Effects of Fluids on the Macro- and Microcirculations.

This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2018. Other selected articles can be found online at https://www.biomedcentral.com/collections/annualupdate2018. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901

Microcirculatory monitoring in septic patients: Where do we stand?

Microcirculatory alterations play a pivotal role in sepsis-related morbidity and mortality. However, since the microcirculation has been a "black box", current hemodynamic management of septic patients is still guided by nnacrocirculatory parameters. In the last decades, the development of several technologies has shed some light on microcirculatory evaluation and monitoring, and the possibility of incorporating nnicrocirculatory variables to clinical practice no longer seems to be beyond reach. The present review provides a brief summary of the current technologies for microcirculatory evaluation, and attempts to explore the potential role and benefits of their integration to the resuscitation process in critically ill septic patients. (C) 2016 Elsevier Espana, S.L.U. y SEMICYUC. All rights reserve

Fluid therapy and the hypovolemic microcirculation

Purpose of review In shock states, optimizing intravascular volume is crucial to promote an adequate oxygen delivery to the tissues. Our current practice in fluid management pivots on the Frank-Starling law of the heart, and the effects of fluids are measured according to the induced changes on stroke volume. The purpose of this review is to evaluate the boundaries of current macrohemodynamic approach to fluid administration, and to introduce the microcirculatory integration as a fundamental part of tissue perfusion monitoring. Recent findings Macrocirculatory changes induced by volume expansion are not always coupled to proportional changes in microcirculatory perfusion. Loss of hemodynamic coherence limits the value of guiding fluid therapy according to macrohemodynamics, and highlights the importance of evaluating the ultimate target of volume administration, the microcirculation. Summary Current approach to intravascular volume optimization is made from a macrohemodynamic perspective. However, several situations wherein macrocirculatory and microcirculatory coherence is lost have been described. Future clinical trials should explore the usefulness of integrating the microcirculatory evaluation in fluid optimizatio

In response to: “understanding elevated P v−a CO 2 gap and P v−a CO 2 /C a−v O 2 ratio in venous hyperoxia condition”

info:eu-repo/semantics/publishedVersio

Prognostic implications of tissue oxygen saturation in human septic shock

Purpose: To analyze the prognostic value of tissue oxygen saturation (StO2) in septic shock patients with restored mean arterial pressure (MAP). Methods: This was a prospective observational study of patients admitted to the ICU in the early phase of septic shock, after restoration of MAP. Demographic data, severity score, hemodynamics, blood lactate, acid-base status, and StO2 were measured at inclusion followed by a transient vascular occlusion test (VOT) to obtain the StO2-deoxygenation (DeOx) and StO2-reoxygenation (ReOx) rates. Sequential organ failure assessment (SOFA) score was measured at inclusion and after 24 h. Results: Thirty-three patients were studied. StO2 was 76 ± 10%, DeOx -12.2 ± 4.2%/min, and ReOx 3.02 ± 1.70%/s. MAP showed a significant correlation with VOT-derived slopes (r = -0.4, p = 0.04 for DeOx; and r = 0.55, p\0.01 for ReOx). After 24 h, 17 patients (52%) had improved SOFA scores. Patients who did not improve their SOFA showed less negative DeOx values at inclusion. The association between DeOx and SOFA evolution was not affected by MAP. Both DeOx and ReOx impairment correlated with longer ICU stay (r = 0.44, p = 0.05; and r = -0.43, p = 0.05, respectively). Conclusions: In a population of septic shock patients with restored MAP, impaired DeOx was associated with no improvement in organ failures after 24 h. Decrements in DeOx and ReOx were associated with longer ICU stay. DeOx and ReOx were linked to MAP, and thus, their interpretation needs to be made relative to MAP. © Copyright jointly held by Springer and ESICM 2012

Central venous-to-arterial carbon dioxide difference and the effect of venous hyperoxia: A limiting factor, or an additional marker of severity in shock?

Central venous-to-arterial carbon dioxide difference (PcvaCO2) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when PcvaCO2 is elevated. PcvaCO2 combination with arterial-venous oxygen content difference (PcvaCO2/CavO2) seems to enhance its performance when assessing anaerobic metabolism. However, the fact that PCO2 values might be altered by changes in blood O2 content (the Haldane effect), has been presented as a limitation of PCO2-derived variables. The present study aimed at exploring the impact of hyperoxia on PcvaCO2 and PcvaCO2/CavO2 during the early phase of shock. Prospective interventional study. Ventilated patients suffering from shock within the first 24 h of ICU admission. Patients requiring FiO2 ≥ 0.5 were excluded. At inclusion, simultaneous arterial and central venous blood samples were collected. Patients underwent a hyperoxygenation test (5 min of FiO2 100%), and arterial and central venous blood samples were repeated. Oxygenation and CO2 variables were calculated at both time points. Twenty patients were studied. The main cause of shock was septic shock (70%). The hyperoxygenation trial increased oxygenation parameters in arterial and venous blood, whereas PCO2 only changed at the venous site. Resulting PcvaCO2 and PcvaCO2/CavO2 significantly increased [6.8 (4.9, 8.1) vs. 7.6 (6.7, 8.5) mmHg, p 0.001; and 1.9 (1.4, 2.2) vs. 2.3 (1.8, 3), p < 0.001, respectively]. Baseline PcvaCO2, PcvaCO2/CavO2 and ScvO2 correlated with the magnitude of PO2 augmentation at the venous site within the trial (ρ -0.46, p 0.04; ρ 0.6, p < 0.01; and ρ 0.7, p < 0.001, respectively). Increased PcvaCO2/CavO2 values were associated with higher mortality in our sample [1.46 (1.21, 1.89) survivors vs. 2.23 (1.86, 2.8) non-survivors, p < 0.01]. PcvaCO2 and PcvaCO2/CavO2 are influenced by oxygenation changes not related to flow. Elevated PcvaCO2 and PcvaCO2/CavO2 values might not only derive from cardiac output inadequacy, but also from venous hyperoxia. Elevated PcvaCO2/CavO2 values were associated with higher PO2 transmission to the venous compartment, suggesting higher shunting phenomena