Low Central Venous Oxygen Saturation Research Articles

#4200 INTERACTIONS BETWEEN INTRADIALYTIC CENTRAL VENOUS OXYGEN SATURATION, RELATIVE BLOOD VOLUME, AND ALL-CAUSE MORTALITY IN HEMODIALYSIS PATIENTS

Abstract Background and Aims In maintenance hemodialysis patients, low central venous oxygen saturation (ScvO2) and small decline in relative blood volume (RBV) have been associated with adverse outcomes [1,2]. Here we explore the interactions between ScvO2 and RBV change in relation to all-cause mortality. Method We conducted a retrospective study in maintenance hemodialysis patients with central venous catheters as vascular access. During a 6-month baseline period, Crit-Line (Fresenius Medical Care, Waltham, MA) was used to measure continuously intradialytic ScvO2 and hematocrit-based RBV. We defined four groups per median change of RBV and median ScvO2. Patients with ScvO2 above median and RBV change below median were defined as reference. The follow up period was 3-years. We constructed a Cox proportional hazards model with adjustment for age, diabetes, and dialysis vintage to assess the association between ScvO2 and RBV and all-cause mortality during follow-up. Results Baseline comprised 5,231 dialysis sessions in 216 patients. The median RBV change was –5.5% and median ScvO2 was 58.8%. During follow-up, 44 patients (20.4%) died. Kaplan-Meier analysis is shown in Figure 1. In the adjusted model, all-cause mortality was highest in patients with ScvO2 below median and RBV change above median (HR 6.32; 95% confidence interval [CI] 1.37 to 29.06), followed by patients with ScvO2 below median and RBV change below median (HR 5.04; 95% CI 1.14 to 22.35) and ScvO2 above median and RBV change above median (HR 4.52; 95% CI 0.95 to 21.36). Conclusion Concurrent combined monitoring of intradialytic ScvO2 and RBV change may provide additional insights into a patient's circulatory status. Patients with low ScvO2 and small changes in RBV may represent a specifically vulnerable group of patients at particularly high risk for adverse outcomes, possibly related to poor cardiac reserve and fluid overload.

Interactions between intradialytic central venous oxygen saturation, relative blood volume, and all-cause mortality in maintenance hemodialysis patients.

In maintenance hemodialysis (HD) patients, low central venous oxygen saturation (ScvO2 ) and small decline in relative blood volume (RBV) have been associated with adverse outcomes. Here we explore the joint association between ScvO2 and RBV change in relation to all-cause mortality. We conducted a retrospective study in maintenance HD patients with central venous catheters as vascular access. During a 6-month baseline period, Crit-Line (Fresenius Medical Care, Waltham, MA) was used to measure continuously intradialytic ScvO2 and hematocrit-based RBV. We defined four groups per median change of RBV and median ScvO2 . Patients with ScvO2 above median and RBV change below median were defined as reference. Follow-up period was 3 years. We constructed Cox proportional hazards model with adjustment for age, diabetes, and dialysis vintage to assess the association between ScvO2 and RBV and all-cause mortality during follow-up. Baseline comprised 5231 dialysis sessions in 216 patients. The median RBV change was -5.5% and median ScvO2 was 58.8%. During follow-up, 44 patients (20.4%) died. In the adjusted model, all-cause mortality was highest in patients with ScvO2 below median and RBV change above median (HR 6.32; 95% confidence interval [CI] 1.37-29.06), followed by patients with ScvO2 below median and RBV change below median (HR 5.04; 95% CI 1.14-22.35), and ScvO2 above median and RBV change above median (HR 4.52; 95% CI 0.95-21.36). Concurrent combined monitoring of intradialytic ScvO2 and RBV change may provide additional insights into a patient's circulatory status. Patients with low ScvO2 and small changes in RBV may represent a specifically vulnerable group of patients at particularly high risk for adverse outcomes, possibly related to poor cardiac reserve and fluid overload.

