Cardiovascular physiology help---Systolic dysfunction vs. Diastolic dysfunction!!!

rsweeney

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    Systolic dysfunction vs. Diastolic dysfunction.

    According to Ganong [a text],

    1) "systolic dysfunction = forward failure = increased preload" AND

    2) "Diastolic dysfunction = backward failure = increased afterload"


    My questions:

    1)Why does diastolic dysfunction = increased afterload?


    2)Why does systolic dysfunction = increased preload?

    Thank you for any help with this concept!

    -Richard
     

    Varblade

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      "systolic dysfunction = forward failure = increased preload"

      systolic dysfunction is an inability for heart to contract for blood ejection. Blood ejection from heart is not complete i.e inefficient. Increased blood accumulates in heart after each cardiac cycle. Preload increases as the initial volume of blood to pump out increases. This can eventually lead to a backward failure.

      "Diastolic dysfunction = backward failure = increased afterload"

      diastolic dysfunction is an inability for heart to relax for blood refilling. Venous blood pooling occurs. Arterial blood stasis is added to the mix. Increase TPR. Increased pressure for heart in pumping blood out. This is increased afterload.


      Oh great medical elites.. .correct me as i smell a mistake in my answer somewhere.:scared:
       

      Al Pacino

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        Systolic dysfunction=increased preload because...when you have increased preload (mitral regurgitation, aortic regurgitation, ischemic heart, etc.) that means there's more blood in the left ventricle right before systole begins. This increased blood volume stretches the ventricle, activating the Frank-Starling effect, and the heart shoots out an increased cardiac output, which is a good thing. However, if the heart is subjected to this increased preload for a long time, the heart "starts to break down." It breaks down because it has to work much harder to pump blood. Thus it fails, and can't get blood moving in the forward direction.

        Diastolic dysfunction=increased afterload because...increased afterload (HTN, Aortic stenosis, hypertrophic cardiomyopathy) forces the heart to hypertrophy to be able to pump against this increased "barrier." It's like a weightlifet who hypertrophies their pectoralis muscles when they have to benchpress great weights. Well, the problem with hypertrophy is that the ventricle becomes "stiff and hard" and no longer fills well. This inability to fill is the definition of diastolic dysfunction of heart failure.
         
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        rsweeney

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          diastolic dysfunction is an inability for heart to relax for blood refilling. Venous blood pooling occurs. Arterial blood stasis is added to the mix. Increase TPR. Increased pressure for heart in pumping blood out. This is increased afterload.

          Does the word diastolic dysfunction refer to left ventricular or right ventricular diastolic dysfunction? I understand that venous blood pooling occurs on the level of the pulmonary vein due to the build-up of blood in the left atrium. Thus, the right ventricle will have to pump against a higher pressure, thus increase afterload in the RIGHT VENTRICLE---is this right? What about the left ventricle? Why does increased afterload in the right ventricle result in increased afterload in the left ventricle---meaning why does stasis occur in the systemic circulation [I see why stasis occurs in the pulmonary circulation--it occurs due to the back-damming on the level of the pulmonary veins]? Was the last post only relevant to the pulmonary circulation?

          Also, is the following correct?

          1) Increased afterload CAUSES diastolic dysfunction and not the other way around.

          2) Increases preload CAUSES systolic dysfunction and not the other way around.

          -Thank you VERY much!!!!
           

          rsweeney

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            So increased afterload is primary to [causes] diastolic dysfunction whereas diastolic dysfunction does not CAUSE increased afterload? I thougtht the book implied that diastolic dysfunction CAUSES increased afterload.

            Also, increased preload causes systolic dysfunction down the road and not the other way around? Is this right?

            Thank you VERY much!!!
             

            rsweeney

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              Since I had to edit the last post are these assumptions still correct?

              1)Increased afterload CAUSES diastolic dysfunction and not the other way around.
              2)Increased preload CAUSES systolic dysfunction and not the other way around.


