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Preoxygenation Physiologic Basis, Benefits, and
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February 2017 • Volume 124 • Number 2 anesthesia-analgesia 507
Copyright © 2016 International Anesthesia Research Society DOI: 10/ANE.
T
he ability of preoxygenation, using a high fraction of inspired oxygen (Fio 2 ) before anesthetic induction and tracheal intubation, to delay the onset of apnea-induced arterial oxyhemoglobin desaturation has been appreciated for many years–3 For patients at risk for aspiration, during rapid sequence induction/intubation where manual ventilation is undesirable, preoxygenation has become an integral compo- nent–7 Preoxygenation is also important, when dificulty with ventilation or tracheal intubation is anticipated and when the patient has limited oxygen (O 2 ) reserves,9 In 2003, guidelines
from the American Society of Anesthesiologists Task Force on the Management of the Dificult Airway included “face mask preoxygenation before initiating management of the dificult airway.” 10 Because the “cannot intubate, cannot ventilate” situation is unpredictable, the need for preoxygenation is desirable in all patients,11 In 2015, guidelines developed by Dificult Airway Society in the United Kingdom for the man- agement of unanticipated dificult intubation included the statement that all patients should be preoxygenated before the induction of general anesthesia. 12 Residual effects of anesthetics or inadequate reversal of muscle relaxants can complicate emergence from anesthesia. These effects can lead to decreased functional activity of the pharyngeal muscles, upper airway obstruction, inability to cough effectively, a 5-fold increase in the risk of aspiration, and attenuation of the hypoxic drive by the peripheral che- moreceptors,14 Hypoventilation, hypoxemia, and loss of airway patency may follow these changes. Preoxygenation can also minimize neostigmine-induced cardiac arrhyth- mias. 15 In accordance, “routine” preoxygenation before the reversal of neuromuscular blockade and tracheal extubation has been recommended, given the potential for airway and
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 dificulties 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 pre- oxygenation before the tracheal extubation has also been recommended. The objective of this article is to discuss the physiologic basis, clinical beneits, and potential concerns about the use of preoxygenation. The effectiveness of preoxygenation is assessed by its eficacy and efi- ciency. Indices of eficacy include increases in the fraction of alveolar oxygen, increases in arte- rial oxygen tension, and decreases in the fraction of alveolar nitrogen. End points of maximal preoxygenation (eficacy) are an end-tidal oxygen concentration of 90% or an end-tidal nitrogen concentration of 5%. Eficiency of preoxygenation is relected in the rate of decline in oxyhemo- globin desaturation during apnea. All investigations have demonstrated that maximal preoxygen- ation 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 humidiied rapid insuflation ventilatory exchange. The beneit 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, absorp- tion atelectasis, production of reactive oxygen species, and undesirable hemodynamic effects. Because the duration of preoxygenation is short, the hemodynamic effects and the accumula- tion of reactive oxygen species are insuficient to negate its beneits. 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, 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. (Anesth Analg 2017;124:507–17)
Preoxygenation: Physiologic Basis, Benefits, and
Potential Risks
Usharani Nimmagadda, MD,*† M. Ramez Salem, MD,*† and George J. Crystal, PhD†
From the *Department of Anesthesiology, Advocate Illinois Masonic Medical Center, Chicago, Illinois; and †Department of Anesthesiology, University of Illinois College of Medicine, Illinois. Accepted for publication July 29, 2016. Funding: None. The authors declare no conlicts of interest. Reprints will not be available from the authors. Address correspondence to Usharani Nimmagadda, MD, Department of An- esthesiology, Advocate Illinois Masonic Medical Center, 836 West Wellington Ave, Chicago, IL 60657. Address e-mail to ushanimm@hotmail.
E SYSTEMATIC REVIEW ARTICLE
Section Editor: Richard Prielipp
Anesthesia Patient Safety Foundation
CME
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ventilation problems. 16 Guidelines for the management of tracheal extubation proposed in 2012 by the Dificult Airway Society in the United Kingdom include the statement that it is vital to preoxygenate before extubation because of various perioperative anatomical and physiologic changes that may compromise gas exchange. 17 Preoxygenation has also been recommended before any interruption of ventilation, such as during open tracheobronchial suctioning. 16 The current review describes the physiologic basis and clinical beneits of preoxygenation. Special considerations for preoxygenation in high-risk patient populations are discussed. Over the years, concerns have been expressed in the literature regarding potential undesirable effects of preoxygenation. These effects include delayed diagnosis of esophageal intuba- tion, tendency to cause absorption atelectasis, production of reactive oxygen species, and adverse hemodynamic changes. We describe these effects and discuss whether they justify modifying preoxygenation in selected clinical situations.
