Publications

Introduction: Post-cardiac arrest (CA) resuscitated patients often develop a "sepsis-like" syndrome, which may be associated with organ dysfunction. We have shown that microcirculation is impaired after CA (1), however the time course of these alterations as well as their association with mortality have not been studied yet. We evaluated the evolution of microvascular reactivity disturbances during time after CA and their association with outcome. Methods: From April 2009 to April 2012, we prospectively studied 60 successfully resuscitated CA patients. Thenar oxygen saturation (StO2) was measured using a tissue spectrometer (InSpectra 650; Hutchinson, USA), and a vaso-occlusive test was performed to evaluate StO2 reperfusion rate (SRR), reflecting microvascular reactivity. Measurements were performed at 5 different time points: within the first 4 hours after CA (T0, n=38) and 4-12 hours (T1, n=49), 12-24 hours (T2, n=58), 24-48 hours (T3, n=50), 48-72 hours (T4, n=40) thereafter. The following variables were recorded: total hemoglobin index (THI), the StO2 desaturation slope during the occlusion (dSlope, %/sec) and the StO2 upslope of the reperfusion phase following the ischemic period (ascSlope, %/sec). Muscle oxygen consumption (NIR VO2; arbitrary units) was calculated as the product of the inverse StO2 desaturation slope and the mean THI over the first minute of arterial occlusion. Analysis of variance (ANOVA) for repeated measurement with correction for missing values was performed. Results: In this cohort, median age was 61 [52-67] years and 48 (80%) patients were men, 44 (73%) had a presumed cardiac origin, 29 (60%) VF/VT as initial rhythm and 55 (91%) an out-of-hospital CA. Median time from collapse to CPR and from collapse to ROSC were 3.5 [3-5] and 15 [10-20] minutes, respectively. Median APACHE II and SOFA score were 26 [22-31] and 7 [5-9] on admission, respectively. Twenty-three (38%) patients presented cardiogenic shock on ICU admission. Overall ICU stay was 4 [2-11] days and 33/60 (55%) eventually died. The cause of death was neurological (ND) in 22 patients and related to cardiac or multiple organ failure (MOF) in 11 patients. Only THI (from 11.8 [9.5-14.6] to 9.6 [8.1-11.9], p=0.02), and dSlope (from -0.11 [-0.18 to -0.09] to -0.14 [-0.20 to -0.11], p=0.004) showed significantly changes during time. When we analysed separately survivors, non-survivors for ND and non-survivors with MOF, we observed a significant differences in THI, nirVO2 and ascSlope between survivors and non-survivors with MOF, while microvascular data between survivors and non-survivors with ND were similar. Conclusions: Alterations in peripheral microvascular reactivity progressively resolved during time and were more pronounced in those patients dying from cardiac or MOF.

An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.

The response of septic patients to a fluid challenge is independent of baseline SvO2. The presence of a high SvO2 does not necessarily exclude the need for further fluid administration.

SCOPUS: no.j

1. Dobutamine has been used to study the relationship between oxygen consumption (VO2) and oxygen delivery (DO2) in critically ill patients, but this has led to concerns that it could consistently increase VO2 in all patients. Although a direct thermogenic effect of the catecholamine has been primarily implicated in this increase in VO2, an increase in blood flow may contribute significantly by increasing the oxygen requirements of the heart and other organs such as the kidney and the liver. If this mechanism is predominant, it should also be observed when blood flow increases during the infusion of non-adrenergic agents. To separate the two mechanisms, we compared the effects of dobutamine with those of sodium nitroprusside on VO2/DO2 relationships in healthy volunteers. 2. Eight healthy volunteers received infusions of dobutamine at doses of 2, 4 and 6 micrograms min-1 kg-1 and nitroprusside at doses of 0.5, 1 and 2 micrograms min-1 kg-1 in an alternate order. 3. VO2 was determined by indirect calorimetry and cardiac output by electrical bioimpedance. Data were analysed by analysis of variance for repeated measurements and individual VO2/DO2 slopes were determined by linear regression. 4. VO2 increased more with dobutamine than with nitroprusside (from 138 +/- 14 to 149 +/- 20 ml min-1 m-2, P < 0.001, and from 131 +/- 14 to 138 +/- 17 ml min-1 m-2, P < 0.001, respectively). However, DO2 also increased more with dobutamine than with nitroprusside (from 531 +/- 186 to 702 +/- 274 ml min-1 m-2, P < 0.001, and from 523 +/- 107 to 610 +/- 122 ml min-1 m-2, P < 0.001, respectively). Individual VO2/DO2 slopes were similar with dobutamine and nitroprusside (6.5 +/- 3.5 compared with 7.1 +/- 4.6%, P not significant). 5. At the doses used, DO2 and VO2 increased more with dobutamine than with nitroprusside in healthy volunteers. However, the VO2/DO2 slopes were similar for both substances. Thus, an increase in VO2 is not exclusively observed with catecholamines. Studies of the effects of therapeutic interventions on oxygen-derived variables should report not only changes in VO2 but also VO2/DO2 slopes.