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

Potential Risks of Preoxygenation

Delayed Diagnosis of Esophageal Intubation

Although an unrecognized esophageal intubation ultimately results in severe hypoxemia, minutes may elapse before this occurs. Preoxygenation extends the time period before hypoxemia ensues and, thus, delays the detection of a misplaced endotracheal tube when SpO2 is being used as an indicator. Cases attributing a delayed diagnosis of esophageal intubation to preoxygenation[85,86] prompted some clinicians to suggest abandoning the maneuver.[84] However, this would seem to be an extreme reaction when the practice has proven benefits. Furthermore, it should be emphasized (1) that normal pulse oximetry readings after intubation should not be regarded as evidence of proper endotracheal tube placement and (2) that a severe fall in SpO2 is a relatively late manifestation of an esophageal intubation. In spite of occasional false-positive and false-negative results, identification of CO2 in the exhaled gas (end-tidal CO2), which is readily available on all anesthesia monitors, is a well-accepted and routinely used indicator of proper endotracheal tube placement. The reader is referred to airway management texts and review articles discussing the methods of verification of endotracheal tube placement.[87]

Absorption Atelectasis

Atelectasis occurs in 75% to 90% of healthy individuals undergoing general anesthesia,[87,88] and absorption atelectasis is the most common side effect of preoxygenation. It is initiated by 2 mechanisms during anesthesia.[89–92] One mechanism is the decrease in the functional residual capacity. Both the supine position and induction of anesthesia reduce lung volume, so that it approximates the residual volume. The end-expiratory volume may be lower than the closing capacity leading to airway closure and collapse of the dependent areas of the lung. The second mechanism is compression atelectasis. This is because of changes in the shape of the chest wall, spine, and diaphragm, which cause an increase in intraabdominal pressure leading to compression of the thoracic cavity and airway closure. Normally, O2 shares alveolar space with other gases, principally N2 which is poorly soluble in plasma and therefore remains in high concentration in alveolar gas. In the presence of a partial or complete airway closure, the gases gradually diffuse out of the alveoli and are not replaced. During air breathing, emptying of the lung is limited by the sluggish diffusion of N2. However, during preoxygenation, the rapid replacement of N2 with O2 promotes loss of gas from the lung to the blood stream resulting in alveolar collapse, that is, absorption atelectasis. Absorption of gas does not in itself cause atelectasis, but in effect accelerates collapse should airway closure occur from either of the above 2 mechanisms.[91,92]

Techniques that have been proposed to decrease the extent of absorption atelectasis following preoxygenation are (1) decreasing the concentration of FIO2 and (2) various recruitment maneuvers. Studies using computer modeling, as well as those involving actual measurements in patients using computerized tomography (CT), have demonstrated that decreasing the value of FIO2 can have a profound effect on the extent of atelectasis.[93–96] Computer model of absorption atelectasis predicted that preoxygenation with an FIO2 of 1.0 would accelerate the collapse of the lung.[93] A CT study found that atelectasis was less when patients were ventilated with 30% O2 during induction of anesthesia than when 100% O2 was used.[94] Another CT study evaluated the effect of stepwise variations in inspired O2 on the extent of atelectasis and the time to arterial desaturation (Table 5).[95] The investigators found (1) that atelectasis was significant in patients receiving 100% O2, but that it was small and virtually absent in patients receiving 80% and 60% O2, respectively and (2) that the time to desaturation fell with decreasing O2 concentration. Studies have also shown that administering 100% O2 during emergence from anesthesia can increase atelectasis. Benoit et al[96] found a 6.8% atelectasis in patients awakened on an FIO2 of 1.0 compared with 2.6% in those awakened on an FIO2 of 0.4.

Recruitment maneuvers are commonly performed in patients under general anesthesia, but they have particular value in conjunction with preoxygenation. These maneuvers include CPAP, PEEP, and/or reexpansion maneuver. A CT study found that the combined use of CPAP (6 cm H2O) during 5 minutes of preoxygenation with face mask while breathing spontaneously, and PEEP (6 cm H2O) during mask ventilation for additional 5 minutes during induction of anesthesia, prevented the marked increase in atelectasis that was evident in a control group.[77] A reexpansion maneuver is a vital capacity maneuver. Rothen et al[97] evaluated the dynamics of reexpansion of atelectasis with a vital capacity maneuver during general anesthesia. They found that reopening of the alveoli occurred mainly during the first 7 to 8 seconds of application of an airway pressure of 40 cm H2O. Typically, this maneuver is used soon after tracheal intubation and before tracheal extubation.

