Pre-oxygenation, do you really know how to do it?

Airway Management Team, Department of Anesthesiology, Wuhan First Hospital

We all know that preoxygenation is needed before induction of general anesthesia, but do you really know the correct way to open preoxygenation? How will you de-nitrogenate your next general anesthesia patient with oxygen?

Why preoxygenate? When do you need to preoxygenate? How does it work? Is preoxygenation the same for every patient? What are the dangers of preoxygenation? How to solve it? The physiology of the respiratory system is actually quite complex, and these are not simple questions to answer.

In the February 2017 issue of Anesthesia & Analgesia, the editors recommend, under the title "Is There Anything New About Preoxygenation? Duh, Yeah!" [1], that Nimmagadda et al. published a concurrent review, "Preoxygenation: Physiologic Basis, Benefits, and Potential Risks" [2]. This article combed through 120 related papers and answered these questions in a more systematic way.

Peter D. Slinger, MD, FRCPC

Preoxygenation: physiologic basis, efficacy, and efficiency

Preoxygenation improves the body's oxygen reserve, primarily by increasing the oxygen content of the functional residual air volume.

Assessment of the effectiveness of preoxygenation includes efficacy and efficiency.

Indicators of efficacy include an increase in alveolar oxygen concentration (FAO2); a decrease in alveolar nitrogen concentration (FAN2); and an increase in partial pressure of arterial oxygen (PAO2).

Efficiency is assessed by the rate of decline in blood oxygen saturation (SaO2) during apnea.

Preoxygenation has two phases: oxygen flow to wash out nitrogen from the circuit; and alveolar ventilation to wash out nitrogen from the functional residual airspace

Commonly Used Preoxygenation Methods

Preoxygenation in High-Risk Individuals

Pregnant Women

In comparison to the general population, pregnant women have a high level of ventilation and a high rate of oxygenation. Compared to the general population, pregnant women have high ventilation and low residual gas volume (VA/FRC), and therefore can achieve washout more quickly. However, precisely because of the low residual air volume and the simultaneous high oxygen consumption, oxygen saturation decreases more rapidly in pregnant women after apnea.SaO2 drops to 95% in 243 seconds (over 4 minutes) for an average woman and 173 seconds (less than 3 minutes) for a pregnant woman. Head elevation of 45° was prolonged in women, but not in pregnant women, probably because the pregnant uterus interferes with diaphragmatic descent. In pregnant women, four deep breaths are not as effective as three minutes of tidal volume breathing and are generally not recommended except in emergencies. Because of the high minute ventilation, a higher oxygen flow rate (10 L/min) is required for preoxygenation.

Morbidly obese patients

Apnea after preoxygenation decreases SaO2 to 90% for an average of 6 min in normal-weight people and 2.7 min in morbidly obese patients (BMI>40 kg/m2). the time can be prolonged by approximately 50 seconds in obese patients in a 25° head-up position. The addition of a nasopharyngeal airway is recommended for mask preoxygenation, or placement of an oxygen tube in the oropharynx for continuous oxygen delivery, with an oxygen flow rate of at least 5 L/min.

Pediatric patients

Studies have shown that pediatric patients require only 2 min of tidal volume respiration to achieve preoxygenation requirements. Again, because of the small residual air volume, oxygen consumption is high and oxygen saturation falls rapidly. Infants decline more rapidly than older children. Most infants SaO2 drops to 90% in 70-90 seconds with or without preoxygenation. Pediatric specialist anesthesiologists have realized that the adult version of rapid sequence induction may not be appropriate for children. A modified version of the induction: appropriate depth of anesthesia, adequate muscle relaxation, high oxygen concentration, gentle manual ventilation, and abandonment of cricoid cartilage compression may be more appropriate for children.

Elderly patients

Structural and physiologic changes of the respiratory system in the elderly include reduced respiratory muscle strength, reduced elasticity of the lungs in solid form, dysfunctional ventilation-to-blood perfusion ratios, and reduced oxygen consumption but also reduced oxygen uptake capacity. In the elderly, tidal volume breathing for 3 minutes or longer is significantly better than 4 deep breaths.

Patients with Lung Disease

In patients with chronic obstructive pulmonary disease (COPD), even a brief period of asphyxia, such as sputum aspiration, can result in a rapid decline in oxygen saturation. However, due to chronic pulmonary hypertension, the pour is not prone to pulmonary atelectasis. In such patients, tidal volume breathing for 5 minutes or more may be required to achieve preoxygenation.

Patients at High Altitude

High altitude does not change the air oxygen concentration (21%), but it does reduce the alveolar and arterial partial pressures of oxygen, PO2, which decreases exponentially with increasing altitude. No studies related to preoxygenation at high altitude have been identified. At high altitude, preoxygenation may take longer, but this needs to be confirmed by experimental studies.

Techniques to improve the efficacy of preoxygenation

Oxygen administration without respiratory diffusion

The method is to give 15 L/min of oxygen continuously through a nasopharyngeal or oropharyngeal airway, or cricothyroid puncture needle, after adequate preoxygenation. Healthy adults without airway obstruction can be provided with adequate oxygen supply for at least 10 min. It has even been reported to maintain Sao2 above 90% for up to 100min[7] . It can be used for bronchoscopy or short acoustic procedures. The problem is that although the oxygen supply is adequate, the PCO2 will remain elevated.

