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ICM-Cardio > Cardio valvular disease > Flashcards

Cardio valvular disease Flashcards

1
Q

right side

A

tricuspid

pulmonary

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2
Q

left side

A

mitral

aortic

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3
Q

3 leaflets

A

tricuspid
aortic
pulmonary

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4
Q

2 leaflets

A

mitral

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5
Q

what is prolapse

A

different version of regurgitation

-valve will open, but don’t close in the proper plane

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6
Q

right sided failure

A
  • increased RV pressure
  • increased RA pressure
  • increased CVP
  • increased JVD
  • hepatomegaly
  • ascites
  • edema (peripheral)
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7
Q

left sided failure

A
  • increased LV pressure
  • increased LA pressure
  • increased PA pressure
  • shortness of breathe (congestion)
  • CHF
  • decreased EF
  • decreased systemic perfusion
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8
Q

go to test for valvular disease

A

Echo

  • TTE
  • TEE
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9
Q

what is a CXR good for looking at?

A

chamber size
aortic dilation
pulmonary edema

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10
Q

cardiac cath is good for looking at?

A

mainly a pre-op tool for coronary artery evaluation

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11
Q

swan ganz catheter is goof for looking at

A

different pressures of the chambers in the heart

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12
Q

treatment

A

observation
medical
precutaneous
surgery

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13
Q

causes for tricuspid stenosis

A

*Rheumatic
congenital
*carcinoid

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14
Q

rheumatic

A

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
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15
Q

hallmark of rheumatic disease

A

commissural fusion

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16
Q

carcinoid

A

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.
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17
Q

symptoms of tricuspid stenosis

A
  • 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
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18
Q

physical exam for tricuspid stenosis

A
  • 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
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19
Q

imaging on tricuspid stenosis

A
  • 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)

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20
Q

tricuspid regurgitation cases

A
  • 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
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21
Q

tricuspid regurgitation

A 
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
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22
Q

symptoms for tricuspid regurgitation

A
  • dyspnea, orthopnea

- prone to having atrial fibrillation

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23
Q

what do you see one echo with regurgitations

A
  • echo-quantitates degree of insufficiency/annular size, see associated lesions and vegetations
  • how much flow is going backward
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24
Q

treatment options for tricuspid disease

A
  1. observation: mild to moderate disease
  2. medical- most time treating left sided valve lesions for functional disease, diuretics, afterload reduciton
  3. valvuloplasty repiar, tricuspid valve ring
  4. commissurotomy
  5. tricuspid valve replacement
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25
Q

when to do tricuspid valve replacement

A

infective endocarditis
carcinoid
tricuspid stenosis

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26
Q

when to do valvuloplasty repair, or tricuspid valve ring

A
  • For symptomatic severe disease of functional MR

- Moderate-severe MR when preforming other concominant valve or coronary procedures

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27
Q

what valve is least likely to be repaired?

A

aortic

-usually replace

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28
Q

when is commissurotomy done

A

congenital lesions

rheumatic disease

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29
Q

pulmonary valve

A

mainly congenital lesions: Tetralogy Fallot, pulmonary atresia
-mainly are children

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30
Q

Ross procedure

A

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
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31
Q

Mitral stenosis

A
  • 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)
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32
Q

mitral valve anatomy

A
  • leaflets: anterior and posterior
  • annulus: attachment point of leaflets
  • chordae tendineae
  • papillary muscle: attached to ventricle
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33
Q

portion of annulus that enlarges in Mitral stenosis

A

posterior part

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34
Q

what is important when operating for mitral stenosis

A

keep chordae tendineae and papillary muscle as attached as possible

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35
Q

mitral stenosis means

A

stiffening of the mitral leaflets

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36
Q

right sided lesions mainly

A

deal with back up into the body

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37
Q

left sided lesions mainly

A

back up into the lungs

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38
Q

clots on the right side can go to

A

lungs

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39
Q

clots on the left side

A

can cause stroke (go to brain)

or go to other parts of body-> like arm and cause ischemia of arm

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40
Q

symptoms of MS

A
  • pulmonary congestion
  • cough
  • hemoptysis (coughing up blood)
  • orthopnea
  • PND
  • pulmondary edema
  • dyspnea on exertion
  • cardiac cachexia: thin, frail, patients
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41
Q

classic symptom of MS

A

dyspnea on exertion

-patients learn to avoid exertion

42
Q

imaging on mitral stenosis

A
  • 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
43
Q

auscultatory Triad in MS

A

apical diastolic rumble
increased 1st heart sound
opening snap

44
Q

why do you see a straight cardiac border on CXR in MS?

A

increased LA and PA obliterates the normal concavity between Aortic and LV

45
Q

exclusive cause of MS

A
  • 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)
46
Q

what does progressive disease result in for MS

A

fibrosis of leaflets, commissures, subvalvular apparatus and calcifies

47
Q

what can calcium cause if it grows in conduction system

A

heart block

48
Q

what is the worst part to get calcifications

A

annulus (mitral valve)

49
Q

what are Kerley’s lines (seen with MS)?

A

seen with severe MS

-engorged pulmonary lymphatics

50
Q

imaging seen with MS

A

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

51
Q

treatment of MS

A
  1. Observation/medical: asymptomatic patients looking for LA thrombus, mitral valve area (MVA), valve gradient, PA pressures
    - anticoagulant for thrombus, emboli, atrial fib,
  2. Precutaneous balloon commissurotomy
  3. 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
52
Q

when do you preform precutaneous balloon commissurotomy

A

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

53
Q

when is a mitral valve commissurotomy or MV replacement performed?

