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How does anemia cause a high cardiac output?

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Horowitz

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Can someone help me please? I can't find the mechanism in several physiology texts (including Costanzo and Guyton):scared:
 

virilep

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tissues need oxygen. if you have anemia, less red bloods cells to get oxygen there. so heart compensates and pumps more and more to get the RBCs back out there with oxygen.
 

Anka

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Normovolemic anemia is believed to cause increased cardiac output by (1) decreased blood viscosity; and (2) increased sympathetic tone (Rossi's principles of transfusion medicine). 1 is belived to predominate.

Anka
 

Horowitz

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tissues need oxygen. if you have anemia, less red bloods cells to get oxygen there. so heart compensates and pumps more and more to get the RBCs back out there with oxygen.

Thanks for the input; I know that's what's supposed to happen, but what is the mechanism/feed back loop?
 

-Goose-

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Thanks for the input; I know that's what's supposed to happen, but what is the mechanism/feed back loop?

Read the above post about viscosity. Thats the big point, I believe.
 

Horowitz

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Normovolemic anemia is believed to cause increased cardiac output by (1) decreased blood viscosity; and (2) increased sympathetic tone (Rossi's principles of transfusion medicine). 1 is belived to predominate.

Anka


Does this sound right?

According to the Poiseuille equation (R = 8nl/(pi)r^4), anemia = reduced viscosity, and therefore = reduced resistance, and = reduced TPR.

Since MAP = CO x TPR and TPR is reduced, MAP is also reduced. Via baroreceptor reflex, sympathetic outflow increases, and CO also increases to compensate for the reduced TPR.
 

Anka

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I think you've got the idea, but just to point it out -- you don't need to invoke a feedback loop really for the effect of viscosity. Factors influencing cardiac output are preload and afterload (both of which are affected directly by blood viscosity, and no feedback loop is necessary) as well as heart rate and contractility (which are accounted for by the sympathetic input, and invoke a feedback loop).

Anka
 

Horowitz

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I think you've got the idea, but just to point it out -- you don't need to invoke a feedback loop really for the effect of viscosity. Factors influencing cardiac output are preload and afterload (both of which are affected directly by blood viscosity, and no feedback loop is necessary) as well as heart rate and contractility (which are accounted for by the sympathetic input, and invoke a feedback loop).

Anka

Thanks Anka!:hardy:
 

Blesbok

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On top of the decreased viscosity, there would also be vasodilation because the tissues are not getting enough oxygen so they want more blood to get more oxygen and I would think those two together would cause it.
 

MattD

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I think you've got the idea, but just to point it out -- you don't need to invoke a feedback loop really for the effect of viscosity. Factors influencing cardiac output are preload and afterload (both of which are affected directly by blood viscosity, and no feedback loop is necessary) as well as heart rate and contractility (which are accounted for by the sympathetic input, and invoke a feedback loop).

Anka

While it may be factually accurate (I'm not gonna go look it up), I'm pretty sure the OP wanted to know the mechanism that accounts for the tachycardia and stroke volume changes. Your points about viscosity are interesting, but I'd point out that if you had a decreased number of red blood cells but a compensating (not compensatory, of course) increased number of 'other' cells, viscosity would remain the same. CO would still increase due to the hypoxemia though.

right?
 

Blesbok

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While it may be factually accurate (I'm not gonna go look it up), I'm pretty sure the OP wanted to know the mechanism that accounts for the tachycardia and stroke volume changes. Your points about viscosity are interesting, but I'd point out that if you had a decreased number of red blood cells but a compensating (not compensatory, of course) increased number of 'other' cells, viscosity would remain the same. CO would still increase due to the hypoxemia though.

right?
If you happen to have a mild anemia and a severe case of essential thrombocythemia, then yes, I suppose the viscosity would stay the same. However, i highly doubt you will ever see a proportional increase in other cells to make up for a few million less RBCs. Now, it would potentially be possible to have a relative increase in the viscosity during anemia, but we call that shock.
 

chrischanx

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anemia->hypoxia->anaerobic glycolysis-->more lactic acid->blood pH decrease->chemoreceptor in carotid/aortic bodies/brain->sympathetic outflow

correct me if I m wrong
 
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had2piknowEM

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anemia->hypoxia->anaerobic glycolysis-->more lactic acid->blood pH decrease->chemoreceptor in carotid/aortic bodies/brain->sympathetic outflow

correct me if I m wrong

I think this is the best response...however I would just add that the carotid and aortic bodies respond more to a decrease in O2 which is found in anemia, and that the CNS receptors respond more to the increase in CO2. Anyways...the result is the same...an increase in sympathetic tone---> tachycardia and increased inotropy.
 

