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Changes in tissue oxygen tension, venous saturation, and Fick‐based assessments of cardiac output during hyperoxia
Author(s) -
Perry Dorothy A.,
Thomson Lindsay M.,
Pigula Frank A.,
Polizzotti Brian D.,
DiNardo James A.,
Nedder Arthur,
Gauvreau Kimberlee,
Kheir John N.
Publication year - 2019
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/aas.13225
Subject(s) - fick principle , hyperoxia , medicine , oxygen , anesthesia , oxygen tension , cardiac output , fraction of inspired oxygen , saturation (graph theory) , oxygenation , cardiology , hemodynamics , lung , chemistry , mechanical ventilation , mathematics , organic chemistry , combinatorics
Background Hyperoxemia (arterial oxygen tension >100 mm Hg) may occur in critically ill patients and have effects on mixed venous saturation (SvO 2 ) and on Fick‐based estimates of cardiac output ( CO ). We investigated the effect of hyperoxemia on SvO 2 and on assessments of CO using the Fick equation. Methods Yorkshire swine (n = 14) were anesthetized, intubated, and paralyzed for instrumentation. SvO 2 (co‐oximetry) and tissue oxygen tension ( tPO 2 , implantable electrodes) in brain and myocardium were measured during systematic manipulation of arterial oxygen tension (PaO 2 ) using graded hyperoxia (fraction of inspired oxygen 0.21 → 0.8). Secondarily, oxygen‐ and carbon dioxide‐based estimates of CO (Fick O2 and Fick CO 2 , respectively) were compared with measurements from a flow probe placed on the aortic root. Results Independent of changes in measured oxygen delivery, cerebral and myocardial tPO 2 increased in proportion to PaO 2 , as did SvO 2 ( P < 0.001 for all). Based on mixed model analysis, each 100 mm Hg increase in PaO 2 resulted in a 4.8 ± 0.9% increase in SvO 2 under the conditions tested. Because neither measured oxygen consumption, arterial oxyhemoglobin saturation or cardiac output varied significantly during hyperoxia, changes in SvO 2 resulted in successively increasing errors in Fick O2 during hyperoxia (34% during normoxia, 72% during FiO 2 0.8). Fick CO 2 lacked the progressively worsening errors present in Fick O2 , but correlated poorly with CO . Conclusion SvO 2 acutely changes following changes in PaO 2 even absent changes in measured DO 2 . 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.