              Lastly:
              Why does the heart continue to fail when it is in systolic dysfunction even after eccentric hypertrophy?
               

              Al Pacino

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                Originally posted by rsweeney
                Since I had to edit the last post are these assumptions still correct?

                1)Increased afterload CAUSES diastolic dysfunction and not the other way around.
                2)Increased preload CAUSES systolic dysfunction and not the other way around.


                Lastly:
                Why does the heart continue to fail when it is in systolic dysfunction even after eccentric hypertrophy?

                The 2 conclusions above are correct. As to your last question, the answer lies in the Law Of Laplace which basically states that wall tension in the ventricle is proportional to pressure generated in the ventricles and the radius of the ventricle and inversely proportional to the ventricle's wall thickness. In systolic dysfunction, we get increased left ventricle wall thickness (i.e hypertrophy) which decreases wall tension--that's a good thing. However, the increase in PRESSURE that the left ventricle generates causes much more "strain" than can be overcome with the increase in wall thickness...
                 

                rsweeney

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                  1) Wall tension = (Pressure x radius)/ wall thickness

                  What I know:
                  -Radius increases as a result of increase preload thus increase muscle fiber stretch. Is it the mere stretching that mechanically causes radius increase.

                  Is the radius increase equivalent to the over-blowing up of a baloon a bunch of times such that the baloon will eventually stay at this larger radius, however with a weakened and THINNER wall? However, in the heart the wall is not thinner because the increased preload caused more thickness [muscle fibers] to be added to the heart wall so more force will be generated? If my above statements are correct, then it almost seems as if the raidus and wall thickness increase proportionally in eccentric hypertrophy. Thus, if they do increase proportionally, then the radius and wall thickness increase should have no NET effect---right? Thus pressure is the only factor left. Is this correct?

                  THUS
                  -What is the chief cause of the pressure increase in systolic dysfunction? This question can be extended to diastolic dysfunction---How exactly is ventricular filling pressure increased in diastolic dysfunction? I know that the decrease in compliance shifts the end systolic pressure relationship (ESVPR) up and to the left----BUT WHY? Thank you very much Al BIG TIME!!!!!!!!! These are the last questions---I promise.

                  -Richard
                   

                  Al Pacino

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                    Originally posted by rsweeney
                    1) Wall tension = (Pressure x radius)/ wall thickness

                    What I know:
                    -Radius increases as a result of increase preload thus increase muscle fiber stretch. Is it the mere stretching that mechanically causes radius increase.


                    Yes, I believe that is accurate.


                    Is the radius increase equivalent to the over-blowing up of a baloon a bunch of times such that the baloon will eventually stay at this larger radius, however with a weakened and THINNER wall? However, in the heart the wall is not thinner because the increased preload caused more thickness [muscle fibers] to be added to the heart wall so more force will be generated?


                    From what I know, yes.


                    If my above statements are correct, then it almost seems as if the raidus and wall thickness increase proportionally in eccentric hypertrophy. Thus, if they do increase proportionally, then the radius and wall thickness increase should have no NET effect---right? Thus pressure is the only factor left. Is this correct?


                    I believe wall thickness increases much more than radius...regardless, it's the HUGE pressure increase that is most important of the 3 variables.


                    THUS
                    -What is the chief cause of the pressure increase in systolic dysfunction?


                    Think of a shot putter. If he needs to throw up a much heavier steal ball, don't you think he needs to "generate more pressure."


                    This question can be extended to diastolic dysfunction---How exactly is ventricular filling pressure increased in diastolic dysfunction? I know that the decrease in compliance shifts the end systolic pressure relationship (ESVPR) up and to the left----BUT WHY? Thank you very much Al BIG TIME!!!!!!!!! These are the last questions---I promise.


