How would decreased venous compliance [meaning more blood returns to the heart] affect the function of the cardiac cycle in terms of preload, afterload, stroke volume, cardiac output, etc.---especially afterload. What would the PV-loop look like compared to the control loop?
Physiology subject question
- Thread starter rsweeney
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Compliance is directly proportional to volume and inversely proportional to pressure. So, it essentially describes how volume changes in response to a change in pressure.
Changes in the capacitance of the veins produce changes in unstressed volume. Such as a decrease in venous capacitance decreases unstressed volume and increases stressed volume by shifting blood from the veins to the arteries.
Preload is equivalent to end-diastolic volume. So in the situation you mentioned, where venous return is INCREASED, the end-diastolic volume also INCREASES and stretches the ventricular muscle fibers.
In other words, increased preload is an increase in end-diastolic volume, which is a result of increased venous return (or a decreased venous compliance). The increased preload results in an increased stroke volume (I'm sure you're falimilar with Frank-Starling relationships). This increase in stroke volume is shows on a pressure-volume loop as a increased width of the loop.
An increased afterload would be the ventricle ejecting blood against a higher pressure, which results in a decrease in stroke volume. Since we've already said that increased preload is an INCREASE in stroke volume, we know that the afterload with a decreased venous compliance is DECREASED.
To sum up:
Decreased venous compliance, or more blood returning to the heart:
Preload: Increased
Afterload: Decreased
End-diastolic volume: Increased
Stroke volume: Increased
P-V Loop: Increased width (due to increased preload)
Changes in the capacitance of the veins produce changes in unstressed volume. Such as a decrease in venous capacitance decreases unstressed volume and increases stressed volume by shifting blood from the veins to the arteries.
Preload is equivalent to end-diastolic volume. So in the situation you mentioned, where venous return is INCREASED, the end-diastolic volume also INCREASES and stretches the ventricular muscle fibers.
In other words, increased preload is an increase in end-diastolic volume, which is a result of increased venous return (or a decreased venous compliance). The increased preload results in an increased stroke volume (I'm sure you're falimilar with Frank-Starling relationships). This increase in stroke volume is shows on a pressure-volume loop as a increased width of the loop.
An increased afterload would be the ventricle ejecting blood against a higher pressure, which results in a decrease in stroke volume. Since we've already said that increased preload is an INCREASE in stroke volume, we know that the afterload with a decreased venous compliance is DECREASED.
To sum up:
Decreased venous compliance, or more blood returning to the heart:
Preload: Increased
Afterload: Decreased
End-diastolic volume: Increased
Stroke volume: Increased
P-V Loop: Increased width (due to increased preload)
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I ought to add that my Cardio/Pulmonary module last semester was taught by two tough-nuts from the University of Kentucky Medical School. I almost walked away from that module with a passing grade.
Sheesh.
Sheesh.
1) What ends up happening to end systolic volume and why?
2)If you do have more blood returing to the heart, then when stroke volume and cardiac output increase shouldn't afterload increase? The reason I ask this is because won't the inc. in cardiac output result in greater arterial pressures, thus greater afterload?
I completely understand your explanation
and it makes total since, but this afterload question is still pounding at my brain
Your afterload explanation makes since, but I feel mine does too, so this is where the main confusion is.
-Thank you Gavin
-Richard
2)If you do have more blood returing to the heart, then when stroke volume and cardiac output increase shouldn't afterload increase? The reason I ask this is because won't the inc. in cardiac output result in greater arterial pressures, thus greater afterload?
I completely understand your explanation
and it makes total since, but this afterload question is still pounding at my brain Your afterload explanation makes since, but I feel mine does too, so this is where the main confusion is.
-Thank you Gavin
-Richard
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The heart and circulatory system is a closed system so with a certain set of parameters there is only one value possible for Cardiac Output and Central Venous Pressure at which they will be in equilibrium.
If you have an increase CVP you will get more venous return and thus a higher CO which will lead to more blood leaving the veins and accumulating on the arterial side which will decrease CVP and decrease CO and so on and so forth. The increases and decreases will continue until the CVP and CO are back at equilibrium.
The major problem with learning and being tested on cardiac and circulatory physiology is distinguishing between a primary effect of a changed parameter and the compensatory effects that lead back toward equilibrium.
So what happens with your afterload? The literal answer is that it both increases and decreases. The decreased afterload would be the primary effect of an increase in CVP and the increased afterload would be due to the compensatory effects of the system trying to reestablish equilibrium.
If you have an increase CVP you will get more venous return and thus a higher CO which will lead to more blood leaving the veins and accumulating on the arterial side which will decrease CVP and decrease CO and so on and so forth. The increases and decreases will continue until the CVP and CO are back at equilibrium.
The major problem with learning and being tested on cardiac and circulatory physiology is distinguishing between a primary effect of a changed parameter and the compensatory effects that lead back toward equilibrium.
So what happens with your afterload? The literal answer is that it both increases and decreases. The decreased afterload would be the primary effect of an increase in CVP and the increased afterload would be due to the compensatory effects of the system trying to reestablish equilibrium.
Ah, I see. So the PV-loop most likely represents the preimary cause. In this case of decreased venous compliance, the CVP increases due to the decrease in compliance. The decrease in compliance resulted from the sympathetic nervous system constricting the smooth muscles around the veins---is this right?
Thank you!!!!
-Richard
Thank you!!!!
-Richard
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What Dan said.
There was a reason I hated that subject, and it's all coming back to me now (the reason, NOT the material)
There was a reason I hated that subject, and it's all coming back to me now (the reason, NOT the material)
So what happens with your afterload? The literal answer is that it both increases and decreases. The decreased afterload would be the primary effect of an increase in CVP and the increased afterload would be due to the compensatory effects of the system trying to reestablish equilibrium.
So, when CVP increases that means the afterload in the aorta simultaneously decreases. Thus, not only will you have an increase in stroke volume, but left ventricuar end-systolic volume will go down too. Thus, the PV-loop be wider with elevated left ventricular end-diastolic volume and decreased left ventricular end-systolic volume? Is this right? Thank you!
So, when CVP increases that means the afterload in the aorta simultaneously decreases. Thus, not only will you have an increase in stroke volume, but left ventricuar end-systolic volume will go down too. Thus, the PV-loop be wider with elevated left ventricular end-diastolic volume and decreased left ventricular end-systolic volume? Is this right? Thank you!
