Protocol for a systematic review of the impact of resuscitation fluids on the microcirculation after haemorrhagic shock in animal models (original) (raw)
Related papers
Revista Brasileira de Terapia Intensiva, 2015
Tissue hypoperfusion and subsequent limited oxygen transport are critical features conducting to organ failure during shock states. Therefore, early identification of tissue hypoperfusion and adequate resuscitation are key for improving the probability of survival after septic shock. (1,2) However, how to identify organ perfusion abnormalities at the bedside and select the type and amount of fluids required to improve tissue hypoxia remain highly controversial. Traditionally, clinical signs, such as reduced blood pressure and urinary output, altered consciousness, and mottled skin, have been used to identify tissue perfusion abnormalities. Consequently, current hemodynamic monitoring during shock states mainly focuses on detection of pressure-derived hemodynamic variables related to systemic circulation. However, it has been largely recognized that monitoring these macro-hemodynamic variables is not sufficient to rule out persistent abnormalities of tissue oxygenation. Indeed, the usefulness of resuscitation targets, such as global oxygen-derived parameters, has been strongly questioned, (3) and recent data have failed to demonstrate beneficial effects of using central venous oxygen saturation as a goal of resuscitation. (4-6) Fluid resuscitation therapy primarily aims to optimize cardiac output on the assumption that increasing macro blood flow can improve the convective transport of oxygen to the tissues and, therefore, maintain cellular respiration and support organ function. (7,8) Thus, fluid therapy targeting central venous pressure has been widely recommended to achieve adequate cardiac performance. (9) However, high positive fluid balances have also been associated with unfavorable clinical outcomes. (10) In this sense, dynamic approaches to assessing volume responsiveness to fluid administration seem to be superior to static variables. (11,12) Unfortunately, macro-hemodynamic optimization guided by either dynamic or static variables does not guarantee adequate tissue perfusion or adequate cellular respiration. Oxygen transport to tissues is governed by convective and diffusive components. The convective component is determined by the microcirculatory blood flow itself, i.e., the number of red blood cells (RBCs) entering the microcirculation, and by oxygen content. In normal conditions, inflow and outflow pressures control the driving pressure at the microvascular level. Thus, the convective transport is regulated upstream at the arteriolar level through microcirculatory inflow changes with subsequent micro-hematocrit
Microcirculation, 2020
Objective: Microcirculatory perfusion disturbances following hemorrhagic shock and fluid resuscitation contribute to multiple organ dysfunction and mortality. Standard fluid resuscitation is insufficient to restore microcirculatory perfusion, however, additional therapies are lacking. We conducted a systematic search to provide an overview of potential non-fluid based therapeutic interventions to restore microcirculatory perfusion following hemorrhagic shock. Methods: A structured search of PubMed, EMBASE and Cochrane Library was performed in March 2020. Animal studies needed to report at least one parameter of microcirculatory flow (perfusion, red blood cell velocity, functional capillary density). Results: The search identified 1269 records of which 48 fulfilled all eligibility criteria. In total, 62 drugs were tested of which 29 were able to restore microcirculatory perfusion. Particularly complement inhibitors (75% of drugs tested successfully restored blood flow), endothelial barrier modulators (100% successful), antioxidants (66% successful), drugs targeting cell metabolism (83% successful) and sex hormones (75% successful) restored microcirculatory perfusion. Other drugs consisted of attenuation of inflammation (100% not successful), vasoactive agents (68% not successful) and steroid hormones (75% not successful). Conclusion: Improving mitochondrial function, inhibition of complement inhibition and reducing microvascular leakage via restoration of endothelial barrier function seems beneficial to restore microcirculatory perfusion following hemorrhagic shock and fluid resuscitation.
