Question about the heart

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sambo

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Can anyone explain to me the difference between aortic insufficiency and aortic stenosis? What would you see w/ each regarding cardiac output, stroke volume, etc.

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In the simplest of terms (caveat: my understanding):

Aortic stenosis is narrowing of the aortic valve that is caused by a failure of the valve leaflets to open properly. The reduction in aortic valve orfice area produces an energy loss because there is a result of turbulent flow. The turbulent flow causes the left ventricle to work harder in order to push blood past the narrowed aortic valve.

Aortic insuffiency is an overall similar end product (left ventricle working harder to push blood past the aortic valve), however the means to the end vary. For example, congenitally malformed aortic valves, connective tissue diseases, infective endocarditis, or aortic stenosis, may lead to aortic insuffiency.
 
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Originally posted by ItsGavinC
Aortic insuffiency is an overall similar end product (left ventricle working harder to push blood past the aortic valve), however the means to the end vary. For example, congenitally malformed aortic valves, connective tissue diseases, infective endocarditis, or aortic stenosis, may lead to aortic insuffiency.


Actually, aortic insufficiency is characterized by incomplete leaflet closing of the aortic valve, leading to regurgitation of blood into the LV during diastole (producing a diastolic murmur). I don't think the LV has to push harder, except for the possibility of a slightly increased preload to due blood leaking back through the valve, but that's gotta be minor.

Did we just do someone's PBL assignment for them? I feel used, and not in a good way. :p

HamOn
 
Here's the real deal between the two....


Aortic stenosis AS: most commonly results from calcific degeneration of the aortic valve (presents 60-70s); can also result from premature degeneration of congenitally bicuspid aortic valve (presents 40-50s). The pathology is remarkable for concentric hypertrophy w/o dilation since there is a pressure overload in the left ventricle. Clinically, presents w/ a sustained PMI, pulsus parvus et tardus, diamond shaped systolic murmur. You'll see LVH on ekg, and hypertrophy on CXR. In terms of CO, CO is ALWAYS maintained at the requisite 5L/min until end stage disease. In any case, SV will be uniformly decreased in aortic stenosis as a result of obstruction to outflow. The net result will be an increase in HR. Remember, CO = HR x SV. LVP will be markedly elevated. Normally during systole, the LVP is only 3-4mm greater than aortic pressure. However, in AS, the LVP can be up to 50-60 mm greater than aortic pressure.

Aortic insufficiency AI: the causes are many but is most commonly due to ascending disease of the aorta (Marfans, syphlitic aortitis, etc), followed by trauma, endocarditis. In any case, the net result is regurgitation of blood flow into the LV during diastole. The pathology is remarkable for hypertrophy w/ dilation since there is a volume overload in the left ventricle. Clinically, presents with a sustained and laterally displaced PMI, rapid carotid upstroke, wedge shaped diastolic murmur. You'll see LVH on EKG, and hypertrophy on CXR. You also have a wide pulse pressure as well (something like 150/40 would not be uncommon). In terms of CO, again, it's always maintained at the requisite 5L/min until end stage disease. In terms of SV, it's markedly increased because there's so much regurgitation back into the LV during diastole. This is the whole reason why the LV dilates, so it can accomodate more blood during diastole, and therefore pump out more blood since a large portion will ultimately regurgitate back in. Anyhow, that's all i can think of off the top of my head. hope you're not using this to copy for your homework assignment.
 
Babinski Bob took the words out of my mouth...although a calcified normal aortic valve usually doesn't cause clinical significance until the 70s-80s.

Rheumatic fever can also cause aortic stenosis, usually in combination with mitral valve pathology however.

Mossjoh
 
Can anyone explain to me the difference between aortic insufficiency and aortic stenosis? What would you see w/ each regarding cardiac output, stroke volume, etc



The big diffrence is that aortic stenosis leads to pressure overload of the left ventricle that leads to concentric hypertrophy. Aortic insufficiency is a volume overload that leads to eccentric hypertrophy. Basically concentric is a thicking of the wall and eccentric is a stretching of the wall. CO will be decreased with stenosis and acutally be higher in early aortic insufficiency due to starlings law of preload vs stroke volume. However once the left ventricle becomes to stetched do to eccentric hypertrophy it will start to lose its ability to pump all of the blood and begin to fail.
 
Way too complicated, guys.


Stenotic=narrowed

Insufficient=leaky

Now I think you can logically see what will happen.
 
Just to add another complication, people with clinically significant aortic stenosis always have some element of aortic regurgitation. The calcified valves cannot close all the way during diastole causing regurgitation.
 
Originally posted by sambo
Can anyone explain to me the difference between aortic insufficiency and aortic stenosis? What would you see w/ each regarding cardiac output, stroke volume, etc.

In the simplest terms, aortic stenosis is a narrowing or obstruction of the blood outflow. Insufficiency refers to a heart valve disease in which the aortic valve weakens or balloons, preventing the valve from closing tightly. This leads to backwards flow of blood (regurgitation) from the aorta into the left ventricle.

Hemodynamic alteration would depend on the degree of the disorder.
 
Originally posted by Mossjoh
Babinski Bob took the words out of my mouth...although a calcified normal aortic valve usually doesn't cause clinical significance until the 70s-80s.

Rheumatic fever can also cause aortic stenosis, usually in combination with mitral valve pathology however.

Mossjoh

RF can cause stenosis or insufficiency... clinically speaking the big difference is the murmur... stenosis presents with a diamondshaped, crescendo-decrescendo, systolic ejection murmor that stops BEFORE S2... to the OP: how would an insuf murmur sound?
 
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