you are right... mean systemic pressure only changes with blood volume and/or venous compliance. The specific examples used of hemorrhage and exercise do influence one or the other. Exercise leads to increased sympathetics, hence venoconstriction. Hemorrhage leads to blood loss, loss of volume. TPR has no influence because mean systemic filling pressure is measured when the heart has stopped or the organism is dead.
in case of hemorrhage, the cardiac function curve should remain unchanged (because the contractility of heart is not affected by hemorrhage), please take a look at first aid 2014 page 269. practically the contractility is increased if you consider the increased sympathetic tone after hemorrhage, so the cardiac function curve should go up. Anyhow, the cardiac function curve should not go down as showed in this video
Great job with the video! Many thanks. One anomaly that I find is that during a compensated heart failure, the renal compensatory mechanisms cause retention of fluid causing venous return to actually increase. Therefore, the VR curve also shifts up and to the right so as to maintain the steady state cardiac output to near normal.
Great video!! Just note that during exercise the venous return curve s`X intercept or mean systemic pressure (10 mmHg) should stay in the same place. Because the total circulating volume was not altered. Greetings!
shobs iyer For those nerds wondering why?There are some flaws in your thinking, let me correct them for you. Follow along. flow characteristics of the systemic venous circulation are dependent on Vo (unstressed[reservoir] volume in veins), Vs(stressed volume in veins), Vt(total volume in veins), C(compliance), and Rv (Resistance to venous flow) recall that venous return; VR= ( Pms-Pra ) / Rv Pms is mean systemic pressure, Pms=Vs/C which can be written as Pms=(Vt-Vo)/C This new equation suggests that Pms can be altered through two basic mechanisms: (1) a change in the total volume in the reservoir(Vt); or (2) a change in the proportion of Vo and Vs. An alteration of autonomic tone, catecholamine stress responses, or infusion of exogenous vasoactive substances will alter the ratio of Vs to Vo without a change in C, thus changing Pms. Your partially right, but you should be thinking>exercise>SNS>increase in HR, venoconstriction in non vital organs and vasodilation in vital organs(heart, brain, muscle)>increased preload>increase in CO-->a change in proportion of Vs and Vo (volume of stressed venous blood vs Volume of unstressed venous blood) >increase in PMS A lot of books will says venoconstriction leads to a decrease venous compliance b/c of inverse relationship between resistance and compliance. They try to generalize it and make it simple, but compliance is way more complicated and depends on so many other factors The way I see it is that compliance in this model should be considered a static, passive mechanical property of veins. why? recall that venous system has two compartments; 1)venules and small veins, which lack smooth muscle layer and cannot constrict and account for 70-80% of bodies total blood reservoir, they have a very large crosssectional area contribute little to Rv and systemic compliance 2)Large veins and Medium sized veins, which can constrict, and contribute to compliance and they have small cross-sectional area and act as a valves. These two compartments work against each other under autonomic stress i.e increased stressed volume and Pms in the reservoir compartment (which increases VR) but decreased mean radius in the vena cava and large veins (which decreases VR). In conclusion its not the compliance/restriction of the vein, that increases Pms, but the change in proportion of Vs ans Vo. Yeah this shit is confusing, and a lot of books don't explain it properly.
Guru Jolly thanks for this explanation. Made me realize I had one misunderstanding about why nitro is used in angina. I always thought that venodialation decreased venous return but I realize it's because nitro causes pooling of blood in the periphery hence causing decreased preload not just because of the venodialation which actually makes alot more sense.
yes there will be release of catacholamines but there will also be vasodilatation of arterioles causing drop in TPR arterioles are the main determinant of TPR and the local adenosine rise due to exercise causes vasodilation and opening of these capillaries ie arterioles also increases perfusion to sk.muscle viz required to the energy requirments of body
well, it seems that the owner of the video doesn't care to correct his/her mistake and choose to continue to give wrong information to other people. clearly MSFP is something that i should explain further to my students next time. i guess cardiovascular physiology is something that we should not over-simplify rather should learn each and every fundamental aspects of it. otherwise, everything will go awry.
Correct, but during sympathetic nerve activation (during exercise) you will also get an increase in venous tone (reduced capacitance) - increasing MSFP.
since u put the value as ~10mmHg. But this is MSFP we are talking about. A deeper concept involved. Even many comments in the journal said that Guyton's VRC has to be carefully interpreted, as it is not universally correct. If u r interested, u may google it. Happy learning...
This explanation is completely wrong. The y axis represents both CO and VR, which are always the same in this steady state graph (the heart cannot put out more than its input!). CO and VR are not separate values. The curves do not represent CO and VR. They represent the positive influence of RAP on CO (the cardiac function curve) and the simultaneous negative influence of CO on RAP (the vascular function curve). e.g. in heart failure the CO is lower for any value of RAP, so the cardiac curve will be shifted down. If there is a compensatory increase in blood volume, the vascular curve will be shifted up, because there is a higher RAP for any value of CO. The intersection of the new curves will show a similar level of CO/ VR but a higher RAP (try drawing it). TPR declines in exercise to deliver higher flow through the tissues, not to the heart. The heart's job is always to match the changing flow from arteries to veins with an equal flow from veins to arteries. The vessels set the pace, the heart keeps up!
