Reviewed and revised 14 November 2016
Both the extremes of hypoxaemia and hyperoxia have the potential to harm critically ill patients and worsen their outcomes
- it is unclear if potential harms from hypoxia/ hyperoxia are due to the timing of the insult, severity and/or duration
- traditionally, many ICU patients have been exposed to hyperoxia through liberal oxygen supplementation practices – this is likely due to a lack of awareness of the potential harms of hyperoxia and failure to specify, or adhere to, an upper limit for the target range
Oxygen saturation measured using pulse oximetry (SpO2) are the preferred means of monitoring oxygenation in most circumstances and are used universally in critical care.
Thoracic Society of Australia and New Zealand (TSANZ) Guidelines recommend that:
- “Pulse oximetry should be available in all clinical situations in which oxygen is used. [GRADE C]”
- “Oxygen saturation measured by pulse oximetry should be considered a ‘vital sign’ and documented with other vital signs in patient assessment and management. [GRADE D]”
The harms of hypoxaemia are well established, however, the importance of hyperoxia is uncertain and is an area of ongoing research
RATIONALE FOR USE OF PULSE OXIMETRY OXYGEN SATURATIONS (SpO2)
Pulse oximetry oxygen saturations are preferred to arterial blood gas analyzers for the following reasons:
- allows immediate, non-invasive, painless, and continuous monitoring
- pulse oximetry usually reads within ± 2% (over the 70–100% SpO2 range)
- oxygen saturation (SO2) is a better measurement of the systemic oxygen delivery to the tissues than oxygen tension (PO2)
- ABG sampling is more difficult and subject to error (eg. venous stab)
- point-of-care ABG analyzers typically calculate, rather than measure, SaO2 from the measured PO2 assuming a normal Hb-O2 dissociation curve
- PaO2 measurement may lead to inappropriate therapy if attempts are made to normalise PaO2, despite adequate SaO2/ SpO2 values
- PaO2 differences in sequential ABGs are often due to random variation, according to Mallat et al (2015) only a PaO2 difference of +/- 9 mmHg between measurements should be considered real.
SpO2 is inadequate in certain circumstances:
- marked hypoxaemia
- unreliable SpO2 trace (e.g. peripheral hypoperfusion)
- dyshaemoglobinaemia (e.g. COHb, MetHb)
- to assess lung function (e.g. PF ratio)
- assessing risk of harm from hyperoxia (correlates with PaO2, which may vary over a wide range while SpO2 remains 100%)
The key limitation of SpO2 is that it is only one component of the determinants of oxygen delivery (DO2), which also depends on haemoglobin concentration and cardiac output. Furthermore, it does not indicate if DO2 is adequate for tissue demands, which can be shown by the oxygen extraction ratio (O2ER).
- Limitations, sources of error and complications of pulse oximetry are described in the Pulse Oximeter CCC entry
CHOICE OF SpO2 TARGETS
- Hypoxaemia is usually defined as SaO2 <90% or PaO2 <60 mmHg
- Definitions of hyperoxaemia vary, PaO2 > 300mHg is commonly used in post-cardiac arrest research but there may be no clear threshold associated witth risk of harm in various settings
Oxygen is liberally administered to many critically ill patients, this risks exposing them to supranormal arterial oxygen levels
- Hyperoxia can have adverse effects on the cardiovascular, pulmonary, CNS and immune systems
- Many of the harmful effects of hyperoxia are likely due to reactive oxygen species (ROS) and hyperoxia-induced vasoconstriction (direct and indirect)
- One problem facing observational studies is that hyperoxia (high PaO2) may simply be a marker of illness severity (e.g. FiO2 may be increased in shocked patients who have a poor SpO2 trace), and may not cause significant harm itself
- Hyperoxia is discussed in great detail in the CCC entry on Oxygen
Choice of the lower SpO2 limit should:
- provide sufficient oxygen delivery to meet the body’s needs (e.g. SaO2 88-92%)
- Older healthy subjects have SaO2 levels of ~90% (Crapo et al, 1999; Hardie et al, 2004)
- Healthy subjects have a mean nadir SpO2 of ~90% during sleep (Gries and Brooks, 1996)
- Adults with sleep disordered breathing commonly tolerate SpO2 levels between 80 and 90% for prolonged periods
- Adults with comorbidities tolerate SpO2 levels between 80 and 90% during long distance flights (Akero et al, 2005)
- A proportion of adults with coronary artery disease develop anaerobic metabolism indicative of myocardial ischaemia with SaO2 between 70 and 85%
- avoid the steep part of the oxygen-haemoglobin dissociation curve (as any further decrease in PaO2 with cause a precipitous fall in SaO2 and oxygen delivery, leading to unplanned episodes of hypoxaemia)
- allow for measurement error (e.g. usually +/-2% for SpO2)
- be in keeping with the usual oxygenation status to which a patient has adapted (where appropriate)
Choice of the upper SpO2 limit should:
- allow the recognition of patient improvement and allow down-titration of oxygen supplementation
- avoid the harmful effects of hyperoxaemia
- be tailored to the patient’s disease process (e.g. avoid CO2 retention in COPD patients)
- be in keeping with the usual oxygenation status to which a patient has adapted (where appropriate)
From Thoracic Society of Australia and New Zealand (TSANZ) Guidelines:
- In COPD [GRADE B] and other conditions [GRADE C] associated with chronic respiratory failure, oxygen should be administered if the SpO2 is less than 88%, and titrated to a target SpO2 range of 88% to 92%.