Production of Reactive Oxygen Species

Oxygen is a paramagnetic atom containing 2 unpaired electrons in its outer shell that usually exists in the form of dioxygen (O2). In biological tissues, the dioxygen molecule can be accidentally or deliberately split, producing reactive oxygen species, which include superoxide anion, hydroxyl radical, and hydrogen peroxide.[98–100] Reactive oxygen species can react with critical molecular components, such as lipids, DNA, and proteins, causing significant cellular damage.[101,102] Although endogenous antioxidant mechanisms are normally sufficient to prevent high tissue concentrations of reactive oxygen species, these mechanisms can become overwhelmed resulting in oxidative stress.[102,103] It is known that prolonged use of FIO2 = 1.0 can cause production of reactive oxygen species. Clinical manifestations are pulmonary edema, acute respiratory distress syndrome, retinal detachment, retinopathy of prematurity, and seizures.[104] The signs of early lung injury begin to appear after 12 hours of high concentrations of O2 breathing.[105] Thus, because of its short duration, cellular injury due to reactive oxygen species would not be applicable to preoxygenation.

Cardiovascular Responses

The cardiovascular responses during preoxygenation have received limited attention and have not been well characterized. But there have been many studies, both in humans and animal models, assessing the steady state cardiovascular responses during high O2 breathing, which may provide insight into the hemodynamic changes during preoxygenation. However, the changes in PaO2 during preoxygenation are dynamic and brief, and, furthermore, they have been demonstrated to vary in different patient populations. Thus, caution should be exercised in extrapolating the experimental findings described below to a given patient undergoing preoxygenation.

Several studies in normal male subjects have demonstrated that breathing 100% O2 causes a modest decrease in heart rate accompanied by a parallel decrease in cardiac output. Systemic vascular resistance and arterial blood pressure increase.[106–108] These changes are attributable to a reflex loop, either chemoreceptor or baroreceptor in origin. Since atropine abolishes the reduction in heart rate, this response is mediated by the vagus nerves.[107]

A number of physiologic studies have assessed the effect of inhalation of 100% O2 in the human coronary circulation.[109–113] Hyperoxia consistently caused a marked decrease in coronary blood flow (reflecting coronary vasoconstriction) accompanied by a decrease in myocardial oxygen consumption. The direct coronary vasoconstrictor effect of hyperoxia is due to the oxidative inactivation of nitric oxide[110,112] and other vasodilators released from the vascular endothelium and to closure of the ATP-sensitive K+ channels.[113,114] Investigations in patients with normal coronary arteries have indicated that, despite the decrease in coronary blood flow, oxygenation at the level of the myocytes remains adequate, as indicated by continued myocardial lactate extraction rather than conversion to production.[108,109] This is likely explained by the ability of the increase in arterial O2 content to blunt the reduction in coronary O2 supply caused by the reduced coronary blood flow combined with a reduction in myocardial O2 demand, secondary to the hyperoxia-induced bradycardia. Metabolic findings in patients with severe coronary artery disease have been inconsistent. Some studies have found that O2 breathing by these patients converts myocardial lactate production to extraction, suggesting a beneficial effect,[108] whereas others have found that O2 breathing precipitates or accentuates myocardial lactate production, implying ischemic changes.[110]

It is well established that inhalation of high O2 can also reduce cerebral blood flow because of vasoconstriction.[115–118] It has been proposed that this effect may be because, at least in part, of the associated decrease in PaCO2 that accompanies high O2 breathing rather than to a direct effect of O2[116] The mechanism for the decrease in PACO2 is as follows. When PaO2 is increased by inhalation of 100% O2, the CO2 dissociation curve for blood is altered (the Christiansen-Douglas-Haldane effect), such that there is a reduction in the affinity of blood for CO2. This produces an increase in cerebral tissue PCO2 and hydrogen ion concentration, which stimulates respiration with a result that PaCO2 decreases causing cerebral vasoconstriction.[117,118] Investigators have also assessed the effect of hyperoxia on cerebral O2 consumption, using a functional magnetic resonance technique.117 They found that hyperoxia causes an approximate 20% decrease in cerebral O2 consumption, reflecting reduced neural activity.[117] It was speculated that the decrease in cerebral O2 consumption was because of the ability of reactive oxygen species to damage lipids and proteins, and, in turn, decrease the enzyme activity in oxidative metabolic pathways.

Studies in animal models have demonstrated that hyperoxia causes vasoconstriction and a decrease in blood flow in peripheral vascular beds, including the kidney, gastrointestinal tract, and hindlimb.[115,119,120] Whether this vasoconstriction is because of a direct effect of O2 on vascular smooth muscle or reflex-mediated via an arterial chemoreceptor/autonomic nerve remains unclear. Regardless, it is doubtful that changes in the peripheral vascular beds would have any important clinical effect during preoxygenation. The cardiovascular findings to date provide no justification for limiting the use of preoxygenation.

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