Valvular Heart Disease: Overview, Stenosis, Pathology Flashcards
What kind of load does a stenosis put on the heart?
pressure
What kind of load does regurgitation put on the heart?
volume
What does stenosis do to pressure load?
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
What does regurgitation do to volume load?
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
What’s the difference between aortic and mitral regurg?
aortic increases wall stress during diastole and systole whereas mitral regurgitation increases diastolic wall stress only
What is the consequence of reduced orifice size in valve stenosis?
need to achieve higher flow velocity to achieve physiologic flow rate –> requires higher pressure gradient –> higher pressure load on upstream chamber
How is the pressure gradient related to the velocity through a valve?
Bernoulli –> pressure is proportional to velocity^2
How does the flow rate change as x-sectional area decreases?
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
How does the flow velocity change as x-sectional area decreases?
it increases linearly as per continuity of flow equation
How is flow rate related to CO and time available for flow?
linear and inversely –> the more CO, the higher the flow rate; the less time, the higher the flow rate
What is the implication of the Gorlin Valve Area equation?
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
Why do we need to measure CO when determining severity of stenosis?
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
What is the heart’s adaptive response to aortic stenosis and how is that response limited?
concentric left ventricular hypertrophy
- limits diastolic compliance/need higher filling pressure
- coronary circulation and CAD limit hypertrophy
- fibrosis degrades myocardial performance
- progression of stenosis severity
How do we get angina pectoris in AS?
increased wall thickness negatively affects perfusion leading to chest pain
How do we get syncope/presyncope in AS?
inadequate CO response to exercise can lead to hypotension/ischemia which can provoke further arrhythmia
How do we get CHF in AS?
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
T/F if a pt is asymptomatic but has AS, their compensatory mechanisms are working
T –> stuff is probably working ok but has reduced exercise capacity
If you have symptomatic AS what should you do?
get a valve replacement asap
What is a “sinking aortic”?
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)
What happens to flow velocity in mitral stenosis?
greater and more sustained diastolic flow velocity with turbulence (vs. slower and uniform flow velocity with decrease in velocity by mid diastole)
How does the LA-LV pressure gradient in MS compare to the LV-Ao pressure gradient in AS?
it is smaller in quantity but still substantial –> attenuated y descent
What is the interaction between MS and heart rate?
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
How does the heart cope with MS?
it can’t
What are the consequences of MS?
- 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
- dilation of LA limits contractility and reduces LV preload
- 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)
- chronic atrial dilation leading to chronic atrial fibrillation –> reduces heart rate regulation
- left atrial enlargement
- sluggish flow –> thrombosis/emboli
How do we deal with sluggish flow in MS?
warfarin once a-fib develops –> thrombus risk from slow flow
Why do mild MS become symptomatic vs mild AS?
don’t have adaptive mechanisms however don’t deteriorate as fast as symptomatic AS (which occurs upon decompensation) –> gradual over years
3 layers of valve leaflets
- fibrosa (back/outflow surface of valve continuous with annulus fibrosis)
- spongiosa (centrally located and comprised of loose connective tissue)
- ventricularis (closest to inflow surface and rich in elastic fibers)
Vascularization of a valve leaflet suggests…
marker of prior inflammation
Aortic stenosis is most often due to
degenerative/dystrophic calcification of a normal or bicuspid valve –> wear and tear/senile
Mitral stenosis is most often due to
chronic rheumatic heart disease
Aortic regurgitation is most often due to
to dilation of the aortic root as a function of old age, atherosclerosis and hypertension
Mitral regurgitation is most often due to
myxomatous degeneration, dilation of mitral valve ring w/ LV dilation due to LV failure
How does dystrophic calcification of valve leaflets occur?
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
Is dystrophic calcification a type of atherosclerosis?
no –> not related to lipid profile
Calcification of the aortic valve leaflets is
most often associated with
aortic stenosis
calcification of the mitral valve annulus can be associated with
mitral regurgitation
Where does calcium get deposited on a leaflet and why is this important?
middle of leaflet protruding into sinuses of valsalva on outflow side –> limits leaflets’ ability to open –> stenosis
Is there fusion of leaflet commissures in dystrophic calcification?
no –> distinguishes this from rheumatic valvular disease
When does aortic valve calcification tend to become symptomatic?
eighth to ninth decade
T/F congenitally deformed aortic valves develop symptomatic calcifications earlier
T –> more turbulence
When do bicupsid aortic valves (abnormal) calcifications tend to become symptomatic?
