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

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?
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
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
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
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.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?
anemia->hypoxia->anaerobic glycolysis-->more lactic acid->blood pH decrease->chemoreceptor in carotid/aortic bodies/brain->sympathetic outflow
correct me if I m wrong
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.
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.
And it skips out on about 10 other mechanisms that would cause changes in perfusion and carciac output.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.
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.