[Ref: SH4:p31]
Induction can be accelerated by concentration effect
Recovery cannot be (one cannot administer negative concentration)
At induction, tissue concentrations are all equal and all zero
At recovery, tissue concentrations all differ, depending on the solubility and duration
At the end of anaesthesia, fat and muscles might not have equilibrated
--> Partial pressure that these tissues may still be lower than Pa
--> AA continues to be transfered from blood into fat and muscles
--> Initially accelerates the decline in PA
The longer the duration
--> More AA is absorbed in high capacity tissues such as fat and muscles
--> Time to recovery is longer
This effect is more pronouced in more soluble AAs
Oil:gas solubility is relevant here, not blood:gas solubility
During induction, rate of rise in PA correlates with the blood:gas partition coefficient.
During recovery, correlation is not as strong.
Increase in PA during induction is not influenced by metabolism
* Not even for highly metabolised AA such as HAL and methoxyflurane
Decline in PA can be due to:
For example,
* PA of HAL decreases faster than iso and en
* PA of methoxyflurane decrease faster than EN (even though methoxyflurane is about 6 times more soluble)
--> Both due to greater metabolism of HAL and methoxyflurane
Elimination of AA depends on
Time needed for a 50% decrease in PA of en, iso, des, and sevo is <5min.
* Primarily a function of alveolar ventilation
* Does not increase significantly with duration
Time needed for a 80% decrease in PA of des and sevo is < 8min
* Does not increase significantly with duration
However,
Time needed for a 80% decrease in PA of EN and iso increases significantly with duration.
Thus,
The major difference in the rate at which des, sevo, iso, and EN are eliminated occur in the final 20% of the elimination process
Diffusion hypoxia occurs when inhalation of N2O is discontinued suddenly
--> High volume of N2O enters alveoli from blood
Two effect:
This movement of N2O is the greatest in the first 1 to 5 minutes.