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Cardio > Valvular Disease > Flashcards

Valvular Disease Flashcards

1
Q

Which are the semilunar valves?

A

aortic, pulmonic

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2
Q

Which are the atrioventricular valves?

A

mitral, tricuspid

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3
Q

What are the characteristics of the semilunar valves?

A

Simple pocket-like structure, supported by circular fibrous ring (annulus)

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4
Q

What are the characteristics of the atrioventricular valves?

A

Leaflets, Subvalvular apparatus (Chordae tendinae, papillary muscles), Annulus is non-circular, non-planar
(mitral annulus is “saddle-shaped”)

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5
Q

What are the 2 kinds of regurgitant lesions?

A
  1. Acute with fulminant, life-threatening symptoms;

2. Chronic with gradually progressive symptoms and long latent period

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6
Q

What is aortic stenosis?

A

Inability of the aortic valve to open appropriately; can be due to:

  1. Thickening and calcification of leaflets
  2. Fusion of commisures
  3. Intrinsically narrowed orifice (congenital)
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7
Q

What happens in aortic stenosis?

A

When opening is decreased by more than 50%, then it becomes flow-limiting; A pressure gradient develops across the valve; Significant elevation of LV systolic pressure may be necessary to drive blood forward into the aorta

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8
Q

What are the etiologies of aortic stenosis?

A

Acquired: Calcific (age-related degenerative change), Rheumatic Heart Disease;
Congenital: Bicuspid (1-2% population), Unicuspid - May be severe at birth
Typically occurs in elderly patients (70-80s or 50s-60s if patient has bicuspid valve)

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9
Q

What does the pressure tracing for aortic stenosis look like?

A

pressure in the aorta is less than in the LV; 
delayed rise in the pressure in the aorta


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10
Q

What is the Laplace relationship? How is it used?

A

Wall thickness (as in concentric LVH): wall stress = (Pressure x radius)/(2 x thickness)

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11
Q

What is compensation in aortic stenosis?

A

Increased pressure (afterload) leads to increased wall thickness (concentric hypertrophy); increases LV pressure generation; normalizes wall stress

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12
Q

What is decompensation in aortic stenosis?

A

Occurs after compensation; Hypertrophy causes decreased LV compliance; Inadequate hypertrophy and afterload mismatch (inotropic state inadequate); Eventual irreversible decreased contractility

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13
Q

What are the cardinal symptoms of aortic stenosis?

A

Angina (chest pain), Syncope (loss of consciousness), Dyspnea (shortness of breath), Congestive heart failure

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14
Q

Why does angina occur in aortic stenosis?

A

Increased myocardial oxygen demand; increased muscle mass, increased afterload (wall stress); Decreased myocardial oxygen supply; Coronary perfusion pressure decreases (= Aortic diastolic pressure – increased LV diastolic pressure); Angina may therefore occur despite normal epicardial coronary arteries

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15
Q

Why does syncope occur in aortic stenosis?

A

CO = HR x SV;
Severe AS and exercise:
Decreased MAP = CO (small increase) x total peripheral resistance (decreased); Elevated LVP leads to LV baroreceptors and decreases total peripheral resistance; Less increase in CO due to inability to augment SV across stenotic valve

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16
Q

Why does dyspnea occur in aortic stenosis?

A

Hypertropy causes Decreased LV compliance, increased LVDP, increased pulmonary venous pressure; Decreased LV contractility and afterload mismatch (inotropic state is inadequate for afterload): Increased LV EDP, increased LV ESV, increased LV EDV; Pulmonary alveolar congestion and heart failure sx

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17
Q

What are the physical exam findings in aortic stenosis?

A

Carotid upstroke delayed and reduced in amplitude (pulsus parvus et tardus), Sustained LV apical impulse (S4), Harsh systolic ejection murmur R 2nd intercostal space, Reduced A2, Paradoxical (reversed) splitting of S2

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18
Q

What are signs of severe aortic stenosis?

A

jet velocity of 4.0+ m/s; mean gradient of 40+ mmHg; aortic valve area of less than 1.0 cm2 (normally 3-4); aortic valve index of less than 0.6

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19
Q

How can aortic stenosis be treated?