- In other acute medical conditions, oxygen should be administered if the SpO2 is less than 92%, and titrated to a target SpO2 range of 92% to 96%. [GRADE C]
Other specific situations:
- no formal guidelines exist regarding the optimal oxygenation target in ARDS
- there are unanswered questions about the safety of permitting subnormal oxygenation targets
- Traumatic brain injury
- BTF guidelines do not specify a target SpO2 for severe TBI
- Ischaemic conditions
- Oxygen therapy should only be used to correct hypoxemia in conditions characterised by tissue ischaemia, such as stroke and acute coronary syndromes
- ANZCOR recommends oxygen therapy only if there is hypoxaemia or shock
- Post-cardiac arrest
- ANZCOR recommends use of 100% oxygen during resuscitation of cardiac arrest
- ANZCOR recommends that “once ROSC has been established and the oxygen saturation of arterial blood (SaO2) can be monitored reliably (by pulse oximetry [SpO2] and/or arterial blood gas analysis [SaO2]), it is reasonable to titrate the inspired oxygen to achieve a target saturation between 94 – 98%”
- Bleomycin or paraquat toxicity
- TSANZ guidelines advise a target of SpO2 85% to reduce potentiation of lung injury by oxygen, given that harm from hypoxaemia at this level has not be demonstrated in these settings.
- Decompression sickness and carbon monoxide poisoning
- treat with high flow oxygen immediately, pending assessment for hyperbaric oxygen therapy
Note that, in general, ANZCOR guidelines recommend a default SpO2 target range of 94-98%, slightly higher than the TSANZ guideline recommendations.
EVIDENCE IN GENERAL ICU PATIENTS
Optimal SaO2 / PaO2 target is unknown in mechanically ventilated ICU patients, more research required according to a Cochrane Systematic Review (Gilbert-Kawai et al, 2014)
- In this group, oxygen administration tends to be more liberal than conservative (Young et al, 2015)
- Observational data is consistent in showing harm from hypoxaemia but is conflicting as to the harms of hyperoxia
- A retrospective analysis of ~35,000 ventilated patients in the Netherlands found a U-shaped relationship with increased mortality above 225 mmHg and below 67.5 mmHg, in the first 24h (de Jonge et al, 2008)
- A retrospective analysis of ~150,000 ventilated patients from the ANZICS database found there was an association between hypoxia and increased in-hospital mortality, but not with hyperoxia, in the first 24h (Eastwood et al, 2012)
- A systematic review of 19 observational studies concluded that arterial hyperoxemia is associated with adverse clinical outcomes, with a crude odds ratio for in-hospital mortality of 1.38. In subgroup analysis, the effect was statistically significant for cardiac arrest and ischemic stroke, but not for TBI, intracranial hemorrhage, or after cardiac surgery. (Helmerhost et al, 2015)
- The CLOSE trial is the first attempt to randomize ICU patients to conservative versus liberal oxygenation targets
CLOSE trial – Panwar et al, 2016
- Small multi-centre, parallel group, randomized trial
- n=104 mostly medical ICU patients from 4 ICUs in Australia, New Zealand and France
- Study population
- Inclusion criteria: Adult ICU patients who were ventilated for < 24 hours and their treating clinician expected ventilation to continue for at least next 24 hours
- Exclusion criteria: pregnancy, those not expected to survive, or if the treating clinician lacked equipoise for patient randomisation
- Intervention/ comparison (continued while patient remained ventilated)
- SpO2 targets of 88 – 92% (conservative oxygenation group; n=53) or
- SpO2 targets of ≥ 96% SpO2 (liberal oxygenation group, n=51)
- Primary outcome: mean area-under-curve (AUC) for SpO2, SaO2, PaO2 and FiO2 on days 0 – 7
- significantly lower in the conservative group compared to the liberal group
