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Clin Med - Cardio I > Valvular Heart Dz > Flashcards

Valvular Heart Dz Flashcards

1
Q

what is more common VHD or CAD

A

CAD

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2
Q

what is the most common cause of CHD in developing countries

A

rheumatic heart dz

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3
Q

all pts with mcahnical/prosthetic cardiac vlave replacement or hz of endocarditis need what for invasive procedures (dental/resp)

A

prophylaxis antibiotics

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4
Q

VHD results in what two pathologies

A
  1. stenosis

2. regurgitation

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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

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6
Q

what is a regurgitant valve

A

fails to completely close allowing backflow of blood

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7
Q

regurgitant valve is usually due to

A

endocarditis and dz of valve cusps

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8
Q

how can regurgitatnt valve disrupt supporting structures

A
  1. aorta, mitral annulus, tendinous cord, paillary muscles, ventricular free wall
  2. can occur abruptly with chordae injjury
  3. can occur gradually with leaflet scarring and retraction
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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
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10
Q

when would you refer a pt with VHD to cardiology

A
  1. presence of murmur
  2. pts who are symptomatic of valvular heart dz
  3. diagnostic studies indicative of valvular dz
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11
Q

aortic stenosis accounts for what % of all VHD cases

A

25%

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12
Q

80% of chronic, symptomatic aortic stenosis are what population

A

male

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13
Q

increased incidence correlates with

A

increased life expectancy

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14
Q

what is the most common indication for surgical valce replacement

A

aortic stenosis

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15
Q

2 etiologies of aortic stenosis

A
  1. congenital: asymptomatic until 50-65yo (younger pts may present with more severe symptoms)
  2. atherosclerotic (degenerative) valvular dz: lipid accumulation, endothelial dysfunction, inflammatory cell activation, fibroblast deposits, cytokine release, calcium deposits
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16
Q

age where atherosclerotic aortic stenosis occurs

A

> 65yo

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17
Q

atherosclerotic AS due to?

A

chronic calcification of aortic valve

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18
Q

risk factors of atherosclerotic AS

A

HTN, hypercholesterolemia, smoking, hypertrophic obstructive cardiomyopathy

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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

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20
Q

symptoms of AS

A

–long latent asymptomatic period efore sympts appear
-common s/s: functional, gradual decline
DOE, angina, syncope

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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
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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)

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23
Q

what are the end effects of AS on:

  1. ventricular function
  2. ejection fraction
  3. overall heart function
A
  1. decreased ventricular function
  2. decreased ejection fraction (SV/EDV: % of blood in ventricles that is pumped out of ventricles)
    - -increased afterload with decreased contracility
  3. leads to heart failure
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24
Q

why is DOE seen with AS?

A
  1. decreased filling capacity of aorta which leads to increased ventricular filling pressure (can’t get enough blood out)
  2. therefore increaed end diastolic volume is necessary to maintain normal ejection fraction
  3. as mitral valve opens in diastole, it is subjected to increaed ventricular diastolic pressure
  4. increased ventricular diastolic pressure is transmitted to atria and then to pulmonary veins and lungs (leads to pulmonary congestion and increased difficulty breathing
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25
Q

what happens to the ejection phase in AS

A

ejection phase is longer in AS - LV trying to get blood out thru obstructed valve

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26
Q

what is exercise induced tachycardia in relation to AS

A

-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

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27
Q

what is angina

A
  • result of myocardial ischemia
  • imbalance bw O2 demand and availability
  • increased O2 demand but not enough available = angina
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28
Q

why is there decreased O2 availability with AS and angina

A
  1. increased LV EDV + delay rate of ventricular relaxation due to hypertrophy results in:
  2. decreased coronary perfusion
  3. decreased blood flow reserve needed to offset increase in O2 demand during exercise or stress
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29
Q

what is syncope

A

transient loss of consciousness due to cerebral hypoperfusion

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30
Q

how does syncope occur with exercise?

A
  • 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
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31
Q

where is the murmur of AS located?