A

“Mechanical problems require
mechanical solutions” - No medical therapy effective in delaying progression or altering outcome of AS; Surgical Aortic Valve Replacement; Transcatheter therapies: Balloon Aortic Valvuloplasty, Transcatheter Aortic Valve Replacement

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20
Q

What is the problem with valve replacements?

A

They often require lifelong anticoagulants

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21
Q

What is aortic regurgitation?

A

Leaking of the aortic valve due to:

  1. Primary abnormality of aortic valve leaflets OR
  2. Dilatation of aortic root
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22
Q

What is the primary difference between acute and chronic aortic regurgitation?

A

Pressure is much higher in acute b/c there is time to adjust in chronic

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23
Q

What is the pathophysiology of acute aortic regurgitation?

A

Normal LV size and compliance; LV diastolic pressure rises rapidly due to filling of LV from the aorta as well as LA; Limited increase in EDV and SV and therefore CO; Rapid rise of LV diastolic pressure closes MV in diastole and further limits forward flow; Fulminant pulmonary congestion and decreased CO can lead to death.

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24
Q

What is the pathophysiology of chronic aortic regurgitation?

A

Compensatory adaptation of the LV to longstanding, gradually progressive AR; normal CO and LVDP allow chronic AR to be asymptomatic; Eccentric LVH (Increased LV chamber size) alters the LV pressure – volume relationship; Increased compliance allows accommodation of large regurgitant volume without significant increase in diastolic pressure; CO is maintained because eccentric hypertrophy -> increased SV; Widened pulse pressure is hallmark of chronic AI; High stroke volume leads to increase aortic systolic BP; Large regurgitant volume leads to decrease diastolic BP; Chronic remodeling eventually leads to LV failure; Pressure load: Increased SV leads to increased SBP; Volume load: Regurgitant Vol leads to Increased LVEDV

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25
Q

How does chronic aortic regurgitation affect the pressure-volume curve?

A

down and to the right - more volume = less pressure

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26
Q

How do you calculate cardiac output in aortic regurgitation?

A

CO = SV (1-RF) x HR

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27
Q

What are the symptoms of chronic aortic regurgitation?

A

Dyspnea (increased pulmonary venous pressure), Fatigue and decreased exercise tolerance (LV failure and decreased CO), Angina - rare (Increased demand due to increased afterload, decreased supply due to decreased coronary perfusion pressure (CPP = Ao diastolic pressure – LVDP))

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28
Q

What are the physical exam findings in acute aortic regurgitation?

A

Sudden shock, respiratory failure

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29
Q

What are the physical exam findings in chronic aortic regurgitation?

A

Wide pulse pressure - Multiple eponymous signs; Blowing, decrescendo diastolic murmur LLSB; Low frequency diastolic rumble (Austin Flint); Displaced, hyperdynamic LV impulse

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30
Q

What is the murmur of aortic regurgitation?

A

diastolic, decrescendo

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31
Q

What are the metrics for regurgitation?

A

regurgitant volume, regurgitant fraction, effective regurgitant orifice

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32
Q

What is regurgitant volume?

A

volume of retrograde flow across valve

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33
Q

What is regurgitant fraction?

A

regurgitant volume/total stroke volume

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34
Q

What is effective regurgitant orifice?

A

a measure of the size of the opening through which regurgitation occurs

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35
Q

What are measures of severe aortic regurgitation?

A

Regurgitant volume of 60+ cc, regurgitant fraction of 50+%, effective regurgitant orifice of 0.30+ cm2

36
Q

What causes chronic aortic regurgitation?

A

Low risk until symptoms or decreased LVEF; Symptom onset or decline LVEF leads to progression to death or irreversible LV dysfunction over 1-5 years

37
Q

What causes acute aortic regurgitation?

A

Pulmonary congestion, low cardiac output, death (over hours to days)

38
Q

How can aortic regurgitation be treated?

A

“Mechanical problems require mechanical solutions”; Surgical Aortic Valve Replacement; Afterload reduction may improve symptoms, but does not delay progression (May be useful in setting of concomitant HTN)

39
Q

What causes aortic dissection?

