Urkiola2 said:Great to talk/discuss with an anesthesiologist. That is very impresive, as I personally have high respect for your field for the huge knowledge of general medicine and physiology involved.
Maybe we are not making our points across.
I know that anthesthesiologists are very concerned always with oxygen delivery since it is a crucial part of your job. Especially important as you better than I know, dealing with hypovolemia and hypovolemic shocks is one of the situations anesthesiologists deal with the most and plasma expanders like Hidroxiethyl Starch (HES), albumin, Gelofusine (Gelatin) or Dextran (branched polysaccharide) are widely used by anesthesiologists under hypovelemic situations. So I understand that from your point of view and your experience hypo and hypervolemia are terms and situations that you control very well. I have no doubt about your knowledge about oxygen carrying capacity and delivering to the tissues.
I believe that what you claim has to do with viscosity and in situations like the one you mention (polycythemia vera) the blood flow will be decreased due to the increased viscosity as we can apply Poiseuille's Equiation.
However the situation in which anesthesiologists work is different than the situation we can observe in athletes like it is the case of the post by rmur17. In general medicine and especially during surgery a Hct of 40% or 50% as you know is pretty much irrelevant since the patient is perfectly stable and oxygenized. However in terms of exercise situation a decrease from a physiological normal Hgb levels of 14g/dL to 13g/dL you could have some consequences in terms of performance. An average citizen will probably not tell such a small decrease but an athlete will defenetely tell it. In that situation we are dealing with neither hypo/hypervolemia but dealing with exercise performance and oxygen delivery to the cells. Since O2 is bound to Hgb, if your Hgb levels decrease your O2 carrying capacity will be drecreased to the tissues and especially important this will be during high intensity exercise. An increase in Cardiac Output will not have an effect to compensate the lower Oxygen carrying capacity since during maximal exercise you will reach your Maximal Cardiac Output with low or high Hgb levels. To me the only thing that can change to compensate the decrease in oxygen carrying capacity is 2,3 DPG (2,3 diphosphoglycerate) which could increase in order to increase the unload of O2 bound to Hgb. However and something that it is my day-to-day thing when an athlete decreases his/her Hgb and Hct they can defenetely tell a decrease in their performance. When these athletes bring back their normal physiological Hgb/Hct their performance goes back to normal.
Same thing happens with EPO or blood transfussions. Even when you can be dealing with a hypervolemia the oxygenation to the tissues will be much larger increased due to a higher levels of Hgb and therefore oxygen carrying capacity.
Cheers.
I didn't say there would be no effect from changing the hct but that it will not be as great as many might think as many different things affect oxygen delivery to the tissues. A 10% increase in hct does not result in a 10% increase in capability and vice-versa. And, there is a point where increasing hct further will not result in an improve performance. There are so many variables it is almost impossible to say what the optimum hct for optimum performance would be. You suggest that maximum cardiac output is fixed and not dependent upon hct. There is no evidence to support that view.
I personally think that filling pressure is a much bigger deal in affecting how an athlete performs than the normal variations in hct. For instance, if an athlete exercises and does not replenish fluids lost through sweat the hct will go up but the filling pressure will go down. Wonder if the potential of the athlete goes up or down as the hct goes up under the situation of dehydration?
The capillaries do not care if the oxygen demand of the tissue is due to athletic demands or some other reason. In fact, the two major areas of concern regarding medical research look at delivery of oxygen to the brain and to the heart. The heart is nothing more than an exercising muscle so what is learned there can be applied directly to what happens in the legs. The major difference between exercising muscle and non-exercising tissue is blood flow can only occur in the muscle when it is relaxed, not during contraction. The physiology of this is pretty well understood and the current best understanding be found in any cardiac anesthesia test. Otherwise, the physiology of blood flow through the capillaries (the only part of the vascular system where oxygen can leave the vessels to get to the tissues) is pretty much the same for all the tissues.
My point is that it is complicated. Changing one thing may have adverse influences on another thing. Many things affect oxygen delivery to the tissues including all the variables that can affect maximum cardiac output, the blood pressure, and all the things that can affect the oxyhemoglobin dissociation curve, and how much right left physiolgic shunting is occuring in the lungs, and how easily the blood flows through the tissues, beyond the simple question of how much hemoglobin is in the blood. And then, exercise can affect other variables like electrolyte concentrations that can adversely affect the ability of the muscles to contract optimally that has nothing to do with hemoglobin concentraiton but everything to do with performance. Wishing it to be simple does not make it so.
It is possible to say if I increase hemgolbin concentration the expected tendency is going to be to improve performance but it is not going to be possible to predict how much.
