|Year : 2016 | Volume
| Issue : 3 | Page : 337-342
Effect of high fractional inspiratory oxygen on postoperative pulmonary function: a randomized–controlled study
Gad S Gad
Department of Anesthesia, Qena University Hospital, Qena, Egypt
|Date of Submission||17-Mar-2015|
|Date of Acceptance||06-Apr-2016|
|Date of Web Publication||31-Aug-2016|
Gad S Gad
Lecturer of Anaesthesia and Intensive Care (MD), Anesthesia Department, Qena University Hospital, P.O. Box 83523, Qena
Source of Support: None, Conflict of Interest: None
Although a high fraction of inspired oxygen (FiO2) could reduce surgical site infection, there is a concern that it could increase postoperative pulmonary complications, including hypoxemia. However, there is an advantage for preoperative high FiO2 before induction of anesthesia as it decreases the incidences of desaturation and wound infection. Our aim was to assess whether different levels of FiO2 affect pulmonary function tests.
Patients and methods
Ninety patients scheduled for elective abdominal hysterectomy were randomized to receive either preoxygenation with 1.0 FiO2 for 3 min, then continued on 1.0 FiO2 till the end of surgery (group A), or preoxygenation with 1.0 FiO2 for 3 min, then continued on 0.4 FiO2 till the end of surgery (group B), or preoxygenation with 0.4 FiO2 then continued on 0.4 FiO2 till the end of surgery (group C). The oxygenation index (PaO2/FiO2) was measured every 30 min during anesthesia and 2 h after extubation. Pulmonary function test was measured on the morning of surgery and 2 h after extubation.
Five minutes after intubation, the median PaO2/FiO2 was 483 (371–490) mmHg in group A, 420 (336–490) mmHg in group B, and 450 (350–485) mmHg in group C (P = 0.24). Two hours after extubation, the PaO2/FiO2 was reduced to 333 (314–342) mmHg in group A, 328 (311–357) mmHg in group B, and 342 (303–316) mmHg in group C (P = 0.55). The median functional vital capacity were 1950 (1600–2120), 1850 (1570–2250), and 1900 (1490–2020) ml at baseline and 1650 (1370–1953), 1670 (1340–2350), and 1711 (1412–2410) ml 2 h after extubation in groups A, B, and C, respectively (P = 0.66).
We found no significant difference in the oxygenation index or pulmonary function tests between patients administered different levels of FiO2.
Keywords: abdominal hysterectomy, anesthesia, fraction of inspired oxygen, functional vital capacity, pulmonary atelectasis, pulmonary function, pulmonary function test
|How to cite this article:|
Gad GS. Effect of high fractional inspiratory oxygen on postoperative pulmonary function: a randomized–controlled study. Ain-Shams J Anaesthesiol 2016;9:337-42
|How to cite this URL:|
Gad GS. Effect of high fractional inspiratory oxygen on postoperative pulmonary function: a randomized–controlled study. Ain-Shams J Anaesthesiol [serial online] 2016 [cited 2021 Apr 14];9:337-42. Available from: http://www.asja.eg.net/text.asp?2016/9/3/337/189090
| Introduction|| |
It is well known that high inspiratory oxygen can cause postoperative pulmonary complications in the form of ventilation–perfusion mismatch, absorption atelectasis, reduced function of surfactant, and postoperative hypoxemia ,,. However, there is an advantage for perioperative high fraction of inspired oxygen as preoxygenation with 100% oxygen (FiO2 1.0) before induction of anesthesia decreases the incidence of desaturation and prolongs the apnea time before intubation ,,,. It also helps decrease the incidence of wound infection and postoperative nausea and vomiting.
Multiple studies have compared the effect of high FiO2 and low FiO2 on the pulmonary function test; however, no clear justification between oxygen tension (PO2) and atelectatic changes during maintenance of general anesthesia has been established and on which level of FiO2 exposure can induce pulmonary atelectasis and hypoxemia .
Atelectasis causes hypoxemia by different mechanisms: reduced gas exchange by decreasing functional residual capacity and intrapulmonary right to left shunt, which can be estimated by the FiO2/PO2 ratio ,. However, preoxygenation with 100% FiO2 has become a standard of care before induction of general anesthesia because it exerts a protective effect against oxygen desaturation during intubation as it prolongs apnea time, decreases postoperative nausea and vomiting, and also decreases the incidence of postoperative wound infection ,. The outweigh of benefit and risk of exposure to high FiO2 during general anesthesia need more investigation.
