)
1
Q
what is more common VHD or CAD
A
CAD
2
Q
what is the most common cause of CHD in developing countries
A
rheumatic heart dz
3
Q
all pts with mcahnical/prosthetic cardiac vlave replacement or hz of endocarditis need what for invasive procedures (dental/resp)
A
prophylaxis antibiotics
4
Q
VHD results in what two pathologies
A
- stenosis
2. regurgitation
5
Q
what is a stenotic valve
A
not able to open completely with obstruction of blood flow going forward
–usually chronic process involving calcification or scarring of valves
6
Q
what is a regurgitant valve
A
fails to completely close allowing backflow of blood
7
Q
regurgitant valve is usually due to
A
endocarditis and dz of valve cusps
8
Q
how can regurgitatnt valve disrupt supporting structures
A
- aorta, mitral annulus, tendinous cord, paillary muscles, ventricular free wall
- can occur abruptly with chordae injjury
- can occur gradually with leaflet scarring and retraction
9
Q
classification of VHD
what is it?
how is it used?
A
1. Stage A: at risk for VHD Stage B: progressive VHD and asympt Stage C: Asympt with severe VHD Stage C, C1: normal LV function Stage C, C2: abnormal LV function Stage D: symp pts due to VHD 2. used to detemine valvular repair/replacement
10
Q
when would you refer a pt with VHD to cardiology
A
- presence of murmur
- pts who are symptomatic of valvular heart dz
- diagnostic studies indicative of valvular dz
11
Q
aortic stenosis accounts for what % of all VHD cases
A
25%
12
Q
80% of chronic, symptomatic aortic stenosis are what population
A
male
13
Q
increased incidence correlates with
A
increased life expectancy
14
Q
what is the most common indication for surgical valce replacement
A
aortic stenosis
15
Q
2 etiologies of aortic stenosis
A
- congenital: asymptomatic until 50-65yo (younger pts may present with more severe symptoms)
- atherosclerotic (degenerative) valvular dz: lipid accumulation, endothelial dysfunction, inflammatory cell activation, fibroblast deposits, cytokine release, calcium deposits
16
Q
age where atherosclerotic aortic stenosis occurs
A
> 65yo
17
Q
atherosclerotic AS due to?
A
chronic calcification of aortic valve
18
Q
risk factors of atherosclerotic AS
A
HTN, hypercholesterolemia, smoking, hypertrophic obstructive cardiomyopathy
19
Q
risk factors for AS at younger ages with rapid progression
A
Paget’s dz, severe familial hypercholesterolemia, endstage renal dz, rheumatic heart dz, lupus erythematosus
20
Q
symptoms of AS
A
–long latent asymptomatic period efore sympts appear
-common s/s: functional, gradual decline
DOE, angina, syncope
21
Q
development of symptoms in AS
A
- left ventricle has to work harder to push blood into stenotic aortic valve
- left ventricle hypertrophies to to able to handle the extra stres of increased afterload with an initial smaller interior chamber = incr LV pressure
- chronic AS causes LV to dilate to be able to hold increased afterload in LV without increasing LV pressure
22
Q
what is LaPlace’s Law equation
A
Wall tension (stress) = LV pressure x Internal Radius / 2xWall thickness
-wall thickness affects how much stress the wall can resist (this is why it hypertrophies)
23
Q
what are the end effects of AS on:
- ventricular function
- ejection fraction
- overall heart function
A
- decreased ventricular function
- decreased ejection fraction (SV/EDV: % of blood in ventricles that is pumped out of ventricles)
- -increased afterload with decreased contracility - leads to heart failure
24
Q
why is DOE seen with AS?