- Secondary safety outcomes: change from baseline SOFA score, changes in PaO2/FiO2, new-onset ARDS, changes in creatinine, incidence of haemodynamic instability (cardiac arrest or addition of ≥ 2 new vasopressor/inotrope agents), vasopressor-free days, arrhythmia-free days, and ventilator-free days until day 28, ICU mortality and 90-day mortality
- no significant differences
- Target SpO2 range was achieved for both groups
- Overall, participants spent a median of 6% [IQR 0 – 25%] time off target
- more time was spent off target in the conservative arm than in the liberal arm (14% vs. 3%, p <0.001)
- Primary outcome: mean area-under-curve (AUC) for SpO2, SaO2, PaO2 and FiO2 on days 0 – 7
- Commentary and Criticisms
- bedside nurse titrated the FiO2 within a range of 0.21 to 0.80 to achieve the SpO2 target, whilst PEEP levels were determined by the treating clinicians
- Randomized using opaque sealed envelopes and unique computer- generated, permuted block randomization
- Good baseline balance (including ventilator strategies, fluid administration and blood transfusion)
- the conservative group had more blood gases performed
- Feasibility study only
- blinding was not possible
- only 103 out of 357 screened patients were enrolled in the study and 69 patients were not randomised due to lack of equipoise
- mean saturations were higher than their target in the conservative group (unable to titrate FiO2 below 0.21) – suggesting that some of the patients did not have severe illness
- conservative and liberal targets are somewhat arbitrary
- unclear if harms from hypoxia/ hyperoxia are likely to be due to timing of the insult, severity and/or duration
- The CLOSE trial establishes that targeting conservative and liberal SpO2 targets is feasible in a research setting, and that a trial powered to detect differences in patient-centered outcomes should be possible.
OXYGEN-ICU trial – Giradis et al, 2016
- Single center non-blinded randomised controlled trial
- n=434 ICU patients at a University Hopsital in Italy (March 2010 – October 2012)
- Study population
- Inclusion criteria: Adults aged ≥18y that were admitted to ICU with expected length of stay of ≥72 hours
- Exclusion criteria: Pregnancy, ICU readmission, decision to withhold life sustaining treatment, immunosupression or neutropenia, ARDS with P/F ratio <150, acute decompensation of COPD, enrollment in another study
- Intervention/ comparison
- Conservative oxygen therapy: Target SpO2 94%-98%, using lowest possible FiO2 to maintain PaO2 of 70-100mmHg (n=236), versus
- Standard oxygen therapy: Target SpO2 97%-100%, using FiO2 of at least 0.4, allowing PaO2 of up to 150mmHg (n=244)
- Primary outcome:
- ICU mortality was significantly lower in conservative oxygen group
- 11.6% vs. 20.2% (Absolute risk reduction [ARR] 8.6%, NNT = 12, 95% C.I. 1.7%-15%, p=0.01)
- Secondary outcomes (conservative versus liberal):
- Median FiO2 was lower 0.36 (IQR 0.30-0.40) vs. 0.39 (IQR 0.35-0.42) (p<0.001)
- Median PaO2 was lower 87mmHg (IQR 79-97) vs. 102mmHg (IQR 88-116) (p<0.001)
- Lower rates of shock, liver failure, bacteraemia (all p<0.05)
- Post-hoc analysis
- Hospital mortality was lower: 24.2% vs. 33.9% (ARR 9.9%, 95% C.I. 1.3%-18.2%, p=0.03)
- Mechanical ventilation free hours (median) was lower: 72 vs. 48, p=0.02
- Primary outcome:
- Commentary and Criticisms
- Standard therapy patients received FiO2 of 1.0 during intubation, airway suction, hospital transfer; conservative therapy received FiO2 0.4 if SpO2 <94%
- Randomised control trial with allocation concealment
- Reporting of intention-to-treat analysis (though also used “modified” intention-to-treat analysis, which yielded similar results)
- Clear separation achieved between median PaO2 for conservative and conventional group
- Single centre, non-blinded
- Stopped early due to an earthquake (!)
