Valvular Heart Disease Flashcards
what typically causes aortic stenosis? (actual issue, not etiology)
calcification of the leaflets impaired valve opening
endothelial dysfunction/ inflammation causes myofibroblasts to transform into osteoblasts, which deposit calcium
normal process of aging
when a young patient (<50) has aortic stenosis, what should you be thinking?
bicuspid aortic valve
calcification of aortic valve leaflets develops over time
when aortic stenosis is caused by rheumatic heart disease, what else will you definitely see?
mitral valve disease will also be present
how does aortic valve stenosis affect Wigger’s diagram?
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
describe why aortic stenosis could lead to atrial fibrillation
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
explain why aortic stenosis causes exertional dyspnea and syncope
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
explain why aortic stenosis can cause angina
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
what is pulsus parvus et tardus in aortic stenosis
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
what abnormal heart sounds/murmurs are heard with aortic stenosis? (5)
- when there is bicuspid valve - early systolic ejection click (sound of opening of bicuspid valve)
- calcified leaflets lower S2 intensity
- single S2 or paradoxical splitting of S2 due to prolonged aortic valve closure (prolonged LV systole to get all the blood through)
- S4: stiff LV
- harsh mid-systolic murmur (when aortic valve opens), loudest at R 2nd ICS, crescendo-decrescendo pattern follows pressure curve of aorta, radiates to neck
how does the murmur of aortic stenosis change as the stenosis worsens?
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!
what do the following combined findings indicate?
- early systolic ejection click
- single S2
- S4
- mid-systolic murmur with crescendo-decrescendo pattern
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)
why would a patient with aortic stenosis be told to stay hydrated and avoid strenuous exercise?
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
how would the Valsalva maneuver affect the murmur of aortic stenosis?
Valsalva maneuver lowers venous return to the heart
this would make the murmur softer because less blood is pushing through the stenotic aortic valve
how can infectious endocarditis cause aortic regurgitation?
bacterial attachment causes degradation of protein in valve and they fail
other primary causes: bicuspid aortic valve, calcification, myxomatous valve disease, rheumatic heart disease
explain why bicuspid aortic valve can be both a primary and secondary cause of aortic regurgitation
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)
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
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
what happens to the systolic and diastolic aortic pressure in aortic regurgitation? explain why this makes sense
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
how is coronary perfusion affected by aortic regurgitation?
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
what will a patient with aortic regurgitation feel if they lay on their left side?
“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
what will the pulse feel like of a patient with aortic regurgitation?
there are a few signs, but one is key
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
how will the position and size of the heart be affected by chronic aortic regurgitation?
LARGE heart (LV eccentric hypertrophy) with lateral displacement of PMI
what abnormal heart sounds/murmurs are heard with aortic regurgitation? (2)
- high frequency early diastolic murmur immediately at A2 (S2) with decrescendo pattern (aortic regurgitation)
- S3: increased LV volume
how will the murmur of aortic regurgitation change as the regurgitation gets worse?
high frequency early diastolic murmur immediately at A2 (S2) with decrescendo pattern
when it gets worse, the murmur lengths in time (more backflow occurring)
how would the handgrip maneuver affect the murmur of aortic regurgitation?
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
what is an Austin-flint murmur
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
what causes mitral valve stenosis
almost ALWAYS
RHEUMATIC HEART DISEASE
causes “fish mouth” deformity
rarely, systemic lupus erythematous
describe how patients with mitral valve stenosis (due to rheumatic heart disease) develop heart failure symptoms
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]
explain why atrial fibrillation worsens symptoms of mitral stenosis
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
what sounds does mitral stenosis make? (3)
- louder S1 intensity
- loud P2 due to high pulmonary vascular pressure (A2 should always be louder)
- 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
how do the heart sounds made by mitral valve stenosis change as the stenosis worsens? why does this happen?
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)
in what position should a patient be to best hear a mitral stenosis murmur?
low-pitched, rumbling diastolic murmur beginning after opening snap (of rigid leaflets)
heard best at the apex with patient in left lateral decubitus position
explain how mitral valve stenosis can lead to tricuspid regurgitation
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
why does it make sense that the murmur of mitral stenosis shows pre-systolic accentuation?
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
how should you pharmacologically manage asymptomatic patients with mitral valve stenosis?
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
how can acute MI cause acute development of primary mitral valve regurgitation?
what is the difference between primary and secondary mitral valve regurgitation?
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)
what is myxomatous degeneration, and how does it cause heart valve degeneration?
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
how is regurgitant fraction calculated when assessing the severity of mitral regurgitation?
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
what sounds does mitral regurgitation make? (3)
increased volume in LV:
1. S3
2. lateral displacement of PMI
- 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
S3 + high-pitched holosystolic murmur that radiates to the axilla =
mitral regurgitation
loud P2 + opening snap + low-pitched rumbling diastolic murmur heard best in left lateral decubitus position =
mitral stenosis
S3 + high frequency decrescendo diastolic murmur beginning immediately after A2 =
aortic regurgitation
early systolic ejection click + single S2 + S4 + harsh mid-systolic crescendo-decrescendo murmur that radiates to neck =
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
explain difference between a low pitched and high pitched murmur
low pitched murmur reflects LOW pressure gradient (ex: mitral stenosis)
high pitched murmur reflects HIGH pressure gradient (ex: mitral regurgitation)
which of the following maneuvers would increase the intensity of mitral regurgitation murmur?
a. inspiration
b. handgrip
c. squatting to standing
d. Valsalva
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
what is the cause of most tricuspid regurgitation?
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
what sound does tricuspid regurgitation make? (1)
where can it be heard?
blowing holosystolic murmur beginning with S1, heard best at lower left sternal border
intensity increases with inspiration (increases venous return to right heart)
mitral valve regurgitation vs prolapse
regurgitation = valve doesn’t fully close
prolapse = valve closes, but then a leaflet buckles and separates - usually at point of highest pressure difference
when do symptoms develop in patients with mitral valve prolapse?
most patients are asymptomatic
symptoms occur when mitral regurgitation develops, or due to cardiac arrhythmia
what sound does mitral valve prolapse make?
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
how would squatting affect the mid-systolic click of mitral prolapse?
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
if a patient had mitral valve prolapse + mitral regurgitation, what kind of murmur would you hear?
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
mid systolic click immediately followed by high-pitched late-systolic murmur =
mitral valve prolapse (click) + regurgitation (murmur)
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
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
