Hypoxia nitrous oxide

Until recent times, the only toxicological hazards attributable to nitrous oxide were those common to asphyxiants, with death or permanent brain injury occurring only under conditions of hypoxia. A number of untoward and toxic effects have now been associated with exposure. One of the earliest findings was that patients given 50% nitrous oxide and 50% oxygen for prolonged periods, to induce continuous sedation, developed bone marrow depression and granuloqn openia. The bone marrow usually returned to normal within a matter of days once the nitrous oxide was removed, but several deaths from aplastic anemia have been recorded. ... 

Nitrous oxide is the only inhalation anesthetic that is a gas. It is chemically inert. Nitrous oxide has little effect on overall cardiovascular function. Disadvantages are that it has no muscle relaxing effect and that it cannot be used on its own because of high Minimal Alveolar Concentration values needed for adequate anesthesia. During recovery there is a risk for hypoxia and anesthesia should be slowly tapered off to prevent this event. 

Nitrous oxide decreases tidal volume and increases the rate of breathing and minute ventilation. Although arterial carbon dioxide partial pressures tend not to be affected the normal ventilatory responses to carbon dioxide and to hypoxia are depressed. Alveolar collapse in structured lung segments may be more rapid in the presence of nitrous oxide than with oxygen due to its greater solubility. Similarly, it depresses mucous flow and chemotaxis. In theory these factors predispose to postoperative respiratoiy complications. 

Diffusion hypoxia describes the rapid movement of nitrous oxide from the blood into the alveoli in the early recovery phase. It is usual to circumvent this problem by administering 100% oxygen for a few minutes at the end of anaesthesia. 

These are shown in Table 3.3. Xenon (MAC 70%) has a potency of about twice that of nitrous oxide (MAC 104%). Thus, it can be given in anaesthetic concentrations in o> gen with less risk of hypoxia. It is highly insoluble in all body tissues with a blood/gas partition coefficient of 0.14 (nitrous oxide, 0.47 sevoflurane, 0.65 desflurane, 0.42). 

Postoperatively, the anesthesiologist withdraws the anesthetic mixture and monitors the immediate return of the patient to consciousness. For most anesthetic agents, recovery is the reverse of induction that is, redistribution from the site of action rather than metabolism underlies recovery. The anesthesiologist continues to monitor the patient to be sure that there are no delayed toxic reactions, for example, diffusion hypoxia for nitrous oxide, and hepato-toxicity with halogenated hydrocarbons. 

The main complications associated with nitrous oxide inhalation occur as a result of hypoxia. Prolonged administration may also be harmful. Nitrous oxide is rapidly absorbed on inhalation. 

Nitrous oxide (laughing gas) has been used as an inhalant anesthetic since 1844 and is still widely used in human anesthesia because of its potent analgesic actions. Although it has many desirable properties, including rapid onset and recovery, limited cardiopulmonary depression and minimal toxicity, it is a weak anesthetic. Its lack of potency, its relatively high cost and its possible contribution to hypoxia and accumulation in gas-filled spaces limits its use in the horse. 

Nitrous oxide is very insoluble in blood and other tissues (Table 13-1). This results in rapid equilibration between delivered and alveolar anesthetic concentrations and provides for rapid induction of anesthesia and rapid emergence following discontinuation of administration. The rapid uptake of N2O from alveolar gas serves to concentrate coadministered halogenated anesthetics this effect (the second gas effect ) speeds induction of anesthesia. On discontinuation of administration, nitrous oxide gas can diffuse from blood to the alveoli, diluting Oj in the lung. This can produce an effect called diffusional hypoxia. To avoid hypoxia, 100% Oj rather than air should be administered when N O is discontinued. 

Respiratory System Nitrous oxide causes modest increases in respiratory rate and decreases in tidal volume in spontaneously breathing patients. The net effect is that minute ventilation is not significantly changed and remains normal. Even modest concentrations of N O markedly depress the ventilatory response to hypoxia. Thus, it is prudent to monitor arterial saturation directly in patients receiving or recovering from nitrous oxide. 

Nitrous oxide i i 1 104% 0.5 Minimal Rapid onset and recovery, no metabolism Diffusional hypoxia Spontaneous abortions j... 

Respiratory effects Rate of respiration may be increased by inhaled anesthetics, but tidal volume and minute ventilation are decreased, leading to an increase in arterial CO tension. Inhaled anesthetics decrease ventilatory response to hypoxia even at subanesthetic concentrations (eg, during recovery). Nitrous oxide has the smallest effect on respiration. 

V 1 1 No effects. Least soluble in blood. Thus, excreted rapidly by expiration of unmetabolized gas. Transient hypoxia following anesthesia. Greater than 100% nitrous oxide to achieve anesthesia in 50% of patients, thus it is almost always used in combination with other... 

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