Resuscitation Targets Research Articles

Venous–arterial CO2 to arterial–venous O2 difference ratio as a resuscitation target in shock states?

Venous–arterial CO2 to arterial–venous O2 difference ratio as a resuscitation target in shock states?

Ischemic Postconditioning during Cardiopulmonary Resuscitation Improves Cardiac Mitochondrial Respiration

Ischemic postconditioning (IPC) during cardiopulmonary resuscitation (CPR) increases neurologically intact survival in a porcine cardiac arrest model. We investigated the effect of IPC on mitochondrial respiration, an important therapeutic target for resuscitation, during CPR in this model. Blood pressure and ECG were continuously recorded. After 15 min of ventricular fibrillation, animals received standard CPR +/‐ IPC. IPC consisted of 3 cycles of 20 sec compression / 20 sec pause for the first 2 min of CPR. Cardiac mitochondria were isolated after 4 min. Closed‐cell respiration was measured for complex I (pyruvate+malate) and II (succinate+rotenone). In IPC‐treated animals vs. standard CPR, complex I and II respiratory control indices (RCI), calculated as the ratio of state 3:4 respiration, were higher (6.7±0.8 and 3.1±0.6 vs. 4.3±0.7 and 2.4±0.2, respectively) and complex I and II state 4 respiration (µmol O2*hr‐1*mg‐1) were lower (1.7±0.2 and 2.7±0.3 vs. 2.3±0.5 and 3.3±0.5, respectively). Blood pressure during CPR did not differ. In conclusion, IPC improved mitochondrial oxidative phosphorylation as early as 4 min after initiation of CPR, suggesting that CPR is a source of reperfusion injury and a critical time for intervention. Supported by NIH (R01 HL123227) and VA (CARA‐026‐10F).

Fluid resuscitation in severe sepsis and septic shock: Shifting goalposts.

Fluid resuscitation in severe sepsis and septic shock: Shifting goalposts.

Should microcirculation monitoring be used to guide fluid resuscitation in severe sepsis and septic shock?

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,

The impact of serial lactate monitoring on emergency department resuscitation interventions and clinical outcomes in severe sepsis and septic shock: an observational cohort study.

Monitoring in the setting of critical illness must be linked to beneficial therapy to affect clinical outcome. Elevated serum lactate is associated with an increase in mortality in emergency department (ED) patients with severe sepsis and septic shock. The reduction of lactate levels toward normal during acute resuscitation is associated with improved clinical outcomes. The majority of data demonstrating the interventions used to achieve a reduction in lactate levels and the associated clinical outcomes have been obtained during protocolized randomized trials. We therefore conducted a retrospective observational cohort study of 243 adult patients with severe sepsis and septic shock to assess the interventions associated with nonprotocolized serial lactate monitoring and to assess clinical outcomes. A multivariable model was used to assess outcome differences between the serial lactate (SL) and no serial lactate (NL) cohorts. The SL group received more crystalloid resuscitation (3.6 L vs. 2.5 L; P < 0.01), central venous oxygen saturation monitoring (30% vs. 12%; P < 0.01), and central venous pressure monitoring (23.5% vs. 11.8%; P = 0.02). By day 28, a total of 31 patients in the SL group (23.5%) and 44 in the NL group (39.6%) had died. Multivariable logistic regression analysis demonstrated that the lack of serial lactate monitoring was independently associated with mortality (adjusted odds ratio, 2.09; 95% confidence interval [CI], 1.12 - 3.89; P = 0.02). The SL group also showed greater improvement in 24-h Sequential Organ Failure Assessment scores (1.16 vs. 0.19; P = 0.03), decreased intensive care unit length of stay in days (4.6 vs. 6.0; P = 0.04), and more ventilator-free (19.9 vs. 16; P = 0.05) and vasopressor-free (21.6 vs. 17.9; P = 0.02) days. In the setting of routine clinical care, serial lactate monitoring is associated with an increase in crystalloid administration, resuscitation interventions, and improved clinical outcomes in ED patients with severe sepsis and septic shock. This suggests that serial lactate monitoring, targeting a reduction in lactate levels to normal, is a generalizable resuscitation target in the ED.

Current controversies in the support of sepsis.

