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Internal Medicine > JH IM Board Review - Valvular Heart Disease I > Flashcards

JH IM Board Review - Valvular Heart Disease I Flashcards

1
Q

What are the 3 main causes of AS?

A
  1. Congenital unicuspid valve.
  2. Congenital bicuspid valve.
  3. Degenerative calcific disease.
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2
Q

What is characteristic about congenital unicuspid valve?

A

It is usually severe—and sx present early in childhood.

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3
Q

What is the age of onset for calcific AS in pts w/ bicuspid valve?

A

Calcific AS starts in pts 30s and 40s.

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4
Q

What is the prevalence of degenerative calcific disease in >65y?

A

25%.

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5
Q

What is the earliest manifestation of degenerative calcific disease?

A

Aortic SCLEROSIS.

==> Defined as thickening of the leaflets, presence of a heart murmur, and a gradient <25mmHg.

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6
Q

What is the percentage of pts w/ aortic sclerosis that will develop AS in the next 10y?

A

20%.

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7
Q

What is the effect of statins and other risk factor tx in degenerative calcific disease?

A

Have NOT led to slower AS progression.

**even though the progression is biologically similar to atherosclerosis + linked to the same risk factors.

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8
Q

What are the 3 major physical signs of AS?

A
  1. Slow-rising carotid upstroke (parvus et tardus) — May be difficult to detect in >70y w/ stiff vessels + wide pulse pressure.
  2. Systolic ejection murmur — crescendo/decrescendo, diamond-shaped.
  3. May be conducted to the apex w/ a musical quality (“Gallavardin murmur”).
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9
Q

What is the importance of murmur’s intensity regarding AS severity?

A

There is none.

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10
Q

What is characteristic about the murmur of severe AS?

A

It is “late-peaking”.

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11
Q

What is the effect of severe calcific AS on the intensity of A2 (aortic closure sound)?

A

Reduced intensity of A2 ==> Single S2.

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12
Q

What is the prognosis of in PREsymptomatic AS pts?

A

Excellent.

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13
Q

What is the prognosis of AS pts w/ sx.

A

50% 3y mortality.

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14
Q

What is helpful regarding the anticipation of sx in AS?

A

Outflow tract velocity on Doppler echo.

==> If velocity >4m/sec (ie peak gradient >64mmHg) — sx likely within 3y.

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15
Q

What is relatively CI in AS?

A

Nitrates — may be dangerous to lower preload.

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16
Q

What is the time for intervention in AS pts?

A

Indicated if LVEF <50% and pts are sx.

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17
Q

What is the target group of TAVR?

A

Older or frail pts.

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18
Q

What is important to keep in mind about AR dx?

A

It has a broad ddx and it is critical to identify the underlying cause before tx.

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19
Q

What are the 3 main valvular diseases that may lead to AR?

A
  1. Bicuspid aortic valve.
  2. Previous endocarditis.
  3. Rheumatic valve disease.
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20
Q

What are the main diseases of the aorta that may lead to AR?

3

A
  1. CTDs — Marfan, familial aortic ectasia(!), Loeys-Dietz etc.
  2. AD.
  3. Inflammatory disorders — Giant cell, takayasu, syphilis.
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21
Q

What are the main diseases affecting aorta and valve that lead to AR?

A

Spondyloarthropathies.

==> AS, Reactive arthritis, PA.

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22
Q

What are the other important causes of wide pulses, in addition to AR?

(3)

A
  1. PDA.
  2. AV fistula.
  3. HCM.
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23
Q

What is the Quincke sign?

A

Nail bed pulsation — chronic AR sign.

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24
Q

What is the Corrigan pulse?

A

Visible carotid pulsation—seen in chronic AR.

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25
Q

What is the de Musset sign?

A

Head bobbing to pulse — sign of chronic AR.

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26
Q

What is the Muller sign?

A

Uvula bobbing to pulse — sign of chronic AR.

