Professional Documents
Culture Documents
ABSTRACT
Background: During emergence from anesthesia, breathing 100% oxygen is frequently used to provide a safety margin
toward hypoxemia in case an airway problem occurs. Oxygen breathing has been shown to cause pulmonary gas exchange dis-
orders in healthy individuals. This study investigates how oxygen breathing during emergence affects lung function specifically
whether oxygen breathing causes added hypoxemia in patients with chronic obstructive pulmonary disease.
Methods: This trial has been conducted in a parallel-arm, case-controlled, open-label manner. Fifty-three patients with chronic
obstructive pulmonary disease were randomly allocated (computer-generated lists) to breathe either 100 or 30% oxygen bal-
anced with nitrogen during emergence from anesthesia. Arterial blood gas measurements were taken before induction and at
5, 15, and 60 min after extubation.
Results: All participants tolerated the study well. Patients treated with 100% oxygen had a higher alveolar–arterial oxygen
pressure gradient (primary outcome) compared with patients treated with 30% oxygen (25 vs. 20 mmHg) and compared with
their baseline at the 60-min measurement (25 vs. 17 mmHg). At the 60-min measurement, arterial partial pressure of oxygen
was lower in the 100% group (62 vs. 67 mmHg). Arterial partial pressure of carbon dioxide and pH were not different between
groups or measurements.
Conclusions: In this experiment, the authors examined oxygen breathing during emergence—a widely practiced maneuver
known to generate pulmonary blood flow heterogeneity. In the observed cohort of patients already presenting with pulmonary
blood flow disturbances, emergence on oxygen resulted in deterioration of oxygen-related blood gas parameters. In the periop-
erative care of patients with chronic obstructive pulmonary disease, oxygen breathing during emergence from anesthesia may
need reconsideration. (Anesthesiology 2014; 120:1146-51)
Submitted for publication April 22, 2013. Accepted for publication December 27, 2013. From the Department of Anesthesiology, Inns-
bruck Medical University, Innsbruck, Austria (A.T.K., I.P., S.T., B.T.); Department of Anesthesiology and CCM II, Klinikum Wels, Wels, Austria
(H.K.); and Department of Anesthesiology and CCM, Hanusch Hospital, Vienna, Austria (A.L.).
Copyright © 2014, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins. Anesthesiology 2014; 120:1146-51
Alveolar–Arterial Oxygen Partial Pressure Difference carotid endarterectomy. The patients we examined were in their
Calculation sixties, had almost normal weight, and all had a smoking history
Aado2 (alveolar–arterial oxygen partial pressure difference) greater than 50 pack-years. Spirometric findings in the examined
was calculated using the common alveolar gas equation: cohort revealed COPD at Global Initiative for Obstructive Lung
Disease stage 2.10 Our main findings were that Pao2 was lower
PaCO 2
PA = FIO 2 ⋅ (Patm − PH2 O) − after general anesthesia and this drop was more pronounced in
0.8 those who had oxygen during emergence from anesthesia.
BL 5’ 15’ 60’
Results are reported as mean ± SD of the mean. 5’ reflects 5 min, 15’ is 15 min, and 60’ is 60 min after extubation.
*P < 0.05 in intergroup comparison; †P < 0.01 in comparison to baseline.
apH = arterial pH; BL = baseline; MAP = mean arterial pressure; Paco2 = arterial carbon dioxide partial pressure; Pao2 = arterial partial pressure of oxygen;
Sao2 = arterial saturation of hemoglobin.
hypoxia causes pulmonary arteries to constrict, diverting The decrease in Pao2 between preanesthetic values and
blood flow from poorly to better-oxygenated lung units.15 those measured at 15 and 60 min after extubation is very
Although HPV is of little importance in the healthy lung large in both groups (P = 0.0001; table 2) and reflects why
(because there are no poorly ventilated units), it is critical for we need to be cautious with general anesthesia in COPD
maintaining a balanced distribution of ventilation and per- patients.
