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Stolmeijer et al.
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
(2025) 33:8
https://doi.org/10.1186/s13049-025-01323-4
Scandinavian Journal of
Trauma, Resuscitation
and Emergency Medicine
*Correspondence:
Ewoud ter Avest
e.ter.avest@umcg.nl
1Department of Acute Care, University Medical Centre Groningen,
Groningen, the Netherlands
2Department of Internal Medicine, University Medical Centre Groningen,
Groningen, The Netherlands
3London’s Air ambulance, London, UK
Abstract
Background As iatrogenic hyperoxia has been related to adverse outcomes in critically ill patients, guidelines advise
to titrate oxygen to physiological levels. In the prehospital setting where partial arterial oxygen (PaO2) values are often
not readily available, titration of oxygen is based on peripheral oxygen saturations (SpO2). In this study we aimed to
investigate the ecacy of SpO2 guided oxygen titration in the prevention of hyperoxia.
Methods In a retrospective observational cohort study of patients included in the Acutelines data- and biobank of
the University Medical Center Groningen between September 2020 and March 2023, we collected blood gas samples
and triage data of sequentially included patients who received oxygen at the moment they were presented in the
emergency department (ED). PaO2 values were compared to (concurrently measured) SpO2 values, and to patient-
and treatment characteristics and P/F ratios were calculated in order to investigate the ecacy of SpO2 based oxygen
titration for various subgroups.
Results Blood gas samples were obtained for 1042 patients, of which 178 (17.1%) had hyperoxia (PaO2
levels > 13.5kPa). SpO2 readings were available for 170 of these, 68 of which (40%) had SpO2 values above the
recommended target range (94–98%; 88–92% for patients with COPD) whereas 102 patients (60%) had SpO2 values
within- or even below the recommended target range. Many of these patients (44.1%) received oxygen through a
low-ow device (nasal canula), and these patients almost invariably (84.4%) were not compromised in their ventilation
(P/F ratio’s > 300).
Conclusion When oxygen is titrated based on SpO2 levels, this results in hyperoxemia in a signicant proportion of
the patients. Health care providers should especially be reluctant to administer (low ow) oxygen as a standard of care
to patients who do not have clear respiratory compromise, as these patients are at a high risk of developing (occult)
hyperoxia.
Keywords Hyperoxia, Pre-hospital, Oxygen, P/F ratio
Peripheral oxygen saturation levels as a guide
to avoid hyperoxia: an observational study
RenateStolmeijer1, Jan C.ter Maaten1,2, JackLigtenberg2 and Ewoudter Avest1,3*
Page 2 of 8Stolmeijer et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2025) 33:8
Background
Acutely ill patients often have an increased oxygen
demand, a compromised oxygen uptake- or transport
or both [1]. Consequently guidelines historically recom-
mended the pragmatic suppletion of oxygen with a high
inspired oxygen fraction (FiO2) in these patients in order
to avoid hypoxia [2, 3].
However, over the past decade it has become obvious
that (too) generous suppletion of oxygen is not without
risk. Prolonged episodes of hyperoxia have been found to
be associated with a diminished self-reliance and a higher
mortality [4–7]. is is likely mediated by reactive oxygen
species (ROS), formed when excess oxygen is adminis-
tered [8–10]. ese ROS aect systemic- and pulmonary
vascular tone, resulting in an unwanted decrease in car-
diac output (CO) [4]. Further, ROS can damage cellular
structures, especially mitochondria, eventually resulting
in permanent endothelial damage. Recognition of these
deleterious eects has resulted in guideline changes, and
several guidelines now recommend to titrate oxygen to
physiological levels [11, 12].
is is often done by measuring partial arterial oxy-
gen pressures (PaO2) obtained through arterial blood gas
analysis (ABGA). However, ABGA is not always available
(as in the prehospital setting) or sometimes undesirable
(as in the ED): Although ABGA is integral to assessing
emergency department (ED) patients with acute respira-
tory or metabolic disease, it is a painful procedure with
potential complications and therefore not standard of
care to all patient in the ED [13]. In these situations, oxy-
gen is administered based on peripheral capillary oxygen
saturation (SpO2) values measured by nger plethys-
mography. Several guidelines recommend to aim for an
SpO2 of 94–98% (or an SpO2 of 88–92% in patients with
chronic obstructive pulmonary disease (COPD) GOLD
III or IV) [11, 12]. Titration of oxygen based on SpO2
readings however, requires a reliable and stable SpO2
trace, which may not always be available, especially when
patients have dysrhythmia’s, when they are in shock, or
when there are movement artefacts (as in the prehospital
setting) [14]. is may aect the ecacy of SpO2 guided
oxygen administration.
erefore, in the present study, we set out to investi-
gate the ecacy of SpO2 guided oxygen titration in the
prevention of hyperoxia, and we tried to identify modi-
able patient- or treatment characteristics associated with
hyperoxia.
