J. Mesquida

Characterization of tissue oxygen saturation and the vascular occlusion test: influence of measurement sites, probe sizes and deflation thresholds

IntroductionTissue oxygen saturation (StO2) and the vascular occlusion test (VOT) can identify tissue hypoperfusion in trauma and sepsis. However, the technique is neither standardized nor uses the same monitoring site. We hypothesized that baseline and VOT StO2 would be different in the forearm (F) and thenar eminence (TH) and that different minimal StO2 values during the VOT would result in different reoxygenation rates (ReO2).MethodsStO2 and its change during the VOT were simultaneously measured in the F and TH, with 15 mm and 25 mm probes, using the 325 InSpectra monitor in 18 healthy, adult volunteers. Two VOTs were done to a threshold thenar StO2 of 40% interchanging the 15 mm and 25 mm probes between sites. Two additional VOTs were done to thresholds of 50% and 30%. Baseline StO2 (BaseO2), the deoxygenation rate (DeO2) and ReO2 were compared between sites, probes and (%O2/minute) thresholds. Results are presented as the median (interquartile range), P-value.ResultsBaseO2, DeO2, ReO2, area under the curve and hyperemia duration values were different when comparing TH vs. F and 15 mm vs. 25 mm probes. ReO2 was different between different thresholds for the TH and 15 mm probes. TH15 mm vs. F15 mm: BaseO2, 90.4 (85.2, 93.5) vs. 85.2 (80.7, 90.2), P = 0.031; DO2, -12.1 (-16.2, -11.3) vs. -8.5 (-10.3, -7.8), P = 0.011; ReO2, 297.2 (213.7, 328.6), P < 0.0001; 15 mm vs. 25 mm probe: BaseO2, 97.2 (89.4, 94.7) vs. 87.3 (81.7, 90.9), P = 0.016; DeO2, -18.0 (-24.1, -14.8) vs. -9.9 (-15.3, -6.5), P < 0.0001; and ReO2, 401.6 (331.7, 543.2) vs. 160.5 (132.3, 366.9), P = 0.012, respectively. TH15 mm vs. TH25 mm: BaseO2, P = 0.020; DeO2, P < 0.0001; and ReO2, P < 0.0001. Threshold StO2 values (15 mm probe only): ReO2, P = 0.003; DeO2, P = 0.60. ReO2 at 40% and 50% StO2 thresholds, P = 0.01.ConclusionsBaseO2, DeO2 and ReO2 were different when measured in different anatomical sites (F and TH) and with different probe sizes, and ReO2 was different with differing VOT release StO2 threshold values. Thus, standardization of the site, probe and VOT challenge need to be stipulated when reporting data.

Central venous-to-arterial carbon dioxide difference combined with arterial-to-venous oxygen content difference is associated with lactate evolution in the hemodynamic resuscitation process in early septic shock.

IntroductionSince normal or high central venous oxygen saturation (ScvO2) values cannot discriminate if tissue perfusion is adequate, integrating other markers of tissue hypoxia, such as central venous-to-arterial carbon dioxide difference (PcvaCO2 gap) has been proposed. In the present study, we aimed to evaluate the ability of the PcvaCO2 gap and the PcvaCO2/arterial-venous oxygen content difference ratio (PcvaCO2/CavO2) to predict lactate evolution in septic shock.MethodsObservational study. Septic shock patients within the first 24 hours of ICU admission. After restoration of mean arterial pressure, and central venous oxygen saturation, the PcvaCO2 gap and the PcvaCO2/CavO2 ratio were calculated. Consecutive arterial and central venous blood samples were obtained for each patient within 24 hours. Lactate improvement was defined as the decrease ≥ 10% of the previous lactate value.ResultsThirty-five septic shock patients were studied. At inclusion, the PcvaCO2 gap was 5.6 ± 2.1 mmHg, and the PcvaCO2/CavO2 ratio was 1.6 ± 0.7 mmHg · dL/mL O2. Those patients whose lactate values did not decrease had higher PcvaCO2/CavO2 ratio values at inclusion (1.8 ± 0.8vs. 1.4 ± 0.5, p 0.02). During the follow-up, 97 paired blood samples were obtained. No-improvement in lactate values was associated to higher PcvaCO2/CavO2 ratio values in the previous control. The ROC analysis showed an AUC 0.82 (p < 0.001), and a PcvaCO2/CavO2 ratio cut-off value of 1.4 mmHg · dL/mL O2 showed sensitivity 0.80 and specificity 0.75 for lactate improvement prediction. The odds ratio of an adequate lactate clearance was 0.10 (p < 0.001) in those patients with an elevated PcvaCO2/CavO2 ratio (≥1.4).ConclusionIn a population of septic shock patients with normalized MAP and ScvO2, the presence of elevated PcvaCO2/CavO2 ratio significantly reduced the odds of adequate lactate clearance during the following hours.