fusion in the lungs of COPD patients.16,17 Oxygen breath- In a survey performed in the United Kingdom and Ire-
ing obviously dampens the HPV as nifedipine does.17 In the land in 2005, 54% of the anesthetists claim to always use
classic experiments performed by Mélot et al., the difference pure oxygen during emergence, 32% say, they mostly use
in Pao2 with a vigorous HPV compared with a dampened it and 10% state, they occasionally use oxygen on extuba-
HPV response is approximately 20 mmHg—roughly the tion.18 And recently, Mackintosh et al.19 published that high
same as in our comparison between 100 and 30% oxygen intraoperative concentrations of oxygen do not alter the
during emergence from anesthesia.
postoperative oxygen requirements in those with healthy
lungs. Emergence on oxygen is still a common practice and
Concept: Oxygen Breathing before Removal of PEEP:
it seems to be harmful for only those with a pre-existing pul-
An Unfortunate Sequence?
monary problem. A recommendation or guideline for those
From the alveolus, oxygen moves into the pulmonary capil-
lary blood. This uptake is usually completed in a quarter of presenting with COPD for general anesthesia might help to
a second. Alveolar nitrogen does not readily move into the establish an adapted and adequate treatment.
blood because there is only a negligible partial pressure gra- When we give thought to postoperative care of a COPD
dient and because it has a low solubility in blood. Nitrogen patient with a low Pao2, we come across the nurse in the
helps to keep an alveolus open. Also, our perioperative treat- postanesthesia care unit. As in the observed cohort, such low
ment helps to keep the alveoli open: PEEP is an airway and Pao2 values indicate that supplemental oxygen is required.
alveolar pressure above the atmospheric pressure at the end It is uncertain how supplemental oxygen affects pulmonary
of expiration. PEEP is considered to keep alveoli open. function of the already compromised COPD lung. Research
When oxygen breathing (partially) washes the nitrogen may thus also be directed on the postoperative care of the
out of the alveoli, the alveolus may become increasingly criti- COPD patient after general anesthesia. Noninvasive ventila-
cal and eventually collapses.13 This occurs when all nitrogen tion via face mask may be a strategy to keep the airways open,
is washed out and all oxygen is taken up by the blood. compensate for the work of breathing and avoid dynamic
When oxygen breathing is applied during emergence from hyperinflation. Positive end-inspiratory pressure could be set
anesthesia, ventilated alveoli first have their nitrogen washed to values at the patient’s intrinsic PEEP,20 and delivering low
out and then after extubation also have the PEEP taken away. oxygen concentrations may help to avoid further redistribu-
In contrast to anesthetic induction, this sequence is now tions in pulmonary blood flow.
inverted leaving oxygen-filled alveoli suddenly unpressurized
and thus prone to become partially emptied by the blood flow. Strengths and Limitations
Regional ventilation will be impaired as alveoli become critical In our study, we examined a homogenous cohort, with indi-
and ventilation–perfusion ratios become lower. So in this con- viduals similar in terms of demographics, spirometry results,
cept, extubation on oxygen may particularly help to develop and treatment received. Postoperative oxygenation deficits
lung units with subnormal ventilation–perfusion ratios. The are thus attributable to the only difference between the two
latter partly explains the observed increases in Aado2. groups: oxygen breathing during emergence.
Some limitations should also be mentioned: First, the
Postoperative Oxygen in the COPD Patient
anesthetist was not blinded in terms of group allocation;
In this experiment, we examined a widely practiced maneu-
however, this is impossible due to patient safety. Second,
ver that generates pulmonary blood flow heterogeneity in a
we examined predominantly men, however, fewer women
cohort of patients already presenting with such a heterogene-
ity. Our patients presented with Pao2 values of approximately with a smoking history present for carotid endarterectomy.