Pathophysiological profile of awake and anesthetized pigs following systemic exposure to the highly lethal ricin toxin

Ricin, a plant-derived toxin originating from the seeds of Ricinus communis (castor bean plant), is one of the most lethal toxins known. To date, no in-depth study of systemic exposure to ricin in a standardized large animal model has been reported. This study details for the first time the pathophysiological hemodynamic profile following systemic/intramuscular exposure to the ricin toxin in a porcine model by comprehensive cardiorespiratory monitoring of awake and anesthetized pigs. Unlike respiratory exposure to ricin, which is characterized by the development of acute respiratory distress syndrome, following intramuscular exposure to ricin respiratory parameters were grossly unaffected, however the hemodynamics of both awake and anesthetize pigs were unsustainably compromised. We show that in the early phase until approximately 24 h post-exposure, cardiac output is not impaired although one of its components, stroke volume, is relatively low. This is due to compensatory increase in heart rate, which eventually becomes insufficient. Later, distributive shock develops, characterized by severe vasodilatation (decreased systemic vascular resistance), low central venous oxygen saturation and elevation of venous-to-arterial carbon dioxide difference indicating increase in tissue oxygen demand not met by cardiac supply. These findings serve as a basis for further studies to evaluate the ability of supportive treatments such as vasoactive and inotropic drugs, to postpone the hemodynamic deterioration and thus expand the therapeutic window for the anti-ricin treatment. Such studies are of crucial importance for judicious treatment of victims of acts of bioterrorism or of intentional self-poisoning.

The oxygen cascade in patients treated with hemodialysis and native high-altitude dwellers: lessons from extreme physiology to benefit patients with end-stage renal disease.

Patients treated with hemodialysis (HD) repeatedly undergo intradialytic low arterial oxygen saturation and low central venous oxygen saturation, reflecting an imbalance between upper body systemic oxygen supply and demand, which are associated with increased mortality. Abnormalities along the entire oxygen cascade, with impaired diffusive and convective oxygen transport, contribute to the reduced tissue oxygen supply. HD treatment impairs pulmonary gas exchange and reduces ventilatory drive, whereas ultrafiltration can reduce tissue perfusion due to a decline in cardiac output. In addition to these factors, capillary rarefaction and reduced mitochondrial efficacy can further affect the balance between cellular oxygen supply and demand. Whereas it has been convincingly demonstrated that a reduced perfusion of heart and brain during HD contributes to organ damage, the significance of systemic hypoxia remains uncertain, although it may contribute to oxidative stress, systemic inflammation, and accelerated senescence. These abnormalities along the oxygen cascade of patients treated with HD appear to be diametrically opposite to the situation in Tibetan highlanders and Sherpa, whose physiology adapted to the inescapable hypobaric hypoxia of their living environment over many generations. Their adaptation includes pulmonary, vascular, and metabolic alterations with enhanced capillary density, nitric oxide production, and mitochondrial efficacy without oxidative stress. Improving the tissue oxygen supply in patients treated with HD depends primarily on preventing hemodynamic instability by increasing dialysis time/frequency or prescribing cool dialysis. Whether dietary or pharmacological interventions, such as the administration of L-arginine, fermented food, nitrate, nuclear factor erythroid 2-related factor 2 agonists, or prolyl hydroxylase 2 inhibitors, improve clinical outcome in patients treated with HD warrants future research.

Venous oxygen saturation in critical illness.

To review clinically relevant features of systemic oxygen delivery and consumption and the technique and use of venous oxygenation monitoring in human and veterinary medicine. Veterinary and human peer-reviewed medical literature including scientific reviews, clinical and laboratory research articles, and authors' clinical research experience. Measurement of venous hemoglobin oxygen saturation (venous oxygenation) provides insight into the balance between oxygen supply and tissue demand. In people, measurement of venous oxygen saturation can reveal decompensation that is missed by physical examination and other routinely monitored parameters. Therefore, measurement of mixed or central venous oxygenation measurement may help guide therapy and predict outcome of critically ill patients. In dogs, low central venous oxygen saturation has been associated with impaired cardiopulmonary function and poor outcome in several small studies of experimental shock or severe clinical illness, suggesting that monitoring this variable may assist the treatment of severe illness in this species as well. Venous oxygenation reflects systemic oxygenation status and can be used to guide treatment and estimate prognosis in critically ill patients. Measurement of venous oxygenation in veterinary patients is feasible and is a potentially valuable tool in the management of patients with severe disease. This review is intended to increase the understanding and awareness of the potential role of venous oxygen measurement in veterinary patients.

