Valvular Heart Disease Flashcards

1
Q

what typically causes aortic stenosis? (actual issue, not etiology)

A

calcification of the leaflets impaired valve opening

endothelial dysfunction/ inflammation causes myofibroblasts to transform into osteoblasts, which deposit calcium

normal process of aging

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2
Q

when a young patient (<50) has aortic stenosis, what should you be thinking?

A

bicuspid aortic valve

calcification of aortic valve leaflets develops over time

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3
Q

when aortic stenosis is caused by rheumatic heart disease, what else will you definitely see?

A

mitral valve disease will also be present

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4
Q

how does aortic valve stenosis affect Wigger’s diagram?

A

obstruction to LV outflow produces a systolic pressure gradient between LV and aorta - the arch of LV pressure far exceeds that of the aorta

increased afterload leads to concentric LV —> decreased compliance, SV declines, increased O2 demand

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5
Q

describe why aortic stenosis could lead to atrial fibrillation

A

high pressure on LV leads to concentric hypertrophy and eventually a stiff LV

this raises atrial pressure, as stiff ventricle requires atrial contraction for effective filling (whereas normally its contribution isn’t as important)

increased atrial pressure raises risk of atrial fibrillation

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6
Q

explain why aortic stenosis causes exertional dyspnea and syncope

A

increased pulmonary capillary pressure due to decreased ability of LV to handle increased volume of blood with exercise —> dyspnea

CO cannot increase during exercise —> syncope (fainting)

remember that aortic stenosis causes concentric hypertrophy of LV and it becomes stiff

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7
Q

explain why aortic stenosis can cause angina

A

aortic stenosis leads to higher LV pressure, LV becomes stiff over time

myocardial O2 demand is higher in LV because of hypertrophied muscle - increased LV systolic pressure decreases coronary perfusion pressures

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8
Q

what is pulsus parvus et tardus in aortic stenosis

A

pulsus parvus et tardus = weak and late pulse

refers to weakened and delayed upstroke of carotid pulse due to obstruction of LV outflow into aorta

smaller SV = weaker pulse

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9
Q

what abnormal heart sounds/murmurs are heard with aortic stenosis? (5)

A
  1. when there is bicuspid valve - early systolic ejection click (sound of opening of bicuspid valve)
  2. calcified leaflets lower S2 intensity
  3. single S2 or paradoxical splitting of S2 due to prolonged aortic valve closure (prolonged LV systole to get all the blood through)
  4. S4: stiff LV
  5. harsh mid-systolic murmur (when aortic valve opens), loudest at R 2nd ICS, crescendo-decrescendo pattern follows pressure curve of aorta, radiates to neck
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10
Q

how does the murmur of aortic stenosis change as the stenosis worsens?

A

crescendo-decrescendo pattern that follows aortic pressure curve

harsh mid-systolic murmur (when aortic valve opens), loudest at R 2nd ICS, radiates to the neck

as stenosis worsens, the peak of the murmur moves later in systole because the valve is getting harder to open!

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11
Q

what do the following combined findings indicate?
- early systolic ejection click
- single S2
- S4
- mid-systolic murmur with crescendo-decrescendo pattern

A

aortic stenosis due to bicuspid aortic valve

  • early systolic ejection click = calcified bicuspid valve opening
  • single S2 = delayed aortic valve closure due to prolonged LV systole
  • S4 = stiff LV
  • mid-systolic murmur with crescendo-decrescendo pattern = aortic stenosis (R 2nd ICS, radiates to neck)
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12
Q

why would a patient with aortic stenosis be told to stay hydrated and avoid strenuous exercise?

A

LV can’t eject blood as efficiently through calcified aortic valve

low volume of blood (via dehydration) will exacerbate lower CO

exercise will put stress on heart that LV can’t handle - may syncope, have dyspnea, etc

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13
Q

how would the Valsalva maneuver affect the murmur of aortic stenosis?

