Concentration effect and Second gas effect
The forward movement of inhalational agent is determined by a series of partial pressure gradients, beginning at the vaporizer of the anaesthetic machine, continuing in the breathing circuit, the alveolar tree, blood, and then tissue. The principal objective of that movement is to achieve equal partial pressures on both sides of each single barrier. The alveolar partial pressure governs the partial pressure of the anaesthetic in all body tissues; they all will ultimately equal the alveolar partial pressure of the gas. After a short period of equillibration the alveolar partial pressure of the gas equals the brain partial pressure. Thus the alveolar partial pressure can be raised by increasing minute ventilation, flow rates at the level of the vaporizer and by using a non-rebreathing circuit.
The Concentration Effect-
The concentration effect describes how the concentration of the gas in the remaining alveolar volume can increase after some of the gas has been transferred into the blood. Thus, the concentration effect states that with higher inspired concentrations of an anaesthetic, the rate of rise in arterial tension is greater.
N2O has a low blood:gas partition coefficient and therefore a rapid onset and offset of action. N2O is about 20 times more soluble than O2 and N2. During induction the volume of N2O entering the pulmonary capillaries is greater than the N2 leaving the blood and entering the alveolus. As a result the volume of the alveolus decreases, thereby increasing the fractional concentration of the remaining gases. This process augments ventilation as bronchial and tracheal gas is drawn into the alveolus to make good the diminished alveolar volume.
The Second Gas Effect-
The second gas effect usually refers to nitrous oxide combined with an inhalational agent. Because nitrous oxide is not soluble in blood, its' rapid absorption from alveoli causes an abrupt rise in the alveolar concentration of the other inhalational anaesthetic agent.
Diffusion Hypoxia
First described by Fink in 1955, this is effectively the reverse of the above. The elimination of a poorly soluble gas, such as N2O, from the alveoli may proceed at as greater rate as its uptake, (The volume of N2O entering the alveolus is greater than the volume of N2 entering the pulmonary capillary blood.), thereby adding as much as 1 l/min to alveolar air. This gas effectively dilutes alveolar air, and available oxygen, so that when room air is inspired hypoxia may result. This is usually only mild and rarely clinically significant although this may occur with any anaesthetic agent, its magnitude is insignificant unless an insoluble agent, such as nitrous oxide, has been inhaled for some time.
Blood:gas coefficient
The solubility of a gas in liquid is given by its Ostwald solubility coefficient. This represents the ratio of the concentration in blood to the concentration in the gas phase (c.f. Bunsen at s.t.p.). This is independent of pressure, obeying Henry's law, serum proteins and RBC's are the major determinants of solubility. Solubility describes the affinity of the gas for a medium such as blood or fat tissue. The blood/gas partition coefficient describes how the gas will partition itself between the two phases after equilibrium has been reached. Isoflurane for example has a blood/gas partition coefficient of 1.36. Thus if the gas is in equilibrium the concentration in blood will be 1.36 times higher than the concentration in the alveoli. A higher blood gas partition coefficient means a higher uptake of the gas into the blood and therefore a slower induction time. It takes longer until the equilibrium with the brain partial pressure of the gas is reached. Lower B:G coefficients are seen with Haemodilution Obesity Hypoalbuminaemia and starvation Higher coefficients are seen in: Adults versus children Hypothermia Postprandially
Effect of cardiac output
A higher cardiac output removes more volatile anaesthetic from the alveoli and hence lowers the alveolar partial pressure of the gas. It will take longer for the gas to reach equilibrium between the alveoli and the brain. Therefore, a high cardiac output prolongs induction time. The alveolar to venous partial pressure difference reflects tissue uptake of the inhaled anaesthetic agent. A large difference is caused by increased uptake of the gas during the induction phase. This facilitates the diffusion of the gas from the alveoli into the blood. The brain/blood coefficient describes how the gas will partition itself between the two phases after equilibrium has been reached. All inhalational anaesthetics have high fat/blood partition coefficients. This means that most of the gas will bind to fatty tissue as times goes by. The partial pressure of the gas in fatty tissue will rise very slowly, thus inhalational anaesthetics stored in such tissue in obese patients may delay awakening at the end of anaesthesia.