Objective: The central venousarterial carbon dioxide pressure to arterial-central venous oxygen content ratio (Pcv-aCO2/Ca-cvO2) is frequently used as a surrogate for tissue oxygenation. We aimed to identify and synthesize literature and quality of evidence supporting Pcv-aCO2/Ca-cvO2 as a predictor of mortality in critically ill patients compared with lactate.
Methods: We searched several databases for studies measuring Pcv-aCO2/Ca-cvO2 in critically ill patients.
The central venous minus arterial carbon dioxide pressure to arterial minus central venous oxygen content ratio (Pcv-aCO2/Ca-cvO2) has been proposed as a surrogate for respiratory quotient and an indicator of tissue oxygenation. Some small observational studies have found that a Pcv-aCO2/Ca-cvO2 > 1.4 was associated with hyperlactatemia, oxygen supply dependency, and increased mortality.
View Article and Find Full Text PDFJ Crit Care
October 2019
Purpose: To characterize the microvascular effects of a brief period of hyperoxia, in patients with septic shock and in healthy volunteers.
Materials And Methods: In 20 patients with septic shock, we assessed systemic hemodynamics, sublingual microcirculation by SDF-videomicroscopy, and skin perfusion by capillary refill time (CRT), central-peripheral temperature (ΔT°), and perfusion index. Measurements were performed at baseline and after 5 min of inspired oxygen fraction of 1.
Background: The identification of anaerobic metabolism in critically ill patients is a challenging task. Observational studies have suggested that the ratio of venoarterial PCO (PCO) to arteriovenous oxygen content difference (CO) might be a good surrogate for respiratory quotient (RQ). Yet PCO/CO might be increased by other factors, regardless of anaerobic metabolism.
View Article and Find Full Text PDFThe alterations in O2 extraction in hemodilution have been linked to fast red blood cell (RBC) velocity, which might affect the complete release of O2 from Hb. Fast RBC velocity might also explain the normal mucosal-arterial Pco2 (ΔPco2). Yet sublingual and intestinal microcirculation have not been completely characterized in extreme hemodilution.
View Article and Find Full Text PDFPurpose: The aims of this study are to determine the general relationship of perfused vessel density (PVD) to mortality and organ dysfunctions and to explore if patients in the lowest quartile of distribution for this parameter present a higher risk of bad outcome and to identify systemic hemodynamic and perfusion variables that enhances the probability of finding a severe underlying microvascular dysfunction.
Materials And Methods: This is a retrospective multicenter study including 122 septic shock patients participating in 7 prospective clinical trials on which at least 1 sublingual microcirculatory assessment was performed during early resuscitation.
Results: Perfused vessel density was significantly related to organ dysfunctions and mortality, but this effect was largely explained by patients in the lowest quartile of distribution for PVD (P = .
Objective: To compare systemic hemodynamics with microcirculatory changes at different vascular beds during progressive hemorrhage.
Setting: University-based research laboratory.
Subjects: Twelve anesthetized, mechanically ventilated sheep.
Objective: To test the hypothesis that persistent villi hypoperfusion explains intramucosal acidosis after endotoxemic shock resuscitation.
Design: Controlled experimental study.
Setting: University-based research laboratory.
Objective: To test the hypothesis that levosimendan increases systemic and intestinal oxygen delivery (DO(2)) and prevents intramucosal acidosis in septic shock.
Design: Prospective, controlled experimental study.
Setting: University-based research laboratory.
Objectives: Levosimendan is an inotropic and vasodilator drug that has proved to be useful in cardiogenic shock. Pretreatment with levosimendan in experimental hypodynamic septic shock in pigs has shown valuable effects in oxygen transport. Our goal was to assess the effects of levosimendan in a normodynamic model of endotoxaemia.
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