A
- decreased filling capacity of aorta which leads to increased ventricular filling pressure (can’t get enough blood out)
- therefore increaed end diastolic volume is necessary to maintain normal ejection fraction
- as mitral valve opens in diastole, it is subjected to increaed ventricular diastolic pressure
- increased ventricular diastolic pressure is transmitted to atria and then to pulmonary veins and lungs (leads to pulmonary congestion and increased difficulty breathing
25
what happens to the ejection phase in AS
ejection phase is longer in AS - LV trying to get blood out thru obstructed valve
26
what is exercise induced tachycardia in relation to AS
-decreases diastolic filling time
-ventricle will reach its limit of preload reserve too early (won't fill up as much)
=decreased CO so HR is increased to try and make up for the loss = DOE because you're not perfusing adequately
27
what is angina
- result of myocardial ischemia
- imbalance bw O2 demand and availability
- increased O2 demand but not enough available = angina
28
why is there decreased O2 availability with AS and angina
1. increased LV EDV + delay rate of ventricular relaxation due to hypertrophy results in:
1. decreased coronary perfusion
2. decreased blood flow reserve needed to offset increase in O2 demand during exercise or stress
29
what is syncope
transient loss of consciousness due to cerebral hypoperfusion
30
how does syncope occur with exercise?
- narrowed AV valve restricts increase in CO necessary to offset associated decrease in peripheral resistance (and increased blood supply to muscles ) with exervise results in decreased BP
- exercise in the setting of very high LV pressure stimulates mechanoreceptors that triggers reflexive vasodepressive response and decreased BP
31
where is the murmur of AS located?
systolic or midsystolic usually after S1
32
timing and shape of AS murmur
during systole blood veolcity accelerates across the valve with increased intensity of the murmur then there's deceleration of blood flow across the valve
-"crescendo-decrescendo"
33
intensity of AS murmur
- as stenosis increases?
- with ventricular hypertrophy?
- as stenosis increases the intensity and pitch increases
| - if there's ventricular hypertrophy and decreased EDV the intensity and pitch may be lower than expected
34
where is the murmur of AS heard best?
-aortic area = right 2nd intercostal space at the sternal border with radiation to carotids and sometimes to the apex
35
special maneuvers for AS murmur
1. isometric handgrip - increases systemic vascular resistance and BP (decreases AS murmur)
2. standing and valsalva - decreases ventricular filling, decresaes AS murmur
36
carotid pulse with AS
small and slow rising (parvus and tardus)
- not allowing blood thru valve
- might palpate a shudder or thrill
37
2 changes in heart sounds with AS
1. Paradoxical splitting of A2 (AV) during S2 (A2P2) - S2 is split from delayed AV closing during expiration rather than inspiration
2. 4th heart sound - S4 (happens right before S1), d/t LV hypertrophy from increased wall stress
- Tennessee
38
why is there a 4th heart sound with AS
- creates low pitch during late diastolic filling and atrial contraction in the setting of decresaed ventricular compliance and increased EDP
- atria contracts against increased LV pressure
39
what is an apical pulse with AS
PMI - there is no change in position, but its impulse is prolonged due to increased ejection time
40
what is the primary and preferred diagnositc tool to evaluate AS
Echocardiogram
1. records hemodynamic meaurements
2. assess anatomic integrity
3. assesses aortic dilation
4. assesses co-existing aortic regurgitation
41
when is echocardiogram used
routine surveillance in stable patients every 3 years
| once/year for pts with mod-severe dz
42
changes seen on CXR with AS
```
rounding of left heart = LVH
LA enlargement
pulm venous enlargement
increased aortic shadow
aortic valve calcification
```
43
what 2 things can you see on the ECG with AS
no specific or sensitive for this
| can see: 1. LV hypertrophy 2. LA hyertrophy
44
when is AV replacement indicated
all symptomatic patients with evidence of significant AS
45
what symptoms of AS correlate with poor prognosis without surgery
syncope, angina, heart failure (50% mortality rate in 3 years)
46
prognosis of AV replacement surgery
- dramatic improvement with reliefe of excessive afterload
| - pts with CAD have poorer outcome
47
drawbacks to AV replacement surgery
- need for anticoagulation with mechanical valves
| - wear and tear with bioprosthetic valves
48
when is AV replacement not recommended
asymtomatic patients
49
when is percutaneous balloon valvuloplasty
what is it?
risks?