Methods
Study setting and design
A retrospective observational cohort study was per-
formed of patients who presented in the ED of the Uni-
versity Medical Center Groningen (UMCG), a tertiary
care facility in the northern part of the Netherlands with
approximately 25.000 ED visits each year, and who were
included in the Acutelines data-and biobank at the time
of their visit Ethical approval was obtained from the Cen-
tral ethical Committee (CTc) of the UMCG), protocol
number 11120.
Study population
Patients were included in the present study when they
met the following criteria:
• Oxygen was administered at the time of
presentation/triage in the ED.
• An arterial blood gas sample was performed at triage
and showed hyperoxemia (PaO2 > 13.5kPa).
• Patients had consented to participate in the
Acutelines data- and biobank during their ED visit.
Patients were excluded when no plethysmographic SpO2
readings were obtained or recorded at the time of their
presentation.
Data acquisition
Data for this cohort study were obtained from the Acute-
lines data- and biobank [15]. Acutelines is a multidisci-
plinary prospective hospital-based cohort study in the
ED of the UMCG. Acutelines is approved by the medi-
cal ethics board of the UMCG and registered under trial
registration number NCT04615065 at ClinicalTrials.gov.
e cohort population is broadly representative of the
population with acute medical conditions in the northern
part of the Netherlands. Primary screening of patients
for eligibility on arrival at the ED is performed 24h a day
by the ED nurse together with a trained research team.
Participants are asked to give written informed consent,
with a proxy if necessary. Data were collected and man-
aged using REDCap (Vanderbilt University, Nashville,
TN, USA) electronic data capture tools hosted at the
UMCG [16, 17]. Bedside monitoring data were automati-
cally captured and stored, and information from other
data sources including the electronic health records of
the hospital was imported via the electronic patient le
(EPIC systems, Boston, MA, USA).
e following variables were collected for all included
patients: Demographic variables, relevant (cardio-pul-
monary) past medical history, smoking status, triage
category (urgency) according to the Netherlands Triage
Standard (NTS), the full set of vital signs obtained during
ED triage, and the concentration of oxygen administered
(FiO2). FiO2 was estimated from the method of oxygen
delivery registered, and the registered oxygen ow (in
case of a nasal cannula) [18]. e ratio’s between PaO2
and FiO2 (P/F ratio) were calculated from the rst ABGA
results after triage to objectify presence- and severity
Page 3 of 8Stolmeijer et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2025) 33:8
of acute respiratory distress syndrome (ARDS). A P/F
ratio < 300 was regarded as indicative of ARDS [19].
Outcomes
Primary outcome was the incidence of occult hyperoxia*
in patients receiving oxygen titrated based on SpO2.
Secondary endpoints were patient-or treatment factors
associated with the occurrence of hyperoxia.
* Occult hyperoxia was dened as hyperoxia (PaO2 > 13.5)
with an SpO2 below the target range of 94–98% (or
88–92% in patients with COPD GOLD III-IV).
Sample size
As the primary purpose of this pilot study was not
hypothesis testing, no formal sample size calculation was
made [20]. We aimed to include at least 100 patients.
Statistical analysis
Results are displayed in numbers, percentages and aver-
ages. Dierences regarding secondary endpoints between
identied subgroups where tested using Chi [2] test,
Kruskal Wallis test or independent sample t-tests where
appropriate. Bonferroni adjustments were applied to
correct for multiple comparisons between subgroups of
patients with obvious- and occult hyperoxemia, with a
p < 0.005 being considered statistically signicant. All sta-
tistical analysis was done with SPSS 23.0 (SPSS Inc, Chi-
cago, Illinois, USA).
Results
In total, 1042 patients met eligibility criteria during the
study period. Normoxia- or hypoxia was present in 864
patients whereas hyperoxia was present in 178 patients
(17,1%). For 8 patients with conrmed hyperoxia no
SpO2 values were registered during triage. Further results
refer to the remaining 170 patients.
