A Randomized Controlled Trial of the Effect of Fixed-dose

Routine Nocturnal Oxygen Supplementation on Oxygen

Saturation in Patients with Acute Stroke

Christine Roffe, MD,*‡ Sheila Sills, MPhil,* Sarah J. Pountain, PhD,‡

and Martin Allen, FRCP†

Background: Mild hypoxia is common in patients with stroke, and associated with
worse long-term outcome. Oxygen supplementation could prevent hypoxia and im-
prove recovery. A previous study of routine oxygen supplementation showed no
benefit after acute stroke, but did not report compliance and the effect on oxygena-
tion. The aim of this study was to assess the effect of routine low-flow oxygen sup-
plementation on oxygen saturation (SpO2) in patients with acute stroke. Methods: In
all, 63 patients with normoxic stroke and no indications for oxygen treatment were
randomized to 2 L/min oxygen supplementation via nasal cannulae overnight or to
control (room air) within 72 hours of symptom onset. Additional oxygen was given
at the discretion of the clinical team, if medically indicated. SpO2 was assessed from
22:00 to 09:00 by pulse oximetry. Compliance with the trial treatment and sleep sta-
tus were recorded by nursing staff. Results: In all, 59 patients were confirmed to have
had a stroke and available for overnight monitoring. Six (2 oxygen, 4 control) had no
or insufficient oximetry data for analysis. The mean nocturnal SpO2 was 2.5% higher
in the oxygen group (n 5 27) than in the control group (n 5 26) (P , .001). More pa-
tients on oxygen than control subjects had SpO2 greater than 90% throughout the
night (59% v 23%). Patients on oxygen had fewer desaturations than control subjects
(oxygen desaturation index 4%, 0.8 v 2.1) (P 5.001). Oxygen was found to be in place
as prescribed in 71%. Oxygen supplementation was not associated with insomnia or
restlessness. No patient in either group was given oxygen for clinical indications.
Conclusions: Nocturnal oxygen supplementation at a rate of 2 L/min increases the
mean nocturnal SpO2 by 2.5% and reduces the number of nocturnal desaturations
in patients with acute stroke. Key Words: Stroke—oxygen—hypoxia—
randomized trials—oxygen saturation—pulse oximetry.
Ó 2010 by National Stroke Association

From the *Stroke Research Group, Keele University, Staffordshire,

United Kingdom, †Department of Respiratory Medicine, University
Hospital of North Staffordshire, Staffordshire, United Kingdom;
and ‡Institute for Life Courses Studies, Keele University, Stafford-
shire, United Kingdom.
Received September 18, 2008; revision received February 3, 2009;
accepted February 11, 2009.
North Staffordshire Medical Institute funded the purchase of the
pulse oximeters.
Address correspondence to Christine Roffe, MD, Stroke Research
office, Royal Infirmary, University Hospital of North Staffordshire,
Stoke-on-Trent, ST4 7LN, United Kingdom. E-mail: christine.roffe@
northstaffs.nhs.uk.
1052-3057/$—see front matter
Ó 2010 by National Stroke Association
doi:10.1016/j.jstrokecerebrovasdis.2009.02.008
Specialist care on stroke departments is effective in pre-
venting death and disability after stroke.1 Although it has
not been established which aspects of stroke care are cru-
cial for improving outcome it has been shown that pa-
tients in a stroke department are more likely to receive
oxygen than in a nonspecialized general department.2
Oxygen treatment may thus be a factor relevant to stroke
outcome. Mild hypoxia is common in patients with stroke
and may have significant adverse effects on the ischemic
brain after stroke.3 Although healthy adults with normal
cerebral circulation can compensate for mild hypoxia by
an increase in cerebral blood flow,4 this is not possible
in the already ischemic brain after stroke.5-7 Sleep apnea

