scuba andy
Registered
Hi,
Ive been reading about the narcotic effects of gases at depth. I cant seem to find answers to some questions after doing some online searching, so here goes...
1. Is it only a minimum partial pressure of O2 in a gas that enables successful external and internal respiration of O2?
e.g. could a mix of 3.5% O2 be breathed as successfully at 6 ATM (nitrogen narcosis aside) as normal air can be breathed at 1 ATM?
2. Why does the pulmonary exchange of CO2 appear to be less efficient than that of O2? - I understand that the blood PO2 increases (150%) from 40mmHg to 100mmHg as it passes through the alveolar capillaries, but that blood PCO2 decreases (only 11.1%) from 45mmHg to 40mmHg. Is it just that the O2 molecule has been made bigger having become CO2 after metabolism?
3. Is the safe (non-narcotic) arterial PCO2 range actually narrower at depth?
4. How quickly canarterial PCO2 increase above safe levels with exertion or deficient breathing? And how quickly can safe homeostasis be re-established after PCO2 spiking into dangerous levels?
Hope the questions arent phrased too poorly to make sense.
thanks,
andy
Ive been reading about the narcotic effects of gases at depth. I cant seem to find answers to some questions after doing some online searching, so here goes...
1. Is it only a minimum partial pressure of O2 in a gas that enables successful external and internal respiration of O2?
e.g. could a mix of 3.5% O2 be breathed as successfully at 6 ATM (nitrogen narcosis aside) as normal air can be breathed at 1 ATM?
2. Why does the pulmonary exchange of CO2 appear to be less efficient than that of O2? - I understand that the blood PO2 increases (150%) from 40mmHg to 100mmHg as it passes through the alveolar capillaries, but that blood PCO2 decreases (only 11.1%) from 45mmHg to 40mmHg. Is it just that the O2 molecule has been made bigger having become CO2 after metabolism?
3. Is the safe (non-narcotic) arterial PCO2 range actually narrower at depth?
4. How quickly canarterial PCO2 increase above safe levels with exertion or deficient breathing? And how quickly can safe homeostasis be re-established after PCO2 spiking into dangerous levels?
Hope the questions arent phrased too poorly to make sense.
thanks,
andy