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Pulmonary Function after Emergence on 100% Oxygen

in Patients with Chronic Obstructive Pulmonary Disease


A Randomized, Controlled Trial
Axel T. Kleinsasser, M.D., Iris Pircher, M.D., Suzan Truebsbach, M.D., Hans Knotzer, M.D.,
Alexander Loeckinger, M.D., Benedict Treml, M.D.

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)

A CCORDING to the World Health Organization,


chronic obstructive pulmonary disease (COPD) reflects
a disease characterized by obstruction of airflow which inter-
What We Already Know about This Topic
• One hundred percent oxygen is frequently administered to
feres with normal breathing and is not fully reversible. In emerging patients to prevent hypoxia after anesthesia
2007, COPD was the fifth leading cause of death worldwide
What This Article Tells Us That Is New
but will become the third leading cause by 2030.1 Patients
• In a case-controlled, open-labeled study of 53 chronic ob-
with COPD often present with increased blood flow to structive pulmonary disease patients, patients breathing
lung units with subnormal ventilation—perfusion ratio.2,3 100% oxygen during emergence had lower arterial oxygen
Loeckinger et al.4 documented the underlying modifications levels after 60 min compared with patients breathing 30%
oxygen balanced with nitrogen
in pulmonary gas exchange: With oxygen breathing during
emergence, pulmonary blood flow is redistributed to lung
units with a subnormal ventilation–perfusion ratio. The atelectasis formation after induction. Benoît et al.6 showed
consequence of oxygen breathing on postanesthetic pulmo- that oxygen breathing during emergence from anesthesia
nary function in COPD patients remains uncertain and may equally results in atelectasis. Amazingly, there is no evidence
involve changes in ventilation–perfusion ratios. base for oxygen breathing,7 and despite long-standing con-
On insertion and removal of artificial airways, the troversies,8,9 this routine remains a confirmed habit. Oxy-
patients’ lungs are routinely ventilated with 100% oxygen. gen is also used in patients with COPD particularly because
This is done to widen the safety margin toward hypoxemia these frequently present with impaired oxygenation. Little is
in case airway problems occur. The gain in safety comes at known about the pulmonary gas exchange after emergence
a price: Oxygen breathing may cause alveolar instability and on oxygen in COPD patients; however, a deterioration of
atelectasis formation. Hedenstierna et al.5 demonstrated pulmonary gas exchange is likely.

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

Anesthesiology, V 120 • No 5 1146 May 2014

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For examining this theory, we hypothesized that in


COPD patients, emergence on 100% oxygen leads to lower
arterial oxygen pressures compared with the arterial oxygen
pressures with emergence on 30% of oxygen.

Materials and Methods


In Brief
In this study, we examined COPD patients after general
anesthesia. All patients were treated with 30% of oxygen
at induction and during anesthesia. One group was treated
with 100% of oxygen during emergence, and the other
group remained on 30% of oxygen in this period. After
the anesthetic, all patients were continued on room air so
that the only difference between groups was the oxygen
concentration during emergence from anesthesia. This is of
Fig. 1. Study outline with regard to enrollment, group alloca-
course not the usual practice but was performed in this trial tion to treatment or control, and time points of measurements.
under supervision and with special attention. Pulse oxy- ABG  =  arterial blood gas; BL  =  baseline; COPD  =  chronic
metry was monitored continuously and arterial blood gas obstructive pulmonary disease; FEV1 = forced expiratory vol-
(ABG) analyses were performed before and 15 and 60 min ume in 1 s; FVC = forced vital capacity; OR = operation the-
after anesthesia. ater; PACU = postanesthesia care unit.