                    Screw the equations. Think of it conceptually, because come Step 1 & 2 time, you're gonna forget the equations but just remember the big picture. For diastolic dysfunction, think of a balloon made of car tire material (this represents hypertrophy) and think of a normal balloon with normal material. Now visually try to blow up the balloon made with tire material. Don't you think trying to blow that piece of sucker will be much harder than blowing up a regular balloon.

                    Similarly, the body has a harder time filling up a heart that has hypertrophied into much stronger "tire" material.
                     

                    omarsaleh66

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                      i was under the impression that increased preload causes diastolic problems such as congestive heart failure. So if u have an increased venous return, u are gonna have right heart (diastolic problems)

                      If u have increased afterload, then the aorta is under alot more pressure and ur stroke volume and left ventricle work is alot harder, so incresaed afterload gives u left ventrcle (systolic) problems.

                      I think this is right, somebody please correct me if im wrong

                      later

                      Omar
                       

                      rsweeney

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                        Hmmmm.....interesting. I guess a result of this increased filling presure [meaning the left artrium is pushing harder into the less compliant, thicker, possibly increased radius ventricle] then the left atrium may itself hypertrophy down the road and lead to some real serious problems. Thank you very much for taking the time to help me out, as I am sure you are very busy. Thank you immensley!!!

                        -Richard
                         

                        Al Pacino

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                          Good. I think you got it. In fact, if the diastolic dysfunction is bad enough, you get the S4 sound -- the sound of the atrial kick. It's the sound of the atrial contraction as the blood hits the severely stiff ventricle.

                          This increased back pressure in diastolic dysfunction affects not only the atria but also the pulmonary veins in the lungs. You get spillage of fluid into the interstitium and into the alveoli -- hence that's why these people come in complaining of dyspnea, cough, and so forth.

                          I love physiology. If you understand this stuff well, you will be better to understand the signs and symptoms of disease. I just finished up junior medicine, and I can't stress enough how important it is to have a good grasp of this stuff. Good luck.
                           
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                          rsweeney

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                            Let's test what you taught me by nit-picking this definition:

                            Here is a definition out of a book: "Diastolic dysfunction = stiff heart requiring higher filling pressure to achieve normal volume. Aggressive volume loading frequently results in backward failure, causing acute pulmonary edma."

                            1) "requiring higher filling pressure to achieve normal volume"--this higher filling pressure is due to the fact that the ventricle is stiff, therefore the atrium has to push harder against the stiff ventricle if normal volume is to be achieved. The higher filling pressure is achieved by the atrium pushing harder. What causes ---is this right? If this is right, what causes the atrium to increase the strength with which is contracts. Is it because the increase "preload" in the atrium causes the atrial fibers to stretch and therefore eject at a stronger force?

                            2) "Aggressive volume loading frequently results in backward failure"--are they referring to excessive loading in the atrium--only this would result in acute pulmonary edema?
                             

                            organic

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                              Originally posted by rsweeney
                              Systolic dysfunction vs. Diastolic dysfunction.

                              According to Ganong [a text],

                              1) "systolic dysfunction = forward failure = increased preload" AND

                              2) "Diastolic dysfunction = backward failure = increased afterload"


                              My questions:

                              1)Why does diastolic dysfunction = increased afterload?


                              2)Why does systolic dysfunction = increased preload?

                              Thank you for any help with this concept!

                              -Richard

                              Hi Richard, I am not sure what you mean by "= " but here are my inputs regarding to your qestion.

                              In ventricular systolic dysfunction, the ventricular preload increases because of the inability of the ventricle to eject normal volumes of blood. This causes blood to "back up" in the ventricle and proximal venous circulation.

                              Acute elevations in blood pressure ( afterload) alter diastolic function because increased afterload limits systolic contraction. This influences relaxation, since elastic recoil significantly contributes to early left ventricular filling.

                              I hope it is helpful. If you could make your " =" more procise, maybe I could have some more stuff to say.
                               

                              rsweeney

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                                The "=" sign in the book stumped me too, because just an "=" sign gives no regard to cause and effect. Nonetheless, your answer is physically logical! Your answer helps a lot---thank you!!!