Patient characteristics
e majority of the included patients (57.6%) was male.
Mean age at the time of presentation was 62 years. Most
included patients visited the ED with complaints attrib-
utable to sepsis (47%). About a third of the patients had
an underlying chronic lung condition. Oxygen was deliv-
ered by nasal cannula (n = 74), venturi mask (n = 11), non-
rebreathing mask (n = 59), or by (non-invasive) assisted
ventilation (n = 26) (Table1).
Table 1 Patient characteristics of patients (n = 170) presented in the ED with hyperoxia (PaO2 > 13,5kPa) in their arterial blood gas
analysis, stratied by SpO2 recorded by nger plethysmogram at presentation
Total
N = 170
Occult hyperoxia
(SpO2 ≤ target range*, n = 102)
Obvious hyperoxia
SpO2 > target range*, n = 68)
p-value
Gender 0.800
- Male
- Female
98 (57.6)
72 (42.4)
58 (56.9)
44 (43.1)
40 (58.8)
28 (41.2)
Age 62.3 (15.8) 63.9 (16.4) 59.7 (14.5) 0.278
O2 delivery device 0.458
- Nasal canula
- Venturi mask
- Non rebreathing mask
- Non invasive ventilation
- Tube or supraglottic airway device
74 (43.5)
11 (6.5)
59 (34.7)
7 (4.1)
19 (11.2)
45 (44.1)
6 (5.9)
39 (38.2)
4 (3.9)
8 (7.8)
29 (42.6)
5 (7.4)
20 (29.4)
3 (4.4)
11 (16.2)
Triage urgency colour code 0.227
- Yellow (urgent)
- Orange (emergent)
- Red (immediate)
- Missing
55 (32.4)
88 (51.8)
23 (13.5)
4 (2.4)
35 (34.3)
54 (52.9)
10 (9.8)
3 (2.9)
20 (29.4)
34 (50)
13 (19.1)
1 (1.5)
Smoker 45 (26.5) 24 (23.5) 21 (30.9) 0.042
Comorbidities**
- Cardiac
- Pulmonary
29 (17)
54 (31.8)
24 (23,5)
27 (26.5)
5 (7.4)
27 (39.7)
0.006
0.069
Suspected diagnosis in ED
- Sepsis
- COPD exacerbation
- Other****
80 (47,1)
12 (7,1)
81 (47,6)
52 (51.0)
3 (2.9)
47 (46.1)
28 (41.2)
9 (13.2)
34 (50)
0.210
0.010
0.616
Legend Table1. Age is represented as mean (SD), all other values are n (%). Abbreviations: SaO2, peripheral oxygen saturation; O2, oxygen; PaO2, partial arterial
oxygen pressure; PCI, percutaneous coronary intervention; CABG, coronary artery bypass grafting; COPD, chronic obstructive lung disease; ED, emergency
department. *; SpO2 target range is 94–98%, except for patients with COPD GOLD III-IV, in which it is 88–92%. **Co-morbidities: Cardiac comorbidities included
heart failure (n = 19), myocardial infarction (n = 9) PCI or CABG (n = 11) or previous hear t valve replacement (n = 3); Pulmonar y comorbidities inclu ded COPD GOLD I-II
(n = 17), COPD GOLD III-IV (n = 15) and other chronic pulmonary conditions (n = 22). ***; Other diagnoses included: intoxications, anaphylaxis and gastro-intestinal
bleed. Af ter Bonferroni adju stment, a p value < 0.005 was reg arded as signicant
Page 4 of 8Stolmeijer et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2025) 33:8
Incidence of hyperoxia
Obvious hyperoxia, with SpO2 values above the generally
recommended target range of 94–98% (88–92% in severe
COPD), was present in 68 (40%) patients, whereas occult
hyperoxia (PaO2 > 13,5kPa but with SpO2 values within
or below the target range) was present in the remaining
102 (60%) of the patients. (Fig.1).
Patient and treatment factors associated with hyperoxemia
Stratication of patients based on their SpO2 at presen-
tation revealed that patients with occult hyperoxia more
often had heart failure or a history of ischemic heart dis-
eases (Table1), whereas patients with obvious hyperoxia
more often had a history of pulmonary diseases (although
signicance was not reached, Table1).
