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Canadian Journal of Anesthesia 49:1040-1043 (2002)
© Canadian Anesthesiologists' Society, 2002
General Anesthesia

Oxygen in air (FIO2 0.4) improves gas exchange in young healthy patients during general anesthesia

[La présence d’oxygène dans de l’air (FiO2 de 0,4) améliore les échanges gazeux chez de jeunes patients en bonne santé pendant l’anesthésie générale]

Anil Agarwal, MD*, Prabhat K. Singh, MD*, Sanjay Dhiraj, MD*, Chandra M Pandey, PhD{dagger} and Uttam Singh, PhD{dagger}

* From the Department of Anesthesia, and
{dagger} Biostatistics, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India.

Address correspondence to: Dr. Anil Agarwal, Type IV/48, SGPGIMS, Lucknow 226 014, India. Fax: +91 522 668017, 668047, 668078; E-mail: aagarwal{at}sgpgi.ac.in


   Abstract
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 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Purpose: One hundred percent O2 is used routinely for preoxygenation and induction of anesthesia. The higher the O2 concentration the faster is the development of atelectasis, an important cause of impaired pulmonary gas exchange during general anesthesia (GA). We evaluated the effect of ventilation with 0.4 FIO2 in air, 0.4 FIO2 in N2O and 100% O2 following intubation on the development of impaired gas exchange.

Methods: Twenty-seven patients aged 18–40 yr, undergoing elective laparoscopic cholecystectomy were administered 100% O2 for preoxygenation (three minutes) and ventilation by mask (two minutes). Following intubation these patients were randomly divided into three groups of nine each and ventilated either with 0.4 FIO2 in air, 0.4 FIO2 in N2O or 100% O2. Arterial blood gases were obtained before preoxygenation and 30 min following intubation for PaO2 analysis. Subsequently PaO2/FIO2 ratios were calculated. Results were analyzed with Student’s t test and one-way ANOVA. P value of # 0.05 was considered significant.

Results: Ventilation of the lungs with O2 in air (FIO2 0.4) significantly improved the PaO2/FIO2 ratio from baseline, while 0.4 FIO2 in N2O or 100% O2 worsened the ratio (558 ± 47 vs 472 ± 28, 365 ± 34 vs 472 ± 22 and 351 ± 23 vs 477 ± 28 respectively; P < 0.05).

Conclusion: Ventilation of lungs with O2 in air (FIO2 0.4) improves gas exchange in young healthy patients during GA.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
GENERAL anesthesia (GA) per-se with or without paralysis causes impairment in gas exchange with decreased blood oxygenation.1–3 Atelectasis is an important cause of this impairment in gas exchange during GA. Atelectasis is caused by two mechanisms and both must be present to produce collapse. The two mechanisms are: loss of respiratory muscle tone causing reduction in functional residual capacity (FRC) and resorption of gases. An alveolus or a lung region that is closed off from the ambient air slowly collapses because of absorption of oxygen (O2) into the blood stream whereas carbon dioxide (CO2) delivered to the closed unit will dissolve in the surrounding tissue. The higher the O2 concentration, the faster is the rate of adsorption and formation of atelectasis.

O2 100% is used routinely for preoxygenation and for ventilation during induction of anesthesia. Use of a high fractional inspiratory O2 concentration (FIO2) allows more time for endotracheal intubation before life-threatening hypoxemia develops.4 This increased safety is obtained at the cost of development of atelectasis. Whether it contributes to postoperative complications has not been analyzed but remains a possibility. Almost 3% of patients undergoing elective abdominal surgery do suffer from postoperative pulmonary complications.5 Even a moderate decrease in the complication rate could reduce the numbers substantially. After induction of anesthesia, patients are usually ventilated with different concentration of O2 in nitrous oxide (N2O) or air. O2 100% and O2 in N2O both favour the development of atelectasis, while O2 in air has been found to retard the development of atelectasis.6 We postulated that ventilation with FIO2 0.4 in air following preoxygenation (three minutes) and mask ventilation (two minutes) with O2 100% would improve pulmonary gas exchange during GA.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
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Following approval from the Institutional Research and Ethic’s Committees, informed consent from all patients was obtained for this study. Twenty-seven patients of both sexes, aged 18–40 yr, ASA class I and II, undergoing elective laparoscopic cholecystectomy in the supine posture were included in this randomized, prospective study. Smokers and patients with abnormal preoperative pulmonary function tests were excluded from the study. Patients were premedicated with ranitidine 150 mg po and lorazepam 2.0 mg on the night prior to and 2.0 hr before surgery. All patients were preoxygenated (three minutes) and ventilated during induction of anesthesia (two minutes) with 100% O2. Anesthesia was induced with fentanyl (3 µg•kg-1 iv) and thiopentone sodium (4–5 mg•kg-1 iv). Intubation was facilitated by vecuronium (0.1 mg•kg-1 iv). Following intubation patients were randomized into three groups A, B and C of nine with the help of a computer-generated table of random numbers and maintained on gas mixtures as follows along with isoflurane (0.6–1%), A: 0.4 FIO2 in air; B: 0.4 FIO2 in N2O and C: 100% O2.