- this is likely to lead to effect overestimation
- under powered – predicted sample size was 660 patients to detect an absolute reduction in mortality of 6% assuming a baseline of 23%, with a false negative rate of 20% and a false positive rate of 5%
- Minor baseline imbalances (age, severity of illness, organ failures) favoured conservative oxygen therapy group
- Low fragility index (3 for primary outcome), means that if 3 patients did not have improved outcome the primary outcome would not have been significant
- This flawed RCT found an almost certainly ‘too good to be true’ ICU mortality benefit from targeting SpO2 94%-98% versus 97-100% in general ICU patients. Interestingly, the conservative arm has higher SpO2 targets than current TSANZ guideline recommendations.
- Further research is needed.
EVIDENCE IN POST-CARDIAC ARREST
Most observational data suggests that both hypoxaemia and hyperoxia are associated with worse outcomes, including mortality and neurological recovery. Some studies, notably those from Australasia (including the largest, most valid analysis to date), did not find significant associations between hyperoxia and worse outcomes.
- A number of animals studies have suggested that harm may result from the use of high concentrations of oxygen in the early resuscitation period
These observational studies suggest harm from both hypoxaemia and hyperoxaemia
- Kilgannon et al, 2010
- a multicenter cohort study using the Project IMPACT critical care database of ICUs at 120 US hospitals involved 6326 adult non-traumatic cardiac arrest patients and found that the hyperoxia group (PaO2 >300 mmHg) had significantly higher in-hospital mortality (OR for death, 1.8; 95% CI, 1.5 to 2.2).
- This study has major flaws: there was no adjustment for illness severity, 27.6% of data were missing, few patients received targetted temperature management, and the first PaO2 in the ICU was used to indicate hyperoxia (a poor indicator of mean PaO2)
- Kilgannon et al, 2011
- another multi-center cohort study using the Project IMPACT post cardiac arrest database, this time involving 4,459 patients, 54% of whom died. Over ascending ranges of PaO2 (continuous variable), there were significant linear trends of increasing in-hospital mortality and decreasing functionally independent survival. The study did not support the use of a single threshold of hyperoxic PaO2 as harmful.
- This study also has major flaws, similar to those described above for Kilgannon et al, 2010
- Jansz et al, 2012
- a retrospective study of 170 patients treated with mild therapeutic hypothermia after cardiac arrest found that higher levels of the maximum measured PaO2 in the first 24h were associated with increased in-hospital mortality (OR 1.439; 95% CI 1.028-2.015; p = .034) and poor neurological status at hospital discharge (OR 1.485; 95% CI 1.032-2.136; p = .033).
- Lee BK et al, 2014
- a small retrospective observational study of 213 adult cardiac arrest patients found a V-shaped independent association between the mean PaO2 and poor neurological outcome at hospital discharge, with worse outcomes associated with the extremes of mean PaO2.
These observational studies suggest harm from hypoxaemia, but did not find evidence of harm from hyperoxaemia
- Bellomo et al, 2011
- Retrospective analysis of 12,108 non-traumatic cardiac arrest patients from the ANZICS database found that hyperoxia (PaO2 >300 mmHg) had no independent association with mortality.
- The assessment of oxygenation status in the first 24 hours was based on the ‘worst’ possible arterial blood gas result in the first 24h, a better measure of mean PaO2 that the method used in the Kilgannon/ EMShockNET studies.
- Ihle J et al, 2013
- a retrospective analysis of 584 OHCA patients from the Victorian Ambulance Cardiac Arrest Registry, using the most abnormal PaO2 level in the first 24 hours of ICU stay, found that hyperoxia in the ICU was not independently associated with increased hospital mortality (OR, 1.2; 95% CI, 0.51 to 2.82; P=0.83).
Evidence from randomised controlled trials is currently lacking
Young et al, 2014 (HOT OR NOT trial)
- This pilot study was stopped early because titration of oxygen in the prehospital period following OHCA was found to be infeasible.
