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stroke volume and venous return

SamarEsawy

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Feb 25, 2013
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    surfing the internet, I found this page about effect of afterload on sv
    http://cvphysiology.com/Cardiac Function/CF008.htm

    my problem is with increasing EDV:

    The effects of afterload on ventricular end-systolic and end-diastolic volumes can be illustrated using pressure-volume loops (Figure 2). If afterload is increased by increasing aortic diastolic pressure, the ventricle has to generate increased pressure before the aortic valve opens. The ejection velocity after the valve opens is reduced because increased afterload decreases the velocity of cardiac fibers shortening as described by the force-velocity relationship. Because there is only a finite time period for electrical and mechanical systole, less blood is ejected (decreased stroke volume), which increases the ventricular end-systolic volume as shown in the pressure-volume loop. Because end-systolic volume is increased, this extra blood within the ventricle is added to the venous return, which increases end-diastolic volume. Ordinarily, in the final steady-state (after several beats), the increase in end-systolic volume is greater than the increase in end-diastolic volume so that the difference between the two, the stroke volume, is decreased (i.e., the width of the pressure-volume loop is decreased).

    ESV is increased that's okay ,,on adding this increased ESV to venous return we have larger EDV ..why??? decreased stroke volume means decreased venous return right?since venous return normally equals cardiac out okay?on adding decreased venous return to increased ESV we obtain the same EDV
    so why EDV volume is increased in this case?
    thanks
     

    gabloammar

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    May 7, 2013
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      [supposition]

      Let's say venous return is 10 mL.
      If ESV is increased then EDV will also be higher than normal. [If this doesn't make sense then stop reading and tell me so I can explain.]

      If EDV is higher, then the next contraction will also be stronger, will it not?

      If it's stronger, then the stroke volume will be higher for that contraction.

      If it's higher, then more blood goes into the systemic arteries.

      If that happens, venous return is higher.

      If venous return is higher, EDV is higher.

      Hope that helped!
       

      zherussianbear

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        **IMHO:

        I think that this has to do pulmonary circulation. At the time of systole, the LV pumps blood through the aorta and into the body, as described by your blurb - call this portion X. As the blurb points out, some blood, Y, remains in the LV. Simultaneously, the RV pumps blood into the lungs; in a normal person this must be X+Y (because it replaces that which the LV puts out, which in a healthy person should be the full ejection fraction, say 60%). When diastole begins, the LA empties into the LV the blood it received from the Lungs (from the RV). So now, the LV, at end-diastole should contain X+2Y the cycle after the pathology kicks-in. The next cycle, 2Y will remain in the LV while X will return; later on, a bit more blood may remain in the LV, and so Y will probably increase with time to a point, and then the real pathology will start.

        Of course, it's important to remember that these moments and volumes are not totally discreet, so Y changes with time, and pathology doesn't really "kick in," it chips away, and the stagnant amount should increase from a little to a significant amount with time.

        Correct me if I'm wrong.
         
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        SamarEsawy

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        Feb 25, 2013
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          If ESV is increased then EDV will also be higher than normal
          that's what I'm trying to understand here
          EDV=ESV+SV
          by increasing ESV ,stroke volume decreases (or venous return decreases) so EDV still constant
          but this is contradictory with what really happens.

          I think that this has to do pulmonary circulation. At the time of systole, the LV pumps blood through the aorta and into the body, as described by your blurb - call this portion X. As the blurb points out, some blood, Y, remains in the LV. Simultaneously, the RV pumps blood into the lungs; in a normal person this must be X+Y (because it replaces that which the LV puts out, which in a healthy person should be the full ejection fraction, say 60%). When diastole begins, the LA empties into the LV the blood it received from the Lungs (from the RV). So now, the LV, at end-diastole should contain X+2Y the cycle after the pathology kicks-in. The next cycle, 2Y will remain in the LV while X will return; later on, a bit more blood may remain in the LV, and so Y will probably increase with time to a point, and then the real pathology will start.
          so x is stroke volume
          y is ESV
          Simultaneously, the RV pumps blood into the lungs; in a normal person this must be X+Y
          blood pumped to the lung is simply stroke volume which is only x
          this is still going over my head
           

          gabloammar

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            Okay let's break that one down a little more.