Most patients (45/102 (44%)) with occult hyperoxia
received oxygen via a nasal canula (low ow oxygen
suppletion) (Table 2). ese patients were considered
less sick (as represented by a lower triage urgency cat-
egory) than patients receiving high ow oxygen (via
NRM or ventimask (VM)) or assisted ventilation). e
vast majority of the patients with a nasal canula (84,4%)
had a P/F ratio > 300, whereas in patients receiving high-
ow oxygen therapy this was the opposite: 75.6% had a
P/F ratio < 300. In 4 patients (all receiving oxygen through
assisted (non-invasive) ventilation), no P/F ratio could be
determined, since no FiO2 was registered.
Figure 2 shows the frequency distribution of SpO2
levels of patients with occult hyperoxia (SpO2 within or
below target range, but PaO2 > 13,5 kPa) stratied by
their P/F ratio. e vast majority of patients with occult
hyperoxia receiving oxygen via a nasal canula (low ow)
had an SpO2 between 95% and 97% and had a high P/F
ratio (Fig.2a). e 7 patients with a low P/F ratio were
all within their SpO2 target range. On the contrary, the
majority of patients receiving oxygen via a high ow
device (ventimask or non-rebreathing mask) had satu-
ration of 97 or 98% and all but 112 patients had a P/F
ratio < 300, indicative of underlying ventilatory compro-
mise (Fig.2b).
Discussion
In this cohort study, we found that when oxygen is
titrated based on SpO2 levels, this results in occult hyper-
oxemia in a signicant proportion of the patients. EMS
personnel should especially be reluctant to administer
(low ow) oxygen as a standard of care to patients who do
not have clear respiratory compromise, as these patients
are at a high risk of developing (occult) hyperoxia.
e potential harmful eects of long-term hyperoxia
on vascular tone and cellular integrity are well known [4,
8]. Animal studies have indicated that even short-term
(1-hour) hyperoxia maybe harmful, inducing functional
and morphological changes in rat brains [21], and long-
term changes in DNA-repair pathways, even at FiO2
Fig. 1 Frequency distribution of SpO2 levels of hyperoxic (PaO2 > 13,5 kPa patients (n = 170)
Page 5 of 8Stolmeijer et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2025) 33:8
levels as low as 0.3 [22]. In humans, brief exposure of
only 15min to a high FiO2 has been shown to result in
an increase in systemic vascular resistance, with poten-
tial eects on CO [23, 24]. Although no studies have been
published so far on the potential negative eects of (ultra)
short exposure to moderate FiO2 levels (as most patients
were exposed to in this study), based on these ndings,
hyperoxia should be avoided if possible.
erefore several treatment guidelines nowadays focus
on the prevention of both hypoxia- and hyperoxia [11,
12]. is study demonstrates however, that awareness
of and/or adherence to these guidelines in the prehos-
pital setting is not yet optimal: In 40% of the patients
presented to the ED who demonstrated hyperoxia in
their ABGA, SpO2 values were above the generally rec-
ommended target range of 94–98% (88–92% in severe
COPD).
Interestingly, in patients with a history of ischemic
heart disease, EMS providers seemed to be more aware
of the potential risks of hyperoxia, as in this subgroup,
obvious hyperoxia was less often present. is could be
explained by the early and explicit emphasis placed by
several societies on the potential deleterious eects of
hyperoxia in patients with an acute coronary syndrome
(ACS) or an out-of-hospital cardiac arrest [25, 26]. Inter-
estingly, for patients with COPD we found the opposite:
obvious hyperoxia (with SpO2 values above 92%) was
encountered more often in this subgroup of patients,
which may be a reection of the generally higher con-
cerns of developing hypoxia in this group.
is study demonstrates that in the majority of the
cases, hyperoxia remains undetected by measuring SpO2
values alone. Over 60% of the patients in our cohort had
occult hyperoxia: ese patients had normal (or even
decreased) SpO2 levels in the presence of an PaO2 > 13,5
Kpa. is may be explained by various reasons. First, the
reliability of the SpO2 relies on the quality of the ple-
thysmogram. In patients wearing nail polish, in shocked
patients with cold extremities, in sick patients who are
shivering or otherwise have movement artefacts, and in
patients with dysrhythmia’s it is dicult to obtain a reli-
able SpO2 trace, and the SpO2 value represented may be
an underestimation of actual values, resulting in unnec-
essary (high amounts of) oxygen administration More
importantly, the relation between SpO2 and PaO2 is
described by the oxygen dissociation curve. is means
that in the upper range of saturations measured, a wide
range in PaO2 values may be present: whereas some
patients will be normoxemic, others will be hyperoxemic.