Persistence of Central Venous Oxygen Desaturation During Early Sepsis Is Associated With Higher Mortality: A Retrospective Analysis of the ALBIOS Trial

Relevance of low (< 70%) central venous oxygen saturation (Scvo2) during early sepsis has been recently questioned by three negative trials (Protocol-Based Care for Early Septic Shock, Australasian Resuscitation in Sepsis Evaluation, and Protocolized Management in Sepsis) on early goal-directed therapy; however, subjects included in those trials had Scvo2 at enrollment as high as 71 ± 13%, 73 ± 11%, and 70 ± 12%. Here we assess the association between Scvo2< 70%at 6h and 90-day mortality in subjects enrolled in the Albumin Italian Outcome Sepsis (ALBIOS) trial, focusing on those with initial Scvo2< 70%. Regardless of treatment assignment (to receive albumin or not), all subjects enrolled in the ALBIOS trial received early goal-directed therapy aiming for Scvo2≥ 70%at 6 h. Using multivariable logistic regression analyses, we tested the association between Scvo2< 70%at 6h and 90-day mortality in those with initial Scvo2< 70%(n= 514) or≥ 70%(n= 961). Scvo2< 70%at 6h was independently associated with higher 90-day mortality in subjects with initial Scvo2< 70%(OR, 1.84; 95%CI, 1.19-2.85; P= .007) but not in those with initial Scvo2≥ 70%(OR, 1.25; 95%CI, 0.79-1.95; P= .357). Scvo2< 70%at enrollment and at 6h was associated with history and/or signs of cardiac dysfunction but not with greater severity of disease or more aggressive resuscitation (required per protocol). In the ALBIOS trial, persistence of low Scvo2 was associated with higher 90-day mortality, possibly because it reflected underlying cardiac dysfunction. Subjects with Scvo2< 70%may benefit most from individually tailored interventions aimed at normalizing the balance between systemic oxygen delivery and consumption. ClinicalTrials.gov; No. NCT00707122; URL: www.clinicaltrials.gov.

Clinical predictors of a low central venous oxygen saturation after major surgery: a prospective prevalence study.

Optimising perioperative haemodynamic status may reduce postoperative complications. In this prospective prevalence study, we investigated the associations between standard haemodynamic parameters and a low central venous oxygen saturation (ScvO2) in patients after major surgery. A total of 201 patients requiring continuous arterial and central venous pressure monitoring after major surgery were recruited. Simultaneous arterial and central venous blood gases, haemodynamic and biochemical data and perfusion index were obtained from patients at a single time-point within 24 hours of surgery. A low ScvO2 (<70%) was observed in 109 patients (54%). Use of mechanical ventilation, mean arterial pressure, central venous pressure, haemoglobin concentrations, arterial pH and lactate concentrations, arterial oxygen (PaO2) and carbon dioxide tensions (PaCO2) were all associated with a low ScvO2 in the univariate analyses. In the multivariate analysis, only a higher perfusion index (odds ratio [OR] 0.87, 95% confidence interval [CI] 0.78 to 0.98), PaO2 (OR 0.98 per mmHg increment, 95% CI 0.97 to 0.99) and PaCO2 (OR 0.88 per mmHg increment, 95% CI 0.82 to 0.95) and a lower central venous pressure (OR 1.14 per mmHg increment, 95% CI 1.04 to 1.25) were significantly associated with a reduced risk of a low ScvO2, all in a linear fashion. In conclusion, PaO2, PaCO2, perfusion index and central venous pressure were significant predictors of a low ScvO2 in patients after major surgery including cardiac surgery.

Prevalence of low central venous oxygen saturation in the first hours of intensive care unit admission and associated mortality in septic shock patients: a prospective multicentre study.