Good video, however i have one remark: The curve that you mark as Cardiac output is actually the Cardiac Function curve. The whole point of the graph is to determine the Cardiac Output which lies at the point where the Cardiac function curve and the venous function curve cross.
Hi I use screen-o-matic which is a free screen recording website. I also use bamboo, which is like a tablet to draw my diagrams. If look onto youtube, you will find plenty of examples of what the are. Good Luck.
@4:35 I am told by my professors that hemorrhage does not in fact affect the cardiac output and so we only see a drop in VR but CO and SV remain the same. Please clarify that point?
Can you increase sympathetic only in veins? I doubt that is possible. But if you increase sympathetic stimulation the TPR increases. TPR is both for arteries and veins. Changing TPR will have effect on both and not only in veins. When you use this graph, think of situations only exclusive to CO and Venous return.
In theory RAP is very low because right atrium has thin walls and the compliance is very high. The pressure is really the pressure of central venous pressure. So, RAP technically is not zero but very low. Think about it, how can the pressure be zero, then it will collapse.
The venous return will actually increase Because of RAAS in kidney will cause fluid retention which increases venous return This usually confuses people because its said that CO=VR but if that was the case in heart failure there wouldn’t have been increased work load on the heart and diuretics would have been useful Thats how i like to think about it, hope i was able to help clear things up
that is perfect nice job explaining it. in Anesthesia school and professor does bad in explaining. the other thing that is important is that if you have a increase in central venous pressure (RAP or LVEDV) you will have a decreased CO like in Failure. You have high pressures with poor CO because your SNS is increasing in venous tone (SNS activation) in order for response of failing CO. This is marvelous. Bottom line increased CVP = decreased contractility
So yes I think that the curve in question (the cardiac function curve) can be called the contractility curve, as it is the curve that demonstrates the Frank-Starling mechanism that can be shifted by changes in contractility. You can do a quick check of wiki for "cardiac function curve" or I can dig through to my costanzo book if necessary.
does anyone know where i can find the video when she about cardiogenic/hypovolemic/etc shock???!!! I saw it but now i cannot find it anymore...she describes how to use a specific formula including pulmonary wedge pressure, SV, etc
well, initially i tried to explain, but i guess it would be difficult if ur basic concepts about cardiac and vascular functions are not profound enough. Please refer to the website (google-->venous return curve-->click "CVphysiology: cardiac and systemic..." link, the 'systemic vascular function curve' aka venous function curve part. Ur explanation is actually right for mean arterial pressure as MAP=COxTPR. But i am assuming ur mean systemic pressure refers to mean systemic filling pressure...
Thank you . Please make another video on anti hypertensive drugs with more details . Your explanation is more simple and interesting . Very informative too.Best regards Dr.Joe , India
I am not so sure. I think you might want to check the venous return curve again. When you change the TPR, the mean systemic pressure shouldn't be affected. The mean systemic pressure only change when you change the blood volume and the venous compliance. correct me if i am wrong. thanks
"mean systemic pressure" you/she are talking is called systemic function pressure which is a measure of venous return ( means at what pressure is VR=0 [check graph]) and is = BV/Complaince and below , what she is trying to explain is called "mean arterial pressure" which is = CO x TPR or HR x SV x TPR
100lurics I know it’s been many moons but we still need u buddy, to make these easy grasping concepts tutorials please. You are one of the few who are good at the game!
+sam s (ss)  This is what I was thinking too... I even thought the curve would go up because of arterial vasodilatation, (causing the afterload to decrease), and a compensatory higher heart frequency and contractility because of sympathetic nervous system activation.. Edit: www.ncbi.nlm.nih.gov/books/NBK54474/
+Rosalie Poldervaart In hemorrhage the TPR increases (body's compensatory mechanism during blood loss is to vasoconstrict to prevent further blood loss) The Cardiac output drops because there isn't enough blood to pump forward (remember CO = SV x HR you may be thinking of increased HR to make up for the decrease in SV but ultimately SV drops so much that the racing heart just can't keep up and CO drops), and the Venous Return also drops, because of the same reason, loss of volume.
Mean systemic filling pressure increases due to sympathetic activation--> contraction of the peripheral vessels. This means that the venous curve shifts to the right up to +17mmHg. However, due to increased venous resistance, the curve also rotates to the left (little bit). The net effect is around a maximum 100% increase in cardiac output before other regulatory measures will decrease it. At the same time the cardiac curve will rotate upwards due to a stronger heart pump.
GREAT explanation. Professors didn't attempt to teach this, and Boards and Beyond was BEYOND confusing. This was perfect. Now I actually understand the variables and can predict how they will change in different situations as well as interpret graphs to know what underlying disease process would give such changes! THANK YOU!!
