Accepted for publication May 20, 1999.

THE purposes of maximally preoxygenating a patient before the induction of general anesthesia and paralysis are to provide the maximum amount of time that a patient can tolerate apnea and for the anesthesia provider to solve a cannot-ventilate, cannot-intubate situation. This issue of ANESTHESIOLOGY contains an intriguing article by Baraka et al.  1that describes a new method of preoxygenation that may be best with regard to both efficacy and efficiency.

Maximal preoxygenation is achieved when the alveolar, arterial, tissue, and venous compartments are all filled with oxygen. However, patients with a decreased capacity for oxygen loading (i.e. , decreased functional residual capacity [FRC], hemoglobin concentration, alveolar ventilation, cardiac output) or an increased oxygen extraction, or both, desaturate during apnea much faster than a healthy patient. 2,3Consequently, in patients with oxygen transport limitations (who desaturate the fastest) and in any patient in whom difficulty in managing the airway is suspected (need to tolerate apnea the longest time), maximal preoxygenation is indicated. Moreover, because the development of a cannot-ventilate, cannot-intubate situation is largely unpredictable, the desirability/need to maximally preoxygenate is theoretically present for all patients. Along this line of thought, the American Society of Anesthesiologists Difficult Airway Algorithm, 4which makes no mention of preoxygenation, should include a requirement for preoxygenation before the induction of general anesthesia whenever possible; obvious exclusion examples are very uncooperative adult patients and pediatric patients. Two major but preventable reasons why a patient will not be maximally preoxygenated are failure to achieve an alveolar fraction of oxygen (FAO2)= 0.87 (i.e., failure to breathe fraction inspired oxygen tension [FIO2]= 1.0 through a sealed system) and insufficient time of preoxygenation.

The major reason for failure to achieve an FIO2= 1.0 and an FAO2= 0.87 is a leak under the mask, allowing inspiratory entrainment of room air. Avoiding a leak between the mask and the face is the most important factor in obtaining maximal preoxygenation because it is the one factor that cannot be compensated for by an increased duration of preoxygenation, and relatively minor degrees of leak may be hard to appreciate. 5,6Using the model of Farmery and Roe, 3it can be shown that when preapnea FAO2is progressively decreased from 0.87 to 0.8, 0.7, 0.6, 0.5, 0.4, 0.3, 0.2, and 0.13 (breathing room air) for a healthy 70-kg patient, apnea times to arterial saturation of oxygen (SaO2)= 60% are progressively decreased from 9.90 to 9.32, 8.38, 7.30, 6.37, 5.40, 4.40, 3.55 and 2.80 min, respectively. Clinical endpoints that indicate a sealed system are movement of the reservoir bag in and out with each inhalation and exhalation, respectively; presence of a normal capnogram and an end-tidal partial pressure of carbon dioxide (PETCO2) and tidal oximetry indicating appropriate inspired and end-tidal values.

The half-time for exponential change in FAO2with a step change in FIO2is given by 0.693 × VFRC/V̇Afor a non-rebreathing system. With VFRCequal to 2.5 l, the half-time is 26 and 13 s when V̇A= 4.0 and 8.0 l/min, respectively. Thus, most of the oxygen that can be stored in the alveolar and arterial spaces can be brought in by hyperventilation FIO2= 1.0 for a short period of time and is the basis for the 4-deep-breath-within-30-seconds method of preoxygenation (termed the “4DB/30 sec method”).

Indeed, three studies have shown that there is no significant difference between the arterial oxygen tension (PaO2) achieved with 3–5 min of normal tidal volume ventilation of FIO2= 1.0 method of preoxygenation (termed the “traditional”[T] method) compared to the 4DB/30 sec method (Table 1). 7–9The similarity in PaO2between the T and 4DB/30 sec methods of preoxygenation has led to the conclusion that the 4DB/30 sec method provides the same amount of preoxygenation as the T method. However, three studies have shown that patients preoxygenated using the 4DB/30 sec method desaturate faster than patients preoxygenated using the T method (Table 2). 10–12There are two possible reasons why the 4DB/30 sec method of preoxygenation results in faster desaturation than the T method.

Table 1. PaO2before and after Fast Track and Traditional Methods of Preoxygenation 

Table 1. PaO2before and after Fast Track and Traditional Methods of Preoxygenation 
Table 1. PaO2before and after Fast Track and Traditional Methods of Preoxygenation 

Table 2. Time to SaO2= 90%(or SaO2= 93%) following Fast Track  versus Traditional Methods of Preoxygenation 

Table 2. Time to SaO2= 90%(or SaO2= 93%) following Fast Track  versus Traditional Methods of Preoxygenation 
Table 2. Time to SaO2= 90%(or SaO2= 93%) following Fast Track  versus Traditional Methods of Preoxygenation 

{tabft}* Statistically significant greater time to SaO2= 90%(and SaO2= 93%) between traditional vs.  fast track methods of preoxygenation.