            Let's say the normal ESV is 50 mL.

            And that EDV is 120 mL.

            Stroke volume is 120-50 = 70 mL.

            After the next contraction, the ESV is 60 mL [because the heart didn't pump the blood out effectively enough].

            The blood that comes back in through the right atrium will be the same [for THIS contraction], and let's say that the EDV in this case is 130 mL.

            If EDV is increased [which in this case, for THIS contraction, is increased], the heart will contract more powerfully due to increased preload.

            The stronger contraction means the stroke volume is higher.

            Hope that made sense to you. Do tell if it didn't.
             

            GadRads

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            Oct 13, 2012
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              surfing the internet, I found this page about effect of afterload on sv
              http://cvphysiology.com/Cardiac Function/CF008.htm

              my problem is with increasing EDV:



              ESV is increased that's okay ,,on adding this increased ESV to venous return we have larger EDV ..why??? decreased stroke volume means decreased venous return right?since venous return normally equals cardiac out okay?on adding decreased venous return to increased ESV we obtain the same EDV
              so why EDV volume is increased in this case?
              thanks

              Ejection fraction (EF) is the fraction of blood pumped out of the ventricle during systole. The blood that now remains is the ESV. Thus EF is the amount of blood pumped out of the heart (called SV) divided by the starting blood volume just PRIOR to systole. This prior blood is the EDV.

              Increased resistance to ejection of blood during systole is termed afterload. Since the ejection time is the same, afterload will decrease the volume of ejected blood due to increased resistance to flow (read : decreased stroke volume), thus creating a bigger leftover of blood in the ventricle (increased ESV). Remember this leftover (ESV) is a sum of EDV1 - SV +"delta" where delta is the decrease in SV (and EDV1 is end diastolic volume from the previous cardiac cycle.

              The same volume of blood (say V) fills the atria and, subsequently, ventricles during the accompanying diastole. This volume is then added to the previously increased ESV. Since the volume of blood at the end of diastole is EDV, this volume will be increased by prior blood from the previously increased ESV. Thus the new EDV2 = "delta"+EDV1-SV + V = ESV +V. More "delta"'s are added during future cycle leading to subsequently increasing EDV assuming pathology remains.

              Finally although pre-load is increased leading to stronger contractions, the EF is less than optimal. Therefore EDV is always increasing. Thus "delta" is not the same each cycle.
               
              Last edited:

              SamarEsawy

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              Feb 25, 2013
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                The same volume of blood (say V) fills the atria
                that's what I'm askin about guys
                what volume of blood?
                if stroke volume decreases, then this would lead to decreased venous return in the next cycle right?
                if so then the increase in ESV is compensated by the decrease in venous return (as a result of decreased SV) so EDV is not changed
                this is my misconception so correct it please and help me understand
                 

                gabloammar

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                  that's what I'm askin about guys
                  what volume of blood?
                  if stroke volume decreases, then this would lead to decreased venous return in the next cycle right?
                  if so then the increase in ESV is compensated by the decrease in venous return (as a result of decreased SV) so EDV is not changed
                  this is my misconception so correct it please and help me understand

                  Venous return would be decreased only if the heart could only hold a constant amount of volume, but it can hold more than the normal value. There's no compensation. There will certainly be a higher amount of blood now because of what I as well as Cyal told you.
                   

                  GadRads

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                    can you get my problem?

                    I corrected some of the equations in my previous post, although it shouldn't alter the overall message.

                    What you are missing is that the circulatory system is a closed circuit with pools of blood all along the vessels and chambers. During ventricular systole, the atria are also filling simultaneously, so the decreased SV doesn't have an immediate effect on venous return. In the long term, it's reasonable to expect effects from decreased venous return, however by this stage the patient should've gotten some kind of heart/pulmonary/systemic pathology.

                    As far as I know, the biggest factors affecting venous return are (1) calf pump--lower limb skeletal muscle contraction around deep veins; and (2) intrapleural and intrabdominal pressures during respiration. Secondly, if there was compensation due to decreased SV (and possibly cardiac output), patients with aortic stenosis (a kind of afterload) would be less likely to have pulmonary edema, but that's not what the evidence shows.
                     
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