Sepsis has a high morbidity, with a mortality rate of over 50% in the septic shock patient. This review provides a comprehensive summary of the latest Surviving Sepsis Campaign and the recent evidence since its publication. The guidelines reflect literature from the past 5 years to optimize outcomes in patients with severe sepsis and septic shock. The most relevant changes in the latest Surviving Sepsis Campaign include the use of a protocolized resuscitation with specific physiologic targets, preference of crystalloids for volume resuscitation, preferential use of norepinephrine as the initial vasopressor, addition of lactate and its clearance as a marker of tissue hypoperfusion, reduced emphasis on corticosteroids, and removal of activated protein C therapy. Since these latest guidelines, there have been many trials published to address the various measures that are advocated. We review the recent data on fluid resuscitation, targets of resuscitation, vasopressors, and trials of protocolized care versus usual care. Severe sepsis remains a significant cause of morbidity and mortality in hospitalized patients. The International Surviving Sepsis Guidelines provide a framework for early recognition and treatment of this condition, with the goal of an improved outcome and mortality in severe sepsis. The recent evidence suggests that early identification, adequate volume resuscitation, and assessment of adequate circulation may be the key elements to decrease morbidity from severe sepsis and septic shock.

The treatment of haematemesis and upper gastrointestinal bleeding in United Kingdom Armed Forces and other deployed units

Upper Gastro-intestinal (UGI) bleeding is a significant cause of morbidity worldwide. United Kingdom Armed Forces (UKAFs) are not immune to this condition. There is a substantial body of conflicting evidence regarding initial management and risk stratification. To provide the background knowledge and treatment pathways required to assess and manage a patient adequately during the first 24 hours of an episode of UGI bleeding. Clinical grading of hypovolaemic shock is inaccurate, but is a broad indicator of severity; the Rockall Score must not be used to assess requirement for intervention. Where laboratory assets are available, the Blatchford score is adequate to assess requirements for intervention. The principles of hypotensive resuscitation (target systolic blood pressure 90 mmHg for the first hour) hold true for UGI bleeds. In areas where endoscopy is available within four hours, a restrictive pattern of packed Red Blood Cell (pRBC) transfusion may be beneficial. Despite limited evidence of benefit, Proton Pump Inhibitors (PPIs) should be given routinely in UKAFs. Where available, in cases of variceal and non-variceal UGI Haemorrhage without locally available endoscopy, administration of tranexamic acid and somatostatin or octreotide should be considered.

Interdisciplinary ICU Cardiac Arrest Debriefing Improves Survival Outcomes*

In-hospital cardiac arrest is an important public health problem. High-quality resuscitation improves survival but is difficult to achieve. Our objective is to evaluate the effectiveness of a novel, interdisciplinary, postevent quantitative debriefing program to improve survival outcomes after in-hospital pediatric chest compression events. Single-center prospective interventional study of children who received chest compressions between December 2008 and June 2012 in the ICU. Structured, quantitative, audiovisual, interdisciplinary debriefing of chest compression events with front-line providers. Primary outcome was survival to hospital discharge. Secondary outcomes included survival of event (return of spontaneous circulation for ≥ 20 min) and favorable neurologic outcome. Primary resuscitation quality outcome was a composite variable, termed "excellent cardiopulmonary resuscitation," prospectively defined as a chest compression depth ≥ 38 mm, rate ≥ 100/min, ≤ 10% of chest compressions with leaning, and a chest compression fraction > 90% during a given 30-second epoch. Quantitative data were available only for patients who are 8 years old or older. There were 119 chest compression events (60 control and 59 interventional). The intervention was associated with a trend toward improved survival to hospital discharge on both univariate analysis (52% vs 33%, p = 0.054) and after controlling for confounders (adjusted odds ratio, 2.5; 95% CI, 0.91-6.8; p = 0.075), and it significantly increased survival with favorable neurologic outcome on both univariate (50% vs 29%, p = 0.036) and multivariable analyses (adjusted odds ratio, 2.75; 95% CI, 1.01-7.5; p = 0.047). Cardiopulmonary resuscitation epochs for patients who are 8 years old or older during the debriefing period were 5.6 times more likely to meet targets of excellent cardiopulmonary resuscitation (95% CI, 2.9-10.6; p < 0.01). Implementation of an interdisciplinary, postevent quantitative debriefing program was significantly associated with improved cardiopulmonary resuscitation quality and survival with favorable neurologic outcome.

Role of 6-hour, 12-hour, and 24-hour lactate clearance in mortality of severe sepsis and septic shock patients

Lactate is one of biomarkers used for risk stratification, resuscitation target, and death prediction in sepsis [1,2]. Interpretation of lactate clearance was proven more superior than single measurement to evaluate resuscitation adequacy and to determine prognosis [3,4]. This study aimed to find out whether mean differences of 6-hour, 12-hour, and 24-hour lactate clearance were observed between nonsurvivors and survivors of acute phase mortality in severe sepsis and septic shock patients.