Although SpO2 is not a perfect tool to guide oxy-
gen suppletion, often it is the only tool available, as it is
important to start oxygen suppletion early to prevent
Table 2 Patients with occult hyperoxia on presentation in the ED, stratied by method of oxygen suppletion
Total
n = 102
Low ow* oxygen
suppletion
N = 45
High ow** oxygen
suppletion
N = 45
Assisted (non-) invasive
ventilation
N = 12
P-
value
Gender 0.393
- Male
- Female
58 (56.9)
44 (43.1)
25 (55.6)
20 (44.4)
24 (53.3)
21 (46.7)
9 (75)
3 (25)
Age 63.9 (16.4) 64.4 (19.2) 64.0 (14.7) 62.3 (11.3) 0.372
Triage colour < 0.001
- Yellow
- Orange
- Red
- Missing
35 (34.3)
54 (52.9)
10 (9.8)
3 (2.9)
25 (55.6)
17 (37.8)
2 (4.4)
1 (2.2)
6 (13.3)
33 (73.3)
4 (8.9)
2 (4.4)
4 (33.3)
4 (33.3)
4 (33.3)
0 (0)
Smoking 24 (23.5) 7 (15.6) 11 (24.4) 6 (50) 0.004
Co-morbidities***
- Pulmonary
- Cardiac
27 (26,5)
24 (23.5)
13 (28,9)
10 (22.2)
9 (20)
10 (22.2)
5 (41,7)
4 (33.3)
0,283
0.695
Suspected ED diagnosis
- COPDexacerbation
- Sepsis
- Other****
3 (2.9)
52 (51.0)
47 (46.1)
1 (2.2)
21 (46.7)
23 (51.1)
1 (2.2)
30 (66.7)
14 (31.1)
1 (8.3)
1 (8.3)
10 (83.3)
0.500
0.001
0.004
P/F ratio < 0.001
- < 300
- > 300
- Missing
47 (46.1)
51 (50)
0 (0)
7 (15.6)
38 (84.4)
0 (0)
34 (75.6)
11 (24.4)
0 (0)
6 (50)
2 (16.7)
4 (33.3)
Legend Table2. Age is represented as mean (SD), all other values are n (%). Abbreviations: PCI, percutaneous coronary intervention; CABG, coronary artery bypass
grafting; COPD, chronic obstructive lung disease; ED, emergency department; P/F ratio, partial arterial oxygen pressure / inspired oxygen fraction ratio. *Low ow
oxygen suppletion is provided by a nasal canula. **High ow oxygen suppletion is provided by a venturi mask or a non-rebreathing mask. ***Co-morbidities:
Pulmonar y comorbidities i ncluded COPD GOLD I- II (n = 17), COPD GOLD III-I V (n = 15) and other chronic pul monary condit ions (n = 22). Cardiac comorbidities included
heart failure (n = 19), myocardial infarction (n = 9) PCI or CABG (n = 11) or previous heart valve replacement (n = 3); ****; Other diagnoses included: intoxications,
anaphylaxis and gastro-intestinal bleed. After Bonferroni adjustment, a p valu e < 0.005 was reg arded as signicant
Page 6 of 8Stolmeijer et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2025) 33:8
hypoxia in many critically ill patients, and guidance
of suppletion by arterial blood gasses (as is done in the
intensive care unit (ICU)) is not always possible or desir-
able in the prehospital setting or the ED. erefore it is
important to establish how occult hyperoxia can be pre-
vented when we only have SpO2 as a guidance, and our
ndings provide some clues:
In patients with occult hyperoxia, the majority (> 75%)
of patients receiving high ow oxygen (by ventimask or
NRM) had a P/F ratio < 300, indicative of ARDS [27, 28].
ese patients are likely also clinically pulmonary com-
promised, and hence oxygen therapy is started liberally
to prevent hypoxia. For further guidance and preven-
tion of hypoxia, blood gas analysis is warranted. In these
Fig. 2 (a) Frequency distribution of SpO2 levels of patients with occult hyperoxia with low ow oxygen suppletion stratied by P/F ratio (n = 45); (b) Fre-
quency distribution of SpO2 levels of patients with occult hyperoxia with high ow oxygen suppletion stratied by P/F ratio (n = 45)
Page 7 of 8Stolmeijer et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2025) 33:8
patients, a brief period of hyperoxia is likely unavoidable.