PREOXYGENATION: PHYSIOLOGIC BASIS,
EFFICACY, AND EFFICIENCY
Preoxygenation increases the body O 2 stores, the main increase occurring in the functional residual capacity. The size of the increases in O 2 volume in the various body tis- sues is dificult to assess with precision, but assuming that the partition coeficient for gases approximates the gas- water coeficients, the estimated increases are appreciable (Table 1; Figure 1).18,19 The effectiveness of preoxygenation is assessed by its eficacy and eficiency. 8 Indices of eficacy include increases in the fraction of alveolar O 2 (Fao 2 ),20– decreases in the fraction of alveolar nitrogen (Fan 2 ),23, and increases in arterial O 2 tension (Pao 2 ).25–27 Eficiency of
preoxygenation is assessed from the decline of oxyhemo- globin desaturation (Sao 2 ) during apnea– Preoxygenation increases Fao 2 and decreases Fan 2 (Figure 2). 31 The key to achieving maximal preoxygenation is the washout of alveolar nitrogen (N 2 ). The terms preoxygen- ation and denitrogenation have been used synonymously to describe the same process. In a subject with normal lung function, the O 2 washin and the N 2 washout are exponen- tial 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 typi- cally 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 low through a container (volume) to equal its capacity. Thus, there are 2 stages of preoxygenation (Table 2), 16 the washout of the circuit by O 2 low and the washout of the functional residual capacity by the alveolar ventilation. After 1 t , the O 2 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 denitro- genation have been deined as an end-tidal O 2 concentration (Eto 2 ) of approximately 90% and an end-tidal N 2 concentra- tion (Etn 2 ) of 5%,20 In an adult subject with a normal func- tional residual capacity and oxygen consumption (Vo 2 ), an Eto 2 > 90% implies that the lungs contain >2000 mL of O 2 , which is 8 to 10 times the Vo 2 .8,32 Because of the obligatory presence of carbon dioxide (CO 2 ) and water vapor in the alveolar gas, an Eto 2 >94% cannot be easily achieved. Many factors affect eficacy and eficiency (Table 3). 16 Factors affecting the eficacy of preoxygenation include the Fio 2 , duration of preoxygenation, and the alveolar ventila- tion/functional residual capacity ratio. Failure to achieve an Fio 2 near 1 can be caused by a leak under the face mask,34, 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 Fio 2. The absence of a normal capnographic tracing, and a lower than expected end-tidal carbon dioxide concentration (Etco 2 ) and Eto 2 should alert the anesthesiologist to the presence of leaks in the anesthetic circuit. 8 Fio 2 can also be inluenced by the duration of breathing, technique of breathing, and the level of the fresh gas low (FGF). 36 Adequate time is needed to achieve maximal preoxygenation. With an Fio 2 near 1, most healthy adults with tidal volume breathing can reach the target level of an Eto 2 > 90% within 3 to 5 minutes. The half-time for an exponential change in the fraction of Fao 2 following a step change in Fio 2 is given by the equation: Fao 2 = 0 × Volume of gas in the functional residual capacity / alveolar ventilation. With a functional residual capacity of 2. L, the half-times are 26 seconds when alveolar ventilation = 4 L/min and 13 seconds when alveolar ventilation = 8 L/min. 8 These indings indicate that hyperventilation can reduce the time required to increase the O 2 stores in the lungs, which provides the basis for using deep breathing as an alternative to tidal volume breathing,37–39 A wide range of preoxygen- ation techniques have been described (Table 4). 16
Table 1. Body O 2 Stores (in mL) During Room Air
and 100% O 2 Breathing
Body Store Room Air 100 % O 2 Lungs 450 3000 Blood 850 950 Dissolved in tissue luids 50 100 Combined with myoglobin 200 200 Total 1550 4250 Adapted from Nunn. 18
Figure 1. Variation in the volume of O 2 stored in the functional residual capacity (□), blood (▲), tissue (○), and whole body (◼) with the duration of preoxygenation. Published with permission from Campbell and Beatty. 19
