Changes in tissue oxygen tension, venous saturation, and Fick-based assessments of cardiac output during hyperoxia.

Abstract

Hyperoxemia (arterial oxygen tension >100 mm Hg) may occur in critically ill patients and have effects on mixed venous saturation (SvO₂ ) and on Fick-based estimates of cardiac output (CO). We investigated the effect of hyperoxemia on SvO₂ and on assessments of CO using the Fick equation. Yorkshire swine (n = 14) were anesthetized, intubated, and paralyzed for instrumentation. SvO₂ (co-oximetry) and tissue oxygen tension (tPO₂ , implantable electrodes) in brain and myocardium were measured during systematic manipulation of arterial oxygen tension (PaO₂ ) using graded hyperoxia (fraction of inspired oxygen 0.21 → 0.8). Secondarily, oxygen- and carbon dioxide-based estimates of CO (Fick_O2 and Fick_CO₂ , respectively) were compared with measurements from a flow probe placed on the aortic root. Independent of changes in measured oxygen delivery, cerebral and myocardial tPO₂ increased in proportion to PaO₂ , as did SvO₂ (P < 0.001 for all). Based on mixed model analysis, each 100 mm Hg increase in PaO₂ resulted in a 4.8 ± 0.9% increase in SvO₂ under the conditions tested. Because neither measured oxygen consumption, arterial oxyhemoglobin saturation or cardiac output varied significantly during hyperoxia, changes in SvO₂ resulted in successively increasing errors in Fick_O2 during hyperoxia (34% during normoxia, 72% during FiO₂ 0.8). Fick_CO₂ lacked the progressively worsening errors present in Fick_O2 , but correlated poorly with CO. SvO₂ acutely changes following changes in PaO₂ even absent changes in measured DO₂ . This may lead to errors in Fick_O2 estimates of CI. Further work is necessary to understand the impact of this phenomenon in disease states.