A

Valsalva maneuver lowers venous return to the heart

this would make the murmur softer because less blood is pushing through the stenotic aortic valve

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14
Q

how can infectious endocarditis cause aortic regurgitation?

A

bacterial attachment causes degradation of protein in valve and they fail

other primary causes: bicuspid aortic valve, calcification, myxomatous valve disease, rheumatic heart disease

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15
Q

explain why bicuspid aortic valve can be both a primary and secondary cause of aortic regurgitation

A

bicuspid aortic valve can calcify such that it never really closes (primary)

or bicuspid aortic valve can develop enlargement of the aortic root such that annulus has stretched (secondary)

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16
Q

describe what is similar in that pathology of how all of the following cause secondary aortic regurgitation:
- bicuspid aortic valve
- Marfan syndrome, Ehlers-Danlos, Osteogenesis imperfecta
- Syphilis
- aortic aneurysms

A

all of these pathologies can cause enlargement/dilation of the aortic root, leading to aortic regurgitation

Marfan/Ehlers-Danlos/Osteogenesis imperfecta: genetic mutations in structural proteins

syphilis: inflamed vaso vasorum don’t supply blood to wall of aorta and it dilates

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17
Q

what happens to the systolic and diastolic aortic pressure in aortic regurgitation? explain why this makes sense

A

aortic systolic pressure rises because regurgitation is cause some blood to go back into LV, which adds to the blood already there from the LA —> a larger amount of blood is ejected on systole, and systolic pressure is determined by SV

aortic diastolic pressure decreases because regurgitation is running blood back into LV, which is causing volume in arterial system to drop, and diastolic pressure is determined by volume in the arterial system

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18
Q

how is coronary perfusion affected by aortic regurgitation?

A

in aortic regurgitation, aortic diastolic pressure drops because diastolic pressure is determined by the amount of blood in the arterial system, and the aorta is dumping some of that blood back in the LV

therefore, there is decreased coronary perfusion - recall that coronary arteries fill during diastole

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19
Q

what will a patient with aortic regurgitation feel if they lay on their left side?

A

“uncomfortable awareness of their own heartbeat” due to large SV being ejected

regurgitation of blood in aorta back into LV is added to the blood volume already there from the atrium - this all gets ejected and SV is therefore large

worse when lying down because venous return to heart is greater - may have paroxysmal nocturnal dyspnea

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20
Q

what will the pulse feel like of a patient with aortic regurgitation?

there are a few signs, but one is key

A

regurgitation of blood in aorta back into LV is added to the blood volume already there from the atrium - this all gets ejected and SV is therefore large

WIDE pulse pressure due to higher SBP (higher SV) and lower DBP (lower aortic volume)

“water-hammer” pulse: very big pulse that goes away quickly, abrupt distention and quick collapse

pistol shot sounds: booming systolic and diastolic sounds over femoral artery

bisferiens pulse: double systolic impulse in carotid or brachial artery

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21
Q

how will the position and size of the heart be affected by chronic aortic regurgitation?

A

LARGE heart (LV eccentric hypertrophy) with lateral displacement of PMI

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22
Q

what abnormal heart sounds/murmurs are heard with aortic regurgitation? (2)

A
  1. high frequency early diastolic murmur immediately at A2 (S2) with decrescendo pattern (aortic regurgitation)
  2. S3: increased LV volume
23
Q

how will the murmur of aortic regurgitation change as the regurgitation gets worse?

A

high frequency early diastolic murmur immediately at A2 (S2) with decrescendo pattern

when it gets worse, the murmur lengths in time (more backflow occurring)

24
Q

how would the handgrip maneuver affect the murmur of aortic regurgitation?