5th to 6th decade –> unequal w/ or w/o raphe on larger
When do unicuspid aortic valves (abnormal) calcifications tend to become symptomatic?
2nd to 4th decade
Where does calcification take place in the mitral valve?
in the valve ring/annulus vs. the leaflets in Ao valve stenosis
Who gets mitral dystrophic calcification?
elderly women w/chronically increased LV pressures or myxomatous degeneration –> usually asymptomatic but can cause regurg, rarely erodes into conduction system
What is acute rheumatic fever?
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
what is the pathology of chronic rheumatic heart disease CRHD?
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
_________is the pathologic hallmark of CRHD
Commissural fusion
Which valves are affected by CRHD?
most often the mitral valve (65-70%),
sometimes with the aortic valve as well (25%), and less commonly the right sided valves.
Pure MS results in
left atrial dilation, atrial fibrillation, atrial thrombus, and possible arterial embolization
MS + MR results in
left atrial dilation, atrial fibrillation, atrial thrombus, and possible arterial embolization PLUS left ventricular hypertrophy
What risk is associated with scarred valves
infection
Most common cause of aortic regurg
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
What kind of hypertrophy results from aortic regurg?
eccentric hypertrophy of LV
Myxomatous degeneration of the mitral valve (and less often other cardiac valves) is characterized
by
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
Is myxomatous degeneration of mitral valve symptomatic?
not commonly
- asymptomatic systolic click
- thrombus formation and endocarditis
- dysrhythmia leading to syncope/sudden death
- mitral regurg and late systolic murmur
What underlying hereditary connective tissue defect may be associated with myxomatous degeneration?
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.
Acute pulmonary effects of LAP increase
venous congestion, stiff lung, interstitial/alveolar edema resulting in SOB
Chronic pulmonary effects of LAP increase
- fibrosis of pulmonary veins and hemosiderin deposition in the lungs from leakage of red blood cells as part of chronic passive congestion
- intimal fibroelastic hyperplasia and medial muscular hypertrophy –> fixed elevation of PVR and permanent increase in pulmonary artery pressure
- right ventricular hypertrophy and right heart
failure - Atherosclerotic lesions in larger pulmonary arteries
T/F All cases of infectious endocarditis are caused by bacteria
F –> most but other microorganisms can also be responsible, such as fungi, rickettsiae (Q fever), chlamydia, or viruses.
What is the pathogenesis of bacterial endocarditis?
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
What causes acute bacterial endocarditis and how does it present?
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
What causes subacute bacterial endocarditis and how does it present?
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
Tx of subacute bacterial endocarditis
iv abs –> curable
Tx of acute bacterial endocarditis
surgery + antibiotics –> 50% mortality
What is non-bacterial thrombotic endocarditis?
NBTE occurs in pts w/o bacterial infection but with endocardial injury due to turbulent blood flow + hypercoagulable state –> can facilitate secondary bacterial infection
What is the pathogenesis of bacterial endocarditis?
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
What causes acute bacterial endocarditis and how does it present?
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
What causes subacute bacterial endocarditis and how does it present?
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
Which organisms associated with endocarditis: IV drug users
Right sided, especially! –> staph aureus, candida, aspergillus
Tx of acute bacterial endocarditis
surgery + antibiotics –> 50% mortality
What is non-bacterial thrombotic endocarditis?
NBTE occurs in pts w/o bacterial infection but with endocardial injury due to turbulent blood flow + hypercoagulable state –> can facilitate secondary bacterial infection
Which organisms associated with endocarditis: normal valves
staph aureus, gram -‘s
Which organisms associated with endocarditis: abnormal valves
strep viridans
Which organisms associated with endocarditis: prosthetic valves
staph epidermidis, staph aureus, strep
Which organisms associated with endocarditis: IV drug users
staph aureus, candida, aspergillus
Which hypercoagulable states predispose to NBTE?
low grade DIC, mucin producing adenocarcinomas, sepsis, burns