Journal of Stroke and Cerebrovascular Diseases, Vol. 19, No. 1 (January-February), 2010: pp 29-35 29
30
is common after stroke, and may lead to nocturnal hyp-
oxia. Up to a quarter of patients with stroke who are con-
sidered normoxic in the day have been shown to develop
hypoxia during the night.8 For all these reasons the use of
oxygen treatment is rapidly increasing in European stroke
departments. A questionnaire survey of United Kingdom
stroke physicians showed that almost 50% of respondents
would start oxygen supplementation after stroke at an ox-
ygen saturation (SpO2) of 95% or above,9 which is well
within the normal physiologic range.10 There are, how-
ever, also reasons for caution. Oxygen treatment is not
without side effects.11 It impedes early mobilization, is as-
sociated with at least minor discomfort, could lead to up-
per and lower airway infection, and may disrupt sleep.12
Although it is likely that oxygen supplementation will in-
crease SpO2 in the blood, it may have a neutral or even
negative effect by causing respiratory depression. There
is only one large randomized study of oxygen supple-
mentation for acute stroke, and this suggests that routine
oxygen treatment to unselected patients with stroke does
not reduce morbidity and mortality.13 The study did not
report compliance with allocated treatment or SpO2 be-
fore and during treatment. It is, therefore, impossible to
say whether the observed lack of effect may have been
a result of poor compliance with treatment, failure to
improve SpO2 on treatment, or oxygen toxicity and free
radical formation in patients with SpO2 at the higher
end of the normal scale. It is, therefore, important to
find out more about the effects of oxygen treatment in
patients with acute stroke.
The aim of this study was to assess the compliance with
and effectiveness of routine low-flow nocturnal oxygen
supplementation in patients with acute stroke. The main
hypotheses were that oxygen supplementation reduces
the time with SpO2 less than 90% and reduces the severity
of desaturations.
Methods
Trial Design, Setting, and Participants
This was a randomized, controlled, single-blind study
comparing the effects of fixed-dose oxygen supplementa-
tion on nocturnal SpO2 with no oxygen. Adult patients
with a clinical diagnosis of acute stroke14 who were not
moribund were recruited within 72 hours of admission
to our university hospital, a large teaching hospital admit-
ting about 800 patients with stroke per year. Patients with
an admission diagnosis of stroke or possible stroke were
identified by a part time research nurse (S.S.), who
checked the medical admissions department log book ev-
ery morning on the days she was working. Patients with
definite indications for oxygen supplementation (SpO2 ,
90%, decompensated congestive cardiac failure, pneumo-
nia with consolidation on the chest radiograph, known
chronic hypoxia requiring long-term oxygen treatment)
were excluded. Other reasons for study exclusion were:
C. ROFFE ET AL.
severe persistent disability from a prior stroke, confusion
and restlessness making probe placement difficult,
reduced peripheral perfusion leading to an unobtainable
or poor oximetry trace, pregnancy, and refusal of consent.
Intervention
Patients were randomized by simple randomization us-
ing a computer-generated random number code to one of
two groups: the oxygen group or the control group. Pa-
tients in the oxygen group were given oxygen via nasal
cannulae at a flow rate of 2 L/min from 21:00 to 09:00 dur-
ing the first night after enrollment. Vital signs incuding
SpO2 were checked once every 8 hours in all patients
and more freqently if necessary, as was routine practice
in the department. If an indication for oxygen treament
developed in the control group, or a different flow rate
was needed in the treatment group, this was prescribed
by the treating medical team as clinically indicated.
Baseline Clinical Assessment and Follow-ups
At baseline, details of the medical history were estab-
lished by interview and consultation of medical notes. Pa-
tients were examined neurologically and classified as
having total anterior circulation syndrome, partial ante-
rior circulation syndrome, lacunar syndrome, or posterior
circulation syndrome using the Oxfordshire Community
Project classification.15 Cause was determined by com-
puted tomography of the head and reported as cerebral
infarct or intracerebral hemorrhage. Hemorrhagic infarcts
were recorded as infarcts. Neurologic deficit was scored
using the Scandinavian Stroke Scale at baseline on day 1
(after the intervention night) and on day 2 (no interven-
tion the night before).
Further Clinical Assessments
The night nurses documented the blood pressure and
temperature at 21:00 on the intervention night and the
night postintervention. Each patient was checked at
02:00 and 03:00 and it was recorded whether the oximeter
was still in place, whether the oxygen cannula was in
place, whether the patient was asleep and resting
(asleep/awake and restful/awake and restless), and
how they were lying (right side/left side/prone/supine)
on each night. The Scandinavian Stroke Scale was
repeated by the researcher after both nights.
Pulse Oximetry
SpO2 and heart rate were assessed using a pulse oxi-
meter (Pulsox-3I, Minolta, Stowood Scientific Instru-
ments, Beckley, Oxford, United Kingdom). Hands were
inspected to ensure that the fingers were warm and well
perfused. Nail varnish was removed and long fingernails
