Rollo

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So my understanding is that the myocardium is hypertrophied while the ventricular volume decreases which results in low, inadequate ventricular filling. So why is the myocardium contracting harder to pump what seems to be a relatively low volume of blood?
 

MilkmanAl

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It has to push that small volume enough to make your blood circulate effectively. That's why heart hypertrophy is a vicious cycle.
 

Rollo

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Wouldn't it make sense for the myocardium to not work as hard to push a small volume of blood through? I'm trying to compare it to how skeletal muscle would work for example, if I were to lift a 5 lb weight vs. a 10 lb weight, my bicep muscles wouldn't work as hard to lift the 5 lb weight as it would to life the 10 lb weight.
 

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Hypertrophic cardiomyopathy is also known as Idiopathic Hypertrophic Subaortic Stenosis (IHSS).. has an increase in ventricular wall size which is larger than the incresaed size of the rest of the ventricular... this causes a subaortic stenosis (stenosis below the aortic valve)....so, it requires more work to pump blood.....hence, only a smaller amount leaves the ventricle.

This is why in IHSS manuvers that increase blood flow back to the ventricles and increase preload (laying down) actually REDUCE the work of the ventricle (reduces the stenosis)....because it expands the outflow tract allowing blood to leave through a larger area.

hopefully, this answered your question.
 

MilkmanAl

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That would dramatically decrease your blood flow. Your tissues still have the same oxygen demand, regardless of what your heart is doing, so it's going to have to get blood to them somehow. If it's pushing a smaller volume, that means pushing that volume harder to equalize the flow. Think of it Bernoulli-style: small volume x high flow rate=large volume x low flow rate.

After typing that, I realize it's not a very med student-friendly explanation. Let's try something else.

First off, it's important to totally do away with the bicep analogy. It's not the same at all. The best thing I can come up with that would force the comparison into making sense is imagining your arm getting longer as you lifted less weight, but...yeah, let's not go there. Scrap it entirely.

Like I said above, you're trying to keep blood flow (particularly to extremities) the same as it was pre-hypertrophic myopathy. Presumably, the patient's BP is going to be high, so the heart has to work harder to push blood and thus hypertrophies. The hypertrophy decreases the intraventricular volume. BP increases because that smaller amount of blood has to get pushed hard enough to move the deoxygenated blood through the capillary beds at a somewhat normal rate. The increase in BP leads to more hypertrophy, and the whole cycle keeps going. Along the way, you'll start having fun conditions like edema (peripheral and pulmonary), aneurysms, MI's, and all that stuff that comes with huge BP's and heart failure.
 

illixir

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Hypertrophic cardiomyopathies often have outflow tract obstruction which an above poster explained; that is a big reason for the increased work/contraction needed by the ventricle.
 

turkeyjerky

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That would dramatically decrease your blood flow. Your tissues still have the same oxygen demand, regardless of what your heart is doing, so it's going to have to get blood to them somehow. If it's pushing a smaller volume, that means pushing that volume harder to equalize the flow. Think of it Bernoulli-style: small volume x high flow rate=large volume x low flow rate.

After typing that, I realize it's not a very med student-friendly explanation. Let's try something else.

First off, it's important to totally do away with the bicep analogy. It's not the same at all. The best thing I can come up with that would force the comparison into making sense is imagining your arm getting longer as you lifted less weight, but...yeah, let's not go there. Scrap it entirely.

Like I said above, you're trying to keep blood flow (particularly to extremities) the same as it was pre-hypertrophic myopathy. Presumably, the patient's BP is going to be high, so the heart has to work harder to push blood and thus hypertrophies. The hypertrophy decreases the intraventricular volume. BP increases because that smaller amount of blood has to get pushed hard enough to move the deoxygenated blood through the capillary beds at a somewhat normal rate. The increase in BP leads to more hypertrophy, and the whole cycle keeps going. Along the way, you'll start having fun conditions like edema (peripheral and pulmonary), aneurysms, MI's, and all that stuff that comes with huge BP's and heart failure.
it sounds like you're describing hypertension-induced concentric hypertrophy more than hypertrophic cardiomyopathy (which, as we all know, is autosomal dominant with reduced penetrance and variable expressivity). A big component of HCM is the genetic defect that leads to irregular myofiber structure and ineffective contraction leading to fibrosis and a predisposition to arrhythmias.
 

Rollo

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Hypertrophic cardiomyopathy is also known as Idiopathic Hypertrophic Subaortic Stenosis (IHSS).. has an increase in ventricular wall size which is larger than the incresaed size of the rest of the ventricular... this causes a subaortic stenosis (stenosis below the aortic valve)....so, it requires more work to pump blood.....hence, only a smaller amount leaves the ventricle.

