Hey
I have a basic question that I've never been able to get my head around.
I know that in hyperventilation there is a decrease in ETCO2, however the physiology behind it gets me really confused.
So in hyperventilation I get that the arterial paC02 decreases as the is increased removal of CO2 as the CO2 is blown off and a resp alkalosis may develop. Surely therefore if more CO2 is being blown off the ETCO2 should be higher (as there will be more CO2 in the expired air?)
Again I know in hypoventilation the ETCO2 rises. Again my brain tells me that with hypoventilation leads to decreased gas exchange and pCO2 rises in the systemic circulation (hence acidosis on an ABG) - if there is decreased gas exchange - why will the end tidal CO2 increase?
I know I am missing something basic but would love some clarity!
Cheers
Adam
I have a basic question that I've never been able to get my head around.
I know that in hyperventilation there is a decrease in ETCO2, however the physiology behind it gets me really confused.
So in hyperventilation I get that the arterial paC02 decreases as the is increased removal of CO2 as the CO2 is blown off and a resp alkalosis may develop. Surely therefore if more CO2 is being blown off the ETCO2 should be higher (as there will be more CO2 in the expired air?)
Again I know in hypoventilation the ETCO2 rises. Again my brain tells me that with hypoventilation leads to decreased gas exchange and pCO2 rises in the systemic circulation (hence acidosis on an ABG) - if there is decreased gas exchange - why will the end tidal CO2 increase?
I know I am missing something basic but would love some clarity!
Cheers
Adam