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27
Q

What is the Duroziez sign?

A

Diastolic bruit w/ compression of the femoral artery at the groin (!).
— sign of chronic AR.

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28
Q

What is the Hill sign?

A

Systolic pressure in the leg >10mmHg higher than the measurement at the brachial artery.

Reflects large SV.

— sign of chronic AR.

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29
Q

What is the Traube sign?

A

Pistol-shot sounds best heard over the femoral artery — sign of chronic AR.

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30
Q

What is the Water-Hammer pulse?

A

Slapping quality of pulse when the hand is held up and the DBP is <25mmHg.

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31
Q

What are the main auscultatory findings in AR?

A
  1. Early diastolic murmur which starts at the instant of aortic closure — usually medium frequency.
  2. Austin-Flint murmur.
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32
Q

What is the time when the early diastolic murmur of AR is longest and loudest?

A

When AR is chronic and the pt is doing well.

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33
Q

What is the Austin-Flint murmur of AR?

A

A 2nd murmur, beginning in mid- or late diastole.

34
Q

What is the cause of the Austin-Flint murmur?

A

Turbulent flow through the mitral orifice.

35
Q

What is the importance of the Austin-Flint murmur?

2

A
  1. Reflects high LV diastolic pressure — thus an adverse hemodynamic situation.
  2. Often indicates the need for surgical valve replacement.
36
Q

What is the role of echo in the dx of AR?

4

A
  1. Differentiates site leading to AR — Valve or aortic wall.
  2. Determines valve morphology.
  3. Detects vegetations and perforations.
  4. Assesses associated disease of other valves — MVP, MS, LV cavity size and function.
37
Q

What are the 3 main points of AR tx?

A
  1. Tx associated medical issues.
  2. No proven direct medical therapies for AR (afterload reduction is NOT beneficial).
  3. Surgery or percutaneous interventions are the only proven treatments.
38
Q

What is the physical course of chronic AR?

A

It is often well tolerated for many yrs but will eventually lead to irreversible LV dilation (cor bovinum) and dysfunction.

39
Q

What are the indications for intervention (ie surgery) for symptomatic AR pts?

(2)

A
  1. First hint of symptoms — dyspnea, palpitations, fatigue.

2. Angina rare w/ AR — may reflect coronary ostial involvement by aortitis or unrelated coronary artery atherosclerosis.

40
Q

What are the 4 main indications for intervention in asymptomatic AR pts?

A
  1. Enlarging LV cavity — LV end-systolic dimension >5.5cm or end-diastolic dimension >7cm.

(implies combination of a large cavity and some reduction in function)

  1. EF <50%.
  2. Aortic ectasia.
  3. Aortic root >5cm in Marfan or Loeys-Dietz syndromes — >5.5cm in other dx.
41
Q

What is the ddx of MR?

8

A
  1. MVP (myxomatous floppy valve).
  2. Ruptured chordae tendinae.
  3. Previous endo.
  4. Papillary muscle dysfunction.
  5. Mitral annulus calcification.
  6. Rheumatic disease.
  7. “Functional” (ie from annulus or LV dilation).
  8. Rarities (eg Libman-Sacks endocarditis caused by lupus).
42
Q

What is the clinical presentation of ACUTE MR?

2

A
  1. Very abrupt tall V wave in the LA.

2. Hence, acute pulmonary edema, low CO, and an unimpressive murmur that may sound like an ejection murmur.

43
Q

What is the clinical presentation of CHRONIC MR?

3

A
  1. Hyperkinetic LV (prominent apical impulse).
  2. Pansystolic murmur.
  3. Signs of HF (eg S3).
44
Q

What is important to keep in mind about the pansystolic murmur of CHRONIC MR?

A

In general, LOUDNESS CORRELATES W/ SEVERITY.

45
Q

What is the role of medical treatment in MR?

A

Afterload-reducting meds can probably help — especially for “functional” MR.