Benefit of achieving lactate clearance versus central venous oxygen saturation target as microcirculation end point resuscitation in severe sepsis and septic shock

In severe sepsis and septic shock patients, lactate clearance >10% and central venous oxygen saturation (ScvO2) >70% are accepted parameters of tissue oxygenation adequacy. There is controversy of which parameters better associate with early mortality, and thus should be implemented as the microcirculation end point resuscitation [1-3]. This study was aimed to address the association of achieving either one or two targets of microcirculatory end point resuscitation and early mortality in severe sepsis and septic shock patients.

Central venous oxygen saturation and carbon dioxide gap as resuscitation targets in a hemorrhagic shock

Fluid resuscitation is still a major challenge. We aimed to describe changes in central venous oxygen saturation (ScvO2 ) and venous-to-arterial carbon dioxide gap (dCO2 ) during an experimental stroke volume (SV) index (SVI)-guided hemorrhage and fluid resuscitation model in pigs. Twelve anesthetized, mechanically ventilated pigs were bled till baseline SVI (Tbsl ) dropped by 50% (T0 ), thereafter fluid resuscitation was performed with balanced crystalloid in four steps until initial SVI was reached (T4 ). Statistical analysis was performed with Statistical Program for Social Sciences version 18.0; data are expressed as mean ± standard deviation. After bleeding, ScvO2 dropped (Tbsl = 78 ± 7 vs. T0 = 61 ± 5% P < 0.05) and oxygen extraction ratio increased (Tbsl = 0.20 ± 0.07 vs. T0 = 0.36 ± 0.05, P < 0.05). By T4 the ScvO2 normalized, but on average it remained 5% lower than at Tbsl (T4 = 73 ± 9% P < 0.05) and oxygen extraction also remained higher as compared with Tbsl (T4 = 0.24 ± 0.09 P = 0.001). ScvO2 showed significant correlation with SVI (r = 0.564, P < 0.001). dCO2 increased during hypovolemia (Tbsl :5.3 ± 2.0 vs. T0 :9.6 ± 2.3 mmHg, P = 0.001), then returned to normal by T4 = 5.1 ± 2.6 mmHg, and it also showed significant correlation with SVI (R = -0.591, P < 0.001) and oxygen extraction (R = 0.735, P < 0.001). In this SV-guided bleeding and fluid resuscitation model, both ScvO2 and dCO2 correlated well with changes in SV, but only the dCO2 returned to its baseline, normal value, while ScvO2 remained significantly lower than at baseline. These results suggest that dCO2 may be a good hemodynamic endpoint of resuscitation, while ScvO2 is not strictly a hemodynamic parameter, but rather an indicator of the balance between oxygen delivery and consumption.

Timing and volume of fluid administration for patients with bleeding

Treatment of haemorrhagic shock involves maintaining blood pressure and tissue perfusion until bleeding is controlled. Different resuscitation strategies have been used to maintain the blood pressure in trauma patients until bleeding is controlled. However, while maintaining blood pressure may prevent shock, it may worsen bleeding. To examine the effect on mortality and coagulation times of two intravenous fluid administration strategies in the management of haemorrhagic hypovolaemia, early compared to delayed administration and larger compared to smaller volume of fluid administered. We searched the Cochrane Injuries Group Specialised Register, Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library, Ovid MEDLINE(R), Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations, Ovid MEDLINE(R) Daily and Ovid OLDMEDLINE(R), Embase Classic + Embase (OvidSP), ISI Web of Science (SCI-Expanded and CPCI-S) and clinical trials registries. We checked reference lists of identified articles and contacted authors and experts in the field. The most recent search was run on 5 February 2014. Randomised trials of the timing and volume of intravenous fluid administration in trauma patients with bleeding. Trials in which different types of intravenous fluid were compared were excluded. Two authors independently extracted data and assessed trial quality. Six trials involving a total of 2128 people were included in this review. We did not combine the results quantitatively because the interventions and patient populations were so diverse. Early versus delayed fluid administration Three trials reported mortality and two reported coagulation data.In the first trial (n = 598) the relative risk (RR) for death with early fluid administration was 1.26 (95% confidence interval (CI) 1.00 to 1.58). The weighted mean differences (WMD) for prothrombin time and partial thromboplastin time were 2.7 (95% CI 0.9 to 4.5) and 4.3 (95% CI 1.74 to 6.9) seconds, respectively.In the second trial (n = 50) the RR for death with early blood transfusion was 5.4 (95% CI 0.3 to 107.1). The WMD for partial thromboplastin time was 7.0 (95% CI 6.0 to 8.0) seconds. In the third trial (n = 1309) the RR for death with early fluid administration was 1.06 (95% CI 0.77 to 1.47). Larger versus smaller volume of fluid administration Three trials reported mortality and one reported coagulation data.In the first trial (n = 36) the RR for death with a larger volume of fluid resuscitation was 0.80 (95% CI 0.28 to 22.29). Prothrombin time and partial thromboplastin time were 14.8 and 47.3 seconds in those who received a larger volume of fluid, as compared to 13.9 and 35.1 seconds in the comparison group.In the second trial (n = 110) the RR for death with a high systolic blood pressure resuscitation target (100 mm Hg) maintained with a larger volume of fluid as compared to a low systolic blood pressure resuscitation target (70 mm Hg) maintained with a smaller volume of fluid was 1.00 (95% CI 0.26 to 3.81). In the third trial (n = 25) there were no deaths. We found no evidence from randomised controlled trials for or against early or larger volume of intravenous fluid administration in uncontrolled haemorrhage. There is continuing uncertainty about the best fluid administration strategy in bleeding trauma patients. Further randomised controlled trials are needed to establish the most effective fluid resuscitation strategy.