A

severe MS with severe symptoms

-MVA less/equal 1.5

54
Q

Mitral regurgitation causes

A
  • 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
55
Q

murmur for MR

A

Loud pansystolic murmur transmitted to axilla

56
Q

MR characteristics

A
  • increased LA pressure/PCWP/pulmonary vein pressure

- can decrease CO

57
Q

papillary muscle most effect my ischemia?

A

posterior medial papillary muscle

  • comes from RCA or Posterior circumflex (depends on dominance)
  • only has a single blood supply
58
Q

symptoms of MR

A

-fatigue, dyspnea, decreased exercise tolerance, palpitations/atrial fib.

59
Q

imaging for MR

A
  • 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

60
Q

acute MR

A

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
61
Q

anterior papillary muscle supplied by

A

LAD and lateral circumflex

-dual blood supply

62
Q

in MR, mitral annulus dilates

A

posteriorly

63
Q

LV function in MR

A

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

64
Q

what do patients with MR have increased risk for?

A

bacterial endocarditis

65
Q

treatment of MR

A

observation
medical treamtent
surgery

66
Q

which patients should be observed?

A

mild disease, serial echo exams to look for evidence of LV decompensation, LA thrombus, degree of regurgitation

67
Q

which patients should get medical treatment

A

diuresis, afterload reduction, rhythm control/possible anticoagulation, possible beta-blockers

68
Q

which patients should receive surgery as a treatment?

A

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
69
Q

Aortic stenosis causes

A
  1. Degenerative/calcific, senile calcific
    - greater in males
    - may affect conduction system if Ca extends to conduction system
  2. congenital-> Bicuspid most common, (age 30-60)
  3. Rheumatic (usually associated with MV)
70
Q

most common cause of aortic stenosis

A
  1. Degenerative/calcific, senile calcific
71
Q

pathology of AS

A
  • 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
72
Q

classic symptoms of AS

A

angina
syncope
CHF (exertional dyspnea)
sudden death (ventricular arrhythmias) (20% present with symptoms)

73
Q

most common fatal valve lesion

A

Aortic stenosis

74
Q

what do most untreated patients with AS die from?

A

CHF (congestive heart failure)

75
Q

natural progression of AS

A
  1. asymptomatic for years prior to symptoms
  2. once clinical symptoms occur the clinical course is malignant
  3. average survivial post onset of symptoms
    CHF: 2 years
    Syncope: 3 years
    Angina: 5 years
76
Q

murmur for AS

A

systolic ejection murmur in right 2nd ICS that radiates to carotids

77
Q

AS diagnosis

A
  1. murmur
  2. carotid pulse has diminished upstroke
  3. ECG: LVH, IVC delays like right/left BBB, AV nodal block or atrial fib
  4. CXR: calcifications of aortic valve/aorta, LVH, post-stenotic aorta enlargement
  5. echo: measure AVA (.8 or less severe), look for associated lesions, EF, wall motion, chamber size, leaflet motion, aortic size
  6. cath: assess coronaries for patients going to surgery, measure gradients, aorta assessment, look for AI
  7. CTA chest with 3D reconstruction: to assess aortic dilation/aneurysm/root
78
Q

AS treatment: observation

A

mild to moderate disease

79
Q

AS treatment: medical treatment

A

control hypertension (careful in severe end stage disease)
control arrhythmias
cautious use of diuretics

80
Q

AS treatment: surgery for symptomatic patients

A

Symptomatic patients with severe AS

  • .8 AVA
  • mean gradient 40mmHG or greater
  • aortic velocity 4.0m/sec or greater
81
Q

AS treatment: surgery for asymptomatic patients

A

asymptomatic with severe AS

  • EF 50% or less
  • undergoing cardiac surgery for another reason
82
Q

types of surgery for AS

A

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.

83
Q

aortic regurgitation causes

A
  • 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
84
Q

most common valvular lesion in blunt chest trauma

A

Aortic regurgitation

85
Q

AR pathology

A
  • 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
86
Q

difference between with AS and AR

A
  • 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)
87
Q

symptoms of AR

A

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

88
Q

murmur/special things in AR

A
  1. diastolic blowing murmur
  2. austin flint murmur
  3. water hammer pulse
  4. De musset’s sign
  5. quincke’s pulse
  6. Duroziez’s sign
  7. Traube’s sign
89
Q

austin flint murmur is from

A

regurgitation jet hits anterior leaflet of mitral valve and tends to close it and causes a murmur at apex

90
Q

water hammer pulse

A

bounding and forceful peripheral pulse

  • Corrigans: carotid artery
  • Waston’s-> limb pulse
91
Q

De musset’s sign

A

bobbing of head with cardiac cycle

92
Q

quincke’s pulse

A

pulsating nail beds

93
Q

Duroziez’s sign

A

systolic/diastolic murmur over femoral arteries

94
Q

Traube’s sign

A

pistol shot sounds over large arteries

95
Q

imaging for AR

A

-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

96
Q

AR treatment: observation

A

mild to moderate, serial echo exams

97
Q

AR treatment: medical

A

afterload reduction, diuretics, treat hypertension

98
Q

AR surgery as treatment

A

AVR (aortic valvular replacement)
occasionally can repair
may need to replace ascending aorta

99
Q

who gets an AVR

A
  • patients with severe regurgitation in symptomatic patients
  • asymptomatic disease with EF of 50% or less, severe LV dilatation (greater than 50mmHg)
100
Q

who tends to recover better, AS or AR patients?

A

AS patients ventricular wall mass, volumes and function recover better overall after surgery compared to AR patients post op

ICM-Cardio (21 decks)

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