Regional venous\u2013arterial CO2 to arterial\u2013venous O2 content difference ratio in experimental circulatory shock and hypoxia

Thiago Domingos Corrêa,Stephan Mathias Jakob,Adriano José Pereira,Jukka Takala

doi:10.1186/s40635-020-00353-9

Abstract

BackgroundVenous–arterial carbon dioxide (CO2) to arterial–venous oxygen (O2) content difference ratio (Cv-aCO2/Ca-vO2) > 1 is supposed to be both sensitive and specific for anaerobic metabolism. What regional hemodynamic and metabolic parameters determine the ratio has not been clarified.ObjectivesTo address determinants of systemic and renal, spleen, gut and liver Cv-aCO2/Ca-vO2.MethodsPost hoc analysis of original data from published experimental studies aimed to address effects of different fluid resuscitation strategies on oxygen transport, lactate metabolism and organ dysfunction in fecal peritonitis and endotoxin infusion, and from animals in cardiac tamponade or hypoxic hypoxia. Systemic and regional hemodynamics, blood flow, lactate uptake, carbon dioxide and oxygen-derived variables were determined. Generalized estimating equations (GEE) were fit to assess contributors to systemic and regional Cv-aCO2/Ca-vO2.ResultsMedian (range) of pooled systemic Cv-aCO2/Ca-vO2 in 64 pigs was 1.02 (0.02 to 3.84). While parameters reflecting regional lactate exchange were variably associated with the respective regional Cv-aCO2/Ca-vO2 ratios, only regional ratios were independently correlated with systemic ratio: renal Cv-aCO2 /Ca-vO2 (β = 0.148, 95% CI 0.062 to 0.234; p = 0.001), spleen Cv-aCO2/Ca-vO2 (β = 0.065, 95% CI 0.002 to 0.127; p = 0.042), gut Cv-aCO2/Ca-vO2 (β = 0.117, 95% CI 0.025 to 0.209; p = 0.013), liver Cv-aCO2/Ca-vO2 (β = − 0.159, 95% CI − 0.297 to − 0.022; p = 0.023), hepatosplanchnic Cv-aCO2/Ca-vO2 (β = 0.495, 95% CI 0.205 to 0.786; p = 0.001).ConclusionIn a mixed set of animals in different shock forms or during hypoxic injury, hepatosplanchnic Cv-aCO2/Ca-vO2 ratio had the strongest independent association with systemic Cv-aCO2/Ca-vO2, while no independent association was demonstrated for lactate or hemodynamic variables.

Highlights

Venous–arterial carbon dioxide (CO2) to arterial–venous oxygen (O2) content difference ratio (Cv-aCO2/Arterial–venous O2 content difference (Ca-vO2)) > 1 is supposed to be both sensitive and specific for anaerobic metabolism
In a mixed set of animals in different shock forms or during hypoxic injury, hepatosplanchnic Venous–arterial CO2 content difference (Cv-aCO2)/Ca-vO2 ratio had the strongest independent association with systemic Cv-aCO2/Ca-vO2, while no independent association was demonstrated for lactate or hemodynamic variables
Our study found that neither arterial lactate, nor lactate disappearance, nor whole-body venous lactate efflux are associated with Respiratory quotient (RQ), potentially suggesting that lactate may be, at least in part, associated to aerobic metabolism in the hypoxia and shock models assessed in this study

Summary

Introduction

Venous–arterial carbon dioxide (CO2) to arterial–venous oxygen (O2) content difference ratio (Cv-aCO2/Ca-vO2) > 1 is supposed to be both sensitive and specific for anaerobic metabolism. Inadequate oxygen delivery may occur with normal perfusion when arterial oxygen content is critically reduced, e.g., in severe respiratory failure or at high altitude In septic shock, both global perfusion and arterial oxygen content can be normal, but the metabolic needs may still be insufficiently met as a result of oxygen extraction and/or utilization abnormalities [2]. Both global perfusion and arterial oxygen content can be normal, but the metabolic needs may still be insufficiently met as a result of oxygen extraction and/or utilization abnormalities [2] In all of these conditions, regional blood flow may be redistributed as a consequence of central (e.g., sympathetic nervous system) and/or peripheral (e.g., nitric oxide, shear stress) adaptive mechanisms [3]. Lactate concentration can increase as a result of impaired ability of the liver to extract lactate [5] or as a consequence of increased aerobic lactate production, e.g., when epinephrine is used to stabilize hemodynamics [6]

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