were clipped, where necessary. The pulse oximeter was
attached to the wrist and the sensory probe was fitted to
FIXED-DOSE OXYGEN SUPPLEMENTATION AFTER STROKE
the index finger. To reduce movement artefact the hemi-
paretic side was used for oximetry.16
Pulse oximetry was performed overnight from 21:00 to
9:00 on the first night after recruitment (during the inter-
vention) and again overnight on night 2 (no intervention).
Pulse oximetry was also performed while the patient was
awake for 5 minutes at recruitment (baseline), after the in-
tervention night (day 1), and after night 2 (no interven-
tion). After completion of the recording, data were
downloaded onto a personal computer using software
(Oximeter DownLoad Software for Windows, Stowood
Scientific Instruments). Values for SpO2 were obtained
by performing a moving average for the last 5 seconds,
updated every second. Desaturations (oxygen desatura-
tion index 4%) were defined as a 4% decrease in satura-
tion from the baseline just before the decrease.
Main Outcomes
Prespecified main outcomes were the time spent with
an SpO2 below 90% during the night (corrected for an
8-hour recording), the lowest SpO2 recorded during the
night, feasibility (the proportion of patients prescribed
oxygen who actually had oxygen in place when checked),
and tolerability (sleep disturbance).
Ethical Approval and Consent
The protocol was approved by our ethics committee
(project number 1168). Written informed consent was
sought from all study participants. Assent from the next
of kin was accepted if the patient agreed to take part
but was unable to give fully informed consent.
Statistical Analysis
All analyses were performed using a statistical soft-
ware package (SPSS, SPSS Inc., Chicago, Illinois, Version
14.0), as detailed in the text.
Results
Recruitment
In all, 214 successive patients within 72 hours of onset
of a first acute stroke who were not moribund were iden-
tified from the admissions log and considered for trial in-
clusion (Figure 1). Of those, 151 (71%) were excluded for
the following reasons: oxygen treatment in progress at the
time of recruitment (n 5 46); and no oxygen treatment in
progress at the time of screening, but potential clinical in-
dications for oxygen (n 5 33) [e.g., chronic obstructive air-
ways disease (n 5 9), chest infection (n 5 11), abnormal
chest radiograph result (n 5 13)]. Not all patients treated
with oxygen had a clinical indication (staff in the emer-
gency admissions department routinely give oxygen to
all patients with stroke whether indicated or not). In 42
patients consent could not be obtained [e.g., refusal of
consent (n 5 9), incompetent to consent and next of kin
31
could not be contacted in time (n 5 33)]. In 6 patients
the oximetry probe could not be placed safely, 23 patients
were too confused to comply with oxygen treatment or
monitoring, and 1 patient was recruited to another study.
In all, 63 patients were randomized. Thirty were allocated
to oxygen and 33 to control. All randomized patients
received the allocated treatment).
One patient in the control group was lost to follow-up
(transfer to another hospital). One patient in the oxygen
group and two patients in the control group were ex-
cluded retrospectively because the initial diagnosis of
stroke was not confirmed (two subdural hemorrhages
and one brain tumor) leaving 59 patients (29 in the oxygen
group and 30 in the control group) with a confirmed diag-
nosis of stroke and available for assessment of outcomes.
Of these, 53 had analyzable pulse oximetry results (27 in
the oxygen group and 26 in the control group).
Baseline Demographic and Clinical Data
The mean age of patients included in the study was 74.9
SD 9.6 years, 35 (59%) were male, 18 (31%) were smokers,
and 17 (29%) had a severe stroke (total anterior circulation
syndrome). Ten (17%) and 16 (27%) had a history of chest
problems and ischemic heart disease, respectively. A com-
parison of baseline characteristics between the two treat-
ment groups is shown in Table 1.
SpO2
Table 2 shows the results of overnight pulse oximetry
for the two groups for night 1. Oximetry was conducted
successfully in 27 of 29 patients in the oxygen group
and 26 of 30 control subjects. The mean nocturnal SpO2
was 2.5% higher in the treatment group than in the control
group (P , .001, t test). There were also 1.3% less desatu-
rations (oxygen desaturation index 4%) in the oxygen
group than in the control group (P 5 .01, Mann Whitney
U test). Patients in either group spent very little time
with SpO2 below 90%. There were no significant differ-
ences between the active and the control groups for the
two prespecified main outcomes (the time spent with
SpO2 , 90% and the lowest nocturnal SpO2, P 5 .2 and
P 5 .2, respectively). More patients in the oxygen group
had normal SpO2 throughout the night. Fig 2 shows the
lowest SpO2 at night for patients in the oxygen and con-
trol groups. In 16 of 27 (59%) and 6 of 26 (23%) patients
in the oxygen and control groups, respectively, the lowest
SpO2 at night was 90% or above. The lowest SpO2 de-
creased below 70% at night in 0 of 27 (0%) patients on ox-
ygen and in 4 of 26 (15%) of the control subjects. There
was no relationship between baseline SpO2 (at recruit-
ment) and the lowest SpO2 in either group.
None of the patients in either group had mean noctur-
nal SpO2 below 90% during either night. Only one patient
in the oxygen group had mean SpO2 greater than 98.5%
(e.g., 99.2%) during the treatment night. The mean
32 C. ROFFE ET AL.

