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Cardiology > Valvular Heart Disease: Overview, Stenosis, Pathology > Flashcards

Valvular Heart Disease: Overview, Stenosis, Pathology Flashcards

1
Q

What kind of load does a stenosis put on the heart?

A

pressure

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2
Q

What kind of load does regurgitation put on the heart?

A

volume

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3
Q

What does stenosis do to pressure load?

A

increases the pressure gradient across the valve –> requires increased pressure from upstream chamber, impairs ability to increase CO

*chronic disorder and the heart’s ability to cope is determined by the upstream chamber’s ability to increase pressure to compensate

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4
Q

What does regurgitation do to volume load?

A

backward flow of blood into upstream chamber –> increases volume load on both chambers, reduce ability to increase CO (but not as much as stenosis)

*acute/chronic and heart’s ability to cope is determined by volume capabilities of both affected chambers

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5
Q

What’s the difference between aortic and mitral regurg?

A

aortic increases wall stress during diastole and systole whereas mitral regurgitation increases diastolic wall stress only

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6
Q

What is the consequence of reduced orifice size in valve stenosis?

A

need to achieve higher flow velocity to achieve physiologic flow rate –> requires higher pressure gradient –> higher pressure load on upstream chamber

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7
Q

How is the pressure gradient related to the velocity through a valve?

A

Bernoulli –> pressure is proportional to velocity^2

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8
Q

How does the flow rate change as x-sectional area decreases?

A

it doesn’t –> fluid is incompressible –> flow rate is constant, flow velocity changes AKA same amount of fluid crosses over a smaller orifice but it has to go faster to ensure same volume/time is passing

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9
Q

How does the flow velocity change as x-sectional area decreases?

A

it increases linearly as per continuity of flow equation

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10
Q

How is flow rate related to CO and time available for flow?

A

linear and inversely –> the more CO, the higher the flow rate; the less time, the higher the flow rate

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11
Q

What is the implication of the Gorlin Valve Area equation?

A

x-sectional area of valve = F/sqrt (pressure difference) –> change in pressure = F^2/kA^2 –> smaller area = higher flow velocity and greater pressure gradient in stenosis

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12
Q

Why do we need to measure CO when determining severity of stenosis?

A

At low flow rates, even with a small orifice area, the valve pressure gradient may be deceptively small –> need to know how velocity changes to figure out how stenotic a valve is –> challenge CO

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13
Q

What is the heart’s adaptive response to aortic stenosis and how is that response limited?

A

concentric left ventricular hypertrophy

  1. limits diastolic compliance/need higher filling pressure
  2. coronary circulation and CAD limit hypertrophy
  3. fibrosis degrades myocardial performance
  4. progression of stenosis severity
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14
Q

How do we get angina pectoris in AS?

A

increased wall thickness negatively affects perfusion leading to chest pain

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15
Q

How do we get syncope/presyncope in AS?

A

inadequate CO response to exercise can lead to hypotension/ischemia which can provoke further arrhythmia

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16
Q

How do we get CHF in AS?

A

inadequacy of LV hypertrophy to normalize systolic wall stress leads to degradation of contractile performance (systolic HF) and diastolic compliance (diastolic HF) resulting in progression of obstruction severity

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17
Q

T/F if a pt is asymptomatic but has AS, their compensatory mechanisms are working

A

T –> stuff is probably working ok but has reduced exercise capacity

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18
Q

If you have symptomatic AS what should you do?

A

get a valve replacement asap

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19
Q

What is a “sinking aortic”?

A

someone with AS who is decompensating like heck –> progressing to cardiogenic shock (low pressure, low cardiac index, tanking pressure gradient b/c of low CO)

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20
Q

What happens to flow velocity in mitral stenosis?

A

greater and more sustained diastolic flow velocity with turbulence (vs. slower and uniform flow velocity with decrease in velocity by mid diastole)

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21
Q

How does the LA-LV pressure gradient in MS compare to the LV-Ao pressure gradient in AS?

A

it is smaller in quantity but still substantial –> attenuated y descent

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22
Q

What is the interaction between MS and heart rate?

A

mitral stenosis is adversely affected by heart rate –> velocity decay decreases as duration of diastole decreases –> makes pressure gradient worse –> progressive rise of left atrial pressure during short cardiac cycles

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23
Q

How does the heart cope with MS?

A

it can’t

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24
Q

What are the consequences of MS?

A
  1. LA pressure> 30 mmhg is poorly tolerated by pulm. capillaries –> venous htn w/ secondary artery htn (SOB, arteriolar constriction leading to destruction of alveoli AKA irreversible increase in PVR) –> right ventricular afterload excess –> rv dilation, tricuspid regurg and systemic venous htn
  2. dilation of LA limits contractility and reduces LV preload
  3. exercise increases heart rate and worsens the atrial state by reducing diastolic filling time and thereby increasing atrial pressures (b/c of slow decay of pressure)
  4. chronic atrial dilation leading to chronic atrial fibrillation –> reduces heart rate regulation
  5. left atrial enlargement
  6. sluggish flow –> thrombosis/emboli
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25
Q

How do we deal with sluggish flow in MS?