Overview Definition of COPD


This single-site study was performed from May 2007 to Chronic obstructive pulmonary disease was defined as a
May 2008 at the hospital of the Medical University in Inns- FEV1/FVC ratio of less than 0.7 and an FEV1 of 80% or
bruck, Austria. The type of the study is two-group, paral- less 15 min after inhalation of 400 μg of salbutamol.10
lel arm. An overview of the study protocol is outlined in
figure 1. Taken together, patients listed for elective carotid Anesthesia
endarterectomy with general anesthesia were asked to par- General anesthesia with intubation was performed. Positive
ticipate in this study. Participants were thus recruited at end-expiratory pressure (PEEP) was set 5 cm H2O. Patients
the preanesthetic visit. After the visit on the day before sur- enrolled in this study received no premedication. In terms
gery, informed consent was obtained and spirometry was of drugs, anesthesia was performed in a total intravenous
performed on potential participants. Those with spirometry manner using fentanyl (0.005 mg/kg), propofol (2.5 mg/kg),
results positive for COPD (see Spirometry) were then fur- and rocuronium (0.6 mg/kg) for induction and continuous
ther enrolled for pre- and postoperative ABG analyses and remifentanil (0.25 μg kg−1 min−1) and propofol (50 to 100
randomly allocated (see Statistical Analysis) to either emer- μg kg−1 min−1) for maintenance. Additional dosing of the
gence on 100% oxygen (100%, n = 26) or to emergence on listed drugs or higher infusion rates was left at the discretion
30% oxygen (30%, n = 27). The duration of emergence was of the anesthetist. Before intubation, lungs were ventilated
measured. After extubation, patients were breathing room using 30% oxygen balanced with nitrogen. This gas mixture
air. The study was approved by the local ethical committee was then used until emergence where—depending on group
and conducted in accordance to their guidelines. The eth- allocation—patients were kept on 30% oxygen or switched
ics committee also served as a data-safety monitoring board to 100% oxygen. Duration of emergence (from stopping the
(Innsbruck, Tirol, Austria). propofol infusion to extubation) was recorded. Before extu-
bation, relaxometry was performed. A train-of-four ratio of
Spirometry greater than 0.9 was accepted for extubation otherwise neo-
After informed consent was obtained, potential partici- stigmine (25 μg/kg) and atropine (0.01 mg/kg) were given.11
pants were given 400 μg of salbutamol by inhalation. Fif-
teen minutes later, patients completed spirometry using Measurements
a hand-held spirometer (Micro Spirometer; CareFu- Arterial blood gas samples were taken using an indwelling radial
sion, Basingstoke, United Kingdom). The best of three arterial catheter before induction and at 5, 15, and 60 min after
attempts was recorded. Parameters obtained included the extubation and immediately analyzed using a Chiron RapidLab
forced expiratory volume in 1 s (FEV1, liters per sec- 860 (Chiron, Fernwald, Germany). The 15 and 60 min mea-
ond), the forced vital capacity (FVC, Liters), and the surements were taken in the postanesthesia care unit (fig. 1).
FEV1/FVC ratio calculated by the device (FEV1/FVC). Samples were immediately analyzed for Pao2, Paco2, pH, frac-
Percent-of-predicted value of FEV1 (FEV1%) was calcu- tion of oxyhemoglobin, bicarbonate, and lactate. Other vari-
lated thereafter. ables recorded included heart rate and blood pressure.

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Extubation on Oxygen in COPD Patients

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.

