scholarly journals Non-invasive capnodynamic mixed venous oxygen saturation during major changes in oxygen delivery

Author(s):  
Anders Svedmyr ◽  
Mark Konrad ◽  
Mats Wallin ◽  
Magnus Hallbäck ◽  
Per-Arne Lönnqvist ◽  
...  

AbstractMixed venous oxygen saturation (SvO2) is an important variable in anesthesia and intensive care but currently requires pulmonary artery catheterization. Recently, non-invasive determination of SvO2 (Capno-SvO2) using capnodynamics has shown good agreement against CO-oximetry in an animal model of modest hemodynamic changes. The purpose of the current study was to validate Capno-SvO2 against CO-oximetry during major alterations in oxygen delivery. Furthermore, evaluating fiberoptic SvO2 for its response to the same challenges. Eleven mechanically ventilated pigs were exposed to oxygen delivery changes: increased inhaled oxygen concentration, hemorrhage, crystalloid and blood transfusion, preload reduction and dobutamine infusion. Capno-SvO2 and fiberoptic SvO2 recordings were made in parallel with CO-oximetry. Respiratory quotient, needed for capnodynamic SvO2, was measured by analysis of mixed expired gases. Agreement of absolute values between CO-oximetry and Capno-SvO2 and fiberoptic SvO2 respectively, was assessed using Bland–Altman plots. Ability of Capno- SvO2 and fiberoptic SvO2 to detect change compared to CO-oximetry was assessed using concordance analysis. The interventions caused significant hemodynamic variations. Bias between Capno-SvO2 and CO-oximetry was + 3% points (95% limits of agreements – 7 to + 13). Bias between fiberoptic SvO2 and CO-oximetry was + 1% point, (95% limits of agreements − 7 to + 9). Concordance rate for Capno-SvO2 and fiberoptic SvO2 vs. CO-oximetry was 98% and 93%, respectively. Capno-SvO2 generates absolute values close to CO-oximetry. The performance of Capno-SvO2 vs. CO-oximetry was comparable to the performance of fiberoptic SvO2 vs. CO-oximetry. Capno-SvO2 appears to be a promising tool for non-invasive SvO2 monitoring.

Author(s):  
Stephan M. Jakob ◽  
Jukka Takala

Adequate oxygen delivery is crucial for organ survival. The main determinants of oxygen delivery are cardiac output, haemoglobin concentration, and arterial oxygen saturation. The adequacy of oxygen delivery also depends on oxygen consumption, which may vary widely. Mixed venous oxygen saturation reflects the amount of oxygen not extracted by the tissues, and therefore provides useful information on the relationship between oxygen delivery and oxygen needs. If not in balance, tissue hypoxia may ensue and arterial lactate concentration increases. This occurs at higher oxygen delivery rates in acute compared with chronic diseases where metabolic adaptions often occur. Arterial and mixed venous oxygen saturation are related to each other. The influence of mixed venous saturation on arterial saturation increases with an increasing intrapulmonary shunt. This chapter discusses interactions between the components of oxygen transport and how they can be evaluated. Various methods for measuring tissue oxygenation and oxygen consumption are also presented, together with their limitations.


2018 ◽  
Vol 97 (2) ◽  
Author(s):  
Karel Van Keer ◽  
Jan Van Keer ◽  
João Barbosa Breda ◽  
Vahid Nassiri ◽  
Johan Van Cleemput ◽  
...  

Author(s):  
Hans Tregear ◽  
Brigid C. Flynn

This chapter evaluates the importance of identifying the oxygen delivery and oxygen consumption balance in critically ill patients. Mixed venous oxygen saturation is a valuable marker of oxygen consumption and delivery in an intensive care unit patient. Organ perfusion can be improved by optimizing all components of the oxygen delivery calculation and decreasing oxygen consumption, if indicated. Several tools that aid in this assessment include pulmonary artery catheter–derived mixed venous oxygen saturation, central venous line–derived central venous saturation, cardiac ultrasonography, and laboratory values such as the arterial blood gas and lactate levels. The chapter also discusses hyperlactatemia. Hyperlactatemia can be due to anaerobic metabolism (type A lactic acidosis) or aerobic metabolism (type B lactic acidosis).


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