A

high frequency early diastolic murmur immediately at A2 (S2) with decrescendo pattern

handgrip maneuver increases arterial pressure —> increased afterload

this puts more backwards pressure on regurgitation, and murmurs sounds louder

25
Q

what is an Austin-flint murmur

A

Austin-flint murmur: mitral valve obstruction secondary to aortic regurgitation

the aortic leaflet being pushed backwards (regurgitating) obstructs the opening of the mitral valve during diastole

26
Q

what causes mitral valve stenosis

A

almost ALWAYS
RHEUMATIC HEART DISEASE

causes “fish mouth” deformity

rarely, systemic lupus erythematous

27
Q

describe how patients with mitral valve stenosis (due to rheumatic heart disease) develop heart failure symptoms

A

mitral valve stenosis makes it take longer for LV to fill

tachycardia shortens filling time —> exertional dyspnea —> increased LA pressure —> increased pulmonary capillary pressure —> RIGHT ventricle pressure increase and symptoms of RIGHT heart failure

[LV is working fine, it’s just not filling as well]

28
Q

explain why atrial fibrillation worsens symptoms of mitral stenosis

A

if LV is filling more slowly due to mitral stenosis, atrial contraction is going to be really important in assisting with filling

if a-fib occurs, that assistance is lost —> acute decompensation (increased HR)

LA enlargement due to stenosis puts it at risk for A-fib! and this can lead to LA thrombus

29
Q

what sounds does mitral stenosis make? (3)

A
  1. louder S1 intensity
  2. loud P2 due to high pulmonary vascular pressure (A2 should always be louder)
  3. opening snap as rigid mitral valve leaflets opens, followed by low-pitch rumble diastolic murmur (heard best at apex in left lateral decubitus position

*interval between S2 and opening snap shortens as severity of stenosis increases

30
Q

how do the heart sounds made by mitral valve stenosis change as the stenosis worsens? why does this happen?

A

interval between S2 and opening snap shortens as severity of stenosis increases

as LA pressure rises (due to hypertrophy), it causes valve to open earlier (because it exceeds LV pressure sooner)

31
Q

in what position should a patient be to best hear a mitral stenosis murmur?

A

low-pitched, rumbling diastolic murmur beginning after opening snap (of rigid leaflets)

heard best at the apex with patient in left lateral decubitus position

32
Q

explain how mitral valve stenosis can lead to tricuspid regurgitation

A

mitral valve stenosis causes pressure to build in LA —> then pulmonary circulation —> then RV

fluid backup causes RV to dilate, which can cause tricuspid valve to stretch —> tricuspid regurgitation develops

33
Q

why does it make sense that the murmur of mitral stenosis shows pre-systolic accentuation?

A

reflects atrial contraction - the atrial “kick” that happens just before LV systole

*note if patient develops A-fib from high LA pressure, this accentuation will be absent!

recall murmur is low-pitched, rumbling diastolic murmur beginning after opening snap (of rigid leaflets), heard best at apex with patient in left lateral decubitus position

34
Q

how should you pharmacologically manage asymptomatic patients with mitral valve stenosis?

A

want to reduce heart rate - more time to LV to fill —> give beta blockers, calcium channel blockers

high LA pressure puts it at risk for LA thrombus —> give anticoagulation

35
Q

how can acute MI cause acute development of primary mitral valve regurgitation?

what is the difference between primary and secondary mitral valve regurgitation?

A

acute MI may cause papillary muscle to rupture —> this can cause mitral valve regurgitation/prolapse

primary = disease of valve structures (ex: Marfans, myxomatous degeneration)
secondary (“functional”) = enlargement of mitral annulus (ex: dilated cardiomyopathy)

36
Q

what is myxomatous degeneration, and how does it cause heart valve degeneration?

A

myxomatous degeneration = collagen in tissue fragments and is replaced by proteoglycan deposition

collagen provided strength, without it, valve breaks down —> elongation and stretching of leaflets and chordae tendineae

37
Q

how is regurgitant fraction calculated when assessing the severity of mitral regurgitation?