                                -Richard
                                 

                                Dr.SpongeBobDDS

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                                  rsweeney, have you ever read anything by Patrick McManus? He always tells stories about his friend "Retch" Sweeney. I always think of that when I see your name on here. Just wonderin'.

                                  BTW, physiology is nice like that. You only have to learn a few key concepts and then you can pretty much reason yourself to a logical answer for most any question - if it's a scantron test you're golden. Biochem, on the other hand... :)
                                   

                                  the big wand

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                                    Didn't realize this thread posted in two different places.... So, I removed my previous answers. :) But I have to say that both preload and afterload are systolic dysfunctions.

                                    In case of preload, the heart muscle is at the upper limit of Frank-Starling curve. This leads to decreased contractility and decreased emptying.

                                    In case of afterload, the heart can't empty efficiently against whatever barrier is there (eg, high systemic pressure or AS), thereby reduced emptying.

                                    Both cases have reduced emptying which occurs during systole, so they're systolic dysfunctions.

                                    I rest my case. :D
                                     

                                    rsweeney

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                                      So then why do texts say that diastolic dysfunction results FROM systolic dysfunction?

                                      "Diastolic Dysfunction: loss of left ventricular compliance impairs it?s ability to receive blood. This disorder most commonly results FROM systolic dysfunction"

                                      1) Diastolic dysfunction: results in concentric hypertrophy [normal chamber radius but increased wall thickness]

                                      2) Systolic dysfunction: results in eccentric hypertrophy [chamber radius and wall thickness increase proportionally]

                                      Thus, if diastolic dysfunction often results from systolic dysfunction, how can the heart go from eccentric hypertrophy to concentric hypertrophy? It does not make physical since :confused:

                                      Texts stink--they are not specific and don't give any regard to these types of obvious questions that will arise. I mean AS SOON as I read it I immediately questioned it--geez :eek: :cool:

                                      I love the new SDN!
                                       

                                      omarsaleh66

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                                        left ventricle and right ventricle have different typed of muscles, due to their different fucntions, so these different types of hypertrophy are pertaining to the fact that they are contained to those respective regions of the heart.

                                        Basically both of these types of hypertrophy are impeding the heart to pump out the blood in both of these areas so it makes sense.
                                         

                                        rsweeney

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                                          left ventricle and right ventricle have different typed of muscles, due to their different fucntions, so these different types of hypertrophy are pertaining to the fact that they are contained to those respective regions of the heart.

                                          Basically both of these types of hypertrophy are impeding the heart to pump out the blood in both of these areas so it makes sense.


                                          I am speaking of just the left ventricle. What the text implies [I believe] is that systolic dysfunction of the left ventricle results in diastolic dysfunction of the left ventricle. I'm sorry Omar but I still don't understand :oops: Lets say you have a decrease in contractility of the left ventricle. Thus, you can longer eject properly in the forward direction. Thus, your ESV increases and preload goes up and up as the problem gets worse--this is systolic dysfunction. Now how will this problem in the left ventricle lead to an increase in afterload, which will then lead to diastolic dysfunction of the left ventricle. Where I am stuck is that since systolic dysfunction essentially keeps cardiac output down, I don't see where the increase in afterload [which leads to diastolic dysfunction] comes from. I apologize for my hard headedness :confused: :(

                                          -Richard
                                           

                                          omarsaleh66

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                                            hey disregard my first post cus i thought u were talking about something else.

                                            Ok lets see if we can make sense out of this...

                                            Ok so if u have a systolic disfunction, ur stroke volume goes down and ur ESV increases like u mentioned.

                                            Ur right heart is pumping the same preload, becuase it is still normal, BUT.. since ur ESV is abnormally increased u are going to have ur EDV be too high cuz normal preload coming in + (abnormal amount of blood still in the heart) so u are gonna have backflow, hence damage the mitral valve which will in turn lead to diastolic problems like abnormal preload or EDV.