Microvascular Perfusion as a Target for Fluid Resuscitation in Experimental Circulatory Shock*

To study regional perfusion during experimental endotoxemic and obstructive shock and compare the effect of initial cardiac output-targeted fluid resuscitation with optimal cardiac output-targeted resuscitation on different peripheral tissues. Controlled experimental study. University-affiliated research laboratory. Fourteen fasted anesthetized mechanically ventilated domestic pigs. Domestic pigs were randomly assigned to the endotoxemic (n = 7) or obstructive shock (n = 7) model. Central and regional perfusion parameters were obtained at baseline, during greater than or equal to 50% reduction of cardiac output (T1), after initial resuscitation to baseline (T2), and after optimization of cardiac output (T3). Regional perfusion was assessed in the sublingual, intestinal, and muscle vascular beds at the different time points and included visualization of the microcirculation, measurement of tissue oxygenation, and indirect assessments of peripheral skin perfusion. Hypodynamic shock (T1) simultaneously decreased all regional perfusion variables in both models. In the obstructive model, these variables returned to baseline levels at T2 and remained in this range after T3, similar to cardiac output. In the endotoxemic model, however, the different regional perfusion variables were only normalized at T3 associated with the hyperdynamic state at this point. The magnitude of changes over time between the different vascular beds was similar in both models, but the endotoxemic model displayed greater heterogeneity between tissues. This study demonstrates that the relationship between the systemic and regional perfusion is dependent on the underlying cause of circulatory shock. Further research will have to demonstrate whether different microvascular perfusion variables can be used as additional resuscitation endpoints.

Treatment of Severe Sepsis-Based on Surviving Sepsis Campaign Guideline

Sepsis is a systemic, deleterious host response to infection. The term “severe sepsis” is used when sepsis is complicated by acute organ dysfunction, and septic shock as sepsis complicated by either hypotension that is refractory to fluid resuscitation or by hyperlactatemia. The number of cases with severe sepsis exceeds 750,000 per year in the United States and the mortality is now closer to 20 to 30% in these days. The principles of the initial management bundle are to provide sufficient hemodynamic resuscitation and early initiation of appropriate antibiotics to mitigate uncontrolled infection. Initial resuscitation requires the use of intravenous fluids and vasopressors. It is very important to achieve the target of initial resuscitation. The supportive cares in ICU are also significant such as blood component transfusion, glucose control, renal replacement therapy, deep vein thrombosis prophylaxis and stress ulcer prophylaxis. The goals of care and prognosis including end-of-life care should be discussed with patients and families as early as feasible. (Korean J Med 2014;86:557-562)

Hemodynamic Directed Cardiopulmonary Resuscitation Improves Short-Term Survival From Ventricular Fibrillation Cardiac Arrest*