A

warfarin once a-fib develops –> thrombus risk from slow flow

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26
Q

Why do mild MS become symptomatic vs mild AS?

A

don’t have adaptive mechanisms however don’t deteriorate as fast as symptomatic AS (which occurs upon decompensation) –> gradual over years

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27
Q

3 layers of valve leaflets

A
  1. fibrosa (back/outflow surface of valve continuous with annulus fibrosis)
  2. spongiosa (centrally located and comprised of loose connective tissue)
  3. ventricularis (closest to inflow surface and rich in elastic fibers)
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28
Q

Vascularization of a valve leaflet suggests…

A

marker of prior inflammation

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29
Q

Aortic stenosis is most often due to

A

degenerative/dystrophic calcification of a normal or bicuspid valve –> wear and tear/senile

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30
Q

Mitral stenosis is most often due to

A

chronic rheumatic heart disease

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31
Q

Aortic regurgitation is most often due to

A

to dilation of the aortic root as a function of old age, atherosclerosis and hypertension

32
Q

Mitral regurgitation is most often due to

A

myxomatous degeneration, dilation of mitral valve ring w/ LV dilation due to LV failure

33
Q

How does dystrophic calcification of valve leaflets occur?

A

turbulent blood flow leads to wear and tear damage –> stromal cells undergo phenotypic change and deposit calcium and fibrosis during repair process

*turbulence is why it affects mitral and aortic valve more

34
Q

Is dystrophic calcification a type of atherosclerosis?

A

no –> not related to lipid profile

35
Q

Calcification of the aortic valve leaflets is

most often associated with

A

aortic stenosis

36
Q

calcification of the mitral valve annulus can be associated with

A

mitral regurgitation

37
Q

Where does calcium get deposited on a leaflet and why is this important?

A

middle of leaflet protruding into sinuses of valsalva on outflow side –> limits leaflets’ ability to open –> stenosis

38
Q

Is there fusion of leaflet commissures in dystrophic calcification?

A

no –> distinguishes this from rheumatic valvular disease

39
Q

When does aortic valve calcification tend to become symptomatic?

A

eighth to ninth decade

40
Q

T/F congenitally deformed aortic valves develop symptomatic calcifications earlier

A

T –> more turbulence

41
Q

When do bicupsid aortic valves (abnormal) calcifications tend to become symptomatic?

A

5th to 6th decade –> unequal w/ or w/o raphe on larger

42
Q

When do unicuspid aortic valves (abnormal) calcifications tend to become symptomatic?

A

2nd to 4th decade

43
Q

Where does calcification take place in the mitral valve?

A

in the valve ring/annulus vs. the leaflets in Ao valve stenosis

44
Q

Who gets mitral dystrophic calcification?

A

elderly women w/chronically increased LV pressures or myxomatous degeneration –> usually asymptomatic but can cause regurg, rarely erodes into conduction system

45
Q

What is acute rheumatic fever?

A

an acute, multisystem inflammatory disease
triggered by an abnormal immune reaction to pharyngitis caused by group A beta hemolytic Streptococcus –> can injure all layers of the heart and sequential episodes can become chronic rheumatic heart disease leading to injury to valves over years

46
Q

what is the pathology of chronic rheumatic heart disease CRHD?

A

fibrosis, thickening, and retraction of the valve leaflets, often with fusion of the commissures (the sites where the free edges of adjacent leaflets attach to the underlying chamber [or arterial] wall) w/also shortening, thickening and fusion of
chordae tendineae

47
Q

_________is the pathologic hallmark of CRHD

A

Commissural fusion

48
Q

Which valves are affected by CRHD?

A

most often the mitral valve (65-70%),

sometimes with the aortic valve as well (25%), and less commonly the right sided valves.

49
Q

Pure MS results in

A

left atrial dilation, atrial fibrillation, atrial thrombus, and possible arterial embolization

50
Q

MS + MR results in

A

left atrial dilation, atrial fibrillation, atrial thrombus, and possible arterial embolization PLUS left ventricular hypertrophy

51
Q

What risk is associated with scarred valves

A

infection

52
Q

Most common cause of aortic regurg

A

Dilation of aortic root is by far the most common cause (old age, medial degeneration, Marfan’s)

can also tear a leaflet in infectious endocarditis, retract a valve leaflet in CRHD, fixate valve leaflets in dystrophic calcification or CRHD

53
Q

What kind of hypertrophy results from aortic regurg?

A

eccentric hypertrophy of LV

54
Q

Myxomatous degeneration of the mitral valve (and less often other cardiac valves) is characterized
by

A

increased deposition of extracellular matrix material (mucopolysaccharides) in the spongiosa layer and
attenuation of the fibrosa layer, associated with elongation and thickening of the valve leaflets and, as well as elongation and thinning of chordae tendineae –> valve prolapse into atrium

*can be due to inherited disorder of structural proteins/increased deposition of ECM/stretching of cordae

55
Q

Is myxomatous degeneration of mitral valve symptomatic?

