Defining the hemodynamic response to volume therapy is integral to managing critically ill patients with acute circulatory failure, especially in the absence of cardiac index (CI) measurement. This study aimed at investigating whether changes in central venous-to-arterial CO difference (Δ-ΔPCO) and central venous oxygen saturation (ΔScvO) induced by volume expansion (VE) are reliable parameters to define fluid responsiveness in sedated and mechanically ventilated septic patients. We prospectively studied 49 critically ill septic patients in whom VE was indicated because of circulatory failure and clinical indices.
View Article and Find Full Text PDFObjectives: To evaluate the ability of central venous-to-arterial carbon dioxide pressure difference, central venous oxygen saturation, and the combination of these two parameters to detect extubation failure in critically ill patients.
Design: Multicentric, prospective, observational study.
Setting: Three ICUs.
Background: Central venous oxygen saturation (ScvO2) is often used to help to guide resuscitation of critically ill patients. The standard gold technique for ScvO2 measurement is the co-oximetry (Co-oximetry_ScvO2), which is usually incorporated in most recent blood gas analyzers. However, in some hospitals, those machines are not available and only calculated ScvO2 (Calc_ScvO2) is provided.
View Article and Find Full Text PDFBackground: To evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (∆PCO) in hemodynamically stable septic shock patients.
Methods: Eighteen mechanically ventilated septic shock patients were prospectively included in the study. We measured cardiac index (CI), ∆PCO, oxygen consumption (VO), central venous oxygen saturation (ScvO), and blood gas parameters, before and 30 min after an increase in alveolar ventilation (increased respiratory rate by 10 breaths/min).
The mixed venous-to-arterial carbon dioxide (CO2) tension difference [P (v-a) CO2] is the difference between carbon dioxide tension (PCO2) in mixed venous blood (sampled from a pulmonary artery catheter) and the PCO2 in arterial blood. P (v-a) CO2 depends on the cardiac output and the global CO2 production, and on the complex relationship between PCO2 and CO2 content. Experimental and clinical studies support the evidence that P (v-a) CO2 cannot serve as an indicator of tissue hypoxia, and should be regarded as an indicator of the adequacy of venous blood to wash out the total CO2 generated by the peripheral tissues.
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