                                            Ok so lets rewind. U got aortic stenosis or something so u have high afterload or high pressure that its messing up the left ventricle so u have decreased SV and increased ESV. That extra blood not being pumped out is going to put too much pressure on the mitral valve, hence screwing up the left heart's EDV or its diastolic filling properties.


                                            I hope this is right and it makes sense. Its kinda hard to discuss cardio physiology on the internet hahahah

                                            gluck

                                            Omar
                                             

                                            beezar

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                                              rsweeney said:
                                              I am speaking of just the left ventricle. What the text implies [I believe] is that systolic dysfunction of the left ventricle results in diastolic dysfunction of the left ventricle. I'm sorry Omar but I still don't understand :oops: Lets say you have a decrease in contractility of the left ventricle. Thus, you can longer eject properly in the forward direction. Thus, your ESV increases and preload goes up and up as the problem gets worse--this is systolic dysfunction. Now how will this problem in the left ventricle lead to an increase in afterload, which will then lead to diastolic dysfunction of the left ventricle. Where I am stuck is that since systolic dysfunction essentially keeps cardiac output down, I don't see where the increase in afterload [which leads to diastolic dysfunction] comes from. I apologize for my hard headedness :confused: :(

                                              -Richard

                                              My 2 cents:

                                              Definitions and keeping things separate are very important:

                                              Heart failure = inability of the heart to pump enough blood to provide adequate oxygen to tissues. Due to either systolic dysfunction, diastolic dysfunction, or both.

                                              Systolic dysfunction = heart does not generate as much force to pump the blood as in a normal individual (ie: contractile failure). Period. Forget about afterload, preload, eccentric hypertrophy, etc. in the definition.

                                              Diastolic dysfunction = heart does not relax as well as in a normal individual leading to less blood inside the heart leading to less blood pumped out of the heart to the tissues. In pure diastolic dysfunction, contractility remains normal. Again, forget about afterload, preload, etc. in the definition.

                                              Eccentric hypertrophy occurs because of VOLUME overload (eg: aortic regurgitation). The increased volume leads to synthesis of new sarcomeres in SERIES with the old. Hence, radius of the ventricle and thickness of the ventricle both increase. Eccentric hypertrophy is a compensation, and its definition should be kept separate from systolic dysfunction and diastolic dysfunction. In fact, BOTH systolic and diastolic dysfunction can be present in a heart that has eccentric hypertrophy.

                                              Concentric hypertrophy occurs because of PRESSURE overload (eg: aortic stenosis). This increased pressure leads to synthesis fo new sarcomeres in PARALLEL with the old. Hence only the thickness of the ventricle increases. Again, the definition of concentric hypertrophy should be kept separate from systolic and diastolic dysfunction. Both systolic and diastolic dysfunctions can occur in a concentric hypertrophied heart as well.

                                              Now, many books equate concentric hypertrophy with diastolic dysfunction. This is simply not true. They are not equivalent. There is a strong relationship between the 2 however. Concentric hypertrophy --> increased wall thickness. This increased wall thickness often impairs the heart's ability to relax, thus causing diastolic dysfunction. In pure diastolic dysfunction, contractility remains normal. However with concentric hypertrophy, you can also have systolic dysfunction at the same time with diastolic dysfunction... if there is contractile failure from whatever cause.

                                              The reason why they associate systolic dysfunction to dilation of the heart is because with continued systolic dysfunction (contractile failure), the heart will not pump out the blood effectively and its volume will increase, eventually leading to dilation of the heart. Thus there is usually a relationship between eccentric hypertrophy and systolic dysfunction. But again, you can have eccentric hypertrophy with BOTH systolic dysfunction and diastolic dysfunction. Diastolic dysfunction will occur in this case if the heart cannot relax well from whatever cause.

