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# What is contractility?

Contractility tells us how many myosin heads are working at the end of systole; a number that goes up or down with the level of sympathetic nerve stimulation. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.

## Want to join the conversation?

• I am a little confused about Rishi's statement at that the same minimum volume (i.e. intersection of volume axis) is reached for both ESPVR curves with different contractilities. He later mentions that the contractility is reflected in the slope of the line. However, I read on the wikipedia page (and have also heard in my cardiac physiology course) on Pressure-volume loop analysis in cardiology (http://en.wikipedia.org/wiki/Pressure-volume_loop_analysis_in_cardiology) that the slope increases *and the ESPVR curve "shifts to the left as inotropy (contractility) increases"*. This seems to indicate that the point of intersection with the volume axis is not the same as the contractility changes. However, I don't know why that would be the case. I'm also confused about the significance of this intersection value. If someone could shed some light on this issue, I would greatly appreciate it. Thanks.
• I think this sentence is mathematically incorrect.
An increase in inotropy causes the the ESPVR to to around the intersection with the volume axis. Which essentially makes the slope steeper. This rotation however makes it look like the line is also shifting to the left at the end-systolic pressure point.
• One thing that I don't understand is how and why 2 or more different preload can have the same contractility?Shouldn't the contractility increase as we increase the volume and the sarcomere lenght?
• at , volume-pressure slope increases as the sympathetic nerve does work.
But I'm confused because in previous lecture of ESPVR , the slope was drawn with assuming all the myosin-actin contract as much as it could. So, to me it's more reasonable that we should stick on first slope. Can anyone help me, I would appreciate it
• We must remimber that everything is variable with time, location, input and circumstance. He is saying, contracting as much as it can in relation, for example: "As much as it can at the current Ca level in the cardiac cells, and at that current affinity for Ca that Trop-C has and at that current permeability the cell has for Ca and at the specific type of cardiac cell, and at the current health of the individual." All of these can be reduced or enhanced via ANS input, as well as other inputs. Plus, he is drawing general graphs, they are not representative graphs in the strictest sense. Don't get caught in the inconsistency between hand drawn graphs. Look online to find different graphs that are pulled from human subjects.
• At , Rishi is explaining that the contraction force is greater because the "workers" or myosin are working harder. I wanted to know if I believed something incorrectly, is it the myosin that are working harder that causes the greater force in contraction or is it the greater number of myosin heads working?

At , this causes a little bit more confusion. Is it the greater number of myosin heads that cause the slope of the ESPVR to increase (as he says), the myosin heads working harder, or both that contribute to the increase of slope in the ESPVR? Thx

P.S. I think this is another one of Rishi's great videos, where he applies this to the world around us and in what cases we may be in to apply this knowledge to real life. Thx Rishi! There should be an up-vote button for videos... :D