First, if the half-minute volume of ventilation is much greater than the half-minute oxygen inflow rate, rebreathing of exhaled nitrogen must occur, which, in turn, will lower the FIO2less than 1.0. 10However, simple calculation (and daily clinical observation of tidal oximetry) shows that the effect of nitrogen rebreathing in a completely oxygen-loaded standard anesthesia circle system is a minor factor causing submaximal preoxygenation. It is not surprising, therefore, that patients preoxygenated by the 4DB/30 sec method using an oxygen inflow rate of 35 l/min still desaturate to an SaO2= 90%, much faster (212 ± 92 s) than patients preoxygenated using the T method (406 ± 75 s). 11 

Another reason why patients preoxygenated with the 4DB/30 sec method desaturate faster is because the tissue and venous compartments need more than 30 s to fill with oxygen; these compartments have the capability of holding a significant amount of additional oxygen above that contained while breathing room air. 13In fact, if during breathing FIO2equal to 1.0, the alveolar arterial, venous, and tissue compartments are all considered, total whole-body oxygen stores can theoretically increase 1,200 and 800 ml from the end of the first half-minute (at 30 s) and first minute (at 60 s), respectively, to the end of the third minute (at 180 s)(fig. 1). 13The 1,200 and 800 ml theoretically gained from the first half-minute and minute to the third minute, respectively, would be worth 3 to 4 min of oxygen consumption during apnea and can certainly account for the observed difference in rates of hemoglobin desaturation during apnea between the 4DB/30 sec and T methods of preoxygenation.

Fig. 1. Variation in volume of oxygen stored in the functional residual capacity (□), the blood (▴), the tissue (○), and the whole body (▪), with duration of preoxygenation. (Reprinted with permission from Campbell and Beatty.  13 ). 

Fig. 1. Variation in volume of oxygen stored in the functional residual capacity (□), the blood (▴), the tissue (○), and the whole body (▪), with duration of preoxygenation. (Reprinted with permission from Campbell and Beatty.  13 ). 

Close modal

The article by Baraka et al.  1is valuable because it not only confirms the previously observed differences between 4DB/30 sec and T methods of preoxygenation, but, more importantly, shows that an 8-deep-breath-in-60-seconds method of preoxygenation (termed “8DB/60 sec”) results in a slower rate of hemoglobin desaturation (to SaO2= 95%) during apnea than the T method. This is a surprising and clinically very important result because one would intuitively think that the 8DB/60 sec method would have results somewhere in between the 4DB/30 sec and T methods. However, because the authors used a relatively small volume Mapleson-D circuit (2.5 l) and a different oxygen flow rate in comparing 4DB/30 sec, 8DB/60 sec, and T methods, these results will require confirmation in a standard anesthesia machine circle system using the same flow rate for all conditions.

The authors hypothesized that the 8DB/60 sec method might result in a greater store of oxygen in the alveolar compartment compared to the T method by either causing an increase in flow rate into or the volume of the compartment. However, it is very unlikely that there was a significant difference in the amount of oxygen in the alveolar compartment (the product of FAO2× FRC) between the T and 8DB/60 sec methods of preoxygenation. Because the PaO2values were nearly equal, the PAO2and FAO2had to be nearly equal for the two groups. Because all patients (who had no lung disease) were paralyzed and tracheally intubated and because the airway was exposed to atmospheric pressure at the beginning of the apnea period, the FRC for the two groups should have been nearly equal. Thus, the amount of oxygen in the alveolar compartment cannot provide the explanation for the different rates of hemoglobin desaturation.

Given that the half-time for decreases in PaCO2with step increases in minute ventilation is 3 min, the 8DB/60 sec method (hyperventilation for 1 min) could result in a significant decrease in PaCO2and an increase in p  H. A significant decrease in PaCO2and an increase p  H could result in a significant change in blood compartment oxygen transport variables, such as the position of the oxyhemoglobin dissociation curve, oxygen consumption, cardiac output, and blood and plasma volumes, which, in turn, could alter the rate of hemoglobin desaturation. Thus, the answer as to why the 8DB/60 sec method resulted in slower hemoglobin desaturation than the T method may reside in the blood compartment rather than in the alveolar compartment. Future areas of useful research will be to determine how oxygen transport parameters, the overall well-being of the patient, and rates of hemoglobin desaturation to levels lower than an SaO2equal to 95% are effected by the 8DB/60 sec method of preoxygenation. Obviously, if the 8DB/60 sec method of preoxygenation clears the system used and the physiologic hurdles, then it will fulfill efficacy and efficiency criteria for being the best method of preoxygenation.

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