pts not able to tolerate open heart procedure
less invasive
risk of restenosis
makes narrowed AV larger - balloon inflated to open up the stenosis
50
2 categories of causes of Aortic regurg
1. valvular
| 2. root dz
51
valvular causes of aortic regurg
1. rheumatic fever
2. infective endocarditis
3. HTN
4. syphilis
5. traumatic
6. myxomatous
52
root disease causes of aortic regurg
1. aortic dissection
2. HTN
3. Marfan's syndrome
4. congenital bicuspid aortic deformity
53
what is the compensatory mechanism in AR
- SV increased to maintain ejection fraction
- -for this reason, pts with AR can be asymptomatic
- regurg increases LV workload which will eventually lead to dilation
54
AR affect on myocardial contractility, ejectino fraction, and what is the end result
myocardial contractility - decreases
ejection fraction - decreases
end result - heart failure
55
where is the murmur hear for AR
AR may only reveal a decrescendo (high pitched) aortic diastolic murmur heard best at the right parasternal 2nd 3rd and/or 4th intercostal space that radiates to the neck (can be heard anywhere along the left sternal border)
-heard during diastole
56
further LV dilation leads to what in end stage AR
further LV failure
57
common s/s with LV failure
DOE, fatigue most common
- PND d/t pulm edema
- syncope (decr BP and brain perfusion)
- angina pectoris
- widened pulse pressure (elevated SBP and low DBP)
- corrigan pulse
58
what is corrigan pulse
rapid rise and fall of pulse (should be uniform)
59
clinical presentation of AR
1. CAD - ischemic heart disease/angina type chest pain
2. Pre-syncope and syncope (less common in AS)
3. Musset sign: head will bob with each pulse
4. Duroziez sign: to and fro murmur over a partially compressed peripheral artery (femoral)
5. Quincke pulses: large stroke volume can produce nailbed capillary pulsations
60
diagnostic studies for AR
1. Echo - LV anatomry and AR integrity assessment as pre surgical determinant - preferred and diagnostic
2. ECG - moderate-severe LVH
3. CXR - cardiomegaly with LV prominence/dilated aorta
4. cardiac MRI/CT - assess for aortic aneurysm and aortic root size
61
indication for surgery in AR
abnormal LV function
| appearance of symptoms dramatically increase the risk of mortality
62
surgery involves AV replacement when?
- in all symptomatic pts
- ejection fraction 5-5.5cm
- even for asymptomatic pts with evidence of valvular dz
- surgical mortality 3-5%
63
main cause of mitral valve stenosis
rheumatic fever (30%)
64
other causes of mitral valve stenosis
congenital mitral valve stenosis
system lupus erythematosus
rheumatoid arthritis
infective endocarditis
65
what is happening to incidence of acute rheumatic fever and why
decreased incidence = decreased MS due to decrease in strep infections
66
what population is MS 3x more common in
women
67
MS remains a major health concern where
developing countries
68
in rheumatic MS, chronic inflammation leads to
narrowing of valve due to:
1. valve leaflets thickening and formation of fibrous deposit
2. mitral commissures and chordae fuse and shorten
3. abnormally close papillary muscles
4. valvular cusps become rigid
69
hallmark orifice size in MS
decreased orifice area from 4-6cm to ~2cm
70
what does the decreased orifice size do to the left AV pressure gradient
blood can only flow from LA to LV with abnormally elevated Left AV pressure gradient (harder to get blood through to the ventricles
71
what orifice size is considered severe MS
72
what does elevated LA pressure have an affect on?
leads to elevated pulm venous and pulm arterial pressures that can reduce pulm compliance which leads to DOE
73
s/s of MS
1. DOE
2. fatigue
3. orthopnea
4. PND
5. palpitations
6. chest pain
7. hemoptysis d/t elvated LV pressure and rupture of small bronchial veins
8. thromboembolism
74
two clinical syndromes of MS
1. mild-moderate MS - pt is either asympt or sympt only with exterme exertion; mitral valve area (MVA) - 1-1.5cm
2. severe MS - MVA is
75
what does severe MS results in
decreased CO & right sided HF
| --ascites, edema, hepatomegaly, JVD
76
what symptoms of MS occur in 50-80% of MS patients
paroxysmal and chronic atrial fibrillation
77
how does atrial fibrillation develop with MS
as LA dilates it is more prone to A fib
78
A fib in MS does not allow for what
maximal diastolic filling in the LV
- this further increases mitral valve pressure gradient
- -that's why its impt to maintain HR control (slower HR allows for greater diastolic filling)
79
all signs of MS can be precipitated by
1. onset of A fib
2. pregnancy (d/t increase CO)
3. exercise (d/t increase HR)
80
how is the murmur of MS described
where is it best heard
what position is the murmur best heard
the murmur of MS is described as an opening snap followed by a diastolic low pitched rumbling decrescendo heard best at the apex in the left lateral decubitus position
81
where can the murmur of MS radiate
left axilla
82
the murmur of MS is best heard with what part of stethoscope
bell (for low pitched sounds)
83
what is the opening snap of the MS murmur due to?
