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ICM > 3: Valvular Disease > Flashcards

3: Valvular Disease Flashcards

1
Q

causes of mitral regurgitation

A
  • rheumatic disease
  • dystrophic/degenerative valves
  • ischemic (secondary to CAD, MI)
  • infective endocarditis - bacterial > fungal
  • cardiomyopathies (dilated/distorted LV)
  • CT disease
  • prolapse
  • myxomatous/Barlows disease
  • trauma
  • papillary mm. rupture/dysfunction/displacement
  • LV aneurysm
  • atrial myxoma
  • effects on annulus, leaflets, chordae, papillary, wall, chamber size
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2
Q

type of murmur seen in mitral regurgitation

A

loud pansystolic murmur transmitted to axilla

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3
Q

where do you get increased pressure with mitral regurgitation?

A

increased LA pressure, PCWP, pulmonary vein pressure

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4
Q

what symptoms will a patient with mitral regurgitation get?

A
  • fatigue
  • dyspnea
  • decreased exercise tolerance
  • palpitations/a fib
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5
Q

what happens to the size of the LA in mitral regurgitation? in gradual onset vs acute onset?

A

increased size - if gradual can accommodate the extra load without pressure rise until late and then becomes symptomatic

acute: (ex: ruptured papillary muscle post MI) then the normal/small LA cannot accommodate with resultant acute pulmonary edema and possible extremis status

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6
Q

what pathologic changes occur in right sided heart failure?

A 
increased RA and RV pressure 
increased CVP 
increased JVD 
hepatomegaly 
ascites 
edema
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7
Q

what pathologic changes occur in left sided heart failure?

A 
increased LA and LV pressure 
increased PA pressure 
SOB 
CHF + pulmonary edema 
decreased EF 
decreased systemic perfusion
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8
Q

what is important when evaluating a potential valvular disease patient?

A
  • H&P
  • EKG
  • CXR - chamber size, aortic dilatation, pulmonary edema
  • **ECHO - TTE, then TEE (this is go-to test for valve disease)
  • Cardiac cath - mainly for pre-op coronary artery eval
  • Swan ganz cath - pressures/waveforms
  • CT/gated MRA - myxoma, aorta size evaluation
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9
Q

general possibilities for valvular disease

A
  • observation
  • medical: diuresis, afterload reduction
  • percutaneous: balloon valvuloplasty, TAVR (valve w/i valve)
  • surgery: repair (mitral mostly, some tricuspid/aortic), replacement (bioprosthetic, mechanical, autograft/homograft)
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10
Q

causes of tricuspid stenosis

A
  • rheumatic disease
  • carcinoid disease
  • congenital (Ebstein’s anomaly, tricuspid atresia)
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11
Q

describe tricuspid stenosis in rheumatic heart disease

A
  • usually associated with acute rheumatic disease
  • not usually an isolated lesion (mitral too)
  • regurgitation w/ variable stenosis
  • *commissural fusion
  • choral thickening, mild fusion
  • NO calcification
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12
Q

describe tricuspid stenosis in carcinoid disease

A
  • secondary to serotonin production from liver mets
  • sx: flushing, diarrhea, palpitations
  • cicatricial deformity in TV, PV (ice-like frozen sheet)
  • fibrous plaques on leaflets and onto endocardium
  • commissure fusion
  • leaflets thicken and shorten
  • chordae thick and fused
  • combined stenosis and regurgitation
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13
Q

symptoms of tricuspid stenosis

A
  • excessive fatigue
  • dyspnea (can be from associated L sided lesions)
  • forward failure (decreased preload LV, SV; salt and water retention from RAA)
  • backward failure (hepatic congestion, peripheral edema)
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14
Q

physical findings with tricuspid stenosis

A
  • mid-diastolic murmur over lower LSB
  • murmur increases with inspiration
  • liver large but NOT pulsatile
  • peripheral edema (if a fib present, rate with NSR)
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15
Q

test findings with tricuspid stenosis: CXR

A

CXR: increased RA, normal pulmonary artery size, clear lung fields (this triad***)