A

Hypertension, Connective tissue disorders - Marfan’s: 1 in 5000

40
Q

What are the parts of the mitral valve?

A

1) Valvular leaflets
2) Annulus
3) Chordae tendinae
4) Papillary muscles
5) Left ventricular wall

41
Q

What are the chordae tendinae?

A

Responsible for the end-systolic position of the leaflets; Arise from the papillary muscles and are classified by their site of insertion on the leaflets: Marginal chordae (primary chordae), Intermediate chordae (secondary chordae), Basal chordae (tertiary chordae)

42
Q

What are the papillary muscles?

A

Provide chordae to both leaflets, generate tension by contracting in systole; Two papillary muscles – arise between the apical and middle thirds of the LV wall:

  1. antero-lateral papillary muscle: one body or head with dual blood supply from LAD and Diag or OM branch of the LCx
  2. postero-medial papillary muscle usually with two bodies or heads with single blood supply from either LCx or RCA; Because of its single blood supply, this papillary muscle is prone to ischemic injury
43
Q

What is mitral stenosis?

A

The mitral valve does not open appropriately

44
Q

What are the etiologies of mitral stenosis?

A

Rheumatic Heart Dz; Congenital causes; Mitral annular calcification; Endocarditis; (left atrial myxoma,
thrombus)

45
Q

What are the mechanisms of mitral stenosis?

A

Commissures fuse; Leaflet thickening (± calcification) and immobilization; Chord thickening and shortening; Annular calcification extension; Mass obstructs inlet

46
Q

What is the pathophysiology of mitral stenosis?

A

Abnormal diastolic pressure gradient across the stenotic mitral valve (between LA and LV); High left atrial pressure needed to maintain flow across the valve; Increased LA pressure leads to increased PCWP, causing pulmonary alveolar edema; Left atrial pressure / volume overload leads to atrial dilitation and predisposes to atrial fibrillation; Left ventricle generally normal

47
Q

What are the 2 kinds of pulmonary hypertension?

A
  1. Passive: backward transmission of elevated LA pressure into pulmonary vasculature
  2. Reactive: Chronic increase PAP causes pulmonary arteriolar constriction (increased PVR), leading reactive medial hypertrophy and intimal fibrosis, further increasing PVR and PAP
48
Q

What are the symptoms of mitral stenosis?

A

Dyspnea and exercise intolerance; Exercise leads to increased flow and increased HR (reduced diastolic filling time), causing increased gradient; Increased LAP = Increased PCWP and pulmonary alveolar edema; hemoptysis; JVD, edema, ascites, hepatic congestion (RV failure); Atrial fibrillation occurs frequently and can tip the balance (pulmonary edema) and is associated with embolic events

49
Q

How do symptoms present in mitral stenosis?

A

Gradual, initially only with exertion (increased CO, HR); Rapid onset or abrupt worsening due to: Atrial Fibrillation, Fever/infection, Hyperthyroidism, Pregnancy, Anemia (increased CO, HR)

50
Q

How does mitral stenosis present on physical exam?

A

Increased S1 due to high pressure in LA forcing leaflets widely open even in end diastole (may disappear as leaflets become immobile); Opening snap in early diastole; Diastolic rumble with presystolic accentuation; Timing of opening snap (earlier) and duration of rumble (longer) reflect increased severity; Signs of pulmonary hypertension (e.g. RV heave, increased P2)

51
Q

What are indications that mitral stenosis is severe?

A

10+ mmHg mean gradient, less than 1.0 MVA, 50+ PASP mmHg

52
Q

What is the natural history of mitral stenosis?

A

Typically long latent period (decades) - May be interrupted by Afib, embolic events; 10-year survival of asymptomatic patient 80+%; 10-year survival after symptom onset about 50% (less than 3 years in the presence of severe PHTN)

53
Q

How is mitral stenosis treated?

A

Diuretics, Rate/rhythm control for AFib, Anticoagulation for Afib; Valvuloplasty - Balloon (catheter-based) if anatomy favorable, Commissurotomy (open surgical); Surgical mitral valve replacement

54
Q

What is mitral regurgitation?

