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Regional venous-arterial CO2 to arterial-venous O2 content difference ratio in experimental circulatory shock and hypoxia.

ABSTRACT: BACKGROUND: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. What regional hemodynamic and metabolic parameters determine the ratio has not been clarified. OBJECTIVES:To address determinants of systemic and renal, spleen, gut and liver Cv-aCO2/Ca-vO2. METHODS:Post 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. RESULTS:Median (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 (??=?0.148, 95% CI 0.062 to 0.234; p?=?0.001), spleen Cv-aCO2/Ca-vO2 (??=?0.065, 95% CI 0.002 to 0.127; p?=?0.042), gut Cv-aCO2/Ca-vO2 (??=?0.117, 95% CI 0.025 to 0.209; p?=?0.013), liver Cv-aCO2/Ca-vO2 (??=?-?0.159, 95% CI -?0.297 to -?0.022; p?=?0.023), hepatosplanchnic Cv-aCO2/Ca-vO2 (??=?0.495, 95% CI 0.205 to 0.786; p?=?0.001). CONCLUSION:In 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.

SUBMITTER: Correa TD

PROVIDER: S-EPMC7596113 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Regional venous-arterial CO<sub>2</sub> to arterial-venous O<sub>2</sub> content difference ratio in experimental circulatory shock and hypoxia.

Corrêa Thiago Domingos TD Pereira Adriano José AJ Takala Jukka J Jakob Stephan Mathias SM

Intensive care medicine experimental 20201029 1

<h4>Background</h4>Venous-arterial carbon dioxide (CO<sub>2</sub>) to arterial-venous oxygen (O<sub>2</sub>) content difference ratio (Cv-aCO<sub>2</sub>/Ca-vO<sub>2</sub>) > 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.<h4>Objectives</h4>To address determinants of systemic and renal, spleen, gut and liver Cv-aCO<sub>2</sub>/Ca-vO<sub>2</sub>.<h4>Methods</h4>Post hoc analysi ...[more]

PMID: 33119834

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Project description:The purpose of the study was to evaluate the behavior of the venous-to-arterial CO2 tension difference (ΔPCO2) over the arterial-to-venous oxygen content difference (ΔO2) ratio (ΔPCO2/ΔO2) and the difference between venous-to-arterial CO2 content calculated with the Douglas' equation (ΔCCO2D) over ΔO2 ratio (ΔCCO2D/ΔO2) and their abilities to reflect the occurrence of anaerobic metabolism in two experimental models of tissue hypoxia: ischemic hypoxia (IH) and hypoxic hypoxia (HH). We also aimed to assess the influence of metabolic acidosis and Haldane effects on the PCO2/CO2 content relationship. In a vascularly isolated, innervated dog hindlimb perfused with a pump-membrane oxygenator system, the oxygen delivery (DO2) was lowered in a stepwise manner to decrease it beyond critical DO2 (DO2crit) by lowering either arterial PO2 (HH-model) or flow (IH-model). Twelve anesthetized and mechanically ventilated dogs were studied, 6 in each model. Limb DO2, oxygen consumption ([Formula: see text]), ΔPCO2/ΔO2, and ΔCCO2D/ΔO2 were obtained every 15 min. Beyond DO2crit, [Formula: see text] decreased, indicating dysoxia. ΔPCO2/ΔO2, and ΔCCO2D/ΔO2 increased significantly only after reaching DO2crit in both models. At DO2crit, ΔPCO2/ΔO2 was significantly higher in the HH-model than in the IH-model (1.82 ± 0.09 vs. 1.39 ± 0.06, p = 0.002). At DO2crit, ΔCCO2D/ΔO2 was not significantly different between the two groups (0.87 ± 0.05 for IH vs. 1.01 ± 0.06 for HH, p = 0.09). Below DO2crit, we observed a discrepancy between the behavior of the two indices. In both models, ΔPCO2/ΔO2 continued to increase significantly (higher in the HH-model), whereas ΔCCO2D/ΔO2 tended to decrease to become not significantly different from its baseline in the IH-model. Metabolic acidosis significantly influenced the PCO2/CO2 content relationship, but not the Haldane effect. ΔPCO2/ΔO2 was able to depict the occurrence of anaerobic metabolism in both tissue hypoxia models. However, at very low DO2 values, ΔPCO2/ΔO2 did not only reflect the ongoing anaerobic metabolism; it was confounded by the effects of metabolic acidosis on the CO2-hemoglobin dissociation curve, and then it should be interpreted with caution.

