TY - JOUR
T1 - Extracorporeal Membrane Oxygenation Physiological Factors Influence Pulse Oximetry and Arterial Oxygen Saturation Discrepancies
AU - HERALD group
AU - Kalra, Andrew
AU - Shou, Benjamin L.
AU - Zhao, David
AU - Wilcox, Christopher
AU - Keller, Steven P.
AU - Kim, Bo Soo
AU - Whitman, Glenn J.R.
AU - Cho, Sung Min
AU - Leng, Albert
AU - Geeza, Andrew
AU - Menta, Arjun Kumar
AU - Akbar, Armaan F.
AU - Brodie, Daniel
AU - Hager, David
AU - Alejo, Diane
AU - Bush, Errol L.
AU - Rando, Hannah J.
AU - Flaster, Harry
AU - Chinedozi, Ifeanyi David
AU - Hwang, Jaeho
AU - Kim, Jiah
AU - Kang, Jin Kook
AU - Capili, Karlo
AU - Sussman, Marc
AU - Mendez-Tellez, Pedro Alejandro
AU - Sun, Philip
AU - Stephens, R. Scott
AU - Rojas, Ramon
AU - Stephen, Scott
AU - Khanduja, Shivalika
AU - Kapoor, Shrey
AU - Feng, Chengyuan Alex
AU - Brown, Trish
AU - Darby, Zachary
N1 - Publisher Copyright:
© 2024 The Society of Thoracic Surgeons
PY - 2024/6
Y1 - 2024/6
N2 - Background: Cannulation strategy, vasopressors, and hemolysis are important physiological factors that influence hemodynamics in extracorporeal membrane oxygenation (ECMO). We hypothesized these factors influence the discrepancy between oxygen saturation measured by pulse oximetry (SpO2) and arterial blood gas (SaO2) in patients on ECMO. Methods: We retrospectively analyzed adults (aged ≥18 years) on venoarterial or venovenous ECMO at a tertiary academic ECMO center. SpO2−SaO2 pairs with oxygen saturation ≥70% and measured within 10 minutes were included. Occult hypoxemia was defined as SaO2 ≤88% with a time-matched SpO2 ≥92%. Adjusted linear mixed-effects modeling was used to assess the SpO2−SaO2 discrepancy with preselected demographics and time-matched laboratory variables. Vasopressor use was quantified by vasopressor dose equivalences. Results: Of 139 venoarterial-ECMO and 88 venovenous-ECMO patients, we examined 20,053 SpO2−SaO2 pairs. The SpO2−SaO2 discrepancy was greater in venovenous-ECMO (1.15%) vs venoarterial-ECMO (−0.35%, P < .001). Overall, 81 patients (35%) experienced occult hypoxemia during ECMO. Occult hypoxemia was more common in venovenous-ECMO (65%) than in venoarterial-ECMO (17%, P < .001). In linear mixed-effects modeling, SpO2 underestimated SaO2 by 9.48% in central vs peripheral venoarterial-ECMO (95% CI, −17.1% to −1.79%; P = .02). Higher vasopressor dose equivalences significantly worsened the SpO2−SaO2 discrepancy (P < .001). In linear mixed-effects modeling, SpO2 overestimated SaO2 by 25.43% in single lumen–cannulated vs double lumen–cannulated venovenous-ECMO (95% CI, 5.27%-45.6%; P = .03). Higher vasopressor dose equivalences and lactate dehydrogenase levels significantly worsened the SpO2−SaO2 discrepancy (P < .001). Conclusions: Venovenous-ECMO patients are at higher risk for occult hypoxemia compared with venoarterial-ECMO. A higher vasopressor requirement and different cannulation strategies (central venoarterial-ECMO; single-lumen venovenous-ECMO) were significant factors for clinically significant SpO2−SaO2 discrepancy in both ECMO modes.
AB - Background: Cannulation strategy, vasopressors, and hemolysis are important physiological factors that influence hemodynamics in extracorporeal membrane oxygenation (ECMO). We hypothesized these factors influence the discrepancy between oxygen saturation measured by pulse oximetry (SpO2) and arterial blood gas (SaO2) in patients on ECMO. Methods: We retrospectively analyzed adults (aged ≥18 years) on venoarterial or venovenous ECMO at a tertiary academic ECMO center. SpO2−SaO2 pairs with oxygen saturation ≥70% and measured within 10 minutes were included. Occult hypoxemia was defined as SaO2 ≤88% with a time-matched SpO2 ≥92%. Adjusted linear mixed-effects modeling was used to assess the SpO2−SaO2 discrepancy with preselected demographics and time-matched laboratory variables. Vasopressor use was quantified by vasopressor dose equivalences. Results: Of 139 venoarterial-ECMO and 88 venovenous-ECMO patients, we examined 20,053 SpO2−SaO2 pairs. The SpO2−SaO2 discrepancy was greater in venovenous-ECMO (1.15%) vs venoarterial-ECMO (−0.35%, P < .001). Overall, 81 patients (35%) experienced occult hypoxemia during ECMO. Occult hypoxemia was more common in venovenous-ECMO (65%) than in venoarterial-ECMO (17%, P < .001). In linear mixed-effects modeling, SpO2 underestimated SaO2 by 9.48% in central vs peripheral venoarterial-ECMO (95% CI, −17.1% to −1.79%; P = .02). Higher vasopressor dose equivalences significantly worsened the SpO2−SaO2 discrepancy (P < .001). In linear mixed-effects modeling, SpO2 overestimated SaO2 by 25.43% in single lumen–cannulated vs double lumen–cannulated venovenous-ECMO (95% CI, 5.27%-45.6%; P = .03). Higher vasopressor dose equivalences and lactate dehydrogenase levels significantly worsened the SpO2−SaO2 discrepancy (P < .001). Conclusions: Venovenous-ECMO patients are at higher risk for occult hypoxemia compared with venoarterial-ECMO. A higher vasopressor requirement and different cannulation strategies (central venoarterial-ECMO; single-lumen venovenous-ECMO) were significant factors for clinically significant SpO2−SaO2 discrepancy in both ECMO modes.
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U2 - 10.1016/j.athoracsur.2023.09.019
DO - 10.1016/j.athoracsur.2023.09.019
M3 - Article
C2 - 37748529
AN - SCOPUS:85174028609
SN - 0003-4975
VL - 117
SP - 1221
EP - 1228
JO - Annals of Thoracic Surgery
JF - Annals of Thoracic Surgery
IS - 6
ER -