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with normal body weight was 6 minutes, whereas that in morbidly obese patients was only 2 minutes. 47 These ind- ings are particularly concerning because morbid obesity is often complicated by obstructive sleep apnea, which can make mask ventilation and intubation more dificult. Rapid oxyhemoglobin desaturation during apnea in morbidly obese patients was attributed to an increased Vo 2 and a markedly reduced functional residual capacity. The supine position enhances this decrease in functional residual capac- ity because of a cephalad displacement of the diaphragm. Placing severely obese patients in the 25° head-up position during preoxygenation has been shown to prolong the time of desaturation by approximately 50 seconds. 48 Some anesthesiologists may prefer awake iberoptic intu- bation rather than rapid sequence induction/intubation in morbidly and super morbidly obese patients (BMI > 50 kg/ m 2 ), especially when they have associated problems. 49 An advantage of this approach is the maintenance of airway patency during spontaneous breathing until an “unhurried” tracheal intubation can be accomplished. Face mask preoxy- genation should precede intubation attempts and should be continued with the placement of a nasal cannula or an O 2 catheter in the oropharynx. O 2 low (up to 5 L/min) through the working channel of the scope has the double advantage of insuflating O 2 and enhancing laryngeal visualization by pre- venting fogging and pushing secretions away. It is important to recognize that airway obstruction can hinder the egress
of gases from the iber-optic scope, which, if prolonged, can result in barotrauma. Thus, caution cannot be overempha- sized when this approach is utilized. Techniques to enhance preoxygenation, which are described later, are especially important in morbidly and supermorbidly obese patients.
Pediatric Patients
Studies have demonstrated that maximal preoxygenation (Eto 2 = 90%) can be accomplished in children faster than in adults,51 With tidal volume breathing, an Eto 2 of 90% can be reached within 100 seconds in almost all children, whereas with deep breathing, it can be reached in 30 sec- onds,51 Nevertheless, because children have a smaller functional residual capacity and a higher Vo 2 than adults, they are at a greater risk for developing hypoxemia, when there is interruption in O 2 delivery, such as during apnea or airway obstruction–54 In a comparison of 3 groups of children who breathed O 2 (Flo 2 = 1) with tidal volume breathing for 1, 2, and 3 minutes before apnea, the time needed for Sao 2 to decrease from 100% to 95% and then to 90% during apnea was least in those who breathed O 2 for 1 minute and there was no difference between those who breathed O 2 for 2 and 3 minutes. 55 Based on these indings, 2 minutes of preoxygenation with tidal volume breathing seems suficient for a maximum beneit and to allow a safe period of apnea. 55 The beneit of preoxygenation is greater in an older child than that in an infant. For example, in an 8-year-old child, the duration of safe period of apnea can be extended from 0 minute without preoxygenation to 5 minutes or longer with preoxygenation. 56 The younger the child, the faster the onset of desaturation,54,57 Most infants reach a Sao 2 of 90% in 70 to 90 seconds after the onset of apnea (in spite of preoxygenation), 58 and this period can be even shorter in the presence of upper respiratory tract infec- tion. 59 Pediatric anesthesiologists have expressed concerns about the use of the “adult” version of the rapid sequence
Table 4. Techniques of Preoxygenation
Tidal volume breathing One vital capacity breath followed by tidal volume breathing Single tidal capacity breath Four deep breaths (4 inspiratory capacity breaths) Eight deep breaths (8 inspiratory capacity breaths) Extended deep breathing (12–16 inspiratory capacity breaths) Adapted from Baraka and Salem. 16
Figure 3. Arterial oxyhemoglobin saturation (SaO 2 ) versus time of apnea in an obese adult, a 10-kg child with low functional residual capac- ity and high ventilation, and a moderately ill adult compared with a healthy adult. FAO 2 indicates frac- tional alveolar oxygen concentration; VE, expired volume. Published with permission from Benumof et al. 28
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induction/intubation technique in children. 60 The concerns include the safe duration of apnea and the potential for cri- coid pressure-induced airway obstruction. A modiied ver- sion of the rapid sequence induction/intubation technique, with emphasis on complete muscular relaxation, gentle manual ventilation using high O 2 concentration without cri- coid pressure and suficient anesthetic depth before intuba- tion would seem more appropriate in children. 61
Elderly Patients
Aging is associated with signiicant structural and physiologic changes in the respiratory system,63 The changes include weakened respiratory muscles and parenchymal alterations within the lungs accompanied by a decrease in the elastic recoil. Lung volumes are decreased with increased closing volume, resulting in ventilation—perfusion mismatch, a reduced pulmonary reserve, and an impaired O 2 uptake at the lung. Even though basal Vo 2 decreases with aging, the impaired O 2 uptake produces a more rapid desaturation dur- ing apnea under anesthesia. 63 In elderly patients, tidal vol- ume breathing for 3 minutes or longer has been shown to be more effective than the 4 deep breathing technique,