EVIDENCE IN ARDS
Subnormal oxygen levels are associated with long-term cognitive impairment in ARDS survivors
- Hopkins et al, 1999
- Using serial pulse oximetry measurements, the amount of time spent below normal saturation values (SpO2 <90%, <85%, and <80%) correlated with decreased cognitive performance. 30% of the 55 patietns that completed neuropsychological testing were cognitively impaired at 1 year.
- Mikkelsen et al, 2012
- In an adjunct study to the ARDSNet Fluid and Catheter Treatment Trial (FACTT) neuropsychological function at 2 and 12 months post-hospital discharge was assessed using avalidated telephone-based neuropsychological test battery.
- Long-term cognitive impairment was present in 41 of the 75 (55%) survivors who completed cognitive testing. These patients had mean daily PaO2 values that were significantly lower compared with nonimpaired survivors (71 mmHg [interquartile range, 67–80 mm Hg] vs. 86 mmHg [interquartile range, 70–98 mm Hg]; P = 0.02). Enrollment in a conservative fluid-management strategy (P = 0.005) was also associated with cognitive impairment.
- It is unclear if hypoxaemia is directly responsible for cognitive impairment (though it is biologically plausible), or it is simply an association with hypoxaemia a marker of more severe disease
EVIDENCE IN TRAUMATIC BRAIN INJURY
Observational studies consistently show that hypoxaemia is associated with worse outcomes including increased mortality following severe TBI. Evidence of harm from hyperoxia is, again, less consistent.
- Davis et al, 2009
- In a registry-based retrospective analysis of 3,420 TBI patients in San Diego, TRISS calculations identified worse outcomes than predicted for both hypoxemia and extreme hyperoxemia. Logistic regression revealed an optimal PaO2 range (110 to 487 mmHg), with an independent association observed between decreased survival and both hypoxemia (OR, 0.54; 95% CI, 0.42 to 0.69; P < 0.001) and extreme hyperoxemia (OR, 0.50; 95% CI, 0.36 to 0.71; P < 0.001).
- Brenner et al, 2012
- In a retrospective cohort of 1,547 patients with traumatic brain injury at Shock Trauma in Baltimore, high PaO2 levels (> 200 mmHg) in the first 24h had significantly higher mortality and lower discharge GCS scores than patients with a normal PaO2 (P < 0.05) after controlling for other variables. Patients with low PaO2 levels (<100 mmHg) in the first 24h also had increased mortality (P < 0.05)
- Rincon et al, 2013
- a retrospective multi-centre cohort study of 1,212 ventilated TBI patients found that mortality was highest in the hypoxic (PaO2<60 mm Hg) group (224/553 [41%], crude OR, 2.3; 95% CI, 1.7 to 3.0, P < 0.0001), followed by hyperoxic (PaO2 ≥300 mm Hg) group (80/256 [32%], crude OR, 1.5; 95% CI, 1.1 to 2.5, P = 0.01), as compared to normoxia (87/403 [23%]). Multivariate analysis found that being exposed to hyperoxia was independently associated with higher in-hospital mortality (adjusted OR, 1.5; 95% CI, 1.02 to 2.4; P = 0.04).
These observational studies found either no harm, or improved outcomes, associated with hyperoxia.
- Asher et al, 2013
- a single-centre retrospective study of 193 patients with severe TBI, found that during the first 72 hours after injury PaO2 thresholds in increments of 50 mmHg between 250 and 486 mm Hg was associated with improved all-cause survival (adjusted OR 3.4; 95% CI 1.5-7.7), independent of hypocarbia or hypercarbia. In-hospital hypoxaemia was also common (24%) and was associated with mortality (survival adjusted OR, 0.46; 95% CI 0.22-0.95).
- Raj et al, 2013
- Retrospective analysis of 1,116 mechanically ventilated patients with a moderate-to-severe TBI patients from the Finnish Intensive Care Consortium database. Hyperoxemia in the first 24 hours of ICU admission after a moderate-to-severe TBI was not independently predictive of 6-month mortality.
EVIDENCE IN ISCHAEMIC CONDITIONS
- Roffe et al, SO2S trial
- this 3-armed multi-centered randomised trial of 8000 non-hypoxaemic stroke patients (yet to be published as of November 2016) found no difference in outcomes between continuous supplemental oxygen therapy, nocturnal oxygen therapy only and no supplemental oxygen therapy (therapies administered for the first 72 hours).