where PA reflects the alveolar pressure of oxygen, Fio2 is the Enrollment


fraction of the inspiratory oxygen, Patm is the atmospheric pres- A total of 76 patients were screened. Fifty-three of 76
sure, PH2O is water vapor pressure, Paco2 is the arterial partial recruited patients had an FEV1/FVC of less than 0.7
pressure of carbon dioxide, and 0.8 is the respiratory quotient. together with an FEV1 of less than 80% of predicted and
were further enrolled and examined for pre- and postopera-
Statistical Analysis tive ABGs. Patients allocated to the 100% (n = 26) and to
This trial was registered in a national database. The analytical the 30% groups (n = 27) had similar anthropomorphic char-
framework was to identify superiority when using 30% oxy- acteristics and spirometric findings (table 1).
gen instead of 100% during emergence. The estimation of the
sample size was based on the comparison of arterial oxygen Physiological Data and ABG Results
tension because Aado2 is difficult to attain. The calculation Physiological data and ABG results are given in table 2.
was based on a two-treatment, parallel design. Assuming that Aado2 is presented in figure 2. Emergence on 100% oxygen
the alternative hypothesis is a reduction in arterial oxygen leads to decrease in Pao2 (table 1) based on an increase in
tension of 8%, we a priori estimated that we needed to enrol Aado2 when compared with emergence on 30% (intergroup)
25 patients in each group (totalling 50) to reach a power of and when compared with baseline (intragroup) at 15 and
80% with a type I error rate of 0.05 if the true difference 60 min after emergence from anesthesia. Paco2 was compa-
between treatments is 0.8 times the standard derivation. rable between groups at all measurements. Other parameters
The nature of the randomization scheme was blocking. including time-to-extubation and circulatory variables were
Randomization was performed by using Research Random- not different between groups.
izer,* a long-standing on-line tool. Randomization to the
30% or the 100% group (1:1 ratio) was prepared for 60 Distribution of the Demographic Data and of the Results
patients before the study using opaque envelopes labeled with All demographic data and all results were normally dis-
the sequential number of the patient enrolled and contain- tributed; hence, a parametric test (ANOVA) was adequate.
ing the allocation information (100 or 30%). Randomization When testing for a correlation between the drop amplitude
and envelope preparation were performed by a colleague who in Aado2 and FEV1% (reduction from 100%), we could not
was not involved in perioperative care or in data acquisition. detect a dependence (Pearson correlation = 0).
Analyses were performed using the Statistical Package for the
Social Sciences (SPSS 15.0; IBM, Armonk, NY). Ahead of the Aado2: ANOVA-specific Results and 60-min
main statistical analysis, results were tested for normal distri- Measurement Point Estimate
bution using Pearson chi-square test. A two-way repeated-mea- In the ANOVA results, group effect had a P value of 0.02,
sures ANOVA was then used to detect inter- and intragroup time effect and group × time interaction had a P value of less
differences. The hypothesis was tested t­wo-tailed. Significant
results were post hoc examined using the Newman–Keuls test. Table 1.  Demographic Characteristics
Primary outcome was a difference in Aado2 at the 60 min mea-
Extubation on Extubation
surement. Secondary outcomes included Pao2, Paco2, pH, frac- 100% on 30%
tion of oxyhemoglobin, bicarbonate and lactate, heart rate, and
No. of patients (male:female) 18:8 21:6
blood pressure. Results are presented as mean ± SD of the mean.
Age (yr) 68 ± 13 65 ± 10
P values less than 0.05 were rendered significant. Body mass index 26 ± 3 25 ± 3
Smoking history (pack-years) 53 ± 5 51 ± 4
Results SpO2 at presentation (%) 94 ± 2 94 ± 2
FVC (l) 3.6 ± 1.1 3.6 ± 0.9
Overview
FEV1 (liters in 1 s) 1.9 ± 0.4 2.0 ± 0.6
The presented data sets are complete. This study involved hypox- FEV1/FVC (ratio) 0.52 ± 0.10 0.56 ± 0.14
emia to a certain degree; however, all participants tolerated the FEV% (of predicted) 61 ± 12 60 ± 12
study well. Data are displayed in tables 1 and 2 and figure 2. In
Results are reported as mean ± SD of the mean.
this study, we examined 53 patients with COPD listed for elective
FEV1  =  forced expiratory volume in 1 s; FVC  =  forced vital capacity;
FEV%  =  the percentage of the predicted value; Spo2  =  arterial oxygen
* Available at: www.randomizer.org. Accessed February 3, 2014. saturation (pulse oxymetry).

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Table 2.  Physiologic Data and Blood Gas Results

BL 5’ 15’ 60’

Heart rate (bpm) Extubation on 100% 73 ± 15 87 ± 16 90 ± 22 77 ± 19


Extubation on 30% 75 ± 14 85 ± 21 85 ± 16 75 ± 16
MAP (mmHg) Extubation on 100% 104 ± 17 107 ± 20 112 ± 23 100 ± 14
Extubation on 30% 110 ± 17 109 ± 21 107 ± 22 99 ± 19
Pao2 (mmHg) Extubation on 100% 81 ± 12 125 ± 7 61 ± 7*† 62 ± 6*†
Extubation on 30% 78 ± 11 61 ± 7 68 ± 7† 67 ± 7†
Paco2 (mmHg) Extubation on 100% 37 ± 3 48 ± 6 44 ± 5 41 ± 3
Extubation on 30% 37 ± 3 47 ± 4 41 ± 3 41 ± 3
apH Extubation on 100% 7.42 ± 0.02 7.31 ± 0.04 7.35 ± 0.04 7.37 ± 0.03
Extubation on 30% 7.42 ± 0.02 7.34 ± 0.03 7.37 ± 0.03 7.38 ± 0.03
Sao2 Extubation on 100% 94 ± 2 94 ± 4 89 ± 4 89 ± 2*
Extubation on 30% 94 ± 2 89 ± 3 92 ± 3 92 ± 3

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.

patients to develop shunt has been first noted by Wagner


et al.2 Previous work from our group where emergence on
oxygen has been examined in anesthetized animals also
indicates blood flow heterogeneity as the leading cause of
decreases in Pao2; however, these have been healthy animals.4

