Preoxygenation before anesthetic induction and tracheal intubation is a widely accepted maneuver, designed to increase the body oxygen stores and thereby delay the onset of arterial hemoglobin desaturation during apnea. Because difficulties with ventilation and intubation are unpredictable, the need for preoxygenation is desirable in all patients. During emergence from anesthesia, residual effects of anesthetics and inadequate reversal of neuromuscular blockade can lead to hypoventilation, hypoxemia, and loss of airway patency. In accordance, routine preoxygenation before the tracheal extubation has also been recommended. The objective of this article is to discuss the physiologic basis, clinical benefits, and potential concerns about the use of preoxygenation. The effectiveness of preoxygenation is assessed by its efficacy and efficiency. Indices of efficacy include increases in the fraction of alveolar oxygen, increases in arterial oxygen tension, and decreases in the fraction of alveolar nitrogen. End points of maximal preoxygenation (efficacy) are an end-tidal oxygen concentration of 90% or an end-tidal nitrogen concentration of 5%. Efficiency of preoxygenation is reflected in the rate of decline in oxyhemoglobin desaturation during apnea. All investigations have demonstrated that maximal preoxygenation markedly delays arterial hemoglobin desaturation during apnea. This advantage may be blunted in high-risk patients. Various maneuvers have been introduced to extend the effect of preoxygenation. These include elevation of the head, apneic diffusion oxygenation, continuous positive airway pressure (CPAP) and/or positive end-expiratory pressure (PEEP), bilevel positive airway pressure, and transnasal humidified rapid insufflation ventilatory exchange. The benefit of apneic diffusion oxygenation is dependent on achieving maximal preoxygenation, maintaining airway patency, and the existence of a high functional residual capacity to body weight ratio. Potential risks of preoxygenation include delayed detection of esophageal intubation, absorption atelectasis, production of reactive oxygen species, and undesirable hemodynamic effects. Because the duration of preoxygenation is short, the hemodynamic effects and the accumulation of reactive oxygen species are insufficient to negate its benefits. Absorption atelectasis is a consequence of preoxygenation. Two approaches have been proposed to reduce the absorption atelectasis during preoxygenation: a modest decrease in the fraction of inspired oxygen to 0.8, and the use of recruitment maneuvers, such as CPAP, PEEP, and/or a vital capacity maneuver (all of which are commonly performed during the administration of anesthesia). Although a slight decrease in the fraction of inspired oxygen reduces atelectasis, it does so at the expense of a reduction in the protection afforded during apnea.
Using a circle absorber system, normal breathing of oxygen for 3-5 min achieves optimal oxygenation of the lungs; whereas 4 deep breaths in 30 s does not. However, extending deep breathing to 1.5-2 min and using a high flow of oxygen improves oxygenation of the lungs to the same degree as normal breathing for 3-5 min. This may have important implications for patient safety.
The circle absorber and NasOral systems were equally effective in achieving maximal preoxygenation during tidal volume breathing. Resuscitation bags differed markedly in effectiveness during preoxygenation; those with duck-bill valves without one-way exhalation valves were the least effective. Thus, the use of these bags should be avoided for preoxygenation.
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