IntroductionIn septic shock patients, the prevalence of low (<70%) central venous oxygen saturation (ScvO2) on admission to the intensive care unit (ICU) and its relationship to outcome are unknown. The objectives of the present study were to estimate the prevalence of low ScvO2 in the first hours of ICU admission and to assess its potential association with mortality in patients with severe sepsis or septic shock.MethodsThis was a prospective, multicentre, observational study conducted over a one-year period in ten French ICUs. Clinicians were asked to include patients with severe sepsis or septic shock preferably within 6 hours of ICU admission and as soon as possible without changing routine practice. ScvO2 was measured at inclusion and 6 hours later (H6), by blood sampling.ResultsWe included 363 patients. Initial ScvO2 below 70% was present in 111 patients and the pooled estimate for its prevalence was 27% (95% Confidence interval (95%CI): 18% to 37%). At time of inclusion, among 166 patients with normal lactate concentration (≤2 mmol/L), 55 (33%) had a low initial ScvO2 (<70%), and among 136 patients who had already reached the classic clinical endpoints for mean arterial pressure (≥65 mmHg), central venous pressure (≥8 mmHg), and urine output (≥0.5 mL/Kg of body weight), 43 (32%) had a low initial ScvO2 (<70%). Among them, 49% had lactate below 2 mmol/L. The day-28 mortality was higher in case of low initial ScvO2 (37.8% versus 27.4%; P = 0.049). When adjusted for confounders including the Simplified Acute Physiology Score and initial lactate concentration, a low initial ScvO2 (Odds ratio (OR) = 3.60, 95%CI: 1.76 to 7.36; P = 0.0004) and a low ScvO2 at H6 (OR = 2.18, 95%CI: 1.12 to 4.26; P = 0.022) were associated with day-28 mortality by logistic regression.ConclusionsLow ScvO2 was common in the first hours of admission to the ICU for severe sepsis or septic shock even when clinical resuscitation endpoints were achieved and even when arterial lactate was normal. A ScvO2 below 70% in the first hours of ICU admission and six hours later was associated with day-28 mortality.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-014-0609-7) contains supplementary material, which is available to authorized users.

Decreased central venous oxygen saturation despite normalization of heart rate and blood pressure post shock resuscitation in sick dogs.

To evaluate traditional and global perfusion parameters in clinical canine shock patients, and to evaluate for occult hypoperfusion as evidenced by low central venous oxygen saturation or high plasma lactate concentrations in clinical patients resuscitated to traditional endpoints. Clinical observational trial designed with a 1-year data entry period and patient follow-up of 28 days posthospital presentation. Large, private urban teaching hospital, and emergency and critical care center. Adult canine patients presenting to the emergency department with untreated shock. None. Patients received fluid resuscitation to normalize perfusion parameters based on physical examination and arterial blood pressure (BP). Monitoring of central venous pressure (CVP) and central venous oxygen saturation (ScvO2 ) was feasible with current standard of care interventions in critically ill, client-owned dogs. Decreased ScvO2 was observed in 37.8% of patients resuscitated to normal traditional perfusion parameters. Hyperlactatemia was commonly recorded. Decreased ScvO2 exists in a significant proportion of critically ill dogs following standard fluid resuscitation for shock, providing a relevant target population for implementation of a more standardized early goal-directed therapy bundle in veterinary patients. Normalization of heart rate, blood pressure, mentation, and perfusion parameters directed by physical examination may be attained despite the persistence of significant tissue hypoperfusion and oxygen debt.

Transfusion of red blood cells is associated with improved central venous oxygen saturation but not mortality in septic shock patients.