Our aim is to investigate the risks and benefits of different levels of FiO2 exposures before induction and during general anesthesia on the pulmonary functions.
| Patients and methods|| |
This study was carried out in the Department of Anesthesia and ICU at Qena University Hospital after hospital ethical board review and approval of the study protocol; written informed consent was obtained from every patient participating in the study. Adult women ranging in age from 18 to 60 years scheduled for abdominal hysterectomy under general anesthesia admitted to our hospital in the time period from June 2012 to May 2013 were included in the study. Exclusion criteria were as follows: diagnosis of chronic obstructive pulmonary diseases (COPD), history of obstructive sleep apnea, morbidly obese BMI (>30), spontaneous pneumothorax, chemotherapy within the last 3 months, heavy smokers, hemoglobin less than 10 g/dl, and patient refusal.
Patients were randomized into three groups using a computer-generated list, 30 patients per group, and scheduled for lower abdominal surgery (abdominal hysterectomy) under general anesthesia. In group A, preoxygenation with 100% O2 for 5 min was performed and then continued on 100% O2 till the end of surgery, in group B, preoxygenation was performed with 100% O2 was done for 5 min and continued on 40% O2 till the end of surgery, and in group C, preoxygenation with 40% O2 was performed and then continued on 40% O2 till the end of surgery.
All patients were monitored intraoperatively for ECG, pulse oximetry, invasive and noninvasive blood pressure, skin and core temperature, and end tidal CO2.
Anesthesia was induced with intravenous administration of 2 mg/kg propofol together with fentanyl 1 μg/kg and atracurium 0.6 mg/kg to facilitate endotracheal intubation. Anesthesia was maintained with 1 MAC isoflurane. After intubation, the patients were ventilated with the allocated fraction of inspired oxygen of each group.
The lungs were ventilated by the volume-controlled mode with a tidal volume of 6 ml/kg and a respiratory rate of 12–16 cycle/min to maintain normocapnia. The level of positive end-expiratory pressure (PEEP) was maintained at 5 cmH2O throughout the operative time.
In all patients, an arterial catheter was inserted into the right or the left radial artery at the wrist joint using a completely aseptic technique.
Fluids were administered to replace deficits and intraoperative blood loss was replaced with colloids 1:1 not exceeding 500 ml more than estimated blood loss .
Ephedrine was used if the mean arterial blood pressure decreased by more than 20% of basal mean arterial blood pressure or systolic blood pressure less than 90 mmHg provided adequate blood and fluid replacement was performed. Neuromuscular block in all patients was assessed using train of four (TOF) monitoring using a TOF guard monitor (Danmeter APS, Odense, Denmark).
After completion of surgery, residual neuromuscular block was reversed with intravenous neostigmine at a dose of 0.04 mg/kg and atropine at a dose 0.01 mg/kg, and patients were extubated where they were fully awake and the TOF ratio of 0.90 or more.
After arrival to the postanesthesia care unit (PACU), patients were kept on a nasal cannula with 3 l/min for all patients to maintain oxygen saturation above 92% and patients were monitored with continuous pulse oximetry; no chest physiotherapy was administered in the PACU. Arterial blood samples were obtained using 2-ml syringes containing heparin from a radial arterial catheter and analyzed immediately in a blood gas analyzer (Radiometer-ABL800, Blood Gas Analyzer-Denmark) in the PACU. Samples were obtained 5 min after intubation, every half hour during surgery, and 2 h after extubation.
Spirometry was performed on the morning of surgery and 2 h postoperatively. Patients were asked to rate their pain at rest in the supine position with 30° upper body elevation on a numeric rating scale of 0–10 (0, no pain; 10, maximum pain). If the pain score was more than 3, pain therapy was optimized before spirometric testing was performed. Measurement of pulmonary function was performed using a spirometer (Viasys Healthcare, Microlab, (England), UK). Patients received detailed instructions on how to perform the tests. Measurements were performed in accordance with the standards of the American Thoracic Society. All measurements were performed in the supine position with 30° upper body elevation. A clip was placed over the nose and the patient breathed through the mouth into a tube connected to the spirometer. First, the patient breathed in deeply and then exhaled as quickly and forcefully as possible into the tube. This was done three times and the best of the three results was recorded as the measure of lung function and selected for analysis .
Preoperative and postoperative chest radiographs were obtained before and after surgery. The results were scored by a radiologist unaware of group assignment using a Radiological Atelectasis Score: 0, clear lung field; 1, plate like atelectasis or slight infiltration; 2, partial atelectasis; 3, lobar atelectasis; and 4, bilateral lobar atelectasis.
