Does increase in preload only affect two right corners of the loop: moving the points where mitral valve closes and aortic valve opens to the right with the same end systolic pressure and volume. Or, does increase in preload change the position of all 4 corners of the pressure volume loop: end systolic pressure and volume are also elevated? What are the arguments/evidence supporting or against each scenario?
It depends on the afterload. In the real life (but not in Starling's preparation) physiological and pathophysiological factors affecting preload might simultaneously affect the afterload in different ways. The same change in preload may so produce different changes in the pressure-volume loop, depending on the changes in afterload.
Añ increase in preload will increase afterload due to the increase in volume.Afterload, wall stress, is a function of pressure,volume and the thickness of the wall
There two view on what explain why afterload increases after a rise in preload. First hypothesis says that increase passive stretch of cardiomyocytes increases actine-myosine binding sites matching, therebay increasing points of force generation. The second, more recent view is that stretching cardiomyocytes triggers regulatory pathway, leading to contractile protein phosphorylation; this pathway relay on the multiples cytoskeleton proteins linking contractiles proteins to sarcolemma.
The second,as Pierre mentioned ,is the slow forcé response and relay on a chain of intracellular signaling steps,leading to añ increase in the calcium transient.Homeometric autoregulation or Anrep effect.The first is due to añ increase in myofilsment responsiveness.Referent to the second or slow forcé response and the chaint of events we published a Review in AJP recently.
In a few words,añ increse in preload increse afterload due to Laplace law and contractility through the Anrep effect.In adittion STROKE volume due to Starling law.
When you expect afterload and inotropy are held constant the explanation is most eloquently given on the following site: http://www.cvphysiology.com/Cardiac%20Function/CF025.htm
However it also depends on the cause of preload increase. For instance an acute venous volume overload (e.g. when to many bags of fluid are pushed into a patient) will shift the entire PV loop to the right and will increase SV (as afterload and inotropy are altered by this approach).
Eloquently?? I think that these lots of graphs are out of debate. The key question raised here is what make that stretching more a cardiomyocyte elicites from this cardiomyocyte a stronger contraction. The answer relies on contractiles proteins and ancillar proteins and, for more sustain contractile stress, transcription factors
Hello Pierre,
it is my opinion that pressure-volume loop does not exist at the integrative level of contractile proteins. It is a functional property which appears only when all the cardiovascular system acts as a whole. Contractile proteins are an important part of the integrated function of cardiovascular system but not the unique component of it. Pressure-volume graphs cannot be considered out of debate.
Consider that the truth is between. Control of force by stretch is a process that rely on the contractile apparatus at the cardiomyocyte level. However, this cellular process is trigger, in physiological conditions and at the scale of the whole organism, by systemic factors, i.e.,, venous return.
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