BackgroundAlthough the optimum hemoglobin (H) concentration for patients with septic shock (SS) has not been specifically investigated, current guidelines suggest that H of 7 - 9 g/dL, compared with 10 - 12 g/dL, was not associated with increased mortality in critically ill adults. This contrasts with early goal-directed resuscitation protocols that use a target hematocrit of 30% in patients with low central venous oxygen saturation (ScvO2) during the first 6 hours of resuscitation of SS.MethodsData elements were prospectively collected on all patients with SS patients (lactic acid (LA) > 4 mmol/L, or hypotension). Out of a total of 396 SS patients, 46 patients received red blood cell (RBC) transfusion for ScvO2 < 70% (RBC group). We then matched 71 SS patients that did not receive RBC transfusion (NRBC group) on the following goals (G): LA obtained within 6 hours (G1), antibiotics given within 3 hours (G2), 20 mL/kg fluid bolus followed by vasopressors (VP) if needed to keep mean arterial pressure > 65 mm Hg (G3), central venous pressure > 8 mm Hg within 6 hours (G4) and ScvO2 > 70% within 6 hours (G5).ResultsIn the RBC group, after one unit of RBC transfusion, ScvO2 improved from average of 63% (± 12%) to 68% (± 10%) (P = 0.02). Sixteen patients required another unit of RBC, and this resulted in increase of ScvO2 to 78% (± 11%) (P < 0.01). The RBC and NRBC groups were matched on sequential organ failure assessment (SOFA) scores and all five goals. There was no difference in mortality between the two groups: 41% vs. 39.4% (OR: 0.8, 95% CI: 0.4 - 1.7, P = 0.6).ConclusionsIn our study, transfusion of RBC was not associated with decreased mortality in SS patients.

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Introduction: Marked elevation of lactate following cardiac surgery is associated with increased morbidity and mortality. While high lactate with low central venous oxygen saturation (ScvO2) suggests global hypoperfusion amenable to interventions that address the imbalance between oxygen supply and demand, the approach to patients with high lactate and normal ScvO2 is less clear. The purpose of this study was to identify differences in perioperative characteristics between cardiac surgery patients with markedly elevated lactate and normal ScvO2 upon intensive care unit (ICU) arrival who experienced major complications (MC) versus those without MC. Methods: A retrospective chart review was conducted on 43 patients who underwent cardiac surgery with cardiopulmonary bypass (CPB) between September 2010 and December 2011 and presented with lactate ≥ 4 mmoL/L and ScvO2 ≥ 70% upon ICU arrival. Perioperative characteristics assessed included preoperative ejection fraction (EF), EUROscore, complete blood count, serum chemistries, CPB time and perfusion rate, aortic cross clamp time, cumulative dose/duration of vasoactive therapy, blood loss, vital signs, urine output, lactate, ScvO2, arterial blood gases, ventilator data, chest x-rays, central venous pressure (CVP) and crystalloids/blood products administered. Results: Of the 43 patients evaluated, 14 had MC and 29 had no MC. The most frequent MC was prolonged mechanical ventilation, which occurred in 11/14 patients, followed by sepsis (3), stroke (3), renal failure (2), and pulmonary embolism (1). Comparing the MC and no MC groups, respectively, perioperative characteristics found to be significantly different included median EF (40 vs. 53%, p = 0.0009), cumulative intraoperative epinephrine (701 vs. 200 mcg, p < 0.0001), PaO2/FiO2 (PF) ratio on day 1 (169 vs. 242, p = 0.031), Lung Injury Score on day 1 (1.4 vs. 1, p = 0.029), Multiple Organ Dysfunction Score on days 1, 2 and 7 (7 vs. 5; 5.5 vs. 2; 3 vs. 0, all p < 0.01), vasopressor duration > 24 hr (42.8 vs. 3.4%, p = 0.003), mean CVP at 8 hr (14 vs. 11 mmHg, p = 0.002) and presence of systemic inflammatory response syndrome on day 7 (42.9 vs. 10.3%, p = 0.040). Additionally, mortality was significantly higher in the MC group (21.4 vs. 0%, p = 0.030). Median EUROscore (9 vs. 6, p = 0.149), CPB time (74 vs. 56 min, p = 0.129), aortic cross clamp time (52 vs. 37 min, p = 0.214), intraoperative blood loss (1,550 vs. 1,000 mL, p = 0.156), PF ratio on day 2 (184 vs. 292, p = 0.076) and incidence of intraoperative hypotension (64.3 vs. 48.3%, p = 0.353) were all numerically higher in the MC group as well. Conclusions: The majority of patients presenting with a markedly elevated lactate level in the setting of a normal ScvO2 upon ICU arrival following cardiac surgery experience an uneventful course. However, significant differences in several perioperative characteristics were identified in patients who experienced MC compared to those without MC. Mild to moderate lung injury and a protracted CPB/vasopressor-induced microcirculatory derangement likely contributed to prolonged mechanical ventilation and other adverse outcomes.