- Rowat et al, 2006
- Hypoxemia is common in stroke patients and hypoxemia in the first few hours after hospital admission is associated with an increased risk of death
- Stub et al, 2015
- a multicenter, prospective, randomized, controlled trial of 441 patients with STEMI found that provision of oxygen (8 L/min) is associated with greater infarct size (a secondary outcome), when compared with room air in patients without hypoxaemia. The primary outcome was negative and this study should be considered hypothesis-generating rather than practice-changing.
EVIDENCE IN COPD AND RESPIRATORY DISEASE
- Austin et al, 2010
- a randomised controlled trial of patients with an acute exacerbation of COPD found mortality is more than halved with pre-hospital oxygen therapy titrated to SpO2 88-92%, compared with high concentration oxygen therapy
CO2 retention with oxygen supplementation is not unique to COPD
- Perrin et al, 2010
- in a small randomised controlled trial, high concentration oxygen therapy causes a clinically significant increase in PtCO2 in patients presenting with severe exacerbations of asthma
- Wijesinghe et al, 2012
- in a small randomised controlled trial — similar to Perrin et al, 2010 — high concentration oxygen therapy increases the PtCO2 in patients with suspected community-acquired pneumonia
EVIDENCE IN NEONATES
- Newnam, 2014
- A systematic review found that three large multicentered, international studies (BOOST II, COT, and SUPPORT), support oxygen saturation target ranges of 87% to 94% until vascular maturation of the retina is achieved
- Two of the 3 studies reported a significant correlation between low saturation limits (85%-89%) and death in the extremely preterm population.
Oxygen saturation targets should be tailored to individual patient circumstances (see above) while avoiding potential harms from hypoxia or hyperoxia
- SpO2 monitoring is the preferred means of assessing oxygenation in routine critical care practice
- Upper and lower SpO2 limits should be specified for critically ill patients (“swim between the flags”)
- In most patients requiring oxygen therapy, SpO2 92-96% is an appropriate target
- For patients with chronic respiratory failure, SpO2 88-92% is generally appropriate
- Harms from hypoxaemia are well established in numerous patient groups and should be always avoided where possible – a potential danger of ‘tighter control’ is unplanned episodes of hypoxaemia
- The importance of hyperoxia is uncertain and is an area of ongoing research
References and Links
- CCC — Co-oximeter
- CCC — Pulse oximeter
- CCC — Blood gas analyser
- CCC — Oxygen Extraction Ratio (O2ER)
- CCC — Oxygen-Haemoglobin Dissociation Curve
- CCC — Oxygen
- CCC — Oxygen and CO2 Retention in COPD
- CCC — Tissue Oxygenation Assessment
- CCC — Hyperbaric oxygen
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- Austin MA, Wills KE, Blizzard L, et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. BMJ. 341:c5462. 2010. [pubmed]
- Bellomo R, Bailey M, Eastwood GM, et al. Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest. Critical care (London, England). 15(2):R90. 2011. [pubmed]
- Brenner M, Stein D, Hu P, Kufera J, Wooford M, Scalea T. Association between early hyperoxia and worse outcomes after traumatic brain injury. Archives of surgery (Chicago, Ill. : 1960). 147(11):1042-6. 2012. [pubmed]
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- Davis DP, Meade W, Sise MJ, et al. Both hypoxemia and extreme hyperoxemia may be detrimental in patients with severe traumatic brain injury. Journal of Neurotrauma. 26(12):2217-23. 2009. [pubmed]
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- Ferguson ND. Oxygen in the ICU: Too Much of a Good Thing? JAMA. 316(15):1553-1554. 2016. [pubmed]
- Gilbert-Kawai ET, Mitchell K, Martin D, Carlisle J, Grocott MP. Permissive hypoxaemia versus normoxaemia for mechanically ventilated critically ill patients. The Cochrane database of systematic reviews. 2014. [pubmed]
- Girardis M, Busani S, Damiani E, et al. Effect of Conservative vs Conventional Oxygen Therapy on Mortality Among Patients in an Intensive Care Unit: The Oxygen-ICU Randomized Clinical Trial. JAMA. 316(15):1583-1589. 2016. [pubmed]