A

systolic or midsystolic usually after S1

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32
Q

timing and shape of AS murmur

A

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”

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33
Q

intensity of AS murmur

  • as stenosis increases?
  • with ventricular hypertrophy?
A
  • 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

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34
Q

where is the murmur of AS heard best?

A

-aortic area = right 2nd intercostal space at the sternal border with radiation to carotids and sometimes to the apex

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35
Q

special maneuvers for AS murmur

A
  1. isometric handgrip - increases systemic vascular resistance and BP (decreases AS murmur)
  2. standing and valsalva - decreases ventricular filling, decresaes AS murmur
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36
Q

carotid pulse with AS

A

small and slow rising (parvus and tardus)

  • not allowing blood thru valve
  • might palpate a shudder or thrill
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37
Q

2 changes in heart sounds with AS

A
  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
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38
Q

why is there a 4th heart sound with AS

A
  • 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
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39
Q

what is an apical pulse with AS

A

PMI - there is no change in position, but its impulse is prolonged due to increased ejection time

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40
Q

what is the primary and preferred diagnositc tool to evaluate AS

A

Echocardiogram

  1. records hemodynamic meaurements
  2. assess anatomic integrity
  3. assesses aortic dilation
  4. assesses co-existing aortic regurgitation
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41
Q

when is echocardiogram used

A

routine surveillance in stable patients every 3 years

once/year for pts with mod-severe dz

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42
Q

changes seen on CXR with AS

A 
rounding of left heart = LVH
LA enlargement
pulm venous enlargement
increased aortic shadow
aortic valve calcification
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43
Q

what 2 things can you see on the ECG with AS

A

no specific or sensitive for this

can see: 1. LV hypertrophy 2. LA hyertrophy

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44
Q

when is AV replacement indicated

A

all symptomatic patients with evidence of significant AS

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45
Q

what symptoms of AS correlate with poor prognosis without surgery

A

syncope, angina, heart failure (50% mortality rate in 3 years)

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46
Q

prognosis of AV replacement surgery

A
  • dramatic improvement with reliefe of excessive afterload

- pts with CAD have poorer outcome

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47
Q

drawbacks to AV replacement surgery

A
  • need for anticoagulation with mechanical valves

- wear and tear with bioprosthetic valves

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48
Q

when is AV replacement not recommended

A

asymtomatic patients

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49
Q

when is percutaneous balloon valvuloplasty
what is it?
risks?

A

pts not able to tolerate open heart procedure
less invasive
risk of restenosis
makes narrowed AV larger - balloon inflated to open up the stenosis

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50
Q

2 categories of causes of Aortic regurg

A
  1. valvular

2. root dz

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51
Q

valvular causes of aortic regurg

A
  1. rheumatic fever
  2. infective endocarditis
  3. HTN
  4. syphilis
  5. traumatic
  6. myxomatous
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52
Q

root disease causes of aortic regurg

A
  1. aortic dissection
  2. HTN
  3. Marfan’s syndrome
  4. congenital bicuspid aortic deformity
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53
Q

what is the compensatory mechanism in AR

A
  • 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
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54
Q

AR affect on myocardial contractility, ejectino fraction, and what is the end result

A

myocardial contractility - decreases
ejection fraction - decreases
end result - heart failure

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55
Q

where is the murmur hear for AR

A

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

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56
Q

further LV dilation leads to what in end stage AR

A

further LV failure

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57
Q

common s/s with LV failure

A

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
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58
Q

what is corrigan pulse

A

rapid rise and fall of pulse (should be uniform)

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59
Q

clinical presentation of AR

A
  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
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60
Q

diagnostic studies for AR

A
  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
Q

indication for surgery in AR

A

abnormal LV function

appearance of symptoms dramatically increase the risk of mortality

62
Q

surgery involves AV replacement when?