Patients With Pulmonary Disease
Both eficacy and eficiency can be adversely affected by pulmonary disease. Signiicant pulmonary disease is associ- ated with a decreased functional residual capacity, appre- ciable ventilation—perfusion mismatch, and an increased Vo 2 , which can reduce the margin of safety. Anesthesia has been shown to cause further impairment to gas exchange in patients with chronic obstructive pulmonary disease. 66 Even brief interruption of ventilation, such as during suctioning can result in signiicant desaturation. However, atelectasis is not a consequence, possibly because chronic hyperinlation of the lungs resists volume decrease and collapse. 67 Maximal pre- oxygenation, which is essential in these patients, may require as much as 5 minutes or longer with tidal volume breathing. 68
Patients at High Altitude
High altitude does not alter the concentration of inspired O 2 (21%), but the reduced barometric pressure produces a decrease in the partial pressure of alveolar and arterial Po 2. 69 For example, in Flagstaff, AZ, with an altitude of 2100 m (approximately 7000 feet above sea level), Pao 2 is reduced from the normal value of 100 mm Hg to approximately 74 mm Hg. 69 As altitude increases, Pao 2 decreases exponen- tially. No studies, to our knowledge, have been performed to assess the effect of high altitude on preoxygenation. This is dificult to predict because of the multiple determinants of preoxygenation and the potential inluence of compensatory mechanisms, especially in acclimatized individuals. It is pos- sible that patients at high altitude will require a longer dura- tion of preoxygenation to achieve an acceptable degree of protection, but this remains to be conirmed experimentally.
TECHNIQUE OF PREOXYGENATION
To provide effective preoxygenation, a methodical approach is necessary. The importance of preoxygenation with a tight- itting mask should be explained to the patient beforehand. Once preoxygenation is initiated, Eto 2 and Fio 2 values
should be monitored closely. If the Eto 2 value does not increase as expected, the anesthesia provider may have to hold the mask with both hands and/or replace the mask with a better-itting one. Whenever possible, the induc- tion should not start until the Eto 2 value approximates or exceeds 90%.
TECHNIQUES TO ENHANCE PREOXYGENATION
Apneic Diffusion Oxygenation
Preoxygenation followed by “apneic diffusion oxygenation” is an effective maneuver for prolonging the safe duration of apnea,70–73 The physiologic basis of this maneuver is as fol- lows. During apnea in adults, Vo 2 averages 230 mL/min, whereas CO 2 delivery to the alveoli is only 21 mL/min. 16 The remaining 90% (or more) of CO 2 is buffered within body tissues. The result is that lung volume decreases ini- tially by 209 mL/min, which creates a pressure gradient between the upper airway and the alveoli, and provided that the airway is not obstructed, O 2 enters the lung via dif- fusion. Because CO 2 cannot be exhaled, Paco 2 rises from 8 to 16 mm Hg in the irst minute of apnea, followed by a linear rise of approximately 3 mm Hg/min. 74 The beneit of apneic diffusion oxygenation is dependent on achieving maximal preoxygenation before apnea, main- taining airway patency, and the existence of a high func- tional residual capacity to body weight ratio. Fraioli et al 75 demonstrated that patients with a low predicted functional residual capacity/body weight ratio (37 ± 9 mL/kg) could not tolerate apneic oxygenation for more than 5 minutes, whereas patients with a high predicted functional residual capacity/body weight ratio (53 ± 8 mL/kg) could toler- ate apneic oxygenation for at least 15 minutes. Although Pao 2 falls in direct relation to Pao 2 , Sao 2 remains greater than 90% as long as the hemoglobin can be reoxygenated in the lungs,71,75 Sao 2 starts to decrease only after the O 2 stores in the lungs are depleted, and Pao 2 falls below 60 mm Hg. When Sao 2 is <80%, the rate of decrease in satura- tion is approximately 30%/min. In the presence of an air- way obstruction, gas volume in the lungs decreases rapidly, and intrathoracic pressure decreases at a rate dependent on lung compliance and Vo 2. When the airway obstruction is relieved, a rapid low of O 2 into the lungs resumes, and with high Fio 2 , preoxygenation is restored. 32 Some studies have demonstrated that, with a patent airway, apneic diffu- sion oxygenation can maintain Sao 2 above 90% for up to 100 minutes. 