Clincal diagnosis of acute stroke Excluded (n= 151)

within 72 h of symptom onset,
not moribund Oxygen related (n=79)
(n= 214) On oxygen already (n=46)
Potential need for oxygen (n=33)
No consent (n= 42)
Consent refused (9)
Included (n=63) Unable to consent (33)
Other reasons (n= 30)
Recruited to another study (1)
Randomized (n=63) Probe placement difficult (6)
Too confused for monitoring (23)

Allocated to oxygen Allocated to control

(n= 30)
Received allocated
intervention (n= 30)
Lost to follow-up (n= 0)
Discontinued intervention
(n= 0)
Not a stroke (n=1)
Allocation (n=33)
Received allocated
intervention (n= 33) Figure 1. Inclusions, exclusions, and drop outs.
N1: Night 1.
Lost to follow-up (n= 1)
(transfer to another hospital)
Discontinued intervention (n= 0)
Follow-Up Not a stroke (n=2)

Included in the analysis Included in the analysis of

of outcome data (n=29) outcome data (n=30)

Pulse oximetry data

unavailable or incomplete Pulse oximetry data unavailable
(n=2) or incomplete (n=4)
Problems with the pulse
Refused to wear
oximeter (n=2)
oximeter (n=1) Analysis Too unwell for study, died
No pulse oximetry during N1 (n=1)
data (n=1) Inadequate pulse oximetry
data (n=1)
Adequate pulse oximetry
data (n=27) Adequate pulse oximetry data
(n=26)

