Anesthesia & Analgesia:
Dosing Oxygen: A Tricky Matter or a Piece of Cake?
Lindahl, Sten G.E. MD, PhD, FRCA; Mure, Margareta MD, PhD
Department of Anesthesiology and Intensive Care Medicine, Karolinska Hospital and Institute, Stockholm, Sweden
July 31, 2002.
Address correspondence and reprint requests to Sten G.E. Lindahl, MD, PhD, FRCA, Department of Anesthesiology and Intensive Care Medicine, Karolinska Hospital and Institute, SE-171 76 Stockholm, Sweden. Address e-mail to firstname.lastname@example.org.
Something is burning in my chest,” the healthy volunteer complains after breathing 100% oxygen for 24 h. “There is an inflammation in the trachea. It is all red,” the bronchoscopist concludes. Classical observations explained in a classical paper on “The Toxicity of Oxygen” by Winter and Smith (1). Just as there are side effects with various invasive interventions and drug treatments, there are also complications with oxygen. Tissue oxygen toxicity is one example, and development of pulmonary atelectasis after acute use of 100% oxygen is another. This issue of Anesthesia & Analgesia presents two interesting investigations concerned with the acute use of high-inspired oxygen concentrations and postoperative complications in the near postanesthesia period (2,3). The studies demonstrate a negative influence on lung function after tracheal extubation preceded by a short period of 100% oxygen breathing—an observation of significant clinical importance because leading postoperative complications today, particularly in the elderly, are pulmonary. One of the studies is based on an experimental design evaluating ventilation/perfusion matching using the multiple inert gas technique. It shows less efficient gas exchange after 100% oxygen breathing before extubation. The other study was performed in patients using the computed tomography scanner to detect increased pulmonary atelectasis at 100% oxygen. Certainly, the two investigations suggest that postoperative pulmonary complications could, at least to some extent, be reduced if routines for 100% oxygen just before extubation were modified.
The two studies are not concerned with the long-term (up to 24 h) use of 100% oxygen, when more than 70% of individuals develop respiratory problems (1). They do not involve retinopathy of prematurity, nor do they highlight patients with chronic obstructive lung disease and hypercarbia. They concern the frequent acute use of 100% oxygen for only brief periods during which time no signs of tissue toxicity have been described. However, there have been several reports on the development of pulmonary atelectasis after breathing 100% oxygen before endotracheal intubation at the induction of anesthesia (4,5). These series put forward careful conclusions suggesting lower inspired oxygen concentrations than before practiced to prevent atelectasis formation early during anesthesia and surgery. Alternatively, effective recruitment of lung tissue is advocated immediately after the intubation or whenever 100% oxygen has been used (6). Similar problems are now described for emergence from anesthesia. Patients do get atelectasis from a few minutes of 100% oxygen breathing. To compensate by doing a recruitment maneuver, up to 40 cm H2O, in a recently extubated patient is definitely not a piece of cake. It seems logical just to change the routines; the knowledge is there! Yet, the tradition is long lived, and we still frequently practice 100% oxygen before extubation.
Why is this routine so persistent? First, anesthesiologists actively cause prolonged pharmacologic-induced apnea for which we have to take full responsibility. Second, experience tells us that we sometimes have a patient that just cannot be ventilated, in which case the extra minutes provided by hyperoxygenation are appreciated. Because the functional residual capacity of the lung is the volume that contains the oxygen reserve, the following reasoning might be helpful: Let us assume a functional residual capacity volume of 2500 mL. At normal air breathing this container holds 500 mL of oxygen. After breathing 100% oxygen for approximately 5 min, you have approximately 2500 mL of oxygen. At an oxygen consumption of 200 mL/min, the oxygen supply is used up after about 2 min breathing air and 10 min later after hyperoxygenation. It is these extra 10 min that support the safety-first strategy, justifying maintained routines, during the induction of anesthesia. At the other end, i.e., emergence from anesthesia, there are fewer chances of being completely surprised by a patient that cannot be ventilated.
There are, as always, two sides of this coin. Several studies report a reduction of postoperative nausea and vomiting as well as improved surgical wound healing after breathing 80% oxygen for a couple of hours after surgery (7,8). Can it be justified then to use 80% oxygen to gain these benefits from oxygen treatment? Although it causes atelectasis, it is clear that 100% oxygen breathing for 2–3 h, under normobaric conditions, does not cause tissue oxygen toxicity (1). Hence, 80% oxygen would be fine in this regard. The controversy is whether lung atelectasis is induced also at 80% oxygen. In 1999, Akca et al. (9) demonstrated an equivalent amount of pulmonary atelectasis breathing 30% or 80% oxygen. These studies clearly speak in favor of using large oxygen concentrations (80%) for a couple of hours after surgery to provide the best possible treatment with the best possible outcome for our patients.
The two investigations in this issue of Anesthesia & Analgesia call for caution with regard to Fio2s of 1.0. Surely, smaller concentrations must be used to avoid unnecessary atelectasis in the early postoperative period. Would an Fio2 of 0.8 be acceptable if the incidence of atelectasis was clearly shown not to be increased? If the answer to the question were yes, the routine use of up to 80% oxygen both at the induction of and emergence from anesthesia would be fine. Not only do you get the benefits from oxygen, but you will also get 8 extra min compared with air breathing should an impossible to ventilate patient appear.
1. Winter PM, Smith G. The toxicity of oxygen. Anesthesiology 1972; 37: 210–41.
2. Benoit Z, Wicky S, Fischer J-F, et al. Effects of increased FiO2 before tracheal extubation on postoperative atelectasis. Anesth Analg 2002; 95: 1777–81.
3. Loeckinger A, Kleinsasser A, Keller C, et al. Administration of oxygen prior to tracheal extubation worsens gas exchange after general anesthesia in an animal model. Anesth Analg. In Press.
4. Rothen HU, Sporre B, Engberg G, et al. Atelectasis and pulmonary shunting during induction of general anaesthesia: can they be avoided? Acta Anaesthesiol Scand 1996; 40: 524–9.
5. Rothen HU, Sporre B, Engberg G, et al. Prevention of atelectasis during general anaesthesia. Lancet 1995; 345: 1387–91.
6. Rothen HU, Sporre B, Engberg G, et al. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82: 832–42.
7. Greif R, Laciny S, Rapf B, et al. Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Anesthesiology 1999; 91: 1246–52.
8. Greif R, Akca O, Horn EP, et al. Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. N Engl J Med 2000; 342: 161–7.
9. Akca O, Podolsky A, Eisenhuber E, et al. Comparable postoperative pulmonary atelectasis in patients given 30% or 80% oxygen during and 2 hours after colon resection. Anesthesiology 1999; 91: 991–8.
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© 2002 International Anesthesia Research Society
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