when a high conc of an anaesthetic agent is administered in the inspired gases a very large conc gradient between the alveoli and blood exists especially if partial denitrogenation is done, regardless of the solubility of the anaesthetic agent.
Nitrous oxide is less soluble but 30 times more soluble than nitrogen.
The total volume of nitrous oxide absorbed into the body over 1-2.5hrs after anaesthesia can be up to 30lts, 5-6lts being absorbed in the first 10minutes.
“ The rate of raise of FA/F1 ration is determined by Fi and alveolar ventilation”
As half of N 2 O is removed from the lung the conc of second gas increases from 1-1.7 although the absolute volume does not change. The relative conc increases because of the reduction in total lung volume.
Second one is – if lung is not allowed to collapse but is replenished with gas containing same conc then more of second gas is brought in to the lung. According to Epstein the increased inspiratory ventilation is the second part of second gas effect. The imp. of conc. vs increased inspired ventilation to the second gas effect depends on the solubility of the second gas. If solubility is more the explanation lies in increased ventilation and if solubility is less the concentrating effect is imp.
Def: condition where no difference in partial pressures of agent exists between two phases such as gas phase in alveoli and the dissolved phase in blood.
Expressed in conc. and not as partial pressures.
The larger the blood/gas par coefficient the more soluble the agent in the blood and larger the uptake by the blood and reduction in partial pressure in the alveoli(PA) and consequent reduction in Pa and Pcns.
Increase in cardiac output slows down the raise of alveolar conc even though the equilibrium is attained faster in between tissue compartments
Effect of increase in cardiac output on FA/FI ratio is more pronounced with soluble agents. Decrease in co with soluble agents can cause high FA/FI ratio and sudden increase in PP in CNS. This is further complicated by increase in alveolar ventilation. Profound depression of CVS and CNS can occur.
In obese patients ERV and FRC are reduced, more so in supine position nearly to closing volumes producing true rt to left shunt.
Smaller FRC theoretically must produce faster equilibration between PI, PA and pa but because of collapse of alveoli and shunting there is a delay in uptake of anaesthetic agent so that Pa/PA ratio is reduced and so induction is delayed.
various areas of brain and spinal cord play an important role in getting equilibrium with anaesthetic agent and by which end result occurs, like loss of consciousness movement, analgesia, depression and blockade of autonomic reflexes and relaxation.
Since brain tissue is highly perfused and raise of tension of anaesethic agent is rapid and uptake ceases with in a short period, the raise is more with poorly soluble agents but depends on pressure gradient between agent, PA, Pcns and CBF.
“ Tissue uptake of anaesthetic is governed by tissue solubility, perfusion, tissue size and tissue saturation” .
Nearly all the factors that govern the rate at which the alveolar conc raises in induction apply to recovery.
The immediate decline of the anaesthetic level is rapid because of the wash out of the FRC.
As the ventilation removes the anaesthetic from the alveoli more and more anaesthetic gets washed into the alveoli from the tissues. This depends on the venous alveolar anesthetic gradient which will be higher for more soluble agents. So the fall in alveolar levels will be slow when compared to less soluble agents.