Implications of the Changes in Aado2


In the observed setting, increases in Aado2 suggest changes
in diffusion, ventilation–perfusion ratio, or in shunt. Shunt,
however, has been shown to be of little importance in patients
with COPD.2,12 In the absence of shunt and with no changes
in diffusion, Aado2 reflects the heterogeneity of pulmonary
Fig. 2. Aado2 refers to alveolar arterial partial pressure differ- blood flow. An increase in Aado2 as in our results indicates
ence where *P < 0.05 in intergroup comparison, †P < 0.01 in increased ventilation–perfusion heterogeneity or—put differ-
intergroup comparison, and ‡P < 0.01 in comparison to the ently—an intensification of the pre-existing pathology.
preanesthetic value.
Oxygen Breathing in Normal Subjects and in COPD
than 0.001. A point estimate was calculated for the differ-
With oxygen breathing in normal subjects, a shunt usu-
ence between the two conditions at the 60-min measurement,
ally develops within 30 min and is also readily reversible.13
where the mean difference was 5.32 (95% CI, 1.05 to 9.98). The mechanism behind is alveolar denitrogenation. In lung
units, where oxygen uptake into the blood exceeds the deliv-
Discussion ery of fresh gas, atelectasis occurs.13
This investigation showed that in COPD patients subjected to In terms of anesthesia, oxygen is not the sole source of
surgery for carotid artery stenosis, general anesthesia impaired atelectasis formation: supine posture, reduction in the func-
postoperative oxygenation in all patients. Those who received tional residual capacity, and airway closure all contribute to
100% oxygen during emergence showed a statistically signifi- the formation of atelectasis.5,14
cant increase in Aado2 and hence lower Pao2 as compared with In COPD patients, lungs may show clinically signifi-
patients receiving 30% oxygen during emergence. cant pulmonary blood flow to lung units with normal and
low ventilation–perfusion ratios.8 In awake oxygen breath-
Comparison of Our Results with Previous Work ing, COPD patients rarely develop intrapulmonary right-
The findings by Gunnarsson et al.12 using the multiple to-left shunt, which might be associated with collateral
inert gas technique showed that COPD patients develop an ventilation, where alveoli ventilate other alveoli distal of an
increase in pulmonary blood flow heterogeneity—but no airway obstruction.2
increase in shunt. This means that our observed changes in Some of the observed changes during oxygen breathing
Aado2 are interpretable as changes in heterogeneity rather may also be attributed to the hypoxic pulmonary vasocon-
than increases in shunt. The relative inability of COPD striction (HPV). HPV is a vascular reflex, where airway

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Extubation on Oxygen in COPD Patients

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.

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Summary 7. Gordon RJ: Anesthesia dogmas and shibboleths: Barriers to


After emergence on oxygen sustained alterations in pulmo- patient safety? Anesth Analg 2012; 114:694–9
nary gas exchange could be observed in patients with COPD. 8. Lindahl SG, Mure M: Dosing oxygen: A tricky matter or a
piece of cake? Anesth Analg 2002; 95:1472–3
Emergence on 30% oxygen also caused gas exchange disor-
9. Lumb AB: Just a little oxygen to breathe as you go off to
ders in these patients, but to a lesser extent. The mechanism sleep: Is it always a good idea? Br J Anaesth 2007; 99:769–71
can be attributed to an increase in pulmonary blood flow 10. Vestbo J, Hurd SS, Agustí AG, Jones PW, Vogelmeier C,

heterogeneity because COPD patients show a relative inabil- Anzueto A, Barnes PJ, Fabbri LM, Martinez FJ, Nishimura M,
ity to develop shunt. The routine use of 100% oxygen dur- Stockley RA, Sin DD, Rodriguez-Roisin R: Global strategy
ing emergence might need reconsideration in the treatment for the diagnosis, management, and prevention of chronic
of COPD patients. obstructive pulmonary disease: GOLD executive summary.
Am J Respir Crit Care Med 2013; 187:347–65
11. Kopman AF, Yee PS, Neuman GG: Relationship of the
Acknowledgments
train-of-four fade ratio to clinical signs and symptoms of
­
Support was provided solely from institutional and/or de- residual paralysis in awake volunteers. Anesthesiology 1997;
partmental sources. 86:765–71
12. Gunnarsson L, Tokics L, Lundquist H, Brismar B, Strandberg
Competing Interests A, Berg B, Hedenstierna G: Chronic obstructive pulmonary
The authors declare no competing interests. disease and anaesthesia: Formation of atelectasis and gas
exchange impairment. Eur Respir J 1991; 4:1106–16

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;
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