Prehospital dynamic tissue oxygen saturation response predicts in-hospital lifesaving interventions in trauma patients.

BACKGROUND: Tissue oximetry (StO2) plus a vascular occlusion test is a noninvasive technology that targets indices of oxygen uptake and delivery. We hypothesize that prehospital tissue oximetric values and vascular occlusion test response can predict the need for in-hospital lifesaving interventions (LSI). METHODS: We conducted a prospective, blinded observational study to evaluate StO2 slopes to predict the need for LSI. We calculated the DeO2 slope using Pearsons coefficients of regression (r2) for the first 25% of descent and the ReO2 slope using the entire recovery interval. The primary outcome was LSI defined as the need for emergent operation or transfusion in the first 24 hours of hospitalization. We created multivariable logistic regression models using covariates of age, sex, vital signs, lactate, and mental status. RESULTS: We assessed StO2 in a convenience sample of 150 trauma patients from April to November of 2009. In-hospital mortality was 3% (95% confidence interval [CI], 1.1–7.6); 31% (95% CI, 24–39) were admitted to the intensive care unit, 6% (95% CI, 2.8–11.1) had an emergent operation, and 10% (95% CI, 5.7–15.9) required transfusion. Decreasing DeO2 was associated with a higher proportion of patients requiring LSI. In the multivariate model, the association between the need for LSI and DeO2, Glasgow Coma Scale, and age persists. CONCLUSION: Prehospital DeO2 is associated with need for LSI in our trauma population. Further study of DeO2 is warranted to determine whether it can be used as an adjunct triage criterion or an endpoint for resuscitation. LEVEL OF EVIDENCE: III, observational study.

Objetivos de la reanimación hemodinámica

Cardiovascular failure or shock, of any etiology, is characterized by ineffective perfusion of body tissues, inducing derangements in the balance between oxygen delivery and consumption. Impairment in oxygen availability on the cellular level causes a shift to anaerobic metabolism, with an increase in lactate and hydrogen ion production that leads to lactic acidosis. The degree of hyperlactatemia and metabolic acidosis will be directly correlated to the development of organ failure and poor outcome of the individuals. The amount of oxygen available at the tissues will depend fundamentally on an adequate level of perfusion pressure and oxygen delivery. The optimization of these two physiologic parameters can re-establish the balance between oxygen delivery and consumption on the cellular level, thus, restoring the metabolism to its aerobic paths. Monitoring variables such as lactate and oxygen venous saturations (either central or mixed) during the initial resuscitation of shock will be helpful to determine whether tissue hypoxia is still present or not. Recently, some new technologies have been developed in order to evaluate local perfusion and microcirculation, such as gastric tonometry, near-infrared spectroscopy and videomicroscopy. Although monitoring these regional parameters has demonstrated its prognostic value, there is a lack of evidence regarding to its usefulness during the resuscitation process. In conclusion, hemodynamic resuscitation is still based on the rapid achievement of adequate levels of perfusion pressure, and then on the modification of oxygen delivery variables, in order to restore physiologic values of ScvO(2)/SvO(2) and resolve lactic acidosis and/or hyperlactatemia.