A

not commonly

  1. asymptomatic systolic click
  2. thrombus formation and endocarditis
  3. dysrhythmia leading to syncope/sudden death
  4. mitral regurg and late systolic murmur
56
Q

What underlying hereditary connective tissue defect may be associated with myxomatous degeneration?

A

Very similar changes occur in the cardiac valves of some patients with systemic defects in connective
tissue (e.g. patients with Marfan’s syndrome), suggesting that some, if not all, patients with myxomatous degeneration of valves may have an underlying hereditary connective tissue defect that predisposes to an abnormal tissue response to the hemodynamic stresses to which valves are normally subjected.

57
Q

Acute pulmonary effects of LAP increase

A

venous congestion, stiff lung, interstitial/alveolar edema resulting in SOB

58
Q

Chronic pulmonary effects of LAP increase

A
  1. fibrosis of pulmonary veins and hemosiderin deposition in the lungs from leakage of red blood cells as part of chronic passive congestion
  2. intimal fibroelastic hyperplasia and medial muscular hypertrophy –> fixed elevation of PVR and permanent increase in pulmonary artery pressure
  3. right ventricular hypertrophy and right heart
    failure
  4. Atherosclerotic lesions in larger pulmonary arteries
59
Q

T/F All cases of infectious endocarditis are caused by bacteria

A

F –> most but other microorganisms can also be responsible, such as fungi, rickettsiae (Q fever), chlamydia, or viruses.

60
Q

What is the pathogenesis of bacterial endocarditis?

A

combination of bacteremia and a preexisting deposit of fibrin on a valvular (or endocardial, endothelial or prosthetic) surface–> bacteria take refuge in the fibrin, proliferate, incite acute inflammation and progressive enlargement of the deposit–> invasion of the organism into underlying valve–> bacteria and/or their antigens are periodically shed–>immune complex formation (e.g. acute nercrotizing glomerulonephritis)–> injury at other remote sites

61
Q

What causes acute bacterial endocarditis and how does it present?

A

virulent bacteria (e.g. Staphylococcus aureus or
enteric gram negative bacteria), has a cataclysmic onset with high fever, chills, aggressive clinical
course (untreated leading to death within a few weeks), and can occur on previously normal
cardiac valves, as well as previously damaged valves

62
Q

What causes subacute bacterial endocarditis and how does it present?

A

less virulent bacteria (e.g. Streptococcus, especially viridans) with a more
subtle onset of symptoms with fever, malaise, weight loss, a clinical course leading to death in a
few months if untreated, and occurring on previously damaged, rather than normal, heart valves –> can be cured w/ IV abs

63
Q

Tx of subacute bacterial endocarditis

A

iv abs –> curable

64
Q

Tx of acute bacterial endocarditis

A

surgery + antibiotics –> 50% mortality

65
Q

What is non-bacterial thrombotic endocarditis?

A

NBTE occurs in pts w/o bacterial infection but with endocardial injury due to turbulent blood flow + hypercoagulable state –> can facilitate secondary bacterial infection

66
Q

What is the pathogenesis of bacterial endocarditis?

A

combination of bacteremia and a preexisting deposit of fibrin on a valvular (or endocardial, endothelial or prosthetic) surface–> bacteria take refuge in the fibrin, proliferate, incite acute inflammation and progressive enlargement of the deposit–> invasion of the organism into underlying valve–> bacteria and/or their antigens are periodically shed–>immune complex formation –> injury at other remote sites

67
Q

What causes acute bacterial endocarditis and how does it present?

A

virulent bacteria (e.g. Staphylococcus aureus or
enteric gram negative bacteria), has a cataclysmic onset with high fever, chills, aggressive clinical
course (untreated leading to death within a few weeks), and can occur on previously normal
cardiac valves, as well as previously damaged valves

68
Q

What causes subacute bacterial endocarditis and how does it present?

A

less virulent bacteria (e.g. Streptococcus, especially viridans) with a more
subtle onset of symptoms with fever, malaise, weight loss, a clinical course leading to death in a
few months if untreated, and occurring on previously damaged, rather than normal, heart valves –> can be cured w/ IV abs

69
Q

Which organisms associated with endocarditis: IV drug users

A

Right sided, especially! –> staph aureus, candida, aspergillus

70
Q

Tx of acute bacterial endocarditis

A

surgery + antibiotics –> 50% mortality

71
Q

What is non-bacterial thrombotic endocarditis?

A

NBTE occurs in pts w/o bacterial infection but with endocardial injury due to turbulent blood flow + hypercoagulable state –> can facilitate secondary bacterial infection

72
Q

Which organisms associated with endocarditis: normal valves

A

staph aureus, gram -‘s

73
Q

Which organisms associated with endocarditis: abnormal valves

A

strep viridans

74
Q

Which organisms associated with endocarditis: prosthetic valves

A

staph epidermidis, staph aureus, strep

75
Q

Which organisms associated with endocarditis: IV drug users

A

staph aureus, candida, aspergillus

76
Q

Which hypercoagulable states predispose to NBTE?

A

low grade DIC, mucin producing adenocarcinomas, sepsis, burns

Cardiology (41 decks)

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