nocturnal SpO2 did not exceed 98.5% in any of the pa-
tients in the control group. SpO2 in the morning after
the end of the intervention was the same in both groups.
Effect on Physiologic Parameters and Stroke Progression
There were no significant differences in any of the
physiologic parameters assessed during the intervention.
Mean results for the oxygen and control groups, respec-
tively, were 153.1 SD 23.4 and 152.6 SD 22.6 mm Hg for
systolic blood pressure, 79.6 SD 14.2 and 80.4 SD 14.4
mm Hg for diastolic blood pressure, 75.6 SD 14.3 and
74.2 SD 20.0 beats/min for heart rate, and 36.9 SD 0.5
and 37.0 SD 0.6 C for temperature (P . .05 for all compar-
isons between oxygen and control). Neurologic function
was slightly imbalanced at baseline, but there was no de-
terioration during or after the intervention in either group
with median (interquartile range) Scandinavian Stroke
Scale scores of 41 (28-46), 41.5 (29-46), and 41 (30-47) in
the oxygen group before, on the first morning after the in-
tervention, and on the second morning after the interven-
tion, respectively, and scores of 26 (18-49), 29.5 (17.5-50),
and 29 (16-47) for the control group, respectively. The dif-
ferences between the groups were not statistically signif-
icant (Mann Whitney U test). One patient in the control
group died during the intervention night; no patients in
the oxygen group died during this time period. During
the first 2 weeks after recruitment 2 (7%) patients in the
oxygen group and 3 (10%) in the control group died.
Effect on Sleep
During the intervention night, sleeping positions and
sleep/awake state were checked by the night nurse at
2:00 and 3:00. At 2:00 and 3:00, 27/29 and 25/29 record-
ings, respectively, were documented in the oxygen group
and 23/30 and 22/30 in the control group for sleep/
awake state. At these time points 18 (62%) and 17 (59%)
FIXED-DOSE OXYGEN SUPPLEMENTATION AFTER STROKE 33

Table 1. Baseline characteristics of study population

Oxygen group N 5 29 Control group N 5 30

Demographic characteristics
Age (mean, y) 74.9 SD 9.6 72.8 SD 8.3
Male sex 15 (52%) 20 (67%)
Body mass index (mean) 24.5 SD 4.2 27.4 SD 5.0*
Smokers 11 (38%) 7 (23%)
Snorers 16 (55%) 16 (53%)
Concomitant medical problems
Hypertension 20 (69%) 18 (60%)
Atrial fibrillation 4 (14%) 2 (7%)
Ischemic heart disease 7 (24%) 9 (30%)
Congestive cardiac failure 3 (10%) 1 (3%)
Diabetes mellitus 4 (14%) 7 (23%)
Chronic obstructive pulmonary disease/asthma 4 (14%) 3 (10%)
Other lung diseases 2 (7%) 1 (3%)
Stroke
Time since stroke (mean, h) 45.6 SD 20.4 50.3 SD 17.8
Stroke pathology (infarcts) 16 (55%) 20 (67%)
Median Glasgow Coma Scale score (IQR) 15 (15-15) 15 (14-15)
Median Scandinavian Stroke Scale score (IQR) 40 (28-46) 26 (18-49)
Partial or total anterior circulation syndrome 14 (48%) 14 (47%)
Dysphagia 10 (34%) 13 (43%)
Dysarthria 6 (21%) 12 (40%)
Other clinical data
Oxygen saturation (%, mean) 94.8 SD 2.0 95.6 SD 1.5
Hemoglobin (g/dL, mean) 13.7 SD 1.4 13.8 SD 1.6
White blood cell count (g/dL, mean) 11.0 SD 4.5 10.1 SD 3.4
Creatinine (mmol/L, mean) 88.8 SD 27.0 95.1 SD 20.6
Urea (mmol/L, mean) 5.8 SD 2.0 5.6 SD 1.9
Glucose (mmol/L, mean) 7.3 SD 2.1 8.0 SD 4.4

Abbreviation: IQR, interquartile range.

