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During nitrous oxide administration, appreciable volumes of nitrous oxide can move into closed gas spaces within the body. This transfer does not influence FA/FI but may have important functional consequences. There are two types of closed gas spaces in the body: those enclosed by
Figure 5-12
In dogs, when only the right lung was ventilated, the
rise of the very soluble anesthetic methoxyflurane in arterial blood was normal (i.e.,
did not deviate from control), but the rise for the poorly soluble anesthetic cyclopropane
was significantly slowed. (Adapted from Stoelting RK, Longnecker DE: Effect
of right-to-left shunt on rate of increase in arterial anesthetic concentration.
Anesthesiology 36:352–356, 1972.)
These theoretical limits may be approached rapidly in patients with pneumothorax or gas emboli. Administration of 75% nitrous oxide in the presence of a pneumothorax may double the pneumothorax volume by 10 minutes and may triple it by 30 minutes[54] ( Fig. 5-13 ). This increase in volume may seriously impair cardiorespiratory function,[55] and the use of nitrous oxide is contraindicated in the presence of a significant pneumothorax.
Figure 5-13
The volume of a pneumothorax created by air injection
is affected little when oxygen subsequently is breathed (lower
two curves). However, if 75% nitrous oxide is breathed, the volume doubles
in 10 minutes and triples in 0.5 hour (upper three curves).
(Adapted from Eger EI II, Saidman LJ: Hazards of nitrous oxide anesthesia
in bowel obstruction and pneumothorax. Anesthesiology 26:61–66, 1965.)
A still more rapid expansion of volume occurs if air inadvertently enters the bloodstream in a patient anesthetized with nitrous oxide. Expansion may be complete in seconds rather than minutes. Munson and Merrick[56] demonstrated that breathing nitrous oxide rather than air decreased the lethal volume of an air embolus in animals ( Fig. 5-14 ). The difference could be entirely explained by expansion of the embolus in the animals breathing nitrous oxide (i.e., the predicted total volume of air plus nitrous oxide in the embolus equaled the volume of air needed to produce death in animals breathing only air). These studies suggest caution in the use of nitrous oxide for procedures in which air embolization is a risk (e.g., posterior fossa craniotomies, laparoscopy). They also suggest that nitrous oxide administration should be immediately discontinued if air embolization is suspected. Conversely, a nitrous oxide "challenge" may be used to test whether air embolization has occurred. [57]
The tracheal tube cuff normally is filled with air and is susceptible to expansion by nitrous oxide.[58] The presence of 75% nitrous oxide surrounding such a cuff can double or triple the volume of the cuff. This results from a more rapid diffusion of nitrous oxide than nitrogen across the cuff; the more rapid diffusion occurs because of the greater solubility of nitrous oxide. The result may be an unwanted increase in pressure exerted on the tracheal mucosa. Similarly, nitrous oxide may expand the cuffs of balloon-tipped (e.g., Swan-Ganz) catheters[59] [60] when the balloons are inflated with air. The expansion is rapid, and a doubling of volume may occur within 10 minutes.
Figure 5-14
An air embolus equaling 0.55 mL/kg killed 50% of rabbits
breathing oxygen. If the inspired gas mixture contained 75% nitrous oxide, only
0.16 mL/kg was required to kill one half of the animals. (Adapted from Munson
ES, Merrick HC: Effect of nitrous oxide on venous air embolism. Anesthesiology
27:783–787, 1966.)
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