rsweeney said:
I am speaking of just the left ventricle. What the text implies [I believe] is that systolic dysfunction of the left ventricle results in diastolic dysfunction of the left ventricle. I'm sorry Omar but I still don't understand
Lets say you have a decrease in contractility of the left ventricle. Thus, you can longer eject properly in the forward direction. Thus, your ESV increases and preload goes up and up as the problem gets worse--this is systolic dysfunction. Now how will this problem in the left ventricle lead to an increase in afterload, which will then lead to diastolic dysfunction of the left ventricle. Where I am stuck is that since systolic dysfunction essentially keeps cardiac output down, I don't see where the increase in afterload [which leads to diastolic dysfunction] comes from. I apologize for my hard headedness
-Richard
My 2 cents:
Definitions and keeping things separate are very important:
Heart failure = inability of the heart to pump enough blood to provide adequate oxygen to tissues. Due to either systolic dysfunction, diastolic dysfunction, or both.
Systolic dysfunction = heart does not generate as much force to pump the blood as in a normal individual (ie: contractile failure). Period. Forget about afterload, preload, eccentric hypertrophy, etc. in the definition.
Diastolic dysfunction = heart does not relax as well as in a normal individual leading to less blood inside the heart leading to less blood pumped out of the heart to the tissues. In pure diastolic dysfunction, contractility remains normal. Again, forget about afterload, preload, etc. in the definition.
Eccentric hypertrophy occurs because of VOLUME overload (eg: aortic regurgitation). The increased volume leads to synthesis of new sarcomeres in SERIES with the old. Hence, radius of the ventricle and thickness of the ventricle both increase. Eccentric hypertrophy is a compensation, and its definition should be kept separate from systolic dysfunction and diastolic dysfunction. In fact, BOTH systolic and diastolic dysfunction can be present in a heart that has eccentric hypertrophy.
Concentric hypertrophy occurs because of PRESSURE overload (eg: aortic stenosis). This increased pressure leads to synthesis fo new sarcomeres in PARALLEL with the old. Hence only the thickness of the ventricle increases. Again, the definition of concentric hypertrophy should be kept separate from systolic and diastolic dysfunction. Both systolic and diastolic dysfunctions can occur in a concentric hypertrophied heart as well.
Now, many books equate concentric hypertrophy with diastolic dysfunction. This is simply not true. They are not equivalent. There is a strong relationship between the 2 however. Concentric hypertrophy --> increased wall thickness. This increased wall thickness often impairs the heart's ability to relax, thus causing diastolic dysfunction. In pure diastolic dysfunction, contractility remains normal. However with concentric hypertrophy, you can also have systolic dysfunction at the same time with diastolic dysfunction... if there is contractile failure from whatever cause.
The reason why they associate systolic dysfunction to dilation of the heart is because with continued systolic dysfunction (contractile failure), the heart will not pump out the blood effectively and its volume will increase, eventually leading to dilation of the heart. Thus there is usually a relationship between eccentric hypertrophy and systolic dysfunction. But again, you can have eccentric hypertrophy with BOTH systolic dysfunction and diastolic dysfunction. Diastolic dysfunction will occur in this case if the heart cannot relax well from whatever cause.
Now clinically, patients hardly ever have pure diastolic or pure systolic dysfunction. They usually have a combo of both. In clinics, you might see a patient with an enlarged heart with ejection fraction of 25% with poor myocardial wall motion. Clearly, he has systolic dysfunction (EF and wall motion are poor thus poor contractility). But does that mean he doesn't have diastolic dysfunction? NO! He can (and most likely does) have this as well, it's just not as clinically apparent from that scenario. We treat it as systolic dysfunction: can be more aggressive with vasodilators and diuretics.
The reason why systolic and diastolic dysfunctions are usually separated are because of treatment: they sort of differ between both. In a patient with a non-dilated heart, thickened walls, EF >50%, but symptoms of heart failure, the patient most likely has mostly diastolic dysfunction. But the patient can also have systolic dysfunction (contractile failure) that is not clinically apparent. But in this case, we treat it as diastolic dysfunction: don't be too aggressive with the vasodilators, and diuretics, etc.
Hope this helps... at least a little.