During cardiopulmonary resuscitation, adequate coronary perfusion pressure is essential for establishing return of spontaneous circulation. Current American Heart Association guidelines recommend standardized interval administration of epinephrine for patients in cardiac arrest. The objective of this study was to compare short-term survival using a hemodynamic directed resuscitation strategy versus chest compression depth-directed cardiopulmonary resuscitation in a porcine model of cardiac arrest. Randomized interventional study. Preclinical animal laboratory. Twenty-four 3-month-old female swine. After 7 minutes of ventricular fibrillation, pigs were randomized to receive one of three resuscitation strategies: 1) Hemodynamic directed care (coronary perfusion pressure-20): chest compressions with depth titrated to a target systolic blood pressure of 100 mm Hg and titration of vasopressors to maintain coronary perfusion pressure greater than 20 mm Hg; 2) Depth 33 mm: target chest compression depth of 33 mm with standard American Heart Association epinephrine dosing; or 3) Depth 51 mm: target chest compression depth of 51 mm with standard American Heart Association epinephrine dosing. All animals received manual cardiopulmonary resuscitation guided by audiovisual feedback for 10 minutes before first shock. Forty-five-minute survival was higher in the coronary perfusion pressure-20 group (8 of 8) compared to depth 33 mm (1 of 8) or depth 51 mm (3 of 8) groups; p equals to 0.002. Coronary perfusion pressures were higher in the coronary perfusion pressure-20 group compared to depth 33 mm (p = 0.004) and depth 51 mm (p = 0.006) and in survivors compared to nonsurvivors (p < 0.01). Total epinephrine dosing and defibrillation attempts were not different. Hemodynamic directed resuscitation targeting coronary perfusion pressures greater than 20 mm Hg during 10 minutes of cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest improves short-term survival, when compared to resuscitation with depth of compressions guided to 33 mm or 51 mm and standard American Heart Association vasopressor dosing.

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Introduction: Advances in cardiopulmonary resuscitation (CPR) have focused on the generation and maintenance of adequate myocardial blood flow to optimize the return of spontaneous circulation and survival. Much of the morbidity associated with cardiac arrest survivors can be attributed to global brain hypoxic-ischemic injury. Methods: Fiber-optic intracranial pressure and brain tissue oxygen tension (PbtO2) probes were placed in the left frontal cortex prior to induction of VF. After 7 minutes of untreated VF, 3 month old female swine were randomized to receive one of three resuscitation strategies (N = 7 for each group): 1) Hemodynamic Directed Care (CPP-20): chest compressions (CCs) with depth titrated to a target systolic blood pressure of 100 mmHg and titration of vasopressors to maintain coronary perfusion pressures (CPP) > 20 mmHg; 2) Depth 33mm(D33): target CC depth of 33mm with standard ACLS epinephrine dosing; or 3) Depth 51mm(D51 – American Heart Association (AHA) optimal care): target CC depth of 51mm with standard ACLS epinephrine dosing. All animals received manual CPR guided by audiovisual feedback for 10 minutes before first shock. Differences in cerebral perfusion pressures (CerePP) and PbtO2 over time and between groups were evaluated using generalized estimating equations. Results: CerePPs were significantly higher in the CPP-20 group compared to both D33 (p<0.01) and D51 (p=0.046), and higher in survivors compared to non-survivors irrespective of treatment group (p<0.01). Only the CPP-20 group was able to consistently generate CerePPs above 30 mm Hg. PbtO2 was also higher in the CPP-20 group compared to both D33 (p<0.01) and D51 (p=0.013), and higher in survivors compared to non-survivors irrespective of treatment group (p<0.01). CPP and CerePP in the minute epoch immediately prior to defibrillation were well correlated across treatment groups and survival status (R2= 0.66). Conclusions: Hemodynamic directed resuscitation targeting CPPs > 20 mmHg following VF arrest produced cerebral perfusion pressures > 30 mm Hg and improved brain tissue oxygen tension compared to optimal AHA care

Near-infrared spectroscopy in the assessment of suspected sepsis in the emergency department

The conventional approach to sepsis resuscitation involves early interventions targeting global oxygenation and macro-haemodynamic variables such as central venous and systemic arterial pressures. There is increasing recognition of the importance of microcirculatory changes in shock states, including sepsis, and the relationship of these to outcome. Near-infrared spectroscopy (NIRS) is a recently developed non-invasive technology that measures tissue oxygen saturations (StO2), which may be an indirect measure of the adequacy of the microcirculation. StO2 measurements, therefore, have the potential to identify patients who are at risk of progressing to organ dysfunction and could be used to guide resuscitation. This article reviews the current state of knowledge of NIRS in the setting of sepsis, examining its application, validity and prognostic value. A search of the relevant literature was performed using Medline, Embase and Cochrane databases, and a qualitative analysis was undertaken. A limited number of observational studies, mostly conducted among patients with severe sepsis, have shown that NIRS may correlate with severity of illness but demonstrate a variable relationship between StO2 and outcome. Outstanding questions still remain as to whether NIRS can help to risk-stratify patients with suspected sepsis in the emergency department and the utility of StO2 as a resuscitation target.