Patients were seen daily by a study investigator and were examined according to routine clinical practice by the attending physician; if they presented with symptoms of pulmonary complications, chest radiographs or computed tomography (CT) were performed when relevant. The radiologist was specifically instructed to evaluate the severity of atelectasis according to the Joyce et al.  modification of the Wilcox severity scoring .
All patients received an infusion of paracetamol (perfalgan) and ketorolac 30 mg intravenous preoperatively and pain was monitored in the PACU using the visual analog scale (1–10); the same analgesic was administered postoperatively if visual analog scale was 4 or more.
The primary outcome was the change in PaO2/FiO2 after induction of anesthesia. The secondary outcomes were change in PaO2/FiO2 during and after extubation, change in forced expiratory volume in 1 s (FEV1)/functional vital capacity (FVC) 2 h after extubation, incidence and severity of atelectasis, and SpO2 within 3 days after surgery.
We found that the number of 30 patients per group and 30 mmHg change were sufficient to detect the difference between groups in PaO2/FiO2 with a power of 80% (Graphpad software StatMate. san diegio California).
Our statistical analyses were carried out using SPSS statistical software (version 20; SPSS Inc., Chicago, Illinois, USA). In this study, analysis of variance (ANOVA) was carried out on the demographic data using the ANOVA test for continuous variables (i.e. age, weight, BMI, and duration of surgery) and the Kruskal–Wallis rank test for American Society of Anesthesiologists status. To study the effects of time and group allocation on each of the variables, repeated-measures ANOVA was used to compare the FVC and FEV1/FVC parameters between baseline values and 2 h postoperatively. When an overall difference was detected, the Student–Newman–Keuls post-test was used to localize significant differences. One-way ANOVA was used between groups and multiple comparisons were made using Dunn's method when the results were significant. The data were expressed as mean ± SD and n (%), and statistical significance was defined as P value less than 0.05.
| Results|| |
We included 90 patients in this study; there was no significant difference between the demographic data of the patients [Table 1]. Five minute after intubation, the median PaO2/FiO2 was 483 (371–490) mmHg in group A, 420 (336–490) mmHg in group B, and 450 (350–485) mmHg in group C (P = 0.24). At the end of anesthesia, the PaO2/FiO2 was 406 (322–490), 399 (280–469), and 395 (315–455) mmHg in groups A, B, and C, respectively (P = 0.19; [Table 2]. Two hours after extubation, the PaO2/FiO2 was reduced to 333 (314–342) mmHg in group A, 328 (311–357) mmHg in group B, and 342 (303–316) mmHg in group C (P = 0.55).
Data on pulmonary function test quality were collected in 90 patients [Table 3]. No significant difference was found between the groups. The median FVC were 1950 (1600–2120), 1850 (1570–2250), and 1900 (1490–2020) ml at baseline and 1650 (1370–1953), 1670 (1340–2350), and 1711 (1412–2410) ml 2 h after extubation in groups A, B, and C, respectively (P = 0.66) [Table 2]. FEV1/FVC showed no significant difference between the three groups (P = 0.70).
Seven (23%) patients in group A developed radiologically verified atelectasis compared with three (9%) patients in group B and two (6%) patients in group C (P = 0.52) [Table 4].
|Table 4 Severity of atelectasis assessed according to the Joyce et al. (13) modification of the Wilcox severity scoring (14)|
Click here to view
| Discussion|| |
We did not find a significant difference in PaO2/FiO2 at the end of surgery between patients administered a high perioperative oxygen fraction (100% oxygen) (group A or group B) and lower oxygen fraction (40%) (group C). Moreover, we did not find a significant difference in FVC or in the calculated changes. The accuracy of the measurements was high because blood samples were obtained in rapid succession at each PaO2 measurement and at established FiO2 levels . Moreover, FVC were calculated as an average of two measurements both before and 2 h after extubation.
The change in the PaO2/FiO2 is not a perfect measurement to quantify the amount of impaired gas exchange. It is affected by numerous factors other than true intrapulmonary right to left shunts caused by atelectasis, such as changes in circulatory blood volume, vasopressor use, positioning of the patient, and body temperature. These factors were, however, not different between the groups. Other factors such as ventilation–perfusion (VA/Q) inequality and hypoxic pulmonary vasoconstriction may have also modified the PaO2/FiO2. Moreover, the PaO2/FiO2 is not correlated linearly to FiO2 ,.