d/t a stiff mitral valve that is forced to open from the high LA pressure
-the murmur increase in length as the stenosis worsens
84
preferred diagnostic study for MS
1. echo/doppler: preferred to assess for degree of MV calcification, LA enlargement, narrow MV orifice with accompanying increase in elevated blood flow velocity thru the MV
85
other diagnostic studies for MS
1. catheterization - reserved for pts with concomitant CAD - not helpful to assess for MVS
2. CXR - LA enlargement
86
treatment of MS
1. mitral valve replacement - percutaneous balloon mitral valvuloplasty
- indicated when both stenosis and regurg are present
87
downsides to mitral valve replacement
1. biosynthetic valves degenerate after 10-15 years (restenosis)
2. mechanical prosthetic valves are prone to thrombosis
3. prostehtic valve need prophylaxis for endocarditis - dental/resp procedures; amox, clinda, azithro
88
which blood thinner is used for MS
warfarin - to treat the A fib and to avoid thrombo embolism and potentially resulting stroke
89
when to refer a pt with MS
all pts with MS for monitoring and timing of treatment intervention
90
what is mitral regurg
disorder of MV closure
| -results in backflow of LV stroke volume into the atrium
91
what are the consequences of mitral regurg
leads to LV and LA enlargement with increased ejection fraction assisted by LV hypertrophy
- overtime the EF decreases due to persistent increased volume overload and decreased contractile function = heart failure and
1. pulm HTN and pulm edema
2. A fib
3. sudden cardiac death (can be asympt for years then develop acute heart failure)
92
2 types of MR
acute and chronic
93
acute causes of MR
```
acute MI
severe myocardial ischemia
blunt trauma
ruptured chordae tendinae, papillary muscle
rheumatic fever
infective endocarditis
flail cusps
myxomatous dz
```
94
chronic causes of MR
```
Marfan's syndrome
structural:
-degenerative
-infectious endocarditis
-rheumatic heart dz
-inflammatory dz (SLE)
-anorectic drugs
-congenital cleft leaflet
functional
-ischemic (CAD)
-nonischemic cardiomyopathy
```
95
murmur of MR - describe, best heard where, and radiates where?
murmur of MR is pansystolic heard best at the apex that radiates to the axilla
96
MR and the carotid pulse changes
brisk upstroke of carotid pulse
97
what other heart sound changes are there in MR other than the murmur?
prominent S3 (heart gallop)
- d/t large volume of blood flowing to he LV in early diastole
- sounds like Kentucky with the cky as S3
98
acute MR changes
normal LA is subjected to extremely high regurgitant volume but the LA has not undergone remodeling hypertrophy or dilation to accommodate increased afterload
- LA pressure rises quickly
- LA and pulm venous pressures rise quickly with resulting pulm edema
99
chronic MR changes
LA enlarges slowly but progressively
- no or little significant rise in LA or pulm venous pressure
- DOE progresses over many years
- leads to elevated LA/LV pressure ad failure (Afib and left heart failure)
100
MR diagnostic studies - preferred
1. echo - will show:
- flail leaflet, prolapse valve, vegetations, cardiomyopathy
echo - will assess
-LV size and function, LA size and function, pulm artery pressure, RV function
101
other MR diagnostic studies
1. transthoracic esophageal echo - reveals cause of MR, used to determine timing of surgery
2. BNP - can ID LV dysfunction in asympt pts with MR (>105 at high risk to develop HF)
3. cardiac cath - assess for CAD prior to valve replacement
102
treatment of MR - when is surgery indicated for:
1. sympt pts
2. asympt pts
3. emergency surgery when?