Thenar oxygen saturation and invasive oxygen delivery measurements in critically ill patients in early septic shock.

This prospective study was aimed to test the hypothesis that tissue hemoglobin oxygen saturation (StO2) measured noninvasively using near-infrared spectroscopy is a reliable indicator of global oxygen delivery (DO2) measured invasively using a pulmonary artery catheter (PAC) in patients with septic shock. The study setting was a 26-bed medical-surgical intensive care unit at a university hospital. Subjects were adult patients in septic shock who required PAC hemodynamic monitoring for resuscitation. Interventions included transient ischemic challenge on the forearm. After blood pressure normalization, hemodynamic and oximetric PAC variables and, simultaneously, steady-state StO2 and its changes from ischemic challenge (deoxygenation and reoxygenation rates) were measured. Fifteen patients were studied. All the patients had a mean arterial pressure above 65 mmHg. The DO2 index (iDO2) range in the studied population was 215 to 674 mL O2/min per m2. The mean mixed venous oxygen saturation value was 61% ± 10%, mean cardiac index was 3.4 ± 0.9 L/min per m2, and blood lactate level was 4.6 ± 2.7 mmol/L. Steady-state StO2 significantly correlated with iDO2, arterial and venous O2 content, and O2 extraction ratio. A StO2 cutoff value of 75% predicted iDO2 below 450, with a sensitivity of 0.9 and a specificity of 0.9. In patients in septic shock and normalized MAP, low StO2 reflects extremely low iDO2. Steady-state StO2 does not correlate with moderately low iDO2, indicating poor sensitivity of StO2 to rule out hypoperfusion.

Monitorización hemodinámica en el paciente crítico. Recomendaciones del Grupo de Trabajo de Cuidados Intensivos Cardiológicos y RCP de la Sociedad Española de Medicina Intensiva, Crítica y Unidades Coronarias

Hemodynamic monitoring offers valuable information on cardiovascular performance in the critically ill, and has become a fundamental tool in the diagnostic approach and in the therapy guidance of those patients presenting with tissue hypoperfusion. From introduction of the pulmonary artery catheter to the latest less invasive technologies, hemodynamic monitoring has been surrounded by many questions regarding its usefulness and its ultimate impact on patient prognosis. The Cardiological Intensive Care and CPR Working Group (GTCIC-RCP) of the Spanish Society of Intensive Care and Coronary Units (SEMICYUC) has recently impulsed the development of an updating series in hemodynamic monitoring. Now, a final series of recommendations are presented in order to analyze essential issues in hemodynamics, with the purpose of becoming a useful tool for residents and critical care practitioners involved in the daily management of critically ill patients.

Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse: can irreversibility be anticipated?

BACKGROUND The causes of cardiovascular collapse (CC) during hemorrhagic shock (HS) are unknown. We hypothesized that vascular tone loss characterizes CC, and that arterial pulse pressure/stroke volume index ratio or vascular tone index (VTI) would identify CC. METHODS Fourteen Yorkshire-Durock pigs were bled to 30 mmHg mean arterial pressure and held there by repetitive bleeding until rendered unable to compensate (CC) or for 90 min (NoCC). They were then resuscitated in equal parts to shed volume and observed for 2 h. CC was defined as a MAP < 30 mmHg for 10 min or <20 mmHg for 10 s. Study variables were recorded at baseline (B0), 30, 60, 90 min after bleeding and at resuscitation (R0), 30, and 60 min afterward. RESULTS Swine were bled to 32% ± 9% of total blood volume. Epinephrine (Epi) and VTI were low and did not change in NoCC after bleeding compared with CC swine, in which both increased (0.97 ± 0.22 to 2.57 ± 1.42 mcg/dL, and 173 ± 181 to 939 ± 474 mmHg/mL, respectively), despite no differences in bled volume. Lactate increase rate (LIR) increased with hemorrhage and was higher at R0 for CC, but did not vary in NoCC. VTI identified CC from NoCC and survivors from non-survivors before CC. A large increase in LIR was coincident with VTI decrement before CC occurred. CONCLUSIONS Vasodilatation immediately prior to CC in severe HS occurs at the same time as an increase in LIR, suggesting loss of tone as the mechanism causing CC, and energy failure as its probable cause.