Transfusion, 2012
BACKGROUND: Disparity between the macro-and microcirculation is thought to occur as a result of (micro)vascular dysfunction in some types of shock. Whether this occurs during hemorrhagic shock, however, is unknown. We therefore investigated both macro-and microcirculatory variables in the heart as a vital organ and the gut as a nonvital organ. We hypothesized that the microcirculation in the gut would follow the macrocirculation in the acute phase of hemorrhagic shock and isovolemic autologous whole blood resuscitation, but that the microcirculation in the heart would be preserved even under conditions of macrocirculatory depression. STUDY DESIGN AND METHODS: Eleven pigs (23 Ϯ 4 kg) were anesthetized and subjected to a controlled hemorrhagic shock (30 and 45% reduction of total blood volume) and isovolemic resuscitation with autologous blood. Quantitative measurement of microvascular oxygen pressures (mpO2) was performed by phosphorimetry on the gut and heart simultaneously. Measurements of systemic hemodynamic and regional oxygen-derived variables as well as mpO2 were performed at baseline, after the first and second phases of hemorrhage, and after resuscitation. RESULTS: Five pigs responded to resuscitation, while six pigs died spontaneously within 20 to 30 minutes after reinfusion of the withdrawn blood, without significant differences in macro-or microcirculatory variables at baseline and after hemorrhage. Correlation analysis showed that microvascular pO2 in the heart and the gut were closely related to macrocirculatory variables (cardiac index, mean arterial pressure, and oxygen delivery) during hemorrhage and resuscitation. CONCLUSIONS: This study demonstrated that the microcirculation in the gut (being a nonvital organ) and heart (being a vital organ) follow the macrocirculation in the acute phase of hemorrhagic shock and isovolemic autologous whole blood resuscitation. ABBREVIATIONS: BE = base excess; MAP = mean arterial blood pressure.
Intensive care medicine experimental, 2016
Traumatic hemorrhagic shock (THS) is a leading cause of preventable death following severe traumatic injury. Resuscitation of THS is typically targeted at blood pressure, but the effects of such a strategy on systemic and microcirculatory flow remains unclear. Failure to restore microcirculatory perfusion has been shown to lead to poor outcomes in experimental and clinical studies. Systemic and microcirculatory variables were examined in a porcine model of complex THS, in order to investigate inter-individual variations in flow and the effect of microcirculatory perfusion on reversal of the shock state. Baseline standard microcirculatory variables were obtained for 22 large white pigs using sublingual incident dark field (IDF) video-microscopy. All animals were subjected to a standardised hind-limb injury followed by a controlled haemorrhage of approximately 35 % of blood volume (shock phase). This was followed by 60 min of fluid resuscitation with either 0.9 % saline or component b...
Microcirculatory Alterations in Shock States
Critical Care Nursing Clinics of North America, 2014
In health, functional components of the microcirculation provide oxygen and nutrients and remove waste products from the tissue beds of the body's organs. Shock states overwhelmingly stress functional capacity of the microcirculation, resulting in microcirculatory failure. In septic shock, there is abundant evidence that inflammatory mediators cause or contribute to hemodynamic instability. In nonseptic shock states, the microcirculation is better able to compensate for alterations in vascular resistance, cardiac output (CO), and blood pressure. Autoregulation at the arteriolar level and the endothelium and erythrocyte at the cellular level maintain oxygen diffusion gradients sufficient to support aerobic metabolism. In comparison with septic shock, hypovolemic and cardiogenic shock states are not challenged with the additional burden of infection and its consequential effects on the microcirculation. Global hemodynamic and oxygen delivery (D : O 2) parameters are appropriate for assessing, monitoring, and guiding therapy in hypovolemic and cardiogenic shock but, alone, are inadequate for septic shock.
Systemic and microcirculatory effects of blood transfusion in experimental hemorrhagic shock
Intensive care medicine experimental, 2017
The microvascular reperfusion injury after retransfusion has not been completely characterized. Specifically, the question of heterogeneity among different microvascular beds needs to be addressed. In addition, the identification of anaerobic metabolism is elusive. The venoarterial PCO2 to arteriovenous oxygen content difference ratio (Pv-aCO2/Ca-vO2) might be a surrogate for respiratory quotient, but this has not been validated. Therefore, our goal was to characterize sublingual and intestinal (mucosal and serosal) microvascular injury after blood resuscitation in hemorrhagic shock and its relation with O2 and CO2 metabolism. Anesthetized and mechanically ventilated sheep were assigned to stepwise bleeding and blood retransfusion (n = 10) and sham (n = 7) groups. We performed analysis of expired gases, arterial and mixed venous blood gases, and intestinal and sublingual videomicroscopy. In the bleeding group during the last step of hemorrhage, and compared to the sham group, there ...
Swiss Medical Weekly, 2019
This review describes the evidence relating to fluid resuscitation in sepsis, septic shock and massive haemorrhage. Beside the scientific evidence based on clinical trials, possible effects on the microcirculation and, therefore, organ function will be illustrated and areas of future research highlighted. The critical appraisal of the existing evidence should enable the reader to choose the optimal volume substitution for an individual patient.