1. surgery indicated for all symp pts especially with pulm HTN
2. surgery indicated for asympt pts with: EF 4cm
3. emergency surgery for abrupt MR in life threatening situations (acute MI, perofation of valve, ruptured chordae tendinae)
103
when to refer pts with MR
pts with more than mild MR
| pts with eF 4cm)
104
MVP is also called
floppy valve syndrome and systolic click murmur
105
etiology of MVP
unknown, but can be genetically linked
- reduced type II collagen has been linked to MVP
- frequently found in Marfan's syndrome & Ehlors-Danlos syndrome
106
can MVP be found in normal healthy patients
yes, found 10% in healthy females on echo
107
does MVP affect men or women more
women
108
what types of pts are at higher risk for MVP
musculo-skeletal deformities
| -pectus excavatum, scoliosis, hyper flexibility of joints
109
significant MVP can develop d/t
1. rupture chordae tendinae (flail leaflet)
2. progressive annular dilation
3. dz progression as part of the aging process (pts greater than 60 yo will need mitral valve replacement)
110
s/s of MVP
usually asympt, but pts can complain of (nonspecific chest pain, dyspnea, fatigue, palpitations)
111
murmur of MVP
- mid systolic clicks (due to multiple chordae or redundant valve tissue)
- followed by late systolic murmur (if leaflet fails to come together)
- with increased prolapsing of valve the murmur becomes prolonged = holosystolic
112
MVP diagnosis
made clinically with the history and physical exam
| --echo is preferred and will show prolapse of leaflets into the LA in systole
113
treatment of MVP
control arrhythmias with beta blockers
| -valve repair of chordae, redundant valve tissue
114
when to refer MVP pts
all pts with MVP and audible murmur for monitoring and timing of surgical repair
115
which is more prevalent MS or TS?
MS, but TS is associated with MS
116
who is more affected in TS men or women?
women
117
usually there is a hx of what with TS?
RHD
118
other risk factors in US for TS
carcinoid dz
| prosthetic tricupsid valve degeneration
119
what is happening is TS
increased diastolic pressure gradient bw the RA and RV d/t narrowed tricupsid valve
120
increased RA pressure increases what
systemic venous congestion
- hepatomegaly
- ascites
- edema
- presystolic liver pulsations can be palpated
121
murmur of TS
diastolic rumble along the left sternal border that increases with inspiration
122
dx studies of TS
EKG - RA enlargement
CXR - cardiomegaly with normal pul artery size, dilated SVC and azygous vein
Echo or cath - pressure gradient in diastole >5mmHg is significant
123
tx of TS
1. diuretics & aldosterone inhibitors - decrease fluid and treat liver engorement, ascites
2. tricupsid replacement is tx of choice - -both tricuspid and mitral valves are replaced at the same time since both are usually defective or may become defective
124
which valves are preferred in TS tx?
- -bioprosthetic valves are preferred and not mechanical
| - mechanical can pose future complications if the pt needs a pacemaker implantation or cat procedure
125
what is happening in TR?
backflow from RV to RA
126
what is TR usually due to?
1. right ventricular dilatation (80% cases) not tricuspid valvular dz
2. LV failure is most common cause of RV dilatation
3. occurs with increased volume overload in the RV associated pulm artery HTN
4. occurs from pacemaker lead placement with injury to the valve - increasing iatrogenic cause of TR
5. dilated cardiomyopathy
127
what kind of damage can also lead to TR?
damage to supporting tissue
1. infarction of RV papillary muscles
2. tricupsid valve prolapse
3. radiation
4. infective endocarditis
5. leaflet trauma
128
s/s of TR
identical to right sided heart failure
1. increased JVP
2. ascites
3. edema of lower extremities
4. associated with LV heart failure or pulm HTN
5. A fib
6. distended neck veins
7. hepatomegaly with systolic pulsations
8. ascites
9. pleural effusions
10. edema
11. postiive hepatojuguluar reflex
12. prominenet RV pulsations/heave/thrills along left parasternal border
129
s/s in severe TR
fatigue, DOE, cervical pulsations, abdominal fullness
130
murmur of TR
blowing holosytoilc murmur along the lower left sternal margin that intensifies with inspration and reduced with expiration or valsalva
131
extra heart sounds in TR
| -what causes it
S3 (kentucky) cardiac gallop - related to high blood flow returning to RA
132
dx of TR
1. echo/doppler is diagnostic - will assess severity of TR, RV function, RV size and systolic pressure and volume overload, flail or scarred tricuspid valve
2. CXR: dilated RA/RV, dilated azygous vein and SVC, pleural effusions
3. cath - confirms regurgitant wave in RA and increased RA pressure
4. EKG - Afib, old MI involving RV, RV hypertrophy, RA enlargement
2.