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- Ihle JF, Bernard S, Bailey MJ, Pilcher DV, Smith K, Scheinkestel CD. Hyperoxia in the intensive care unit and outcome after out-of-hospital ventricular fibrillation cardiac arrest. Critical Care and Resuscitation. 15(3):186-90. 2013. [pubmed]
- Janz DR, Hollenbeck RD, Pollock JS, McPherson JA, Rice TW. Hyperoxia is associated with increased mortality in patients treated with mild therapeutic hypothermia after sudden cardiac arrest. Critical care medicine. 40(12):3135-9. 2012. [pubmed]
- Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 303(21):2165-71. 2010. [pubmed]
- Kilgannon JH, Jones AE, Parrillo JE, et al. Relationship between supranormal oxygen tension and outcome after resuscitation from cardiac arrest. Circulation. 123(23):2717-22. 2011. [pubmed]
- Lee BK, Jeung KW, Lee HY, et al. Association between mean arterial blood gas tension and outcome in cardiac arrest patients treated with therapeutic hypothermia. The American journal of emergency medicine. 32(1):55-60. 2014. [pubmed]
- Mallat J, Lazkani A, Lemyze M. Repeatability of blood gas parameters, PCO2 gap, and PCO2 gap to arterial-to-venous oxygen content difference in critically ill adult patients. Medicine. 94(3):e415. 2015. [pubmed]
- Mikkelsen ME, Christie JD, Lanken PN. The adult respiratory distress syndrome cognitive outcomes study: long-term neuropsychological function in survivors of acute lung injury. American journal of respiratory and critical care medicine. 185(12):1307-15. 2012. [pubmed]
- Newnam KM. Oxygen saturation limits and evidence supporting the targets. Advances in neonatal care. 14(6):403-9. 2014. [pubmed]
- Perrin K, Wijesinghe M, Healy B, et al. Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma. Thorax. 66(11):937-41. 2011. [pubmed]
- Raj R, Bendel S, Reinikainen M, et al. Hyperoxemia and long-term outcome after traumatic brain injury. Critical care. 17(4):R177. 2013. [pubmed]
- Rincon F, Kang J, Vibbert M, Urtecho J, Athar MK, Jallo J. Significance of arterial hyperoxia and relationship with case fatality in traumatic brain injury: a multicentre cohort study. Journal of neurology, neurosurgery, and psychiatry. 85(7):799-805. 2014. [pubmed]
- Roffe C, Nevattee T, Buttery A et al. Stroke Oxygen Study: A multi-centre, prospective, randomised, open, blinded-endpoint study to assess whether routine oxygen treatment in the first 72 hours after a stroke improves long-term outcome. http://www.so2s.co.uk/ Accessed Nov 2016
- Rowat AM, Dennis MS, Wardlaw JM. Hypoxaemia in acute stroke is frequent and worsens outcome. Cerebrovascular diseases. 21(3):166-72. 2006. [pubmed]
- Stub D, Smith K, Bernard S. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction. Circulation. 131(24):2143-50. 2015. [pubmed]
- Wijesinghe M, Perrin K, Healy B, Weatherall M, Beasley R. Randomized controlled trial of high concentration oxygen in suspected community-acquired pneumonia. Journal of the Royal Society of Medicine. 105(5):208-16. 2012. [pubmed]
- Young P, Bailey M, Bellomo R, et al. HyperOxic Therapy OR NormOxic Therapy after out-of-hospital cardiac arrest (HOT OR NOT): a randomised controlled feasibility trial. Resuscitation. 85(12):1686-91. 2014. [pubmed]
- Young PJ, Beasley RW, Capellier G, Eastwood GM, Webb SA, et al. Oxygenation targets, monitoring in the critically ill: a point prevalence study of clinical practice in Australia and New Zealand. Critical care and resuscitation. 17(3):202-7. 2015. [pubmed]
FOAM and web resources
- ANZCOR Guidelines — ANZCOR Guideline 11.6.1 – Targeted Oxygen Therapy in Adult Advanced Life Support; January 2016
- PulmCrit – Top 10 reasons pulse oximetry beats ABG for assessing oxygenation (2016)
- PulmCrit Wee — Oxygen-ICU trial: 100% isn’t an A+ (2016)
- Thoracic Society of Australia and New Zealand (TSANZ) — Oxygen Guidelines for Acute Oxygen Use in Adults; October 2015 [pdf]
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of LITFL.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of two amazing children.
On Twitter, he is @precordialthump.