Isolated High Lactate or Low Central Venous Oxygen Saturation After Cardiac Surgery and Association With Outcome

To determine if isolated abnormally low central venous oxygen saturation (ScvO2) or elevated lactate levels on admission to an intensive care unit (ICU) are associated with increased morbidity and length of stay (LOS) after cardiac surgery. Retrospective, observational. Academic tertiary care hospital. Six hundred twenty-nine adult, on-pump cardiac surgery patients with ScvO2 and arterial lactate obtained on admission to the ICU. None. Comparing outcomes across the isolated low ScvO2 and high lactate categories, no significant differences in ICU/hospital LOS, ICU readmission rate, length of mechanical ventilation, or incidence of major complications were observed in patients with ScvO2<70% and lactate < 2 mmol/L or in those with lactate 2-3.9 mmol/L and ScvO2 ≥ 70%. However, patients with lactate ≥ 4 mmol/L and ScvO2 ≥ 70% exhibited significantly longer median ICU LOS (p = 0.018), hospital LOS (p = 0.032), length of mechanical ventilation (p = 0.0001), and higher incidence of major complications (p = 0.008). Multivariate analysis identified isolated elevated lactate levels ≥ 4 mmol/L as an independent predictor for major complications (OR 4.29, p = 0.0008). Low ScvO2 with normal lactate or moderately elevated lactate with normal ScvO2 upon ICU admission after cardiac surgery was not associated with increased morbidity or length of stay. Markedly elevated lactate levels in the setting of a normal ScvO2 was associated with significantly higher incidence of major complications and prolonged length of stay. Additionally, a lactate level ≥ 4 mmol/L was an independent predictor of major complications.

Supporting hemodynamics: what should we target? What treatments should we use?

Assessment and monitoring of hemodynamics is a cornerstone in critically ill patients as hemodynamic alteration may become life-threatening in a few minutes. Defining normal values in critically ill patients is not easy, because 'normality' is usually referred to healthy subjects at rest. Defining 'adequate' hemodynamics is easier, which embeds whatever pressure and flow set is sufficient to maintain the aerobic metabolism. We will refer to the unifying hypothesis proposed by Schrier several years ago. Accordingly, the alteration of three independent variables - heart (contractility and rate), vascular tone and intravascular volume - may lead to underfilling of the arterial tree, associated with reduced (as during myocardial infarction or hemorrhage) or expanded (sepsis or cirrhosis) plasma volume. The underfilling is sensed by the arterial baroreceptors, which activate primarily the sympathetic nervous system and renin-angiotensin-aldosterone system, as well as vasopressin, to restore the arterial filling by increasing the vascular tone and retaining sodium and water. Under 'normal' conditions, therefore, the homeostatic system is not activated and water/sodium excretion, heart rate and oxygen extraction are in the range found in normal subjects. When arterial underfilling occurs, the mechanisms are activated (sodium and water retention) - associated with low central venous oxygen saturation (ScvO2) if underfilling is caused by low flow/hypovolemia, or with normal/high ScvO2 if associated with high flow/hypervolemia. Although the correction of hemodynamics should be towards the correction of the independent determinants, the usual therapy performed is volume infusion. An accepted target is ScvO2 >70%, although this ignores the arterial underfilling associated with volume expansion/high flow. For large-volume resuscitation the worst solution is normal saline solution (chloride load, strong ion difference = 0, acidosis). To avoid changes in acid-base equilibrium the strong ion difference of the infused solution should be equal to the baseline bicarbonate concentration.