133
tx of TR
1. tricupsid valve replacement for severe TR - mechanical valves predisposes pts to thrombotic events
2. diuretics to treat edema
3. aldosterone antagonist for ascites
4. if LV failure is cause - must address to decrease pulm and RV pressures and resolve TR
5. treat pulm HTN
134
causes of pulmonary valve stenosis
essentially a congenital disorder
| valve is typically domed and smooth with fusion of commissures
135
pathophys of PS
systolic pressure gradient bw the RV and PA
- RV hypertrophy develops d/t obstruction of blood flow and a prolonged systolic ejection
- increased resistance from RV blood flow and a prolonged systolic ejection
- increased resistance from RV blood flow to the lungs increase RV pressure thus decreasing pulm blood flow (severe stenosis causes peripheral cyanosis)
136
s/s of PS
1. asympt in mild dz
2. mod-severe - DOE, fatigue, syncope, anginal chest pain, syncope with severe obstruction and eventual RV failure
3. other signs - hepatomegaly, ascites, edma appear in advanced dz (signs of right sided heart failure)
137
murmur of PS
loud, harsh, crescendo-decrescendo, systolic ejection murmur with a palpable thrill in 2nd interspace radiating to shoulder that increases with intensity with inspiration
138
dx of PS
1. echo is diagnostic - assess pressure gradient across valve and dress of stenosis; assesss RV function PA pressures
2. ECG - right axis deviation, RVH and RA enlargement in severe PS
3. CXR - RA enlargement, filling of retrosternal airspace d/t RA enlargement of lateral film
139
on echo, pulmonary pressure should be?
low
140
on echo what are the cutoffs of severity of stenosis for PS
mild PS 60mmHg
141
tx of PS
treat all symp pts
treat all pts with pressure gradient >60mmHG regardless of sympts
diuretics indicated to treat symptoms of right sided heart failure
tx of choice: pulmnoary balloon valvolotomy for symp pts with peak pressure greadient >50mmHg and asympt pts with peak pressure gradient >60mmHg
142
two types of PR
high pressure PR
| low pressure PR
143
what is high pressure PR
| -murmur
mostly due to pulm HTN
-pulm descrescendo, diastolic murmur caused by dilated pulm annulus (murmur is increased with inspiration and decreased with valsalva
144
what is low pressure PR
most d/t valvular dz (congenital, pulm valva nnulus dialtion)
- no murmur can be detected due to low pressure gradient bw the PA and RV
- pts tolerate PR well if RV pressure is low
145
pathophys of PR
sever PR causes RV enlargement and hypertrophy
- this causes both an increase in preload and afterload
- as diastolic pressure increases there is enlargement of the RV and RA with JVD and decreased blood flow to the lungs
146
s/s of PR
most pts are sympt
- some have RHF d/t RV overload
- hyperdynamic RV (RV lift)
147
ausculation of PR
S2 is split d/t prolonged RV systole and associated delayed pulm valve closure P2
-theres a pulm valve systolic click
pulm decrescendo, diastolic murmur
148
dx studies of PR
1. echo - assess pulm valve anatomy and function
2. ECG - RBBB, RVH, RA enlargement
3. CXR - enlarged RV and PA
4. cardiac MRI/CT - assess regurgitant fraction; helps quantify degree of pulm valve resistance
149
tx of PR
1. need to reduce PA HTN (vasodilator, diuretics - also for right sided heart failure)
2. surgical valve replacement - transcatheter pulm valve replacement (bioprosthetic used usually) need to first trate the condition causing PR
