Correspondence  |   February 2018
Avoidance of Hyperoxemia during Cardiopulmonary Bypass: Why Does Pathophysiology Not Always Translate into Clinical Outcome?
Author Notes
  • University of Manitoba, Winnipeg, Manitoba, Canada (H.P.G.). hgrocott@sbgh.mb.ca
  • This letter was sent to the author of the original article referenced above, who declined to respond.—Evan D. Kharasch, M.D., Ph.D., Editor-in-Chief.
    This letter was sent to the author of the original article referenced above, who declined to respond.—Evan D. Kharasch, M.D., Ph.D., Editor-in-Chief.×
  • (Accepted for publication October 26, 2017.)
    (Accepted for publication October 26, 2017.)×
Article Information
Correspondence
Correspondence   |   February 2018
Avoidance of Hyperoxemia during Cardiopulmonary Bypass: Why Does Pathophysiology Not Always Translate into Clinical Outcome?
Anesthesiology 2 2018, Vol.128, 419. doi:10.1097/ALN.0000000000001990
Anesthesiology 2 2018, Vol.128, 419. doi:10.1097/ALN.0000000000001990
The safety of hyperoxemia during cardiopulmonary bypass (CPB) has long been debated, with some evidence suggesting it induces vasoconstriction that may reduce organ (e.g., myocardial, kidney) perfusion.1  Even though the mechanism of this purported hyperoxic vasoconstriction is only partially understood, the production of reactive oxygen species (ROS) seems to play a pivotal role. Nevertheless, despite the excessive production of ROS enhancing ischemia/reperfusion (IR) injury, recent studies2,3  have thus far failed to demonstrate any relationship between avoidance of hyperoxemia during CPB and clinical outcomes. So why do apparently obvious pathologic mechanisms fail to translate into clinical outcome?
First Page Preview
First page PDF preview
First page PDF preview ×
View Large