Low central venous oxygen saturation is associated with increased mortality in critically ill dogs

To investigate relationships between central venous oxygen saturation (ScvO(2)) and survival to hospital discharge in dogs. Central venous oxygen saturation is an accessible measure of the balance between systemic oxygen delivery and consumption. Prospective observational cohort study, enrolling 126 client-owned dogs with central venous catheters. Central venous oxygen saturation was measured over the 24 hours following intensive care unit admission. Poor outcome was defined as death or euthanasia performed for moribund status. Regression analysis identified independent predictors of non-survival and physiologic parameters associated with central venous oxygen saturation. Area under the receiver operator curve analysis identified a cut-off point of central venous oxygen saturation, below which central venous oxygen saturation decrease was associated with increased mortality risk. Mortality risk was 30·9%. Low central venous oxygen saturation was associated with poor outcome (P<0·05). Area under the receiver operator curve analysis selected a central venous oxygen saturation of 68% as the point below which a fall in central venous oxygen saturation was associated with increased mortality risk. For each 10% drop in central venous oxygen saturation below 68%, odds of non-survival increased by 2·66 times (P=0·0002, 95% confidence interval of odds ratio=1·45 to 4·85). Central venous oxygen saturation was equivalent to lactate in predicting non-survival. Predictors of central venous oxygen saturation (packed cell volume, mean arterial blood pressure, fever, % arterial haemoglobin saturation as measured by pulse oximeter) were consistent with hypothesised physiologic mechanisms. Central venous oxygen saturation was a strong mortality predictor. Further work is needed to determine if therapy targeting central venous oxygen saturation can reduce mortality in canine intensive care unit patients.

Low central venous oxygen saturation in haemodynamically stabilized trauma patients is associated with poor outcome

Central venous oxygen saturation (ScvO(2)) is suggested to reflect the adequacy of oxygen delivery, and the main objective of the present study was to determine whether ScvO(2) is associated with outcome in haemodynamically stabilized trauma patients. Haemodynamically unstable trauma patients receiving a central venous line within 1 h of admission were eligible for inclusion in this prospective observational study. The mean arterial pressure (MAP), lactate and ScvO(2) were recorded at inclusion and every 6 h for 36 h or until lactate was <2.0 mmol/l and ScvO(2) was >75% in two consecutive measurements. Patients with a MAP of ≥70 mmHg were considered to be haemodynamically stabilized. The outcome measure was complications defined as infections, delta sequential organ failure assessment score of >0, and mortality. Fifty patients with a median new injury severity score of 27 (17-34) were analysed. Complications occurred in 33 patients. An association between ScvO(2) following resuscitation to MAP ≥70 mmHg and complications was detected with an odds ratio of 0.94 (95% confidence interval; 0.89-0.99). This association was also significant when adjusted for injury severity. The result implies that a low ScvO(2) value is associated with more complications. The optimal cut-off for ScvO(2) to discriminate between patients who did or did not develop complications was found to be 66.5% (56-86%). These data suggest that low ScvO(2) in haemodynamically stabilized patients is associated with a poor outcome and that ScvO(2) represents a potential endpoint of resuscitation in trauma patients.

Thenar oxygen saturation measured by near infrared spectroscopy as a noninvasive predictor of low central venous oxygen saturation in septic patients

Thenar oxygen saturation measured by near infrared spectroscopy as a noninvasive predictor of low central venous oxygen saturation in septic patients

Influence of Central Venous Oxygen Saturation on In-hospital Mortality of Surgical Patients

