TY - JOUR
T1 - Unmasking the Impact of Oxygenator-Induced Hypocapnia on Blood Lactate in Veno-Arterial Extracorporeal Membrane Oxygenation
AU - Kharnaf, Mousa
AU - Abplanalp, William A.
AU - Young, Courtney
AU - Sprague, Cassandra
AU - Rosenfeldt, Leah
AU - Smith, Reanna
AU - Wang, Dongfang
AU - Palumbo, Joseph S.
AU - Morales, David L.S.
N1 - Publisher Copyright:
Copyright © ASAIO 2024.
PY - 2024/9/1
Y1 - 2024/9/1
N2 - Extracorporeal membrane oxygenation (ECMO) is often associated with disturbances in acid/base status that can be triggered by the underlying pathology or the ECMO circuit itself. Extracorporeal membrane oxygenation is known to cause hypocapnia, but the impact of reduced partial pressure of carbon dioxide (pCO2) on biomarkers of tissue perfusion during veno-arterial (VA)-ECMO has not been evaluated. To study the impact of low pCO2 on perfusion indices in VA-ECMO, we placed Sprague–Dawley rats on an established VA-ECMO circuit using either an oxygen/carbon dioxide mixture (O2 95%, CO2 5%) or 100% O2 delivered through the oxygenator (n = 5 per cohort). Animals receiving 100% O2 developed a significant VA CO2 difference (pCO2 gap) and rising blood lactate levels that were inversely proportional to the decrease in pCO2 values. In contrast, pCO2 gap and lactate levels remained similar to pre-ECMO baseline levels in animals receiving the O2/ CO2 mixture. More importantly, there was no significant difference in venous oxygen saturation (SvO2) between the two groups, suggesting that elevated blood lactate levels observed in the rats receiving 100% O2 were a response to oxygenator induced hypocapnia and alkaline pH rather than reduced perfusion or underlying tissue hypoxia. These findings have implications in clinical and experimental extracorporeal support contexts.
AB - Extracorporeal membrane oxygenation (ECMO) is often associated with disturbances in acid/base status that can be triggered by the underlying pathology or the ECMO circuit itself. Extracorporeal membrane oxygenation is known to cause hypocapnia, but the impact of reduced partial pressure of carbon dioxide (pCO2) on biomarkers of tissue perfusion during veno-arterial (VA)-ECMO has not been evaluated. To study the impact of low pCO2 on perfusion indices in VA-ECMO, we placed Sprague–Dawley rats on an established VA-ECMO circuit using either an oxygen/carbon dioxide mixture (O2 95%, CO2 5%) or 100% O2 delivered through the oxygenator (n = 5 per cohort). Animals receiving 100% O2 developed a significant VA CO2 difference (pCO2 gap) and rising blood lactate levels that were inversely proportional to the decrease in pCO2 values. In contrast, pCO2 gap and lactate levels remained similar to pre-ECMO baseline levels in animals receiving the O2/ CO2 mixture. More importantly, there was no significant difference in venous oxygen saturation (SvO2) between the two groups, suggesting that elevated blood lactate levels observed in the rats receiving 100% O2 were a response to oxygenator induced hypocapnia and alkaline pH rather than reduced perfusion or underlying tissue hypoxia. These findings have implications in clinical and experimental extracorporeal support contexts.
KW - carbon dioxide removal
KW - extracorporeal support
KW - hypocapnia
KW - lactate
KW - venous oxygen saturation
UR - http://www.scopus.com/inward/record.url?scp=85202906475&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85202906475&partnerID=8YFLogxK
U2 - 10.1097/MAT.0000000000002191
DO - 10.1097/MAT.0000000000002191
M3 - Article
C2 - 38483814
AN - SCOPUS:85202906475
SN - 1058-2916
VL - 70
SP - 795
EP - 802
JO - ASAIO Journal
JF - ASAIO Journal
IS - 9
ER -