Pushing harder, pushing faster, minimizing interruptions… But falling short of 2010 cardiopulmonary resuscitation targets during in-hospital pediatric and adolescent resuscitation

AimThe objective of this study was to evaluate the effect of instituting the 2010 Basic Life Support Guidelines on in-hospital pediatric and adolescent cardiopulmonary resuscitation (CPR) quality. We hypothesized that quality would improve, but that targets for chest compression (CC) depth would be difficult to achieve. MethodsProspective in-hospital observational study comparing CPR quality 24 months before and after release of the 2010 Guidelines. CPR recording/feedback-enabled defibrillators collected CPR data (rate (CC/min), depth (mm), CC fraction (CCF, %), leaning (%>2.5kg)). Audiovisual feedback for depth was: 2005, ≥38mm; 2010, ≥50mm; for rate: 2005, ≥90 and ≤120CC/min; 2010, ≥100 and ≤120CC/min. The primary outcome was average event depth compared with Student's t-test. Results45 CPR events (25 before; 20 after) occurred, resulting in 1336 thirty-second epochs (909 before; 427 after). Compared to 2005, average event depth (50±13mm vs. 43±9mm; p=0.047), rate (113±11CC/min vs. 104±8CC/min; p<0.01), and CCF (0.94 [0.93, 0.96] vs. 0.9 [0.85, 0.94]; p=0.013) increased during 2010. CPR epochs during the 2010 period more likely to meet Guidelines for CCF (OR 1.7; CI95: 1.2–2.4; p<0.01), but less likely for rate (OR 0.23; CI95: 0.12–0.44; p<0.01), and depth (OR 0.31; CI95: 0.12–0.86; p=0.024). ConclusionsInstitution of the 2010 Guidelines was associated with increased CC depth, rate, and CC fraction; yet, achieving 2010 targets for rate and depth was difficult.

Target blood pressure for hypotensive resuscitation

BackgroundGood outcomes have resulted from hypotensive resuscitation of hemorrhagic shock patients. We hypothesized that mean arterial pressure (MAP) 60mmHg is the target blood pressure for hypotensive resuscitation during uncontrolled hemorrhagic shock in trauma. MethodsTo determine the effective target MAP for hypotensive resuscitation during uncontrolled hemorrhagic shock, we randomly assigned 80 rats to one of 8 treatment groups (n=10 for each group). We then observed the effects of different target MAPs (control, 40, 50, 60, 70, 80, 90mmHg, and sham) on fluid resuscitation of uncontrolled hemorrhagic shock. Blood pressure, serum lactate, hematocrit, fluid therapy, blood loss, and plasma cytokine levels were measured at 0, 30, 90, 120, 180, 240, 300min after the start of the surgical procedure. ResultsA target MAP of 90, 80 and 70mmHg had increased blood loss and decreased hematocrit and IL-6 and TNF-α production. A target MAP of 60, 50 and 40mmHg had lower blood loss, good hematocrit, higher IL-6 and TNF-α production, and decreased animal survival. Only target MAPs of 40 and 50 had and decreased animal survival. The differences in blood loss, hematocrit, lactate, post-resuscitation MAP, survival, IL-6, IL-10, and TNF-α production between rats with a target MAP of 60mmHg and those with a target MAP of 70mmHg were not significant. The amount of fluid therapy in the BP 60 groups was less than in the BP 70 groups (P<0.001). ConclusionA MAP of 60mmHg should be considered for evaluation in human studies as a target for hypotensive resuscitation.

Interactions macro- et microcirculatoires dans le choc

Microcirculatory alterations, frequently observed in shock states, are associated with the development of multiple organ failure and death. These microcirculatory alterations occur even when systemic hemodynamic variables are within resuscitation goals. In this review, we discuss the link between the microcirculation and systemic hemodynamics. Several studies suggested that microvascular perfusion may be dependent from systemic hemodynamics in severely hypotensive patients. However, the threshold of blood pressure at which this occurs is not well defined and it is difficult to define which mean arterial pressure target should be reached. The microcirculation is usually independent of systemic hemodynamics in the usual range of systemic hemodynamic values encountered when resuscitation targets are met. Fluids and vasoactive agents affect the microcirculation independently of their systemic effects.