Project description:OBJECTIVE:To evaluate the prognostic value of the difference between peripheral venous and arterial partial pressure of carbon dioxide in patients with septic shock following early resuscitation. METHODS:This prospective study was conducted among the patients with septic shock treated in our department during the period from May, 2017 to May, 2018. Peripheral venous, peripheral arterial and central venous blood samples were collected simultaneously and analyzed immediately at bedside after 6-h bundle treatment. Arterial blood lactate concentration (Lac) and the arterial (PaCO2), peripheral venous (PpvCO2) and central venous partial pressure of carbon dioxide (PcvCO2) were recorded. The differences between PpvCO2 and PaCO2 (Ppv-aCO2) and between PcvCO2 and PaCO2 (Pcv-aCO2) were calculated. Pearson correlation analysis was used to test the agreement between Pcv-aCO2 and Ppv-aCO2. Multivariable logistic regression analysis was performed to analyze the possible risk factors for 28-day mortality, and the receiver-operating characteristic curve (ROC) was plotted to assess the prognostic values of these factors for 28-day mortality. RESULTS:A total of 62 patients were enrolled in this study, among who 35 survived and 27 died during the 28-day period. Compared with the survivor group, the patients died within 28 days showed significantly higher Acute Physiology and Chronic Health Evaluation ? (APACHE ?) score (24.2±6.0 vs 20.5±4.9, P=0.011), sequential organ failure assessment (SOFA) score (14.9±4.7 vs 12.2±4.5, P=0.027), PcvaCO2 (5.5±1.6 vs 7.1±1.7, P < 0.001), PpvaCO2 (7.1±1.8 vs 10.0±2.7, P < 0.001), and arterial lactate level (3.3±1.2 vs 4.2±1.3, P=0.003) after 6-h bundle treatment. Pearson correlation analysis showed that Ppv-aCO2 was significantly correlated with Pcv-aCO2 (r=0.897, R2= 0.805, P < 0.001). Multiple logistic regression analysis identified Ppv-aCO2 (?=0.625, P=0.001, OR=1.869, 95% CI: 1.311-2.664) and lactate level (?=0.584, P=0.041, OR=1.794, 95%CI: 1.024-3.415) as the independent risk factors for 28-day mortality. The maximum area under the ROC (AUC) of Ppv-aCO2 was 0.814 (95%CI: 0.696- 0.931, P < 0.001), and at the best cut- off value of 9.05 mmHg, Ppv-aCO2 had a sensitivity of 70.4% and a specificity of 88.6% for predicting 28-day mortality. The AUC of lactate level was 0.732 (95%CI: 0.607-0.858, P=0.002), and its sensitivity for predicting 28-day mortality was 70.4% and the specificity was 74.3% at the best cut-off value of 3.45 mmol/L; The AUC of Pcv-aCO2 was 0.766 (95%CI: 0.642-0.891, P < 0.001), and its sensitivity was 66.7% and the specificity was 80.0% at the best cut-off value of 7.05 mmHg. CONCLUSIONS:A high Ppv-aCO2 after early resuscitation of septic shock is associated with poor outcomes. Ppv-aCO2 is well correlated with Pcv-aCO2 and can be used as an independent indicator for predicting 28-day mortality in patients with septic shock.

Project description:BackgroundGuidelines recommend a restrictive red blood cell transfusion strategy based on hemoglobin (Hb) concentrations in critically ill patients. We hypothesized that the arterial-venous oxygen difference (A-V O2diff), a surrogate for the oxygen delivery to consumption ratio, could provide a more personalized approach to identify patients who may benefit from transfusion.MethodsA prospective observational study including 177 non-bleeding adult patients with a Hb concentration of 7.0-10.0 g/dL within 72 h after ICU admission. The A-V O2diff, central venous oxygen saturation (ScvO2), and oxygen extraction ratio (O2ER) were noted when a patient's Hb was first within this range. Transfusion decisions were made by the treating physician according to institutional policy. We used the median A-V O2diff value in the study cohort (3.7 mL) to classify the transfusion strategy in each patient as "appropriate" (patient transfused when the A-V O2diff > 3.7 mL or not transfused when the A-V O2diff ≤ 3.7 mL) or "inappropriate" (patient transfused when the A-V O2diff ≤ 3.7 mL or not transfused when the A-V O2diff > 3.7 mL). The primary outcome was 90-day mortality.ResultsPatients managed with an "appropriate" strategy had lower mortality rates (23/96 [24%] vs. 36/81 [44%]; p = 0.004), and an "appropriate" strategy was independently associated with reduced mortality (hazard ratio [HR] 0.51 [95% CI 0.30-0.89], p = 0.01). There was a trend to less acute kidney injury with the "appropriate" than with the "inappropriate" strategy (13% vs. 26%, p = 0.06), and the Sequential Organ Failure Assessment (SOFA) score decreased more rapidly (p = 0.01). The A-V O2diff, but not the ScvO2, predicted 90-day mortality in transfused (AUROC = 0.656) and non-transfused (AUROC = 0.630) patients with moderate accuracy. Using the ROC curve analysis, the best A-V O2diff cutoffs for predicting mortality were 3.6 mL in transfused and 3.5 mL in non-transfused patients.ConclusionsIn anemic, non-bleeding critically ill patients, transfusion may be associated with lower 90-day mortality and morbidity in patients with higher A-V O2diff.Trial registrationClinicalTrials.gov, NCT03767127. Retrospectively registered on 6 December 2018.