46
Q

What is the only proven beneficial intervention for most types of MR?

A

Surgery.

47
Q

What is the natural history of MR?

What is important to keep in mind?

A

Chronic MR is tolerated even better than AR.

==> Hence, there has been a tendency to operate too late, at a point when the LV is irremediably damaged.

— It is important to follow LV SIZE carefully! — Be alert for subtle changes in effort tolerance, stamina etc.

48
Q

What is the importance of palpitations in a pt w/ MR?

A

May be caused by a-fib ==> INDICATION FOR SURGERY.

49
Q

What are the indications for surgical evaluation in asx pts?

4

A
  1. EF <60% (!).

(EF should be higher than normal because the LV needs to pump blood adequate for systemic perfusion in addition to regurgitant volume)

  1. End-systolic dimension greater than 4.5cm (ie LV has enlarged).
  2. Consider if pulmonary HTN or a-fib.
  3. If other heart surgery needed.
50
Q

What is important to keep in mind about interventional treatment of MR?

A

Remains investigational — In contrast to AV interventions.

51
Q

What is the prevalence of MVP?

A

2-3%.

52
Q

What are the conditions under which MVP can occur in a normal valve?

(2)

A
  1. Hyperkinetic circulation with excessive SNS stimulation.

2. Underfilled LV.

53
Q

What are the 2 main auscultatory findings in MVP?

A
  1. Midsystolic click.

2. Late systolic murmur heard best at the apex.

54
Q

What are the infrequent complications of MVP?

5

A
  1. Slightly increased risk of endocarditis—abx proph is not recommended.
  2. Progressive valve degeneration leading to severe regurgitation occurs in approx. 10% of pts.
  3. Atrial/ventricular arrhythmias.
  4. Sudden death — extremely rare, hence virtually unpredictable.
  5. Stroke — very rare, thus no routine antiplatelet or anticoagulant prophylaxis.
55
Q

What are the 4 main auscultatory findings in MS?

A
  1. Loud S1.
  2. Opening snap (follows S2).
  3. Low pitched middiastolic rumble (loudest apex)—accentuates in late diastole caused by atrial contraction.
  4. Palpable P2.
56
Q

What is the physical finding a/w severe MS?

A

Softening of S1, dull or absent snap, and soft but long murmur.

57
Q

What is the role of TEE in dx of MS?

A

Needed before percutaneous balloon valvotomy because LA thrombus precludes treatment.

58
Q

What is the prognosis of asx MS?

A

80% at 10y.

59
Q

What is the tx of asx MS?

A

No specific medical tx — percutaneous valvotomy if technically feasible in those with moderate or severe MS.

60
Q

What is the prognosis of sx MS?

A

15% survival rate at 10y.

61
Q

What is the tx of sx MS?

4

A
  1. No specific medical tx.
  2. Percutaneous valvotomy or MV replacement/repair.
  3. Percutaneous balloon valvotomy preferable as long as there is pure MS (w/o significant MR) w/ favorable valve characteristics and no LA thrombus by TEE.
  4. Surgery preferable for calcified, immobile valve or subvalvular chordal disease.
62
Q

What is important to keep in mind about pregnancy and MS?

A
  1. Common to have clinical decompensation caused by combined effects of increased blood volume and CO.
  2. Careful preconception assessment is indicated.
63
Q

What is to be considered in a pregnant woman w/ new-onset pulmonary edema?

A
  1. MS.

2. Peripartum cardiomyopathy.

64
Q

What is the main association of pulmonary stenosis?

A

Other congenital abnormalities — Noonan syndrome.

65
Q

What are the main etiologies of PR?

3

A
  1. MC caused by previous pulmonary outflow tract surgery (ie Fallot repair).
  2. PHTN.
  3. Previous endocarditis.
66
Q

What is the degree of severity of PR in asx pts?

A

Mild to moderate PR.

