Harmful Effects of Hyperoxia in Postcardiac Arrest, Sepsis, Traumatic Brain Injury, or Stroke: The Importance of Individualized Oxygen Therapy in Critically Ill Patients
Table 1
Some recent clinical studies on the risks of hyperoxia after cardiac arrest or myocardial infarction, in traumatic brain injury, stroke, sepsis, and mixed ICU patients.
Prospective, randomized, controlled trial, 9 hospitals, 441 patients with STEMI
Patients with an SpO2 > 94% were randomized to receive 8 L/min of oxygen or no supplemental oxygen from arrival of paramedics until transfer to the cardiac care unit
An increased rate of recurrent myocardial infarction, an increase in the frequency of cardiac arrhythmias, and an increase in myocardial infarct size at 6 months on magnetic resonance imaging in the supplement group
Retrospective analysis of a high-resolution database, single-centre, 184 patients postcardiac arrest
Mean hourly exposure in first 24 h. Normoxia: PaO2 60–100 mmHg; Moderate hyperoxia: PaO2 101–299 mmHg; Severe hyperoxia: PaO2 300 mmHg
Severe hyperoxia was associated with decreased survival (OR 0.83 [0.69–0.99] per hour exposure); moderate hyperoxia was not associated with survival but with improved SOFA score 24 h (OR 0.92 [0.87–0.98])
Conservative group had a shorter ICU length of stay; no difference in the proportion of survivors discharged from hospital with good neurological outcome compared to conventional group
A PaO2 value of 110–487 mmHg was considered optimal. Extreme hyperoxia had an independent association with decreased survival (OR 0.50 [0.36, 0.71]) compared to optimal range
Retrospective study, single-centre, 1547 severe TBI patients
Mean PaO2 in first 24 h hospital admission: Hyperoxia: PaO2 > 200 mmHg Normoxia: PaO2 100–200 mmHg
Both low and high PaO2 had increased mortality. Patients with hyperoxia had higher hospital mortality (OR 1.50 [1.15–1.97]) and lower discharge GCS scores at discharge (OR 1.52 [1.18–1.96])
PaO2 AUC by observation time until delayed cerebral ischemia (DCI). Hyperoxia: PaO2 ≥ 173 mmHg (upper quartile)
Hyperoxia group had a higher incidence of DCI (OR 3.16 [1.69 to 5.92]) and poor outcome (modified Rankin Scale 4–6 at 3 months after subarachnoid haemorrhage) (OR 2.30 [1.03 to 5.12])
Retrospective analysis using 2 databases, 432 ventilated patients (subarachnoid haemorrhage)
Time-weighted average PaO2 during the first 24 hours Low PaO2 < 97.5 mmHg; Intermediate PaO2 97.5–150 mmHg; High PaO2 >150 mmHg
Patients with an unfavorable outcome had significantly higher PaO2, but high PaO2 has no effect on 3-month neurological outcomes (OR 1.09 [0.61–1.97]) or mortality (OR 0.73 [0.38–1.40])
Worst PaO2 in first 24 h. Hyperoxia: PaO2 ≥ 123 mmHg (upper quintile) compared with PaO2 between 67 and 80 mmHg
In-hospital mortality was linearly related to FiO2 value and had a U-shaped relationship with PaO2. Hyperoxia had a higher mortality (OR 1.23 [1.13–1.34])
First PaO2 at ICU admission Mild hyperoxia: PaO2 120–200 mmHg Severe hyperoxia: PaO2 > 200 mmHg
Severe hyperoxia was associated with higher mortality rates and fewer ventilator-free days in comparison to both mild hyperoxia and normoxia Time spent in hyperoxia had a linear and positive relationship with hospital mortality
OR: odds ratio; SOFA: sequential organ failure assessment; ROSC: return of spontaneous circulation; DIC: delayed cerebral ischemia; AUC: area under the curve; STEMI: ST-segment elevated myocardial infarction.