A

regurgitant fraction = regurgitation volume / total LV stroke volume

higher regurgitant fraction correlates with worse MR

heightened with increased afterload due to higher resistance to aortic outflow

38
Q

what sounds does mitral regurgitation make? (3)

A

increased volume in LV:
1. S3
2. lateral displacement of PMI

  1. high-pitched holosystolic murmur immediately after S1, continuing to/obscuring A2, heard best at apex and radiates to axilla

*when severe, there is a thrill

39
Q

S3 + high-pitched holosystolic murmur that radiates to the axilla =

A

mitral regurgitation

40
Q

loud P2 + opening snap + low-pitched rumbling diastolic murmur heard best in left lateral decubitus position =

A

mitral stenosis

41
Q

S3 + high frequency decrescendo diastolic murmur beginning immediately after A2 =

A

aortic regurgitation

42
Q

early systolic ejection click + single S2 + S4 + harsh mid-systolic crescendo-decrescendo murmur that radiates to neck =

A

aortic stenosis

*single S2 because delayed aortic valve closure causes A2/P2 to happen at the same time, and S2 intensity will also be lower

43
Q

explain difference between a low pitched and high pitched murmur

A

low pitched murmur reflects LOW pressure gradient (ex: mitral stenosis)

high pitched murmur reflects HIGH pressure gradient (ex: mitral regurgitation)

44
Q

which of the following maneuvers would increase the intensity of mitral regurgitation murmur?
a. inspiration
b. handgrip
c. squatting to standing
d. Valsalva

A

handgrip: increases afterload, pushing blood backwards into regurgitated valve

inspiration: increase venous return to R side of heart (R sided murmurs get louder on inspiration)
Valsalva: decreased venous return to heart, softer murmur
squatting to standing: decreases afterload and venous return, softer murmur

45
Q

what is the cause of most tricuspid regurgitation?

A

mostly due to functional/secondary regurgitation, due to right heart failure - will see sign/symptoms of RHF (JVD, hepatomegaly, ascites, lower extremity edema, etc)

primary causes (uncommon): infective endocarditis, carcinoid syndrome

46
Q

what sound does tricuspid regurgitation make? (1)

where can it be heard?

A

blowing holosystolic murmur beginning with S1, heard best at lower left sternal border

intensity increases with inspiration (increases venous return to right heart)

47
Q

mitral valve regurgitation vs prolapse

A

regurgitation = valve doesn’t fully close

prolapse = valve closes, but then a leaflet buckles and separates - usually at point of highest pressure difference

48
Q

when do symptoms develop in patients with mitral valve prolapse?

A

most patients are asymptomatic

symptoms occur when mitral regurgitation develops, or due to cardiac arrhythmia

49
Q

what sound does mitral valve prolapse make?

A

mid systolic ejection click - snapping of mitral chordae as valve leaflets bow into left atrium

timing varies with volume: higher volume = later click, lower volume = earlier click

less volume = earlier/lengthened murmur due to less tension on the leaflets

50
Q

how would squatting affect the mid-systolic click of mitral prolapse?

A

timing varies with volume: higher volume = later click, lower volume = earlier click

less volume = earlier/lengthened murmur due to less tension on the leaflets

therefore, squatting would increase volume in heart and click would be later/shorter

51
Q

if a patient had mitral valve prolapse + mitral regurgitation, what kind of murmur would you hear?

A

high-pitched late systolic murmur beginning immediately after click of prolapse

later than isolated regurgitation because prolapse occurs when pressure gradient is highest (mid-systole), and THEN regurgitation is occurring

heard best at apex

52
Q

mid systolic click immediately followed by high-pitched late-systolic murmur =

A

mitral valve prolapse (click) + regurgitation (murmur)

53
Q

which of the following would shorten the duration of a murmur caused by mitral valve prolapse?
a. decrease VL preload
b. increase LV contractility
c. increase LV afterload
d. increase HR
e. decrease LV volume

A

systolic click of mitral valve prolapse occurs later when there is MORE volume in the heart (more tension on leaflets), causing its duration to be shorter

c. increase LV afterload - this would increase volume in the heart