A
  • in all symptomatic pts
  • ejection fraction 5-5.5cm
  • even for asymptomatic pts with evidence of valvular dz
  • surgical mortality 3-5%
63
Q

main cause of mitral valve stenosis

A

rheumatic fever (30%)

64
Q

other causes of mitral valve stenosis

A

congenital mitral valve stenosis
system lupus erythematosus
rheumatoid arthritis
infective endocarditis

65
Q

what is happening to incidence of acute rheumatic fever and why

A

decreased incidence = decreased MS due to decrease in strep infections

66
Q

what population is MS 3x more common in

A

women

67
Q

MS remains a major health concern where

A

developing countries

68
Q

in rheumatic MS, chronic inflammation leads to

A

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
Q

hallmark orifice size in MS

A

decreased orifice area from 4-6cm to ~2cm

70
Q

what does the decreased orifice size do to the left AV pressure gradient

A

blood can only flow from LA to LV with abnormally elevated Left AV pressure gradient (harder to get blood through to the ventricles

71
Q

what orifice size is considered severe MS

A
72
Q

what does elevated LA pressure have an affect on?

A

leads to elevated pulm venous and pulm arterial pressures that can reduce pulm compliance which leads to DOE

73
Q

s/s of MS

A
  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
Q

two clinical syndromes of MS

A
  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
Q

what does severe MS results in

A

decreased CO & right sided HF

–ascites, edema, hepatomegaly, JVD

76
Q

what symptoms of MS occur in 50-80% of MS patients

A

paroxysmal and chronic atrial fibrillation

77
Q

how does atrial fibrillation develop with MS

A

as LA dilates it is more prone to A fib

78
Q

A fib in MS does not allow for what

A

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
Q

all signs of MS can be precipitated by

A
  1. onset of A fib
  2. pregnancy (d/t increase CO)
  3. exercise (d/t increase HR)
80
Q

how is the murmur of MS described
where is it best heard
what position is the murmur best heard

A

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
Q

where can the murmur of MS radiate

A

left axilla

82
Q

the murmur of MS is best heard with what part of stethoscope

A

bell (for low pitched sounds)

83
Q

what is the opening snap of the MS murmur due to?

A

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
Q

preferred diagnostic study for MS

A
  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
Q

other diagnostic studies for MS

A
  1. catheterization - reserved for pts with concomitant CAD - not helpful to assess for MVS
  2. CXR - LA enlargement
86
Q

treatment of MS

A
  1. mitral valve replacement - percutaneous balloon mitral valvuloplasty
    - indicated when both stenosis and regurg are present
87
Q

downsides to mitral valve replacement

A
  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
Q

which blood thinner is used for MS

A

warfarin - to treat the A fib and to avoid thrombo embolism and potentially resulting stroke

89
Q

when to refer a pt with MS

A

all pts with MS for monitoring and timing of treatment intervention

90
Q

what is mitral regurg

A

disorder of MV closure

-results in backflow of LV stroke volume into the atrium

91
Q

what are the consequences of mitral regurg

A

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
Q

2 types of MR

A

acute and chronic

93
Q

acute causes of MR

A 
acute MI
severe myocardial ischemia
blunt trauma
ruptured chordae tendinae, papillary muscle
rheumatic fever
infective endocarditis
flail cusps
myxomatous dz
94
Q

chronic causes of MR

A 
Marfan's syndrome
structural:
-degenerative
-infectious endocarditis
-rheumatic heart dz
-inflammatory dz (SLE)
-anorectic drugs
-congenital cleft leaflet
functional
-ischemic (CAD)
-nonischemic cardiomyopathy
95
Q

murmur of MR - describe, best heard where, and radiates where?

A

murmur of MR is pansystolic heard best at the apex that radiates to the axilla

96
Q

MR and the carotid pulse changes

A

brisk upstroke of carotid pulse

97
Q

what other heart sound changes are there in MR other than the murmur?