EKG: prominent p waves unless a fib present

echo: RA enlargement, leaflet thickening, measure gradient, look for associated lesions
cath: identify gradient/CAD eval pre-op

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16
Q

causes of tricuspid regurgitation

A
  • rheumatic disease
  • endocarditis (infective - IV drug abuse; non - LSE)
  • trauma (penetrating, blunt, pacemakers)
  • carcinoid
  • myxoma
  • diffuse collagen disorders
  • fibroelastosis
  • congenital: Ebstein’s anomaly
  • due to MV disease mainly (MR) - functional disease
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17
Q

physical findings in tricuspid regurgitation

A
  • pansystolic murmur maximal over LSB
  • increases with inspiration
  • enlarged liver + systolic pulsations, tender
  • JVD
  • hepato-jugular reflex present
  • edema
  • ascites
  • anasarca (extreme generalized edema)
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18
Q

which murmurs increase with inspiration? which increase with expiration?

A

R sided problems - increase with inspiration
“it’s right to inspire”

L sided problems - increase with expiration

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19
Q

symptoms of tricuspid regurgitation

A
  • depend on etiology
  • may have dyspnea, or orthopnea
  • majority get a fib
  • echo: quantitates degree of insufficiency/annular size, see associated lesions and vegetations
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20
Q

tricuspid valve treatment: observation and medical

A

observation: mild/moderate asymptomatic disease

medical:
- depends on etiology
- generally treat left sided valve lesion for functional disease
- diuretics
- possible afterload reduction

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21
Q

tricuspid valve treatment: surgery options (3)

A

ring valvuloplasty/repair:

  • for symptomatic severe disease of functional MR
  • for moderate-severe MR when performing other concominant valve or coronary procedures

commissurotomy:
- for some rheumatic disease, congenital
- knife to leaflet at commissure, cut apart fusions

replacement:
- for infective endocarditis
- for carcinoid
- for tricuspid stenosis

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22
Q

causes of pulmonary valve disease

A

-mainly congenital: tetralogy of Fallot, pulmonary atresia

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23
Q

what is the 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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24
Q

pathologic findings in mitral stenosis

A
  • decreased flow of blood to LV
  • decreased CO (fatigue, muscle wasting, weakness)
  • LA hypertrophy (a fib, mural thrombi, systemic emboli)
  • pulmonary HTN
  • increased pulm vasculature resistance
  • pulmonary edema + alveolar hemorrhage
  • LA hypertrophy and dilation can compress esophagus - dysphagia for solid foods
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25
Q

symptoms of mitral stenosis

A
  • pulmonary congestion
  • cough
  • hemoptysis
  • orthopnea
  • PND
  • pulmonary edema
  • dyspnea on exertion (classic symptom)***
  • cardiac cachexia
26
Q

physical findings in mitral stenosis

A
  • heart size (LV) normal or small

- ausculatory triad: apical diastolic rumble, increased S1, opening snap*****

27
Q

test findings in mitral stenosis: CXR, other, echo, cath

A

CXR: increased LA, normal cardiac size, straight left heart border (increased LA and PA obliterates normal concavity between Ao and LV)

often MV is calcified - see on CXR, echo, cath, CT

Kerley’s lines with severe MS (engorged pulmonary lymphatics)

echo: LA enlargement, leaflet thickness, vegetations, valve area, EF, associated lesions, thrombus, calcification, leaflet ‘doming’ secondary to restrictive opening of stenotic valve
cath: mainly for CAD eval pre-op

28
Q

causes of mitral stenosis

A

rheumatic disease is nearly the exclusive cause of mitral stenosis

exceptions: rare congenital lesions, extra-valvular causes like myxoma and severe senile calcific disease (this is increasing though)

29
Q

mitral stenosis treatment: observation and medical

A

observation: centered around following echo exams on asymptomatic patients looking for:
- LA thrombus
- mitral valve area (MVA)
- valve gradient
- PA pressures

Medical:

  • anticoagulation for thrombus, emboli, a fib
  • medical tx of a fib and HR control
30
Q

mitral stenosis treatment: surgery options

A

percutaneous balloon commissurotomy:
-symptomatic patients w/ MVA less than/= to 1.5, minimal calcium, and favorable anatomy in absence of LA thrombus and mod-severe MR

commissurotomy or replacement:
-severe MS (MVA less than 1.5) w/ severe sx or if undergoing other concominant cardiac surgery

repair:
- rheumatic MS more difficult, but not routinely done secondary to significant fibrosis
- obliterate left atrial appendage if thrombus present

31
Q

what happens to the mitral annulus in mitral regurgitation?

A

dilates posteriorly (posterior 2/3 dilates up)

32
Q

what happens to LV function in mitral regurgitation?

A

in chronic forms of MR, usually remains adequate for a long period of time even with severe MR, but eventually decompensates with LV dilatation and decreased EF

33
Q

what are patients with MR more susceptible to?

A

bacterial endocarditis

34
Q

CXR in MR

A

enlarged LA and eventually LV

various degrees of pulmonary congestion

35
Q

MR treatment: observation and medical

A

observation:
- mild disease
- serial echos to look for LV decompensation, LA thrombus, degree of regurgitation

medical:
- diuresis
- afterload reduction
- rhythm control/possible anticoagulation
- possible B blockers

36
Q

MR treatment: surgery options

A

MV repair/annuloplasty ring:

  • for symptomatic patients with severe MR
  • for asymptomatic patients with severe MR
  • for LVESD greater than/equal to 40 mm and EF below 60
  • for asymptomatic moderate MR with concomitant cardiac valve/coronary artery procedure

replacement:
- if unable to perform adequate repair
- posterior leaflet chords preserved to preserve LV geometry and function**

37
Q

treatment for acute MR

A

usually deteriorates quickly and needs urgent/emergent surgery

38
Q

causes of aortic stenosis

A
  • degenerative/calcific - senile calcific most common*, more in males, may affect conduction system
  • congenital: bicuspid most common*, occurs at earlier age (30-60y/o)
  • rheumatic - usually has associated MV disease
39
Q

AS pathology

A
  • increased afterload + secondary impaired LV emptying
  • concentric LV hypertrophy- increased mm mass + increased O2 demands + decreased subendocardial flow in diastole = mismatch (angina)
  • LVH may eventually lead to LV failure chronically
  • resultant microinfarcts occur with resultant myocardial scarring/muscle loss and decreased ventricular function
40
Q

what happens to the maintenance of CO as LV gets more compliant in AS?

A

atrial systole becomes more important for LV filling and maintaining CO - therefore, if a fib develops, can suddenly worsen clinical symptoms

41
Q

AS symptoms

A

classic: angina, syncope, CHF (exertional dyspnea)

- sudden death (ventricular arrhythmias)

42
Q

what is the most common ‘fatal’ valve lesion?

A

AS - most untreated AS patients die of CHF

43
Q

AS natural history

A

-asymptomatic for years prior to symptoms
-once clinical symptoms occur, the clinical course is malignant
-average survival post onset of symptoms:
CHF 2 years
syncope 3 years
angina 5 years

44
Q

diagnosis of AS: murmur, pulses, EKG, CXR, echo, cath, CTA

A
  • systolic ejection murmur in 2nd ICS that radiates to carotids
  • carotid pulse with diminished upstroke
  • EKG: LVH, may see IVC delays like R/LBBB, AV nodal block, or a fib
  • CXR: calcification or aortic valve/aorta, LVH, post-stenotic aorta enlargement
  • echo: measure AVA (0.8 or less is severe), look for associated lesions, EF, wall motion, chamber size, leaflet motion, aorta size
  • cath: assess CAD/Ao, measure gradients, look for AI
  • CTA: chest w/ 3D reconstruction to assess aortic dilation/aneurysm/root
45
Q

AS Treatment: observation and medical

A

observation:
- mild to moderate disease

medical:
- control HTN (be careful in severe end stage disease)
- control arrhythmias
- cautious use of diuretics

46
Q

AS treatment: surgery for who?