Project description:BackgroundThe origin of low frequency cerebral hemodynamic fluctuations (CHF) in the resting state remains unknown. Breath-by breath O2-CO2 exchange ratio (bER) has been reported to correlate with the cerebrovascular response to brief breath hold challenge at the frequency range of 0.008-0.03Hz in healthy adults. bER is defined as the ratio of the change in the partial pressure of oxygen (ΔPO2) to that of carbon dioxide (ΔPCO2) between end inspiration and end expiration. In this study, we aimed to investigate the contribution of respiratory gas exchange (RGE) metrics (bER, ΔPO2 and ΔPCO2) to low frequency CHF during spontaneous breathing.MethodsTwenty-two healthy adults were included. We used transcranial Doppler sonography to evaluate CHF by measuring the changes in cerebral blood flow velocity (ΔCBFv) in bilateral middle cerebral arteries. The regional CHF were mapped with blood oxygenation level dependent (ΔBOLD) signal changes using functional magnetic resonance imaging. Temporal features and frequency characteristics of RGE metrics during spontaneous breathing were examined, and the simultaneous measurements of RGE metrics and CHF (ΔCBFv and ΔBOLD) were studied for their correlation.ResultsWe found that the time courses of ΔPO2 and ΔPCO2 were interdependent but not redundant. The oscillations of RGE metrics were coherent with resting state CHF at the frequency range of 0.008-0.03Hz. Both bER and ΔPO2 were superior to ΔPCO2 in association with CHF while CHF could correlate more strongly with bER than with ΔPO2 in some brain regions. Brain regions with the strongest coupling between bER and ΔBOLD overlapped with many areas of default mode network including precuneus and posterior cingulate.ConclusionAlthough the physiological mechanisms underlying the strong correlation between bER and CHF are unclear, our findings suggest the contribution of bER to low frequency resting state CHF, providing a novel insight of brain-body interaction via CHF and oscillations of RGE metrics.

Project description:BackgroundMean circulatory filling pressure (Pmcf) provides information on stressed volume and is crucial for maintaining venous return. This study investigated the Pmcf and other determinants of venous return in dysrhythmic and asphyxial circulatory shock and arrest.MethodsTwenty Landrace/Large-White piglets were allocated into two groups of 10 animals each. In the dysrhythmic group, ventricular fibrillation was induced with a 9 V cadmium battery, while in the asphyxia group, cardiac arrest was induced by stopping and disconnecting the ventilator and clamping the tracheal tube at the end of exhalation. Mean circulatory filling pressure was calculated using the equilibrium mean right atrial pressure at 5-7.5 s after the onset of cardiac arrest and then every 10 s until 1 min post-arrest. Successful resuscitation was defined as return of spontaneous circulation (ROSC) with a MAP of at least 60 mmHg for a minimum of 5 min.ResultsAfter the onset of asphyxia, a ΔPmca increase of 0.004 mmHg, 0.01 mmHg, and 1.26 mmHg was observed for each mmHg decrease in PaO2, each mmHg increase in PaCO2, and each unit decrease in pH, respectively. Mean Pmcf value in the ventricular fibrillation and asphyxia group was 14.81 ± 0.5 mmHg and 16.04 ± 0.6 mmHg (p < 0.001) and decreased by 0.031 mmHg and 0.013 mmHg (p < 0.001), respectively, for every additional second passing after the onset of cardiac arrest. With the exception of the 5-7.5 s time interval, post-cardiac arrest right atrial pressure was significantly higher in the asphyxia group. Mean circulatory filling pressure at 5 to 7.5 s after cardiac arrest predicted ROSC in both groups, with a cut-off value of 16 mmHg (AUC = 0.905, p < 0.001).ConclusionMean circulatory filling pressure was higher in hypoxic hypercapnic conditions and decreased at a lower rate after cardiac arrest compared to normoxemic and normocapnic state. A Pmcf cut-off point of 16 mmHg at 5-7.5 s after cardiac arrest can highly predict ROSC.

Dataset Information

Regional venous-arterial CO2 to arterial-venous O2 content difference ratio in experimental circulatory shock and hypoxia.

Publications

Regional venous-arterial CO<sub>2</sub> to arterial-venous O<sub>2</sub> content difference ratio in experimental circulatory shock and hypoxia.

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