MattD

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If you happen to have a mild anemia and a severe case of essential thrombocythemia, then yes, I suppose the viscosity would stay the same. However, i highly doubt you will ever see a proportional increase in other cells to make up for a few million less RBCs. Now, it would potentially be possible to have a relative increase in the viscosity during anemia, but we call that shock.

Hey, I didn't say it was a realistic scenario, just an exercise for the brain :)
 

dr1day

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OK. We're in the neuro block right now, so I kept reading the thread title as "How does AMNESIA cause high cardiac output" :laugh: I got really worried for a minute because our test is on Friday and I didn't remember any lecturer talking about anything relating the two topics.

Maybe it's time for me to take a break from studying :)
 

kpod

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I think this is the best response...however I would just add that the carotid and aortic bodies respond more to a decrease in O2 which is found in anemia, and that the CNS receptors respond more to the increase in CO2. Anyways...the result is the same...an increase in sympathetic tone---> tachycardia and increased inotropy.

Actually, I think we need to be careful about this because the carotid and aortic chemoreceptors shouldn't respond in anemia becuase the pO2 should still remain at 100%--its simply that there isn't enough Hb.
 

Blesbok

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Actually, I think we need to be careful about this because the carotid and aortic chemoreceptors shouldn't respond in anemia becuase the pO2 should still remain at 100%--its simply that there isn't enough Hb.
And it skips out on about 10 other mechanisms that would cause changes in perfusion and carciac output.
 

treva

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Actually, I think we need to be careful about this because the carotid and aortic chemoreceptors shouldn't respond in anemia becuase the pO2 should still remain at 100%--its simply that there isn't enough Hb.

Assuming the anemia caused a metabolic acidosis you would still get chemoreceptor response, however the peripheral chemoreceptors would pre-dominate over the central chemoreceptors, because central chemoreceptors detect pH in the context of CO2 levels (which would be elevated). However things such as lactate floating around in the blood would strongly stimulate the peripheral chemoreceptors.

Correct me if I'm wrong, but aren't we just talking about the respiratory chemoreceptors here? This would explain why you see an increased RR (and SoB) with anaemia. I can't make the connection in my head between these respiratory controls and an increased cardiac output.

I haven't done cardio yet (next block) but doesn't the heart use baroreceptors in the carotid sinus to detect blood pressure in the artery? In a normocytic anemia caused by a hemmorhage this could explain an increase in CO (due to drop in BP), but what if you have a micro / macrocytic anemia?
 

Anka

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Anemia usually doesn't cause a metabolic acidosis unless it is hypovolemic. Think about it -- if a physiologic insult is bad enough to cause metabolic acidosis due to tissue malperfusion, the person is in shock. If the anemia is that bad, you've got problems other than high output cardiac failure.

Hypoxia indeed has a vasodilator effect (except in the pulmonary bed, where it is vasoconstrictive), but this is, at least from what I've read, not the primary mechanism by which cardiac output is increased in chronic, normovolemic anemia. Again, this kind of makes sense given that most people think this works through an ATP/ADP balance mechanism, so if you're tissue is not oxygenated enough to maintain ATP/ADP within normal, you're going to be really sick.

I included a reference so you could look it up... Rossi's principles of transfusion medicine (which is available on Amazon in searchable form... so it shouldn't be to hard to read over their very nice description). It's fun to go through all of the possible physiologic mechanisms, but at some point you actually have to read (or do an experiment) to find out which of the possible mechanisms is primary, and which aren't important.
 
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