A

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
Q

acute MR changes

A

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
Q

chronic MR changes

A

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
Q

MR diagnostic studies - preferred

A
  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
Q

other MR diagnostic studies

A
  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
Q

treatment of MR - when is surgery indicated for:

  1. sympt pts
  2. asympt pts
  3. emergency surgery when?
A
  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
Q

when to refer pts with MR

A

pts with more than mild MR

pts with eF 4cm)

104
Q

MVP is also called

A

floppy valve syndrome and systolic click murmur

105
Q

etiology of MVP

A

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
Q

can MVP be found in normal healthy patients

A

yes, found 10% in healthy females on echo

107
Q

does MVP affect men or women more

A

women

108
Q

what types of pts are at higher risk for MVP

A

musculo-skeletal deformities

-pectus excavatum, scoliosis, hyper flexibility of joints

109
Q

significant MVP can develop d/t

A
  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
Q

s/s of MVP

A

usually asympt, but pts can complain of (nonspecific chest pain, dyspnea, fatigue, palpitations)

111
Q

murmur of MVP

A
  • 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
Q

MVP diagnosis

A

made clinically with the history and physical exam

–echo is preferred and will show prolapse of leaflets into the LA in systole

113
Q

treatment of MVP

A

control arrhythmias with beta blockers

-valve repair of chordae, redundant valve tissue

114
Q

when to refer MVP pts

A

all pts with MVP and audible murmur for monitoring and timing of surgical repair

115
Q

which is more prevalent MS or TS?

A

MS, but TS is associated with MS

116
Q

who is more affected in TS men or women?

A

women

117
Q

usually there is a hx of what with TS?

A

RHD

118
Q

other risk factors in US for TS

A

carcinoid dz

prosthetic tricupsid valve degeneration

119
Q

what is happening is TS

A

increased diastolic pressure gradient bw the RA and RV d/t narrowed tricupsid valve

120
Q

increased RA pressure increases what

A

systemic venous congestion

  • hepatomegaly
  • ascites
  • edema
  • presystolic liver pulsations can be palpated
121
Q

murmur of TS

A

diastolic rumble along the left sternal border that increases with inspiration

122
Q

dx studies of TS

A

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
Q

tx of TS

A
  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
Q

which valves are preferred in TS tx?

A
  • -bioprosthetic valves are preferred and not mechanical

- mechanical can pose future complications if the pt needs a pacemaker implantation or cat procedure

125
Q

what is happening in TR?

A

backflow from RV to RA

126
Q

what is TR usually due to?

A
  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
Q

what kind of damage can also lead to TR?

A

damage to supporting tissue

  1. infarction of RV papillary muscles
  2. tricupsid valve prolapse
  3. radiation
  4. infective endocarditis
  5. leaflet trauma
128
Q

s/s of TR

A

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
Q

s/s in severe TR

A

fatigue, DOE, cervical pulsations, abdominal fullness

130
Q

murmur of TR

A

blowing holosytoilc murmur along the lower left sternal margin that intensifies with inspration and reduced with expiration or valsalva

131
Q

extra heart sounds in TR

-what causes it

A

S3 (kentucky) cardiac gallop - related to high blood flow returning to RA

132
Q

dx of TR

A
  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
Q

tx of TR

A
  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
Q

causes of pulmonary valve stenosis

A

essentially a congenital disorder

valve is typically domed and smooth with fusion of commissures

135
Q

pathophys of PS

A

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
Q

s/s of PS

A
  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
Q

murmur of PS

A

loud, harsh, crescendo-decrescendo, systolic ejection murmur with a palpable thrill in 2nd interspace radiating to shoulder that increases with intensity with inspiration

138
Q

dx of PS

A
  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
Q

on echo, pulmonary pressure should be?

A

low

140
Q

on echo what are the cutoffs of severity of stenosis for PS

A

mild PS 60mmHg

141
Q

tx of PS

A

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
Q

two types of PR

A

high pressure PR

low pressure PR

143
Q

what is high pressure PR

-murmur

A

mostly due to pulm HTN
-pulm descrescendo, diastolic murmur caused by dilated pulm annulus (murmur is increased with inspiration and decreased with valsalva

144
Q

what is low pressure PR

A

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
Q

pathophys of PR

A

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
Q

s/s of PR

A

most pts are sympt

  • some have RHF d/t RV overload
  • hyperdynamic RV (RV lift)
147
Q

ausculation of PR

A

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
Q

dx studies of PR

A
  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
Q

tx of PR

A
  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

Clin Med - Cardio I (7 decks)

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