Patients were ventilated in volume-controlled mode with a tidal volume of 8 mL•kg-1. Respiratory rate was adjusted so as to keep the end tidal carbon dioxide levels at 35–40 mmHg as measured by Datex Ohmeda 5250 capnograph. Blood gas analysis (ABG) was performed without any temperature correction by i STAT, Abbott, USA, before preoxygenation and 30 min following intubation (end of the study period) for determination of PaO2. Subsequently, PaO2/FIO2 ratios were calculated and analyzed as an indicator of pulmonary gas exchange. Surgical intervention started only after the end of the study period.

Assuming 10% variability in PaO2 and 99% power, the minimum sample size required in each group was six. Anticipating some dropouts we included nine subjects in each group. Student’s t test was applied to determine the significance between the control and final PaO2/FIO2 ratios of the same group. Means for groups in homogeneous subsets were compared by one-way ANOVA. Post hoc analysis for inter-group difference was carried out using Student-Newman-Keuls test. A P value # 0.05 was considered significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Patients of the three groups were comparable with respect to demographic variables (Table IGo). PaO2 and PaO2/FIO2 ratios of the three groups were also comparable at baseline (Table IGo). A significant increase in the PaO2/FIO2 ratio was observed 30 min after induction of anesthesia in patients maintained with 0.4 FIO2 in air (Group A) when compared to baseline values. On the contrary, a significant decrease in PaO2/FIO2 ratio was observed 30 min after induction of anesthesia in patients maintained with 0.4 FIO2 in N2O or 100% O2 (Groups B and C) when compared to baseline values (Table IIGo; Figure).


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  		TABLE I Patient characteristics
 

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  		TABLE II PaO2 and PaO2/FiO2 ratios in the various groups
 
One-way ANOVA revealed a similar baseline PaO2/FIO2 ratio in all three groups, however a significant difference in the final PaO2/FIO2 ratios was observed in the three groups. Post hoc test demonstrated that Groups B and C were similar while Group A was significantly different from the other two groups. A significant increase in final PaO2/FIO2 ratio was observed in Group A when compared to final PaO2/FIO2 ratios of Groups B and C. However, no difference was observed in the final PaO2/FIO2 ratios of Groups B and C. The best PaO2/FIO2 ratios were observed in patients ventilated with FIO2 of 0.4 in air (Table IIGo).


   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Ventilation of the lungs with 0.4 FIO2 in air significantly improved the PaO2/FIO2 ratio in relation to baseline values, following preoxygenation (three minutes) and mask ventilation (two minutes) with O2 100% during induction of anesthesia. On the contrary, ventilation of the lungs with 0.4 FIO2 in N2O or 100% O2 significantly worsened the PaO2/FIO2 ratio in relation to baseline values. The best PaO2/FIO2 ratio was achieved in the group of patients ventilated with FIO2 of 0.4 in air during GA. Therefore, our study suggests that the composition of gases used for ventilating the lungs during GA plays an important role on subsequent pulmonary gas exchange.

Computed tomography (CT) of lungs densities developing during GA is the available evidence suggesting the occurrence of atelectasis. These studies also successfully established the relationship between the oxygen concentration used for ventilating the lungs and the extent of atelectasis.

There have also been attempts to prevent and correct atelectasis during GA. Studies have suggested that the use of 100% O2 during standard anesthesia induction needs to be re-evaluated.6 Approaches might include the use of a gas mixture containing air during induction of anesthesia.7 Alternatively, re-expansion by hyperinflation should be considered to eliminate atelectasis during GA.8,9

In this study, the PaO2/FIO2 ratio was used to estimate the extent of impaired gas exchange during GA,10 since absolute PaO2 values obtained at different FIO2 cannot be compared. Atelectasis results in intrapulmonary shunting and mismatching of ventilation/perfusion (VA/Q), leading to impaired gas exchange. The PaO2/FIO2 ratio reflects the mismatching of VA/Q and intrapulmonary shunting. However, there are other factors, apart from atelectasis, such as displacement of blood from the thorax to the abdomen, reduction in the thoracic diameter and displacement and dysfunction of the diaphragm, which can also contribute to impairment of oxygenation.11–13

Rothen et al. studied the effect of gas composition on the recurrence of atelectasis after lung re-expansion during GA. They observed that if the lungs are ventilated with 0.4 FIO2 in air, re-expansion of atelectasis is sustained with respect to atelectasis, shunt, and PaO2. However, lung collapse reappears within a few minutes if the lungs are ventilated with 100% O2.14