Fluid therapy and the hypovolemic microcirculation

Purpose of reviewIn 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 findingsMacrocirculatory 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. SummaryCurrent 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 optimization.

Thenar oxygen saturation during weaning from mechanical ventilation: an observational study

Our aim was to determine whether thenar tissue oxygen saturation (StO2), measured by noninvasive near-infrared spectroscopy, and its changes derived from an ischaemic challenge are associated with weaning outcome. Our study comprised a prospective observational study in a 26-bed medical–surgical intensive care unit. Patients receiving mechanical ventilation for >48 h, and considered ready to wean by their physicians underwent a 30-min weaning trial. StO2 was measured continuously on the thenar eminence. A transient vascular occlusion test was performed prior to and at the end of the 30-min weaning trial, in order to obtain StO2 deoxygenation and reoxygenation rates, and estimated local oxygen consumption. 37 patients were studied. Patients were classified as weaning success (n=24) or weaning failure (n=13). No significant demographic, respiratory or haemodynamic differences were observed between the groups at inclusion. Patients who failed the overall weaning process showed a significant increase in deoxygenation and in local oxygen consumption from baseline to 30 min of weaning trial, whereas no significant changes were observed in the weaning success group. Failure to wean from mechanical ventilation was associated with higher relative increases in deoxygenation after 30 min of spontaneous ventilation. Failure to wean from mechanical ventilation is associated with increases in deoxygenation after spontaneous ventilation http://ow.ly/pUn5B

Near-infrared spectroscopy StO2 monitoring to assess the therapeutic effect of drotrecogin alfa (activated) on microcirculation in patients with severe sepsis or septic shock

BackgroundSepsis is a leading cause of death despite appropriate management. There is increasing evidence that microcirculatory alterations might persist independently from macrohemodynamic improvement and are related to clinical evolution. Future efforts need to be directed towards microperfusion monitoring and treatment. This study explored the utility of thenar muscle oxygen saturation (StO2) and its changes during a transient vascular occlusion test (VOT) to measure the microcirculatory response to drotrecogin alfa (activated) (DrotAA) in septic patients.MethodsA prospective, observational study was performed in three general intensive care units at three university hospitals. We studied 58 patients with recent onset of severe sepsis or septic shock and at least two organ dysfunctions. Thirty-two patients were treated with DrotAA and 26 were not treated because of formal contraindication. StO2 was monitored using near-infrared spectroscopy (NIRS), and VOT was performed to obtain deoxygenation (DeOx) and reoxygenation (ReOx) slopes. Measurements were obtained before DrotAA was started and were repeated daily for a 96-hour period.ResultsPatients’ characteristics, outcome, severity, and baseline values of StO2, DeOx, and ReOx did not differ between groups. Treated patients significantly improved DeOx and ReOx values over time, whereas control patients did not. In treated patients, ReOx improvements were correlated to norepinephrine dose reductions. Early clinical response (SOFA improvement after 48 hours of treatment) was not associated to changes in VOT-derived slopes. In the treated group, the relative improvement of DeOx within 48 hours was able to predict mortality (AUC 0.91, p < 0.01).ConclusionsIn patients with severe sepsis or septic shock, DrotAA infusion was associated with improvement in regional tissue oxygenation. The degree of DeOx amelioration after 2 days in treated patients predicted mortality with high sensitivity and specificity. Thus, StO2 derived variables might be useful to evaluate the microcirculatory response to treatment of septic shock.