                                              Now clinically, patients hardly ever have pure diastolic or pure systolic dysfunction. They usually have a combo of both. In clinics, you might see a patient with an enlarged heart with ejection fraction of 25% with poor myocardial wall motion. Clearly, he has systolic dysfunction (EF and wall motion are poor thus poor contractility). But does that mean he doesn't have diastolic dysfunction? NO! He can (and most likely does) have this as well, it's just not as clinically apparent from that scenario. We treat it as systolic dysfunction: can be more aggressive with vasodilators and diuretics.

                                              The reason why systolic and diastolic dysfunctions are usually separated are because of treatment: they sort of differ between both. In a patient with a non-dilated heart, thickened walls, EF >50%, but symptoms of heart failure, the patient most likely has mostly diastolic dysfunction. But the patient can also have systolic dysfunction (contractile failure) that is not clinically apparent. But in this case, we treat it as diastolic dysfunction: don't be too aggressive with the vasodilators, and diuretics, etc.

                                              Hope this helps... at least a little.
                                               

                                              beezar

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                                                Another thing... increase in preload can lead to increases in afterload.

                                                You have to remember that afterload is the force that the heart must generate in order to empty the contents of the heart. Afterload = surface tension that the heart generates during systole.

                                                If you have increased preload which leads to increased end-diastolic pressure, the surface tension (and hence afterload) will be higher because of Laplace's law:

                                                surface tension = (pressure x radius) / (2 x wall thickness)

                                                Increased EDP --> increase pressure --> increased surface tension which is equal to increased afterload.

                                                Makes sense because the heart has to squeeze against a higher pressure within the heart (higher preload) in order to pump out the blood. Hence higher afterload.
                                                 

                                                rsweeney

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                                                  WOW! I think I understand it now--actually I know I do! Thank you so much!

                                                  One thing though: Generally afterload is defined in texts as aortic pressure, or the pressure the heart contracts against.

                                                  If wall tension increases does that mean afterload increases, too? [whether the increased wall tension is caused by an increased preload or higher aortic pressure]

                                                  SO these two things increase afterload:
                                                  1)increased end-diastolic volume [or preload--same thing] because the extra volume increases wall tension

                                                  2)increased aortic pressure [but aortic pressure will also go up due to number one above because the increased preload-->increased wall tension [same as wall stretch?]-->increase stroke volume-->increased cardiac output-->increased aortic pressure.

                                                  I guess both are equally valid? Are wall stretch [Frank-Starling] and wall tension equal? I remember from physics that tension relates to force. Does the increased wall stretch in effect increase wall tension via the Frank-Starling mechanism?

                                                  Thank you so much for the extremely thorough and detailed responses! They are a HUGE help!!

                                                  -Richard
                                                   

                                                  BostonSean

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                                                    [/QUOTE]I am speaking of just the left ventricle. What the text implies [I believe] is that systolic dysfunction of the left ventricle results in diastolic dysfunction of the left ventricle. Lets say you have a decrease in contractility of the left ventricle. Thus, you can longer eject properly --this is systolic dysfunction. Now how will this problem in the left ventricle lead to an increase in afterload, which will then lead to diastolic dysfunction of the left ventricle. Where I am stuck is that since systolic dysfunction essentially keeps cardiac output down, I don't see where the increase in afterload [which leads to diastolic dysfunction] comes from. I apologize for my hard headedness :confused: :(

                                                    -Richard[/QUOTE]

                                                    Great post Beezar!!!
                                                    Richard,
                                                    The body will do everything and anything to maintain mean arterial pressure. MAP=TPR*CO....So if one is experiencing systolic dysfunction and one's contractility is reduced, the stroke volume will decrease. Thus CO will be hindered (CO=SV*HR). In response to this the body will increase the TPR by vasoconstricting and thus cause the afterload to increase. A chronic vasoconstrictive state will lead to chronic afterload and potentially diastolic dysfunction.
                                                    :thumbup:
                                                    -BS
                                                     
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