80 mmHg which is at the lower end of the normal range Another limitation is our failure to perform measurements
(80 to 105 mmHg). After extubation on either 100 or 30% later than 60 min after extubation. This is in part due to the
oxygen, we observed a consistent difference in Pao2. The fact that we did not expect such long-term changes. Last, it
observed values (table 2) are all relatively low, and given that has to be noted that induction at 30% of oxygen is uncom-
a Pao2 of 60 mmHg is generally considered as an indication mon, and some may even consider it dangerous. However,
for intubation, this issue deserves attention, because oxygen having done proper airway assessment (i.e., anesthetic his-
breathing leads to Pao2 values of approximately 60 mmHg. tory and Mallampati score), we were able to induce anes-
Furthermore, these Pao2 values are on the steep section of the thesia with 30% safely. It also needs to be mentioned that
oxygen dissociation curve, where a small decrease in oxygen omitting supplemental oxygen after general anesthesia is not
partial pressure results in a large drop in saturation. the usual practice in the European Union.
Correspondence 13. Wagner PD, Laravuso RB, Uhl RR, West JB: Continuous
distributions of ventilation-perfusion ratios in normal sub-
Address correspondence to Dr. Kleinsasser: Department of jects breathing air and 100 per cent O2. J Clin Invest 1974;
Anesthesiology, Innsbruck Medical University, Anichstreet 54:54–68
35, 6020 Innsbruck, Austria. axel.kleinsasser@i-med.ac.at.
14. Lumb AB, Greenhill SJ, Simpson MP, Stewart J: Lung recruit-
Information on purchasing reprints may be found at www.
ment and positive airway pressure before extubation does
anesthesiology.org or on the masthead page at the begin-
not improve oxygenation in the post-anaesthesia care unit: A
ning of this issue. Anesthesiology’s articles are made freely
randomized clinical trial. Br J Anaesth 2010; 104:643–7
accessible to all readers, for personal use only, 6 months
from the cover date of the issue. 15. Von Euler US, Liljestrand G: Observations on the pulmonary
arterial blood pressure in the cat. Acta Physiol Scand 1946;
12:301–20
References
16. Mélot C, Naeije R, Rothschild T, Mertens P, Mols P, Hallemans
1. Mannino DM, Buist AS: Global burden of COPD: Risk factors, R: Improvement in ventilation-perfusion matching by almi-
prevalence, and future trends. Lancet 2007; 370:765–73
trine in COPD. Chest 1983; 83:528–33
2. Wagner PD, Dantzker DR, Dueck R, Clausen JL, West JB:
Ventilation-perfusion inequality in chronic obstructive pul- 17. Melot C, Hallemans R, Naeije R, Mols P, Lejeune P: Deleterious
monary disease. J Clin Invest 1977; 59:203–16 effect of nifedipine on pulmonary gas exchange in chronic
3. Rodríguez-Roisin R, Drakulovic M, Rodríguez DA, Roca J, obstructive pulmonary disease. Am Rev Respir Dis 1984;
Barberà JA, Wagner PD: Ventilation-perfusion imbalance 130:612–6
and chronic obstructive pulmonary disease staging severity. 18. Rassam S, Sandbythomas M, Vaughan RS, Hall JE: Airway
J Appl Physiol 2009; 106:1902–8 management before, during and after extubation: A survey
4. Loeckinger A, Kleinsasser A, Keller C, Schaefer A, Kolbitsch of practice in the United Kingdom and Ireland. Anaesthesia
C, Lindner KH, Benzer A: Administration of oxygen before 2005; 60:995–1001
tracheal extubation worsens gas exchange after general
19. Mackintosh N, Gertsch MC, Hopf HW, Pace NL, White J,
anesthesia in a pig model. Anesth Analg 2002; 95:1772–6
Morris R, Morrissey C, Wilding V, Herway S: High intraop-
5. Hedenstierna G: Oxygen and anesthesia: What lung do we
erative inspired oxygen does not increase postoperative
deliver to the post-operative ward? Acta Anaesthesiol Scand
supplemental oxygen requirements. Anesthesiology 2012;
2012; 56:675–85
117:271–9
6. Benoît Z, Wicky S, Fischer JF, Frascarolo P, Chapuis C, Spahn
DR, Magnusson L: The effect of increased FIO2 before tra- 20.
Marini JJ: Dynamic hyperinflation and auto-positive
cheal extubation on postoperative atelectasis. Anesth Analg end-expiratory pressure: Lessons learned over 30 years. Am J
2002; 95:1777–81 Respir Crit Care Med 2011; 184:756–62