Continuous positive airway pressure and positive end-expiratory pressure

CPAP alone does not prolong the onset of hypoxia in obese patients because once the mask is removed, the functional residual air volume returns to pre-CPAP levels. However, CPAP followed by facemask-pressurized mechanical ventilation giving 5 min of PEEP delayed the onset of hypoxia.

Non-invasive Biphasic Positive Airway Pressure

BiPAP combines the advantages of pressure-controlled ventilation and CPAP to keep the alveoli open throughout the entire respiratory circuit (inspiratory and expiratory phases).

Transnasal Humidified Rapid Inflatable Exchange Ventilation

THRIVE combines the advantages of breathless diffusive oxygen delivery and CPAP to reduce carbon dioxide accumulation by flushing the dead space with gas flow. Through a specialized nasal cannula, oxygen flow of up to 70 L/min can be delivered, allowing for sustained oxygenation and avoiding elevated carbon dioxide after intravenous induction with inotropes.

Potential Risks of Preoxygenation

Delayed Diagnosis of Esophageal Intubation

This is not really a problem because catheter insertion into the esophagus is not judged solely by a drop in SPO2. Excluding occasional false positives and false negatives, it is easy to determine catheter position by EtCO2.

Absorptive pulmonary atelectasis

Pulmonary atelectasis occurs in 75% to 90% of healthy individuals undergoing general anesthesia, and the most significant side effect of preoxygenation is absorptive pulmonary atelectasis. Normally, N2 is not absorbed into the bloodstream and alveolar tone can be maintained. Preoxygenation washes the nitrogen out and the oxygen is absorbed into the bloodstream causing alveolar atrophy.

The solution is either to reduce the concentration of inhaled oxygen or to manipulate the lungs to reopen. Several studies have confirmed that inhalation of pure oxygen can lead to significant pulmonary atrophy; inhalation of 80% oxygen, pulmonary atrophy is significantly reduced; inhalation of 60% oxygen is almost no pulmonary atrophy. However, as the oxygen concentration decreases, the time of decrease in oxygen saturation decreases progressively. Manipulative ventilation is particularly beneficial for preoxygenation, and it includes CPAP, PEEP, and manipulative lung resuscitation. A CT study showed that spontaneous respiration for 5 min with concomitant administration of CPAP (6 cmH2O) followed by oxygen administration for 5 min with PEEP mask pressure at 6 cmH2O resulted in a significantly lower incidence of pulmonary atelectasis than in the control group [8] Rothen et al. demonstrated that alveolar recanalization occurred predominantly in the first 7-8 seconds when given at a pressure of 40 cmH2O [9] . It is recommended to puff the lungs both immediately after intubation and before extubation.

Generation of reactive oxygen species

Stabilized oxygen molecules may be broken down in biological tissues into reactive oxygen species components, including negative superoxide ions, hydroxyl groups, and hydrogen peroxide. These reactive oxygen components act on lipids, proteins, and DNA to cause cellular damage. Prolonged inhalation of pure oxygen produces reactive oxygen components. However, early signs of lung injury only begin to appear after 12 h of inhalation of highly concentrated oxygen. So a short period of pure oxygen preoxygenation is not harmful.

Cardiovascular response

The cardiovascular response during preoxygenation has not received much attention, but these experimental results are worth noting.

Induction of pure oxygen in the general population results in a mild slowing of heart rate and a corresponding decrease in cardiac output, systemic vasoconstriction, and an increase in arterial blood pressure. These changes are induced by chemoreceptor and pressure receptor feedback. Atropine prevents the decrease in heart rate, so it should be a vagal reflex.

Pure oxygen can cause a significant fall in coronary blood flow (due to coronary constriction), accompanied by a fall in myocardial oxygen consumption. In normal people, coronary blood flow falls, cardiomyocytes rely on lactate for energy, oxygen consumption is reduced, while the heart rate slows down, so the oxygen supply is sufficient. However, in patients with severe coronary artery disease, there are conflicting findings on myocardial metabolism. Some studies suggest that oxygen inhalation can lead to greater lactate decomposition than production, which is beneficial to myocardial oxygen supply; other studies show that oxygen inhalation promotes lactate production, suggesting myocardial ischemia.

Inhaling high levels of oxygen reduces cerebral blood flow and also reduces cerebral oxygen consumption by 20%.

Animal models have shown that high concentrations of oxygen constrict blood vessels, leading to a decrease in blood flow in the peripheral vascular bed.

In any case, it is questionable whether these changes during preoxygenation are clinically meaningful. To date there is no definitive evidence to limit the implementation of preoxygenation.

Conclusions

This article provides strong evidence that preoxygenation, whether implemented before induction or extubation, prolongs the onset of hypoxia. For this reason, preoxygenation is required for all general anesthesia patients. And preoxygenation is required whenever there is a possibility of interruption of oxygen supply, such as before tracheal suctioning, before and during awake fibreoptic intubation, especially in high-risk patients, such as those with severe obesity. The procedure must be performed correctly and EtO2 routinely monitored.The effectiveness of preoxygenation in high-risk patients may be compromised, and the clinician needs to have a variety of strategies at his or her disposal to improve oxygenation. Absorptive lung atelectasis caused by preoxygenation is easily resolved and should not be a barrier limiting this technique.