The estimated time to collapse of completely closed off lung units from ambient air is six to nine hours if the unit contains air (21% O2 in N2), about three hours if it contains 30% O2 in N2, and about eight minutes if it contains 100% O2.15,16 Because of the high solubility of N2O a lung unit will collapse even faster if it contains a mixture of O2 and N2O.15 The composition of inspired gases may also influence the formation of atelectasis in conscious subjects breathing at low lung volumes (i.e., close to residual volumes). For example, despite chest strapping, which reduces FRC by 0.6 L, no atelectasis was found with CT in subjects breathing air.17 Conscious subjects breathing 100% O2 at reduced lung volumes, by contrast, showed direct or indirect evidence of atelectasis, although no CT was done.18,19

To conclude, ventilation of the lungs with 0.4 FIO2 in air significantly improved PaO2/FIO2 ratio during anesthesia. Keeping the patient’s safety in mind, we suggest that the practice of using 100% O2 during preoxygenation and induction of anesthesia should be continued. However, the deleterious effect of such a practice on gas exchange can be countered effectively thereafter by ventilating the lungs with an FIO2 0.4 in air. Further studies to determine the optimal FIO2 in air for ventilation during GA are recommended.



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  		FIGURE Mean PaO2/FiO2 ratios at baseline and 30 min after ventilation (final) in various groups. *Newman-Keul (post hoc test) P # 0.05.

 
Revision received September 6, 2002. Accepted for publication June 4, 2002.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Strandberg A, Tokics L, Brismar B, Lundquist H, Hedenstierna G. Atelectasis during anaesthesia and in the postoperative period. Acta Anaesthesiol Scand 1986; 30: 154–8.[Medline]

2 Cote CJ, Goldstein EA, Cote MA, Hoaglin DC, Ryan JF. A single-blind study of pulse oximetry in children. Anesthesiology 1988; 68: 184–8.[Medline]

3 Moller JT, Johannessen NW, Berg H, Espersen K, Larsen LE. Hypoxaemia during anaesthesia–an observer study. Br J Anaesth 1991; 66: 437–44.[Abstract/Free Full Text]

4 Videira RL, Neto PP, do Amaral RV, Freeman JA. Preoxygenation in children: for how long? Acta Anaesthesiol Scand 1992; 36: 109–11.[Medline]

5 Pedersen T, Viby-Mogensen J, Ringsted C. Anaesthetic practice and postoperative pulmonary complications. Acta Anaesthesiol Scand 1992; 36: 812–8.[Medline]

6 Hedenstierna G, Edmark L, Aherdan KK. Time to reconsider the pre-oxygenation during induction of anaesthesia. Minerva Anestesiol 2000; 66: 293–6.[Medline]

7 Rothen HU, Sporre B, Engberg G, Wegenius G, Reber A, Hedenstierna G. Prevention of atelectasis during general anaesthesia. Lancet 1995; 345: 1387–91.[Medline]

8 Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993; 71: 788–95.[Abstract/Free Full Text]

9 Shambaugh GE, Harrison WG, Farrell JI. Treatment of respiratory paralysis of poliomyelitis in respiratory chamber. JAMA 1930; 94: 1371–3.

10 Marino PL. Hypoxia and hypercarbia. In: Zinner SR (Ed.). The ICU Book, 2nd ed. Baltimore: Williams & Wilkins, 1998: 339–54.

11 Hedenstierna G, Strandberg A, Brismar B, Lundquist H, Svensson L, Tokics L. Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation. Anesthesiology 1985; 62: 247–54.[Medline]

12 Krayer S, Rehder K, Vettermann J, Didier EP, Ritman EL. Position and motion of the human diaphragm during anesthesia–paralysis. Anesthesiology 1989; 70: 891–8.[Medline]

13 Klineberg PL, Rehder K, Hyatt RE. Pulmonary mechanics and gas exchange in seated normal men with chest restriction. J Appl Physiol 1981; 51: 26–32.[Abstract/Free Full Text]

14 Rothen HU, Sporre B, Engberg G, Wegenius G, Hogman M, Hedenstierna G. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82: 832–42.[Medline]

15 Joyce CJ, Baker AB, Kennedy RR. Gas uptake from an unventilated area of lung: computer model of absorption atelectasis. J Appl Physiol 1993; 74: 1107–16.[Abstract/Free Full Text]

16 Webb SJ, Nunn JF. A comparison between the effect of nitrous oxide and nitrogen on arterial PO2. Anaesthesia 1967; 22: 69–81.[Medline]

17 Tokics L, Hedenstierna G, Brismar B, Strandberg A, Lundquist H. Thoracoabdominal restriction in supine men: CT and lung function measurements. J Appl Physiol 1988; 64: 599–604.[Abstract/Free Full Text]

18 Nunn JF, Williams IP, Jones JG, Hewlett AM, Hulands GH, Minty BD. Detection and reversal of pulmonary absorption collapse. Br J Anaesth 1978; 50: 91–100.[Abstract/Free Full Text]

19 Baker AB, McGinn A, Joyce C. Effect on lung volumes of oxygen concentration when breathing is restricted. Br J Anaesth 1993; 70: 259–66.[Abstract/Free Full Text]




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