Factors that could cause postoperative hypoxemia include absorption, compression, and loss of surfactant atelectasis; increased ventilation/perfusion mismatch, hypoventilation caused by opioids, other drugs, or pain; pulmonary edema; and other patient comorbidities. Although we did not measure any of these directly, absorption atelectasis is most likely to be different, given that the only difference between the groups was FiO2.
We measured the change in the PaO2/FiO2 from samples drawn at three different FiO2 levels in each patient in groups A, B, and C, respectively. However, the mean difference between the groups in PaO2/FiO2 change from 30 min after intubation to the end of surgery (measured at the same FiO2 level in each group) was only 20 mmHg (P = 0.35). We therefore consider it most likely that any difference in PaO2/FiO2 must be related to the induction of anesthesia including the change from 1.0 to the allocated FiO2.
The application of PEEP = 5 cmH2O may have reduced the amount of intraoperative atelectasis and improved the oxygenation . Hedenstierna et al.  showed in a study of 12 patients a trend toward reoccurrence of atelectasis within 5 min after discontinuation of PEEP. In contrast, a Cochrane review from 2010 indicated that intraoperative PEEP of 5–10 cmH2O may reduce postoperative atelectasis and improve postoperative gas exchange (PaO2/FiO2) .
We found a mean reduction in FVC of 12%, and this is less than the 20% reduction measured shortly after intubation , but in accordance with the 12% reduction found on the first day after lower abdominal surgery .
Our results in FVC may have been too small to affect the PaO2/FiO2 which comparable to a previous study noted by Dueck et al. . Their study showed only a small effect of FVC reduction on the degree of pulmonary shunt.
A postoperative reduction in FVC may not solely be caused by collapse of some lung units (atelectasis) but also by a general change in intrathoracic volumes caused by reflex diaphragmatic dysfunction, shallow breathing, mechanical disruption of the abdomen, pulmonary edema, increased abdominal blood volume, or postoperative incisional pain ,.
In our study, 12 (13%) patients developed radiologically verified atelectasis in addition to pulmonary symptoms (7, 3, and 2 in groups A, B, and C, respectively). With this definition of atelectasis, no significant difference in atelectasis was found among the 1400 patients included in the PROXI trial (7.9 vs. 7.1% in the 80 and 30% oxygen group, respectively; P = 0.60) .
Akca et al.  found no significant difference in the incidence of atelectasis assessed by CT (64 vs. 94%; P = 0.12) in patients administered 30 or 80% oxygen, respectively. Such high incidences are related to the high sensitivity of a CT scan. Edmark et al.  showed that the benefit of using 80% oxygen compared with 100% oxygen during induction of anesthesia to reduce atelectasis decreased gradually with time.
We did not find a significant difference in the degree of atelectasis in each group (P = 0.52). We did not measure atelectasis directly; thus, we cannot draw direct conclusions on the degree of atelectasis or the contribution of absorption atelectasis toward fraction oxygen requirement. The standard measure of atelectasis is CT . CT scans are expensive; require transport of a patient when careful monitoring is critical; do not measure the contribution of absorption atelectasis; are not validated because there is no true gold standard measure of atelectasis; usually rely on a single cut; and may be confounded by fluid in the lung, variations in blood supply, and dense tissue adjacent to the lung .
| Conclusion|| |
Ventilation with 100% oxygen for 2 h was not significantly associated with changes in the perioperative oxygenation index or the pulmonary functional test compared with ventilation with 40% till the end of surgery, and there was no significant difference among the groups in oxygen saturation and radiological changes over the next 3 days postoperatively.
This study suggests that absorption atelectasis induced by high inspired oxygen is not sufficient to induce postoperative hypoxemia beyond that associated with anesthesia/surgery-induced atelectasis, at least in patients with relatively normal pulmonary function. Our study provides helpful information for the debate on appropriate intraoperative inspired oxygen levels. We recommend preoxygenation with 100% oxygen for 5 min to prevent desaturation before intubation, followed by oxygenation with 40% oxygen intraoperatively to avoid the risk of postoperative pulmonary absorption atelectasis.
This study was supported by the Qena University Hospital fund.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Duggan M, Kavanagh BP. Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology 2005; 102:838-854.
Agarwal A, Singh PK, Dhiraj S, Pandey CM, Singh U. Oxygen in air (FiO 2
0.4) improves gas exchange in young healthy patients during general anesthesia. Can J Anaesth 2002; 49:1040-1043.
Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 2003; 98:28-33.
Edmark L, Auner U, Enlund M, Ostberg E, Hedenstierna G. Oxygen concentration and characteristics of progressive atelectasis formation during anaesthesia. Acta Anaesthesiol Scand 2011; 55:75-81.
Lumb AB, editor. Nunn's applied respiratory physiology
. 6th ed. Philadelphia, PA: Butterworth-Heinemann/Elsevier; 2005.
Akça O, Podolsky A, Eisenhuber E, Panzer O, Hetz H, Lampl K, et al
. Comparable postoperative pulmonary atelectasis in patients given 30% or 80% oxygen during and 2 hours after colon resection. Anesthesiology 1999; 91:991-998.
Magnusson L, Spahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth 2003; 91:61-72.
Hedenstierna G, Edmark L. Mechanisms of atelectasis in the perioperative period. Best Pract Res Clin Anaesthesiol 2010; 24:157-169.
Hopf HW, Hunt TK, West JM, Blomquist P, Goodson WH III, Jensen JA, et al
. Wound tissue oxygen tension predicts the risk of wound infection in surgical patients. Arch Surg 1997; 132:997-1004.
Greif R, Akca O, Horn EP, Kurz A, Sessler DI. Outcomes Research Group. Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. N Engl J Med 2000; 342:161-167.
Meyhoff CS, Wetterslev J, Jorgensen LN, Henneberg SW, Simonsen I, Pulawska T, et al.
PROXI Trial Group. Perioperative oxygen fraction - effect on surgical site infection and pulmonary complication after abdominal surgery: a randomized clinical trial. Rationale and design of the PROXI trial. Trials 2008; 9:58.
[No authors listed]. Standardization of spirometry, 1994 update. American Thoracic Society. Am J Respir Crit Care Med 1995; 152:1107-1136.
Joyce CJ, Baker AB, Chartres S. Influence of inspired nitrogen concentration during anaesthesia for coronary artery bypass grafting on postoperative atelectasis. Br J Anaesth 1995; 75:422-427.
Wilcox P, Baile EM, Hards J, Müller NL, Dunn L, Pardy RL, Paré PD. Phrenic nerve function and its relationship to atelectasis after coronary artery bypass surgery. Chest 1988; 93:693-698.
Karbing DS, Kjaergaard S, Smith BW, Espersen K, Allerød C, Andreassen S, Rees SE. Variation in the PaO 2
ratio with FiO 2
: mathematical and experimental description, and clinical relevance. Crit Care 2007; 11:R118.
Whiteley JP, Gavaghan DJ, Hahn CE. Variation of venous admixture, SF6 shunt, PaO 2
, and the PaO 2
ratio with FIO 2
. Br J Anaesth 2002; 88:771-778.
Rusca M, Proietti S, Schnyder P, Frascarolo P, Hedenstierna G, Spahn DR, Magnusson L. Prevention of atelectasis formation during induction of general anesthesia. Anesth Analg 2003; 97:1835-1839.
Hedenstierna G, Tokics L, Lundquist H, Andersson T, Strandberg A, Brismar B. Phrenic nerve stimulation during halothane anesthesia. Effects of atelectasis. Anesthesiology 1994; 80:751-760.
Imberger G, McIlroy D, Pace NL, Wetterslev J, Brok J, Møller AM. Positive end-expiratory pressure (PEEP) during anaesthesia for the prevention of mortality and postoperative pulmonary complications. Cochrane Database Syst Rev 2010; 9:CD007922.
Wahba RW. Perioperative functional residual capacity. Can J Anaesth 1991; 38:384-400.
Drummond GB, Littlewood DG. Respiratory effects of extradural analgesia after lower abdominal surgery. Br J Anaesth 1977; 49:999-1004.
Dueck R, Prutow RJ, Davies NJ, Clausen JL, Davidson TM. The lung volume at which shunting occurs with inhalation anesthesia. Anesthesiology 1988; 69:854-861.
Craig DB. Postoperative recovery of pulmonary function. Anesth Analg 1981; 60:46-52.
Meyhoff CS, Wetterslev J, Jorgensen LN, Henneberg SW, Høgdall C, Lundvall L, et al
. PROXI Trial Group. Effect of high perioperative oxygen fraction on surgical site infection and pulmonary complications after abdominal surgery: the PROXI randomized clinical trial. JAMA 2009; 302:1543-1550.
[Table 1], [Table 2], [Table 3], [Table 4]