Preoxygenation: Physiologic Basis, Benefits, and Potential Risks

Usharani Nimmagadda, MD; M. Ramez Salem, MD; George J. Crystal, PhD

Disclosures

Anesth Analg. 2017;124(2):507-517. 

In This Article

Preoxygenation: Physiologic Basis, Efficacy, and Efficiency

Preoxygenation increases the body O2 stores, the main increase occurring in the functional residual capacity. The size of the increases in O2 volume in the various body tissues is difficult to assess with precision, but assuming that the partition coefficient for gases approximates the gas-water coefficients, the estimated increases are appreciable (Table 1; Figure 1).[18,19] The effectiveness of preoxygenation is assessed by its efficacy and efficiency.[8] Indices of efficacy include increases in the fraction of alveolar O2 (FAO2),[20–22] decreases in the fraction of alveolar nitrogen (FAN2),[23,24] and increases in arterial O2 tension (PaO2).[25–27] Efficiency of preoxygenation is assessed from the decline of oxyhemoglobin desaturation (SaO2) during apnea.[28–30]

Figure 1.

Variation in the volume of O2 stored in the functional residual capacity (□), blood (▴), tissue (^), and whole body (▪) with the duration of preoxygenation. Published with permission from Campbell and Beatty.19

Preoxygenation increases FAO2 and decreases FAN2 (Figure 2).[31] The key to achieving maximal preoxygenation is the washout of alveolar nitrogen (N2). The terms preoxygenation and denitrogenation have been used synonymously to describe the same process. In a subject with normal lung function, the O2 washin and the N2 washout are exponential functions and are governed by the time constant (t) of the exponential curves. This constant is proportional to the ratio of alveolar ventilation to functional residual capacity. Because preoxygenation before anesthetic induction is typically performed using a semiclosed circle absorber circuit, the washout of the circuit must also be considered using the time constant of the circuit, which is the time required for flow through a container (volume) to equal its capacity. Thus, there are 2 stages of preoxygenation (Table 2),[16] the washout of the circuit by O2 flow and the washout of the functional residual capacity by the alveolar ventilation. After 1 t, the O2 in the functional residual capacity will be increased by 63%; after 2 t, by 86%; after 3 t, by 95%; after 4 t, by approximately 98%. The end points of maximal preoxygenation and denitrogenation have been defined as an end-tidal O2 concentration (EtO2) of approximately 90% and an end-tidal N2 concentration (EtN2) of 5%.[19,20] In an adult subject with a normal functional residual capacity and oxygen consumption (VO2), an EtO2 > 90% implies that the lungs contain >2000 mL of O2, which is 8 to 10 times the VO2.[8,32] Because of the obligatory presence of carbon dioxide (CO2) and water vapor in the alveolar gas, an EtO2 >94% cannot be easily achieved.

Figure 2.

Comparison of mean end-tidal O2 and N2 concentration obtained at 30-second intervals during 5-minute period of spontaneous tidal volume oxygenation using the circle absorber and NasOral systems in 20 volunteers. Data are mean ± SD. Published with permission from Nimmagadda et al.31

Many factors affect efficacy and efficiency (Table 3).[16] Factors affecting the efficacy of preoxygenation include the FIO2, duration of preoxygenation, and the alveolar ventilation/functional residual capacity ratio. Failure to achieve an FIO2 near 1.0 can be caused by a leak under the face mask,[34,35] rebreathing of exhaled gases, and the use of resuscitation bags incapable of delivering high FIO2.[31]

Bearded patients, edentulous patients, elderly patients with sunken cheeks, use of the wrong size face mask, improper use of head straps, and the presence of gastric tubes are common factors causing air entrainment and a lower FIO2. The absence of a normal capnographic tracing, and a lower than expected end-tidal carbon dioxide concentration (EtCO2) and EtO2 should alert the anesthesiologist to the presence of leaks in the anesthetic circuit.[8] FIO2 can also be influenced by the duration of breathing, technique of breathing, and the level of the fresh gas flow (FGF).[36] Adequate time is needed to achieve maximal preoxygenation. With an FIO2 near 1.0, most healthy adults with tidal volume breathing can reach the target level of an EtO2 > 90% within 3 to 5 minutes. The half-time for an exponential change in the fraction of FAO2 following a step change in FIO2 is given by the equation: FAO2 = 0.693 × Volume of gas in the functional residual capacity/alveolar ventilation. With a functional residual capacity of 2.5 L, the half-times are 26 seconds when alveolar ventilation = 4 L/min and 13 seconds when alveolar ventilation = 8 L/min.[8] These findings indicate that hyperventilation can reduce the time required to increase the O2 stores in the lungs, which provides the basis for using deep breathing as an alternative to tidal volume breathing.[27,37–39] A wide range of preoxygenation techniques have been described (Table 4).[16]

Increasing the FGF from 5 to 10 L does not increase appreciably the FIO2 during tidal volume breathing, although it does so during deep breathing.[36] Because of the breathing characteristics of the circle system, the minute ventilation during deep breathing may exceed the FGF, resulting in rebreathing of N2 in the exhaled gases, consequently decreasing the FIO2. However, during tidal volume breathing, rebreathing of N2 in the exhaled gases is negligible and thus increasing the FGF from 5 to 10 L has minimal effect on FIO2.[36] Regardless of the technique used, the goal is to reach the end point of maximal preoxygenation, which can be easily measured with most anesthesia monitors.

All investigations have demonstrated that preoxygenation markedly delays arterial oxyhemoglobin desaturation during apnea.[8,21,23,28] The extent of this delay in desaturation depends on the efficacy of preoxygenation, the capacity for O2 loading, and the VO2.[33] Patients with a decreased capacity for O2 transport (decreased functional residual capacity, PaO2, arterial O2 content, or cardiac output) or those with an increased VO2 develop oxyhemoglobin desaturation more rapidly during apnea than healthy patients.[8,28] Farmery and Roe[40] developed and validated a computer model describing the rate of oxyhemoglobin desaturation during apnea. The model is particularly useful for analyzing oxyhemoglobin desaturation values below 90%. These values are dangerous to allow in human subjects, because below 90%, there will be a steep decline of PaO2 because of the sigmoid shape of oxyhemoglobin dissociation curve. In a healthy 70-kg patient, when FAO2 is progressively decreased from 0.87 (FIO2 of 1.0) to 0.13 (air), the apnea time to 60% SaO2 is decreased from 9.9 to 2.8 minutes (Figure 3).[28]

Figure 3.

Arterial oxyhemoglobin saturation (Sao2) versus time of apnea in an obese adult, a 10-kg child with low functional residual capacity and high ventilation, and a moderately ill adult compared with a healthy adult. FAO2 indicates fractional alveolar oxygen concentration; VE, expired volume. Published with permission from Benumof et al.28

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