*P , .05. Where not otherwise indicated, differences were not significant statistically.

patients on oxygen and 14 (47%) and 15 (50%) patients in
the control group were found to be asleep at 2:00 and 3:00
respectively. Six (21%) and 4 (14%) patients on oxygen
and 4 (13%) and 3 (10%) control subjects were awake
and restful, at 2:00 and 3:00 respectively. Two (7%) and
1 (3%) patients on oxygen, and 5 (17%) and 5 (17%)
control subjects were awake and restless at 2:00 and 3:00
respectively. None of the differences between the treat-
ment groups is significant, but there was a trend (P 5
.1) toward more control subjects being awake and restless
at 3:00 AM.
and 20 (69%) patients in the oxygen group at the two
time points, respectively, and correctly not in place in all
patients in the control group. For both of these observa-
tions, probe placement and oxygen treatment, the number
of observations for the oxygen group at 2:00 and 3:00 re-
spectively, were 28/29 and 26/29 and for the control
group 23/30 and 22/30. None of the patients in the oxy-
gen group was given oxygen over and above the trial
treatment and none of the patients in the control group
were prescribed oxygen for clinical reasons during the
trial period.

Compliance with Monitoring and Trial Treatment Discussion

During the intervention night accurate probe place-
ment and oxygen treatment were checked (and replaced
as necessary) at 2:00 and 3:00 for each patient. The oxi-
meters were recorded to be correctly in place in 25
(86%) and 24 (83%) patients in the oxygen group and 23
(77%) and 18 (60%) in the control group at 2:00 and 3:00
respectively. Oxygen was correctly in place in 21 (72%)
The results of this study show that oxygen supplemen-
tation at a rate of 2 L/min results in a mean increase in
nocturnal SpO2 of 2.5%. Oxygen supplementation also
reduces the number of desaturations.
Patients in either group spent very little time with SpO2
of less than 90%. This may be a result of the selection cri-
teria, because patients who were hypoxic or had definite
34 C. ROFFE ET AL.

Table 2. Effect of routine nocturnal oxygen supplementation at a rate of 2 L/min on oxygen saturation

Oxygen group (N 5 27) Control group (N 5 26) P value

Mean nocturnal 96.6 (95.3-97.5) 94.1 (93.7-95.2) .000

SpO2, median (IQR)
Lowest nocturnal 88.0 (84.5-91.0) 87.0 (81.3-89.0) .181
SpO2%, median (IQR)
ODI 4%/h, (median (IQR) 0.8 (0.4-2.4) 2.1 (1.2-3.9) .012
Tc , 90%, h:mm median (IQR) 0:00 (0:00-0:04) 0:02 (0:00-0:06) .149
Tc , 80%, h:mm median (IQR) 0:00 (0:00-0:00) 0:00 (0:00-0:00) .442
Next-day daytime 95.5 (93.6-96.7) 95.7 (95.2-96.1) .783
SpO2, median (IQR)

Abbreviations: IQR, interquartile range; ODI, oxygen desaturation index; SpO2, oxygen saturation; Tc , 90%, analysis time spent with
SpO2 , 90% (normalized for 8 hours); Tc , 80%, analysis time spent with SpO2 , 80% (normalized for 8 hours);
Nocturnal measurements were taken from 21.00-09.00, with analysis from 23.00-07.00 hours. The next day, daytime oxygen saturation was
5-min mean taken in the morning without oxygen supplementation. Statistical significance was determined by Mann-Whitney U test.

