Hi everyone, Im having my physiology exams in 3 day's times n Im desperate for some help in this question, will someone please give me some advice on these questions? Im desperate! I have coloured my questions blue and placed them alongside my reasoning, so that you can better understand the context of my questions: Question 1 Continuous and severe vomitting may lead to metabolic alkalosis due to hypochloremic alkalosis and hypovolemic alkalosis. I understand the physiology of these 2 causes. However, this also occurs: CO2 + H20 <=> H+ + HCO3- During prolonged vomitting, excess HCO3- is released into the blood stream, thus pushing the equation to the left, decreasing [H+] and increasing PCO2. Here's what Im confused about: Wouldnt the increased PCO2 cause increased ventilation, and in so doing cause the equation to shift left even more, aggravating the alkalosis? Does transient alkalosis and hyperventilation and this occur in this patient in real life? I shall call this effect A. However, if we were to look at it the other way, any increased [HCO3-] and pushing of the equation to the left will also cause plasma [H+] to drop, which will stimulate peripheral chemoreceptors at the aortic and carotid bodies, causing hypoventilation, thus increasing PCO2 and correcting the situation. (Is H+ in the plasma important at all in stimulating the central chemoreceptors in the brain to cause ventilation? Or is [H+] mainly, if not only, detected at peripheral chemoreceptors only?) I shall call this effect B. Relating back to real life scenarios in the hospital, patients suffering from prolonged vomiting thus metabolic alkalosis usually hypoventilate, not hyperventilate, to correct the alkalosis. Does this mean that effect B is more significant than effect A, which implies that the triggering of hypoventilation by plasma [H+] is more powerful than the triggering of hyperventilation by excess CO2? (I find this wierd, as I was taught that CO2 is always the more powerful stimulant in triggering off ventilation, not H+) Effects A and B are my self-formed hypotheses. Now, what I was taught in uni was this: As long as the lungs are functioning well, PCO2 in our blood is always kept very constant (with a very rapid response time, usually within seconds) despite changes in CO2 production in our body. As long as the kidney is working fine, [HCO3-] is also kept constant despite changes to its rate of metabolic production or external ingestion, although the response time is longer (days to weeks - am I correct to say this?). With this in mind, I was told that during prolonged vomitting, the excess HCO3- produced by the stomach will be quickly removed by the kidneys (doesnt it take days to weeks for the kidneys to compensate for any [HCO3-] imbalance in the body? I dont find point very valid), and the excess CO2 produced as a result of effect A (see above) will also be removed quickly by hyperventilation. Thus, only [H+] will drop, with little change in [HCO3-] or PCO2. This drop in [H+] will then push the equation to the right, decreasing PCO2, trigger hypoventilation and correct the alkalosis. I find this explanation rather wierd, because of the question I raised above (the previous question regarding HCO3- compensation by the kindeys). Question 2 Again, we look at this equation: CO2 + H20 <=> H2CO3 <=> H+ + HCO3- It is commonly said, for example, that if PCO2, [H+] or [HCO3-] changes, the equation shifts left or right to buffer the changes etc. However, isnt it true that the components of this equation cannot freely equilibrate in the plasma (as the reversible reaction does not take place readily without carbonic anhydrase), but only do so where there is abundant carbonic anhydrase to catalyse the reversible equation, such as in RBCs? Why then can we still assume that the equation is freely equilibrating in the plasma, allowing for rapid or almost instantaneous right-left and left-right shifts in the plasma during buffering reactions? Is it because RBCs are so abundant in the plasma that any excess HCO3-, H+ or CO2 in the plasma will be rapidly acted upon by carbonic anhydrase in RBCs, allowing for rapid equilibration in the plasma? I know that the questions are long, but would someone please please help me out? I really dont want to fail my exams but as you can see, I may just be on my way to it. I would greatly appreciate your help!