This is why in IHSS manuvers that increase blood flow back to the ventricles and increase preload (laying down) actually REDUCE the work of the ventricle (reduces the stenosis)....because it expands the outflow tract allowing blood to leave through a larger area.

hopefully, this answered your question.
Makes sense!!

One more dot that I'm not quite connecting yet is why increasing the preload will reduce the work of ventricles?
 

FutureDoc4

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The reason increased preload will decrease the "work" of the ventricle is that, the increase volume will "open up" the outflow tract.. making LESS resistance for the ventricle to pump blood (remember the stenosis is BELOW the valve, so any expansion in ventricular volume, will increase the radius of the out flow tract (decreasing resistance and therefore, decreasing work the ventricle has to do to pump blood).
 

Rollo

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So essentially, there is more blood volume available to ventricles. It's almost as if reduced ventricular volume was compensated for and now the EDV is somewhat back to its normal value?
 

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In hypertrophic cardiomyopathy, and probably a reason you see athletes succumb to this condition, compensation can only do so much. Never think of compensation as a short term fix (yes there are situations where you have short term compensations but overall compensation happens over a period of time). So basically increasing preload in an attempt to increase cardiac output works as you say: An increase in preload means higher venous return to the left heart and therefore more blood can be pumped from LA to LV to Aorta. In hypertrophic cardiomyopathy the potential space is smaller so no matter how much is compensated for, it would be hard to maintain a normal EDV. My understanding (correct me if I'm wrong) is that in this condition the sarcomeres of the myocardium add in parallel mimicking a pressure overload condition such as aortic stenosis. Therefore to compensate for all of this (the higher pressures, reduced potential space, reduced EDV and attempted increase in preload) the heart has to work that much harder to ensure that whatever volume is contained within actually makes it out into the aorta and then the systemic circulation.
 

Bacchus

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Slide 38 of the power point :).
 

cpants

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The only way to really understand HCM is to look at a diagram or animation of what the ventricals are doing. Basically the hypertrophy at the top the ventricle reduces the radius of the outflow tract making it more difficult to push the blood out of the ventricle. As the heart contracts the radius decreases further.
 

Rollo

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In hypertrophic cardiomyopathy, and probably a reason you see athletes succumb to this condition, compensation can only do so much. Never think of compensation as a short term fix (yes there are situations where you have short term compensations but overall compensation happens over a period of time). So basically increasing preload in an attempt to increase cardiac output works as you say: An increase in preload means higher venous return to the left heart and therefore more blood can be pumped from LA to LV to Aorta. In hypertrophic cardiomyopathy the potential space is smaller so no matter how much is compensated for, it would be hard to maintain a normal EDV. My understanding (correct me if I'm wrong) is that in this condition the sarcomeres of the myocardium add in parallel mimicking a pressure overload condition such as aortic stenosis. Therefore to compensate for all of this (the higher pressures, reduced potential space, reduced EDV and attempted increase in preload) the heart has to work that much harder to ensure that whatever volume is contained within actually makes it out into the aorta and then the systemic circulation.
Makes sense.

Thanks for the help everyone.
 

degoo_

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So my understanding is that the myocardium is hypertrophied while the ventricular volume decreases which results in low, inadequate ventricular filling. So why is the myocardium contracting harder to pump what seems to be a relatively low volume of blood?
Myocardium hypertrophies because it must work harder to eject the the blood past a stenosed left ventricular outflow tract (LVOT). The left ventricular outflow tract (essentially the aortic valve) is stenosed because focal septal hypertrophy has occurred in this region. Why does it occur at this region? Well, as someone said HCM is also known as idiopathic hypertrophic subaortic stenosis. There is evidence of mutations in genes encoding sarcomeric proteins (MHC, MYBPC3 etc), that lead to myocardial disorder which may precipitate this idiopathic hypertrophy... which can occur at many different ages. In fact, this hypertrophy can occur at different areas of the septum and ventricular walls as well, and there are many different kinds of HCM, LVOT affecting HCM (classic IHSS, HOCM), midventricular HCM, apical HCM, mixed...

As the myocardium hypertrophies, the amount of diastolic filling is reduced- both because of decrease in LV volume, and also impaired relaxation from a now stiffened LV. The heart still needs to pump hard to get this relatively reduced amount of blood out.

Medically increasing preload stretches the ventricles more, reducing the stenosis at the outflow tract by getting the hypertrophied myocardium out of the way. Surgically removing this tissue or ablating it interventionally are also used in later stage, when the hypertrophy at the LVOT is so great that even with increased filling it is still tough to eject blood.
 

NRAI2001

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Hypertrophic cardiomyopathies often have outflow tract obstruction which an above poster explained; that is a big reason for the increased work/contraction needed by the ventricle.
Thats exactly correct. HCM (hypertrophic cardiomyopathy) is considered a "Dynamic Obstruction to flow" --> bisferans pulse.