A

The mitral valve leaks

55
Q

What are the 2 types of mitral regurgitation?

A
  1. Functional (dilation of ventricle and annulus) OR
  2. Structural (leaflets and chords): Degenerative (myxomatous [Barlow’s], fibroelastic deficiency), Endocarditis, Rheumatic heart disease, Rupture chords or papillary muscles
56
Q

What is the pathophysiology of mitral regurgitation?

A

During systole, a portion of the LV stroke volume is ejected backward into the low pressure left atrium; Consequence include: Elevated left atrial volume and pressure, Reduction of forward cardiac output, Volume stress on LV due to return of regurgitated volume to LA and LV in addition to normal pulmonary venous return

57
Q

What determines the severity of mitral regurgitation?

A

The size of the regurgitant orifice; The systolic pressure gradient between LV – LA; The systemic vascular resistance (opposes forward flow from LV); Compliance of the left atrium (changes with chronicity); Duration of regurgitation during each systole

58
Q

How do you distinguish acute and chronic regurgitation?

A

Acute: high LA pressure and pulmonary edema; chronic: dilated LA with less elevated pressure

59
Q

What happens in acute mitral regurgitation?

A

Regurgitation into normal size, noncompliant LA, causing marked increase in LA pressure and increased PCWP, which ultimately leads to acute pulmonary edema; Sudden increase in Pulmonary Venous Pressure also leads to acute pulmonary hypertension and RV failure

60
Q

Is mitral regurgitation cause for concern?

A

Acute MR is an emergency! It can lead to pulmonary edema, shock, and even death; if LV systolic function abnormal, such as after MI, severe MR is even more poorly tolerated; Indication for emergent surgical MVR

61
Q

What is the time-pressure gradient characterized by in mitral regurgitation?

A

Tall v wave (rise in systole)

62
Q

What is the pathophysiology of chronic MR?

A

LA enlargement allows accommodation of regurgitant volume without significant pressure elevation; LV dilates (eccentric hypertrophy), allowing accommodation of large regurgitant volume at normal LV diastolic pressure (i.e. shift of LV diastolic P-V relationship); Forward CO maintained by Frank-Starling mech; MR alters the usual measures of systolic function (EF, SV) - Greater than normal while myocardial contractility is maintained, May decrease to “normal” with abnormal contractility; When systolic function worsens, decrease in forward SV and CO and further increase in LVEDV and LA pressure

63
Q

What are the symptoms of chronic MR?

A

Fatigue and weakness on exertion (Low output state due to preferential ejection into low pressure LA – path of least resistance); Dyspnea (elevated LA pressure, PCWP); Atrial fibrillation (LA volume, pressure overload); late symptoms of right heart failure (elevated LA pressure transmitted back to PA)

64
Q

What are the findings of MR on physical exam?

A

Holosystolic murmur at apex, radiating to axilla (worsens with fist clench – afterload); Peripheral signs will vary with acuity and degree of compensation; With chronic severe MR, apex will be displaced and diffuse; S3 (audible and palpable)

65
Q

What is the murmur associated with MR?

A

holosystolic; In severe MR, may be decrescendo and in MVP, may be mid-late systolic

66
Q

How is mitral regurgitation severity determined?

A

regurgitant volume: 60+ cc; regurgitant fraction 50+%; effective regurgitant orifice: 0.40+

67
Q

How should mitral regurgitation be treated?

A

Diuretics; Afterload reduction - certainly in acute, chronic only if hypertensive; in structural MR: Mitral repair/replacement; in functional MR: treatment of underlying ventricular dysfunction; Role of valve replacement remains unclear

68
Q

What are the mechanical treatments for mitral valves?

A

Mechanical valves - durable, thrombogenic; Tissue valves - less durable, less thrombogenic; Repair with own tissue preferred; Percutaneous mitral repair also possible

69
Q

How does aortic stenosis change the pressure-volume loop?

A

shifts up (taller) and to the right - more volume and more pressure

70
Q

How does aortic regurgitation change the pressure-volume loop?

