Predicting arterial blood gas and lactate from central venous blood analysis in critically ill patients: a multicentre, prospective, diagnostic accuracy study.

BACKGROUND: The estimation of arterial blood gas and lactate from central venous blood analysis and pulse oximetry [Formula: see text] readings has not yet been extensively validated. METHODS: In this multicentre, prospective study performed in 590 patients with acute circulatory failure, we measured blood gases and lactate in simultaneous central venous and arterial blood samples at 6 h intervals during the first 24 h after insertion of central venous and arterial catheters. The study population was randomly divided in a 2:1 ratio into model derivation and validation sets. We derived predictive models of arterial pH, carbon dioxide partial pressure, oxygen saturation, and lactate, using clinical characteristics, [Formula: see text], and central venous blood gas values as predictors, and then tested their performance in the validation set. RESULTS: In the validation set, the agreement intervals between predicted and actual values were -0.078/+0.084 units for arterial pH, -1.32/+1.36 kPa for arterial carbon dioxide partial pressure, -5.15/+4.47% for arterial oxygen saturation, and -1.07/+1.05 mmol litre(-1) for arterial lactate (i.e. around two times our predefined clinically tolerable intervals for all variables). This led to ∼5% (or less) of extreme-to-extreme misclassifications, thus giving our predictive models only marginal agreement. Thresholds of predicted variables (as determined from the derivation set) showed high predictive values (consistently >94%), to exclude abnormal arterial values in the validation set. CONCLUSIONS: Using clinical characteristics, [Formula: see text], and central venous blood analysis, we predicted arterial blood gas and lactate values with marginal accuracy in patients with circulatory failure. Further studies are required to establish whether the developed models can be used with acceptable safety.

Brachial cuff measurements of blood pressure during passive leg raising for fluid responsiveness prediction.

OBJECTIVE: The passive leg raising maneuver (PLR) for fluid responsiveness testing relies on cardiac output (CO) measurements or invasive measurements of arterial pressure (AP) whereas the initial hemodynamic management during shock is often based solely on brachial cuff measurements. We assessed PLR-induced changes in noninvasive oscillometric readings to predict fluid responsiveness. STUDY DESIGN: Multicentre interventional study. PATIENTS AND METHODS: In ICU sedated patients with circulatory failure, AP (invasive and noninvasive readings) and CO measurements were performed before, during PLR (trunk supine, not modified) and after 500-mL volume expansion. Areas under the ROC curves (AUC) were determined for fluid responsiveness (>10% volume expansion-induced increase in CO) prediction. RESULTS: In 112 patients (19% with arrhythmia), changes in noninvasive systolic AP during PLR (noninvasiveΔ(PLR)SAP) only predicted fluid responsiveness (cutoff 17%, n=21, positive likelihood ratio [LR] of 26 [18-38]), not unresponsiveness. If PLR-induced change in central venous pressure (CVP) was at least of 2 mm Hg (n=60), suggesting that PLR succeeded in altering cardiac preload, noninvasiveΔ(PLR)SAP performance was good: AUC of 0.94 [0.85-0.98], positive and negative LRs of 5.7 [4.6-6.8] and 0.07 [0.009-0.5], respectively, for a cutoff of 9%. Of note, invasive AP-derived indices did not outperform noninvasiveΔ(PLR)SAP. CONCLUSION: Regardless of CVP (i.e., during "blind PLR"), noninvasiveΔ(PLR)SAP more than 17% reliably identified fluid responders. During "CVP-guided PLR", in case of sufficient change in CVP, noninvasiveΔ(PLR)SAP performed better (cutoff of 9%). These findings, in sedated patients who had already undergone volume expansion and/or catecholamines, have to be verified during the early phase of circulatory failure (before an arterial line and/or a CO measuring device is placed).