A
  • symptomatic patients with severe AS: 0.8 AVA, mean gradient 40 mmHg or greater, aortic velocity 4.0m/s or greater
  • asymptomatic patients with severe AS: + EF 50% or less or undergoing cardiac surgery for another reason
47
Q

AS treatment: what surgery?

A

AVR (replacement) if patient is an acceptable surgical risk

TAVR (transcatheter AV replacement) is performed when surgical risks are too high and patient has a life expectancy greater than 1year

48
Q

AR causes

A
  • mixed AS/AR
  • degenerative calcific AV disease
  • rheumatic disease
  • congenital- usually bicuspid
  • annuloaortic ectasia (abnormal dilatation of annulus, root)
  • marfans
  • myxoid degeneration aortic leaflets
  • aortic dissection
  • bacterial endocarditis
  • rheumatoid arthritis
  • ankylosing spondylitis
  • blunt/penetrating trauma
  • VSD - supracristal defects, from prolapse of leaflet/cusp
  • atrial myxomas
49
Q

most common valvular lesion in blunt chest trauma

A

AR

50
Q

AR pathology

A
  • volume overload of LV
  • increased LVEDP/LV diastolic volume/ wall stress
  • leads to progressive LV dilatation
  • eccentric hypertrophy of LV
  • may get massive dilatation of LV - cor bovinum
  • subendocardial ischemia from decreased diastolic coronary blood flow, increased diastolic ventricular pressure, LVH, and increased workload
  • may get angina in face of normal coronaries
51
Q

describe the progressive LV dilatation and failure in AR

A

fall in contractility and EF until forward CO cannot be maintained and patient expires from progressive CHF

52
Q

AR symptoms

A
  • dyspnea, orthopnea, PND, angina (less than 50%), syncope (rare)
  • may be asymptomatic for years with moderate to severe AR, but when symptoms begin they herald LV dysfunction with frank CHF coming usually several years later
53
Q

what is an Austin Flint murmur?

A

when regurgitant jet hits anterior leaflet of mitral valve, it tends to close and causes murmur at apex

54
Q

what is water hammer pulse?

A

bounding and forceful peripheral pulse:

  • Corrigans = carotid artery
  • Watsons = limb pulse
55
Q

physical findings in AR (many, many)

A
  • widened pulse pressure (increased SBP + decreased DBP)
  • diastolic blowing murmur
  • Austin Flint murmur
  • water hammer pulse
  • DeMusset’s sign (bobbing of head with cardiac cycle)
  • Quincke’s pulse (pulsating nail beds)
  • Duroziez’s sign (systolic/diastolic murmur over femoral aa)
  • Traube’s sign (pistol shot sounds over large arteries)
  • lateral displacement of LV apical pulse
56
Q

AR tests: CXR, EKG, echo, cath, CT

A
  • CXR: LV enlargement, enlarged ascending aorta, pulmonary edema, increased LA
  • EKG: LVH
  • Echo: regurgitant jet, EF, chamber sizes, also helps define etiology
  • Cath: CAD eval pre-op, evaluate aorta/root
  • CT: evaluate aorta
57
Q

AR treatment: observation and medical

A

observation:
- mild to moderate
- serial echo exams

medical:
- afterload reduction
- diuretics
- treat HTN

58
Q

AR treatment: surgery

A
  • usually AVR
  • occasionally repair/re-suspend valve/commissures
  • may need to replace ascending aorta dependent on etiology of AR and size of aorta
59
Q

when to use AVR for AR

A
  • severe regurgitation in symptomatic patients
  • severe asymptomatic disease with EF 50% or less, or severe LV dilatation (LVESD greater than 50mm)
  • moderate to severe disease and undergoing another cardiac or aortic surgery
60
Q

describe AVR recovery AS vs. AR

A

AS patients ventricular wall mass, volumes, and function recover better overall post-op than AR

ICM (26 decks)

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