A

shifts to the right - more volume

71
Q

How does mitral stenosis affect pressure-volume loop?

A

shifts to the left - less volume

72
Q

How does mitral regurgitation affect pressure-volume loop?

A

Makes it bigger - more and less volume (less filling - normal systolic function, but inadequate volume from diastole)

73
Q

What can cause tricuspid regurgitation?

A
  1. Functional: results from RV dilitation to due pressure or volume overload (frequently PH);
  2. Endocarditis: typically Staphylococcus aureus in setting of intravenous drug abuse;
  3. Carcinoid syndrome: neuroendocrine tumor of small bowel, metastatic to liver releases serotonin metabolites that lead to formation of endocardial plaques right side of the heart
74
Q

What is acute rheumatic fever?

A

Immunologically mediated, following 1-6 weeks after pharyngitis with Group A Streptococcus in 3% of those infected; Antibodies against streptococcal M proteins cross-react with similar antigenic determinants in joints, heart, skin, CNS.

75
Q

How is acute rheumatic fever diagnosed?

A

Need 2+ of the following major manifestations:
1. Migratory polyarthritis in 75%
2. Carditis in 50%
3. Sydenham’s chorea in 10%(involuntary, rapid, purposeless movements – caudate)
4. Erythema marginatum of skin in 10% (brown/pink with pale center)
5. Subcutaneous nodules (0.5 – 2 cm; extensor surfaces, occur late)
OR 2 minor + 1 major manifestation (Arthralgia, fever, increased ESR or CRP)
ALSO need supportive evidence of streptococcal infection: ASO Ab, anti-DNAase B, positive throat culture

76
Q

What is the prognosis of rheumatic fever?

A

Excellent prognosis: 1% mortality - cardiac

77
Q

What kind of carditis can rheumatic fever cause?

A

Pancarditis
Pericarditis
Myocarditis (Aschoff body)
Endocarditis with sterile vegetations

78
Q

What does rheumatic carditis look like in path?

A

Aschoff body of acute rheumatic carditis: a cardiac granuloma - found in myocardium; Chronic rheumatic heart disease presents with fibrosis and fusion of mitral valve chordae tendineae

79
Q

What is chronic rheumatic heart disease?

A

Follows Acute Rheumatic Heart Disease by decades.
MV 65-70%
MV & AV 25%
Mitral stenosis, aortic stenosis.
Arrhythmias (Atrial fibrillation with left atrial enlargement).
Heart failure.
Predisposed to infective endocarditis.

80
Q

What might be seen in pathology of chronic rheumatic heart disease?

A

“Fishmouth” deformity of the mitral valve; Fusion thickening and shortening of MV chordae tendineae

81
Q

What is mitral valve prolapse?

A

Most are asymptomatic; bimodal distribution (women in 20s, men in 50s); causes mid-systolic click; Rarely: chest pain, dyspnea, fatigue, or psychiatric manifestations

82
Q

What are potential complications of mitral valve prolapse?

A 
~3% have complications:
Infective endocarditis
Mitral insufficiency
Thrombus formation with embolization
Arrhythmia/sudden death (unknown mechanism)
83
Q

What does mitral valve prolapse look like on pathology?

A

Myxomatous, prolapsing mitral valve (2 layers mixed together)

84
Q

What is Non-bacterial thrombotic endocarditis (NBTE)?

A

Small (1-5 mm) sterile masses of fibrin on lines of closure.; Hypercoagulable state: patients are often debilitated (“marantic” endocarditis) or may have malignancy (mucinous adenocarcinoma), renal failure, sepsis; May embolize to brain, kidney, heart; With bacteremia, may be converted to infectious endocarditis.

85
Q

What are potential complications of heart valve prostheses?

A

Mechanical: component failure; Bioprostheses: degeneration with calcification; Both: Paravalvular leak, endocarditis.; Thrombosis and tissue overgrowth are less common in bioprostheses than in mechanical valves.

86
Q

What are carcinoid tumors of the heart valves?

A

Serotonin and kallikrein are secreted by the tumor and are normally metabolized in the liver and inactivated in the lung; rare cause of valve disease

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