indications for oxygen supplementation at baseline were
not included. Oxygen supplementation did not reduce
the time spent with saturation of less than 90%. Because
the median time spent with saturation below 90% was
so small, and because most patients remained persistently
above 90%, this result may not be representative. A larger
study would be required to confirm this.
Although the total time patients spent with SpO2 below
90% was low, it is of concern that in 15% of patients in the
control group the lowest SpO2 was below 70%. Further-
more, the desaturations were not recorded as events in
the patients’ notes and no treatment was initiated. These
results confirm findings of an earlier study that even in
patients who are normoxic at enrollment nocturnal hyp-
oxia is not unusual, but commonly missed in routine clin-
ical practice with intermittent assessment of vital signs.
Such very deep desaturations were not seen in the oxygen
group. There was no relationship between baseline SpO2
and the lowest nocturnal SpO2 (Fig 2). Therefore, deep
Oxygen Group
100.0
LowestSpO2
nocturnal desaturations cannot be predicted from day-
time SpO2. Continuous monitoring of SpO2 with appro-
priate alarm settings may be necessary to detect such
desaturations. It has previously been shown that hypoxia
is common early after the stroke, especially during trans-
fers between the emergency department and the ward or
the head scanner, and that such early hypoxia is associ-
ated with worse overall outcome.17
Although oxygen supplementation increased the mean
nocturnal SpO2 in the current study, it did not prevent the
lowest SpO2 decreasing below 90% in all treated patients.
Taken together with the finding that the mean time spent
with an SpO2 below 90% was also not affected it could be
hypothesized that a dose of 2 L/min is sufficient to pre-
vent very severe hypoxia (70%) but not milder hypoxia
(90%). Higher doses may be required to keep nocturnal
SpO2 persistently above 90%. However, higher doses of
oxygen are likely to also increase the mean SpO2 and
push the highest SpO2 closer to 100%. Supernormal
SpO2 may increase the risk of free radical formation and
associated tissue injury in the ischemic brain.13
The effectiveness of the dose of oxygen given may have

90.0
been underestimated because the sample contained indi-
80.0
viduals who, at least for some of the time, did not get ox-
70.0
ygen (oxygen was found correctly in place in 69% and
60.0
72% of patients at the two time points in the night when
50.0
90.0 92.0 94.0 96.0 98.0 100.0
correct administration was checked). Although this has
Baseline SpO2 potentially affected the results, and such inaccuracy could
have been prevented by observing the patient continu-
Control Group ously and replacing the oxygen as soon as it came off,
100.0
such intensive observation is unlikely to happen in the
Lowest SpO2

90.0
busy environment of an acute stroke department. The
80.0
results, therefore, reflect the treatment effect that can be
70.0
achieved in ordinary clinical practice.
60.0
Routine oxygen supplementation after acute myocar-
50.0
90.0 92.0 94.0 96.0 98.0 100.0 dial infarction has been shown to increase the heart
Baseline SpO2 rate.18 This may have been a result of increased stress as-
Figure 2. Lowest SpO2 at night for oxygen (top) and control (bottom) sociated with oxygen treatment. In the group of patients
groups. with acute stroke studied here oxygen supplementation
FIXED-DOSE OXYGEN SUPPLEMENTATION AFTER STROKE
did not affect blood pressure or heart rate. Oxygen did not
keep patients awake at night, and was not associated with
an increase in restlessness and agitation requiring treat-
ment. Oxygen treatment did not have a prolonged posi-
tive or negative effect on SpO2 once discontinued. On
the morning after the intervention, at least 1 hour after
discontinuation of SpO2, in both the oxygen and control
groups levels were the same. We found no significant dif-
ference in neurologic outcomes and mortality, but the
study was not powered to address these issues. A previ-
ous, relatively large, study of routine oxygen supplemen-
tation at 3 L/min over 24 hours did not show any benefit
on overall outcome at 3 months.13 A more recent, much
smaller, study of high-flow oxygen treatment over 8 hours
resulted in transient improvement of clinical deficits and
magnetic resonance imaging abnormalities within the
first 24 hours of acute ischemic stroke, but there was no
long-term benefit at 3 months.19 However, this study
only included 16 patients and was, therefore, too small
to exclude any but very large long-term treatment effects.
A larger study is ongoing.
In conclusion, nocturnal oxygen treatment is tolerated
well by the majority of patients with stroke. A dose of 2
L/min significantly increased mean nocturnal SpO2 and
reduced the severity of nocturnal desaturations without
exposing the patient to supernormal SpO2. Although
oxygen supplementation increases SpO2 it is as yet
unknown whether it also improves long-term outcome.
We would like to thank Dr. M. Abd El Halim for his help in
recruiting patients.
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