71 When Fio 2 is at a high level, a small increment can produce a profoundly disproportionate delay in hemo- globin desaturation; the delay in hemoglobin desaturation achieved by increasing Fio 2 from 0 to 1 was greater than that achieved by increasing Fio 2 from 0 to 0 (Figure 4). 76 Apneic diffusion oxygenation can be achieved by maxi- mal face mask preoxygenation followed by O 2 insuflation up to 15 L/min through a nasopharyngeal or an oropharyn- geal cannula or through a needle inserted in the cricothyroid membrane. In healthy patients with an unobstructed airway, this technique can provide at least 10 minutes of adequate oxygenation. The clinical applications include patients who are dificult to intubate or ventilate and patients with lim- ited oxygen reserves. The technique can also be used dur- ing bronchoscopy and can provide adequate time for short
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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 Fio 2 can have a profound effect on the extent of atelectasis–96 Computer model of absorp- tion atelectasis predicted that preoxygenation with an Fio 2 of 1 would accelerate the collapse of the lung. 93 A CT study found that atelectasis was less when patients were ventilated with 30% O 2 during induction of anesthesia than when 100% O 2 was used. 94 Another CT study evaluated the effect of stepwise variations in inspired O 2 on the extent of atelectasis and the time to arterial desaturation (Table 5). 95 The investigators found (1) that atelectasis was signif- icant in patients receiving 100% O 2 , but that it was small and virtually absent in patients receiving 80% and 60% O 2 , respectively and (2) that the time to desaturation fell with decreasing O 2 concentration. Studies have also shown that administering 100% O 2 during emergence from anesthesia can increase atelectasis. Benoit et al 96 found a 6% atelec- tasis in patients awakened on an Fio 2 of 1 compared with 2% in those awakened on an Fio 2 of 0. Recruitment maneuvers are commonly performed in patients under general anesthesia, but they have particular value in conjunction with preoxygenation. These maneu- vers include CPAP, PEEP, and/or reexpansion maneuver. A CT study found that the combined use of CPAP (6 cm H 2 O) during 5 minutes of preoxygenation with face mask while breathing spontaneously, and PEEP (6 cm H 2 O) 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 reexpan- sion 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 irst 7 to 8 seconds of application of an airway pressure of 40 cm H 2 O. 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 (O 2 ). 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–100 Reactive oxygen spe- cies can react with critical molecular components, such as lipids, DNA, and proteins, causing signiicant cellular dam- age,102 Although endogenous antioxidant mechanisms are normally suficient to prevent high tissue concentrations of reactive oxygen species, these mechanisms can become overwhelmed resulting in oxidative stress,103 It is known that prolonged use of Fio 2 = 1 can cause production of reactive oxygen species. Clinical manifestations are pulmo- nary 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 O 2 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 charac- terized. But there have been many studies, both in humans and animal models, assessing the steady state cardiovascu- lar responses during high O 2 breathing, which may provide insight into the hemodynamic changes during preoxygen- ation. However, the changes in Pao 2 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 experimen- tal indings described below to a given patient undergoing preoxygenation. Several studies in normal male subjects have demon- strated that breathing 100% O 2 causes a modest decrease in heart rate accompanied by a parallel decrease in cardiac
Figure 5. The OptiFlow high-low humidi- ied O 2 delivery system. The O 2 humidi- ication unit (A) received O 2 from a standard O 2 regulator and delivers humidiied O 2 to a custom-built transna- sal O 2 cannula (B and C) like a standard nasal O 2 cannula (D). Published with permission from Patel and Nouraei. 82
Table 5. Effect of FIO 2 Before Induction of
Anesthesia on Time for SaO 2 to Reach 90%, Along
With the Associated Atelectasis
FIO 2 Before Induction Time (s) to SaO 2 = 90% % Atelectasis 0 213 (69) 0 (0) 0 303 (59) 1 (1) 1 411 (84) 5 (3) Data are mean (SE). Abbreviations: FIO 2 , fraction of inspired oxygen; SaO 2 , arterial oxyhemoglobin saturation. Adapted from Edmark et al. 95