67
Q

What are the indications for surgery consideration in PR pts?

(6)

A
  1. Sx related to PR, including arrhythmias.
  2. Decr. RV systolic function (EF<40%).
  3. Progressive RV dilation.
  4. Decline in functional aerobic capacity.
  5. 2o severe TR related to progressive annular dilatation.
  6. Severe PR in a pt requiring another cardiac operation.
68
Q

What is the group of PR pts in which we should be concerned about risk of arrhythmia?

A

Pts w/ prolonged or increasing QRS duration — total QRS 180ms or QRS duration increase of >3.5ms/year.

69
Q

What are the 4 indications for abx prophylaxis to prevent IE?

(4)

A
  1. Prosthetic heart valves (including bioprosthetics) or valve repair w/ additional prosthetic material.
  2. Hx of IE.
  3. CCHD (unrepaired or incompletely repaired or repaired using prosthetic material).
  4. Any valve disease in a transplanted heart.
70
Q

What is the recommendation for abx proph in relatively low-risk valvular disorders?

A

Not recommended — MVP, bicuspid AV, acquired AV/MV disorders, HCM.

71
Q

What are the 5 main procedures which require abx proph?

A
  1. Dental procedures that involve manipulation of gingival tissue or periapical tooth region or mucosal perforation.
  2. Respiratory tract procedures that involve incision or biopsy.
  3. Procedures in pts with GI or GU tract infections.
  4. Procedures on infected skin or tissue.
  5. Surgery to implant prosthetic valves or prosthetic intravascular or intracardiac
72
Q

What is the standard abx regimen for most dental and respiratory procedures?

A

Amoxicillin 2g given 30-60min before procedure.

==> Alternatives for penicillin-allergic pts include cephalexin, azithromycin, clarithromycin, clindamycin.

73
Q

What is the group of pts in which bioprosthetic valves deteriorate more rapidly?

(3)

A
  1. Young pts.
  2. Those w/ kidney disease.
  3. Those on CS.
74
Q

What are the indications to consider biologic valves rather than the more durable mechanical prostheses?

A
  1. Plans for future pregnancy—and anticoagulants undesirable.
  2. Anticoagulation is undesirable or risky.
  3. Pts are >60y — bioprosthesis should last long enough.
  4. In setting of high endocarditis risk because they are less likely to require removal in event of recurrent endocarditis.
75
Q

What are the 3 main findings in prosthetic malfunction?

A
  1. Produces the same murmurs as in native valves — exception is paraprosthetic MR, which can be silent.
  2. Consider in a pt w/ hemolysis.
  3. TEE often required for confirmation and assessing severity.
76
Q

What is important to keep in mind when considering interrupting anticoagulants?

A
  1. Relatively safe in pts w/ aortic prostheses.
  2. Should generally use heparin (or LMW heparin) for bridging pts w/ mitral, tricuspid, or pulmonary prostheses.

==> Heparin bridging is needed for older, more thrombogenic valves (eg ball-in-cage).

77
Q

What are the effects of Valsalva (during continuous strain) on the valvular murmurs?

A

ALL DECREASE.

EXCEPT ==> HCM (increase).

+ MVP ==> Moves click and murmur onset closer to S1.

78
Q

What are the effects of amyl nitrite on the valvular murmurs?

A

AS + HCM + MS ==> Increase.

Chronic AR + MR ==> Decrease.

MVP ==> Moves click and murmur onset closer to S1.

79
Q

What are the effects of handgrip on the valvular murmurs?

A

Chronic AR + chronic MR + MS ==> Increase.

AS + HCM ==> Decrease.

MVP ==> Moves click and murmur onset closer to S2.

80
Q

What are the effects of squatting on the valvular murmurs?

A

Chronic AR + Chronic MR + MS + AS ==> Increase.

HCM ==> Decrease.

MVP ==> Moves click and murmur onset closer to S2.

Internal Medicine (106 decks)

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