36 A. Saini et al.: J Extra Corpor Technol 2026, 58, 32 – 38
Figure 1. Scatter plot of patient survival by severity of hyperoxia. Each dot represents an individual patient, with survivors in red and non-survivors in black. The colored dashed lines represent the PaO 2 threshold levels of 100( red), 200( blue), and 300( green).
Table
3. Outcomes of patients undergoing VA – ECLS using a univariable and multivariable regression analysis.
Variables |
OR( 95 % CI) |
p-value |
aOR a( 95 % CI) |
Adjusted p-value |
Mortality Mild vs Ref. |
1.2( 0.6 – 2.3) |
0.43 |
1.3( 0.6 – 2.8) |
0.66 |
Moderate vs Ref. |
1.2( 0.6 – 2.5) |
0.47 |
1.3( 0.6 – 3.1) |
0.70 |
Severe vs Ref. |
2.7( 1.0 – 7.4) |
0.04 |
2.5( 0.9 – 7.4) |
0.10 |
Any Cardiovascular or Renal complication |
Mild vs Ref. |
0.9( 0.6 – 2.3) |
0.12 |
0.8( 0.4 – 2.4) |
0.06 |
Moderate vs Ref. |
0.8( 0.6 – 2.5) |
0.12 |
0.9( 0.3 – 2.4) |
0.23 |
Severe vs Ref. |
4.3( 0.9 – 20.7) |
0.04 |
4.6( 0.9 – 23.0) |
0.03 |
Stage II / III AKI ** Mild vs Ref. |
0.9( 0.4 – 2.1) |
0.16 |
0.9( 0.4 – 2.4) |
0.19 |
Moderate vs Ref. |
0.8( 0.3 – 1.9) |
0.09 |
0.9( 0.3 – 2.4) |
0.14 |
Severe vs Ref. |
6.5( 0.8 – 53.9) |
0.06 |
6.2( 0.7 – 53.5) |
0.07 |
Reference group = Normoxia( PaO 2 100). Mild Hyperoxia( PaO 2 = 101 – 200 mmHg); Moderate Hyperoxia( PaO 2 = 201 – 300 mmHg); Severe Hyperoxia( PaO 2 > 300 mmHg). ** Stage II AKI: Stage 2: serum creatinine increase of 2 – 2.9 times baseline, or UO < 0.5 mL / kg / h for 12 h; Stage III AKI: serum creatinine increase 3 times baseline or 4 mg / dL, or UO < 0.3 mL / kg / h for 24 h or anuria 12 h, or need for renal replacement therapy. a Adjusted for age group, BSA, indication for ECLS.
functional status at discharge was noted based on hyperoxia severity.
Our study adds to the growing body of literature on the impact of early hyperoxia on outcomes in patients undergoing VA – ECLS. The first 48 h after initiating VA-ECLS are often characterized by a profound systemic inflammatory response, which can be exacerbated by hyperoxia. This early phase of ECLS is therefore a period of significant vulnerability to hyperoxia mediated organ injury. Our findings suggest a potential threshold effect with PaO 2 greater than 300 mmHg, associated with adverse outcomes. The duration of exposure above this threshold may also play a role, but quantifying this clinically remains challenging. Despite technological refinements, mortality among patients supported by VA – ECLS remains high. Identifying modifiable risk factors such as hyperoxia is crucial for improving outcomes. Mitigating exposure to hyperoxia remains an important target for intervention. In the absence of robust literature, PaO 2 targets vary across centers and among providers. There is significant heterogeneity in the definition of hyperoxia and the thresholds at which its deleterious effects manifest. Therefore, a collaborative effort to standardize PaO 2 targets during VA – ECLS and prospectively evaluate its impact on outcomes is warranted.
Limitations
Our study is limited by its single-center retrospective design. The PaO 2 targets on ECLS varied based on the provider’ s discretion. Although PaO 2 measurements were obtained