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output. Systemic vascular resistance and arterial blood pres- sure increase–108 These changes are attributable to a relex 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% O 2 in the human coronary circula- tion–113 Hyperoxia consistently caused a marked decrease in coronary blood low (relecting coronary vasoconstric- tion) accompanied by a decrease in myocardial oxygen consumption. The direct coronary vasoconstrictor effect of hyperoxia is due to the oxidative inactivation of nitric oxide110,112 and other vasodilators released from the vascular endothelium and to closure of the ATP-sensitive K+ chan- nels,114 Investigations in patients with normal coronary arteries have indicated that, despite the decrease in coro- nary blood low, oxygenation at the level of the myocytes remains adequate, as indicated by continued myocardial lactate extraction rather than conversion to production, This is likely explained by the ability of the increase in arte- rial O 2 content to blunt the reduction in coronary O 2 sup- ply caused by the reduced coronary blood low combined with a reduction in myocardial O 2 demand, secondary to the hyperoxia-induced bradycardia. Metabolic indings in patients with severe coronary artery disease have been inconsistent. Some studies have found that O 2 breathing by these patients converts myocardial lactate production to extraction, suggesting a beneicial effect, 108 whereas oth- ers have found that O 2 breathing precipitates or accentu- ates myocardial lactate production, implying ischemic changes. 110 It is well established that inhalation of high O 2 can also reduce cerebral blood low because of vasoconstric- tion–118 It has been proposed that this effect may be because, at least in part, of the associated decrease in Paco 2 that accompanies high O 2 breathing rather than to a direct effect of O 2. 116 The mechanism for the decrease in Pac o 2 is as follows. When Pao 2 is increased by inhalation of 100% O 2 , the CO 2 dissociation curve for blood is altered (the Christiansen-Douglas-Haldane effect), such that there is a reduction in the afinity of blood for CO 2. This produces an increase in cerebral tissue Pco 2 and hydrogen ion con- centration, which stimulates respiration with a result that Paco 2 decreases causing cerebral vasoconstriction, Investigators have also assessed the effect of hyperoxia on cerebral O 2 consumption, using a functional magnetic resonance technique. 117 They found that hyperoxia causes an approximate 20% decrease in cerebral O 2 consumption, relecting reduced neural activity. 117 It was speculated that the decrease in cerebral O 2 consumption was because of the ability of reactive oxygen species to damage lipids and pro- teins, and, in turn, decrease the enzyme activity in oxida- tive metabolic pathways. Studies in animal models have demonstrated that hyper- oxia causes vasoconstriction and a decrease in blood low in peripheral vascular beds, including the kidney, gastrointes- tinal tract, and hindlimb,119,120 Whether this vasoconstric- tion is because of a direct effect of O 2 on vascular smooth muscle or relex-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 indings to date provide no justiication for limiting the use of preoxygenation.
CONCLUSIONS
The literature provides overwhelming evidence that preox- ygenation, whether instituted before induction or to emer- gence from anesthesia, delays the onset of hypoxemia during apnea. On that basis, preoxygenation should be performed in all patients given general anesthesia. Preoxygenation should also be performed whenever there is an anticipated interruption of O 2 delivery, such as during open tracheo- bronchial suctioning, and before and during awake iber- optic intubation, especially in high-risk patients, such as the supermorbidly obese. The technique should be performed correctly, with monitoring of Eto 2. Because the advantage of preoxygenation may be blunted in high-risk patients, vari- ous maneuvers are available to prolong its effectiveness. The clinician should be familiar with these maneuvers. Absorption atelectasis during preoxygenation can be read- ily minimized, and thus it should not be a deterrent to the
routine use of the technique. E
DISCLOSURES Name : Usharani Nimmagadda, MD. Contribution : This author helped write the manuscript. Name : M. Ramez Salem, MD. Contribution : This author helped write the manuscript. Name : George J. Crystal, PhD. Contribution : This author helped write the manuscript. This manuscript was handled by: Richard C. Prielipp, MD, MBA, FCCM.
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Preoxygenation Physiologic Basis, Benefits, and
Asignatura: Filología - Alemán (1a2b3c)
Universidad: Universidad Nacional de Colombia
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