Low central venous oxygen saturation (ScvO₂) indicates an imbalance between cellular oxygen supply and consumption and, consequently, worse prognosis for critical patients. However, it is not clear what the value of this marker in surgical patients. The objective of the present study was to evaluate whether low perioperative ScvO₂ determines a worse prognosis. This is a 6-month observational study carried on in a tertiary hospital. Patients who needed to be in the intensive care unit (ICU) postoperatively, with age ≥ 18 years, who underwent large surgeries, were included. Patients who underwent palliative surgeries and those with severe heart failure were excluded. Levels of ScvO₂ were measured before the surgery, during the procedure, and after the surgery in the ICU. Sixty-six patients were included in this study, but 25.8% of them did not survive. Mean ScvO₂ levels were higher intraoperatively, 84.7 ± 8.3%, than preoperatively and in the ICU, 74.1 ± 7.6% and 76.0 ± 10.5% (p = 0.0001), respectively. However, only preoperative SvcO₂ levels of non-surviving patients were significantly lower than those who survived. By logistic regression, preoperative ScvO₂, OR = 0.85 (95% CI 0.74-0.98) (p = 0.02), was an independent factor of in-hospital mortality. Patients with preoperative ScvO₂ < 70% had greater need of intraoperative blood transfusion (80.0% versus 37.0%, p = 0.001) and volume replacement, 8,000.0 (6,500.0-9,225.0) mL versus 6,000.0 (4,500.0-8,500.0) mL (p = 0.04), with greater chances of postoperative complications (75% versus 45.7%, p = 0.02) and longer time in the ICU, 4.0 (20.0-5.0) days versus 3.0 (1.7-4.0) days (p = 0.02). Intraoperative ScvO₂ levels are higher than those both in the pre- and postoperative period. However, low preoperative ScvO₂ determines worse prognosis.

A prospective multicenter cohort study of the association between global tissue hypoxia and coagulation abnormalities during early sepsis resuscitation

Coagulation activation is an integral part of sepsis pathogenesis. Experimental data suggest that endothelial exposure to hypoxia activates coagulation. We aimed to test the hypothesis that the quantity of exposure to global tissue hypoxia is associated with the degree of coagulation activation during early sepsis resuscitation. Prospective, multicenter cohort study. Emergency department and intensive care unit of three academic hospitals. Inclusion criteria were age older than 17, acute infection with two or more signs of systemic inflammation, hypotension despite fluid challenge (or lactate >4 mM), and continuous central venous oxygen saturation (Scvo2) monitoring for quantitative resuscitation. Exclusion criteria were anticoagulant or blood product administration. We recorded central venous oxygen saturation continuously for 0 to 6 hrs of resuscitation and calculated the area under the curve for central venous oxygen saturation <70%. We defined hypoxia exposure as exceeding the median area under the curve for the entire cohort. At 0, 6, and 24 hrs, we measured conventional coagulation biomarkers plus thrombin-antithrombin complex, plasmin-antiplasmin complex, tissue plasminogen activator, plasminogen activator inhibitor-1, protein C, antithrombin, and endothelial markers (E-selectin, intracellular adhesion molecule-1, thrombomodulin). We compared changes during 0 to 6 hrs and 0 to 24 hrs in biomarkers between hypoxia exposure and nonexposure groups. We enrolled 40 patients (60% requiring vasopressors; 30% mortality). We found that exposure to hypoxia alone was not associated with a significant degree of coagulation activation. However, in secondary analyses we found that exposure to arterial hypotension induced E-selectin and thrombin-antithrombin complex, whereas concomitant exposure to both hypotension and hypoxia was associated with amplification of E-selectin and thrombomodulin, and a reduction in protein C. In this sample of patients undergoing quantitative resuscitation for sepsis, we found that exposure to global tissue hypoxia (as quantified by low central venous oxygen saturation) was not associated with major coagulation activation. Further investigation to elucidate the clinical factors that trigger or intensify the procoagulant response to sepsis is warranted.

The importance of low central venous oxygen saturation levels in patients after cardiac surgery

Objectives: Reduced venous oxygen saturation reflect global tissue hypoxia. This has been associated with increased risk of morbidity and mortality. This observation was started to characterize low central venous oxygen saturation in patients after cardiac surgery.

Early changes in lactate and central venous saturation combinations do not predict subsequent changes in organ performance

High lactate (LCT) identifies critically ill patients, predicts risk of mortality and guides resuscitation. Low central venous oxygen saturation (SvO2) is associated with mortality and is used as a resuscitation target. A change in LCT, but not in SvO2, has been shown to relate to outcome. It is physiologically plausible that those with low SvO2 and high LCT do worse versus those with only one of SvO2 or LCT abnormal, or with both normal. Early changes in these combinations may also determine subsequent changes in organ performance. We hypothesised that changes in combinations in SvO2 and LCT from day 1 to day 2 predicted changes in total SOFA between day 2 and day 4.