In contrast, > 75% of the patients receiving low ow oxy-
gen had a P/F ratio > 300. is shows that in patients who
are likely clinically less compromised from a pulmonary
perspective, and in whom oxygen is started (e.g. to meet
increased metabolic demands or for comfort [29, 30])
through a nasal cannula, are at a particular high risk of
developing hyperoxia. In these patients, who are gener-
ally also only moderately sick (judged by their average
triage category), prehospital and ED clinicians should
carefully weight potential risks and benets of oxygen
administration, and overall be more reluctant before
starting oxygen.
Limitations
is study had several limitations. First, as this was a
proof-of-principle descriptive study, no sample size esti-
mation was performed. Some trends may therefore have
remained undetected or may have yielded non-signicant
results.
Second, patients were selected from the Acutelines
data-, image and biobank of a single university hospital
in the Netherlands. Only patients with the most-urgent
NTS triage categories were included (as only these were
included in the biobank). is may have aected the gen-
eralizability of our ndings, although patients with the
lowest triage categories rarely receive oxygen suppletion.
Further, FiO2 levels for calculation of P/F ratio’s were
estimated (based on the method of oxygen delivery and
the amount of oxygen given) and not measured. Although
it is often assumed that the fraction of oxygen that is
inspired (above the normal atmospheric level) increases
by 4% for every additional liter of oxygen ow adminis-
tered there may be inter- patient variability in the actual
administered FiO2, depending on respiration rate, and
pattern (mouth open or closed) [31]. Also, since no FiO2
values were noted in patients receiving non-invasive ven-
tilation (NIV), no conclusion can be drawn about these
patients concerning their P/F ratios.
Finally, as the primary outcome in our study was the
number of patients with occult hyperoxia, and as we
only included patients with conrmed hyperoxia in their
ABGA, confounding by indications may be present.
erefore our ndings should be interpreted with cau-
tion: Although our results demonstrate that hyperoxia
remains undetected by SpO2 guided oxygen titration in a
signicant number of cases, no conclusions can be drawn
regarding overall prevalence of hyperoxia in cohorts were
SpO2 guided titration is used.
Conclusion
When oxygen is titrated based on SpO2 levels, this results
in occult hyperoxemia in a signicant proportion of
the patients. Healthcare providers should especially be
reluctant to administer (low ow) oxygen as a standard of
care to patients who do not have clear respiratory com-
promise, as these patients are at a high risk of developing
(occult) hyperoxia.
Abbreviations
ABGA Arterial blood gas analysis
ACS Acute coronary syndrome
ARDS Acute respiratory distress syndrome
CABG Coronary artery bypass grafting
CO Cardiac output
COPD Chronic obstructive pulmonary disease
CTc Central ethical committee
ED Emergency department
EMS Emergency medical service
FiO2 Inspired oxygen fraction
ICU Intensive care unit
NIV Non-invasive ventilation
NRM non rebreathing mask
NTS Netherlands triage standard
O2 Oxygen
PaO2 Partial arterial oxygen pressure
PCI Percutaneous coronary intervention
P/F Partial arterial oxygen pressure / inspired oxygen fraction
ROS Reactive oxygen species
SpO2 Peripheral capillary oxygen saturations
UMCG University medical center Groningen
VM Ventimask
Acknowledgements
The data used in this manuscript are provided by Acutelines. The authors
would like to thank the Acutelines study team for collection and provision of
the data.
Author contributions
All authors fullled the ICMJE criteria for authorship. RS and EtA conceived the
study. RS acquired the data. RS, JtM and JL and EtA interpreted the data. RS
and EtA drafted the manuscript. All authors revised the manuscript critically
and gave nal approval to submission of the manuscript.
Funding
The establishment of Acutelines has been made possible by funding of the
University Medical Center Groningen.
Data availability
The dataset used and/or analysed during the current study are available from
the corresponding author, after consulting with the board of Acutelines, on
reasonable request.
Declarations
Ethics approval and consent to participate
The ethical review board (CTc) of the University Medical Centre Groningen
(UMCG), has approved the current study ()protocol number 11120) All
participants provided written consent to participate in the Acutelines data-
and biobank and. Acutelines is approved by the medical ethics board of
the UMCG and registered under trial registration number NCT04615065 at
ClinicalTrials.gov.”
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Received: 3 October 2024 / Accepted: 9 January 2025
Page 8 of 8Stolmeijer et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2025) 33:8
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