Examinando por Autor "Salomon, T."

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    Effect of a lung rest strategy during ECMO in a porcine acute lung injury model
    (SpringerOpen, 2015-10) Araos, J.; Cruces, P.; Tapia, P.; Alegria, L.; García, P.; Salomon, T.; Rodriguez, F.; Amthauer, M.; Castro, G.; Erranz, B.; Soto, D.; Carreño, P.; Medina, T.; Damiani, F.; Bugedo, G.; Bruhn, A.
    Introduction ECMO is used to treat patients who develop refractory hypoxemia and to provide a more protective ventilation. Several guidelines recommend “lung rest” strategies based on variable ventilatory parameters. However, there is limited evidence to support this strategy. Objectives To compare the effect of a lung rest strategy based on near-apneic ventilation (Vt 1-2 ml/kg, PEEP 10, respiratory rate-RR 5 min) versus conventional (Vt 10ml/kg, PEEP 5, RR 20/min), and standard protective ventilation (Vt 6ml/kg, PEEP 10, RR 20/min). Methods Twenty-four domestic pigs (26-36 kg) were anesthetized, mechanically ventilated (Vt 10 ml/kg, PEEP 5, O2 1.0) and invasively monitored. Six animals were used as Sham. In the other 18 lung injury was induced by saline lavages (30 ml/kg per lavage) performed repeatedly in both supine and prone position until PaO2/FiO2 dropped below 250. They were then subjected to a 2-hour injurious ventilation with PCV, PEEP = 0, Pinsp = 40 cmH2O, RR = 10/min, I:E = 1:1, one hour in prone and the other in supine. After completing lung injury (time 0) animals were connected to a saline primed-MEDOS Hilite ECMO circuit by inserting a AVALON 23F double-lumen cannula through the external jugular vein. Blood flow was set at 60-70% of cardiac output. Animals were randomized into one of the three groups and ventilated according to randomization for the following 24 hours. Respiratory and hemodynamic data were collected at times 0, 3, 6, 12, 18 and 24h. After euthanizing animals at time 24h, tissue samples were extracted from the lungs and injury evaluated and scored by light microscopy. Total lung water content was estimated by the wet-dry weight ratio. Results PaO2 decreased significantly in all groups after injury, but was progressively restored after ECMO start, despite the study group. Mean arterial pressure remained within normal limits throughout the study period, whereas MPAP increased significantly after injury but reached values close to SHAM soon after ECMO initiation. Lung wet-dry weight ratio and histological injury score increased significantly in all study groups compared to SHAM. Although non-significant, there was a trend towards a better histological injury score when Vt was reduced. Conclusions In this preliminary analysis, we found no clear advantage of reducing Vt when applying ECMO to support a double-hit animal model of ARDS in regard to resolution of lung edema or gas exchange. However, further work is required to determine if the non-significant reduction in lung injury observed in the near-apneic strategy may be relevant in providing further protection to the injured lungs supported by ECMO. © 2015 Araos et al.
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    Ítem
    Influence of tidal volume on pulse pressure variation and stroke volume variation during experimental intra-abdominal hypertension
    (BioMed Central Ltd., 2015-09) Díaz, F.; Erranz, B.; Donoso, A.; Salomon, T.; Cruces, Pablo
    Background: Pulse pressure variation (PPV) and stroke volume variation (SVV) are frequently used to assess fluid responsiveness in critically ill patients on mechanical ventilation (MV). There are many factors, in addition to preload that influence the magnitude of these cyclic variations. We sought to investigate the effect of tidal volume (VT) on PPV and SVV, and prediction of fluid responsiveness in a model of intra-abdominal hypertension (IAH). Methods: Twelve anesthetized and mechanically ventilated piglets on continuous pulse contour cardiac output monitoring. Hypovolemia was ruled out with 2 consecutive fluid boluses after instrumentation. IAH was induced by intraperitoneal instillation of colloid solution with a goal of reducing respiratory system compliance by 50 %. Subjects were classified as fluid responders if stroke volume increased >15 % after each fluid challenge. SVV and PPV were recorded with tidal volumes (VT) of 6, 12 and 18 ml/kg before IAH after IAH induction and after a fluid challenge during IAH. Results: VT influenced PPV and SVV at baseline and during IAH, being significantly larger with higher VT. These differences were attenuated after fluid administration in both conditions. After IAH induction, there was a significant increase in SVV with the three-tested VT, but the magnitude of that change was larger with high VT: with 6 ml/kg from 3 % (3, 4) to 5 % (4, 6.25) (p = 0.05), with 12 ml/kg from 5 % (4, 6) to 11 % (8.75, 17) (p = 0.02) and 18 ml/kg from 5 % (4,7.5) to 15 % (8.75, 19.5) (p = 0.02). Similarly, PPV increased with all the tested VT after IAH induction, being this increase larger with high VT: with 6 ml/kg from 3 % (2, 4.25) to 6 % (4.75, 7) (p = 0.05), with 12 ml/kg from 5 % (4, 6) to 13.5 % (10.25, 15.5) (p = 0.02) and 18 ml/kg from 7 % (5.5, 8.5) to 24 % (13.5, 30.25) (p = 0.02). One third of subjects responded to fluid administration after IAH, but neither SVV nor PPV were able to identify the fluid responders with the tested VT. Conclusion: IAH induction in non-hypovolemic subjects significantly increased SVV and PPV with the three tested VT, but the magnitude of that change was higher with larger VT. This observation reveals the dependence of functional hemodynamic markers on intrathoracic as well intra-abdominal pressures, in addition to volemic status. Also, PPV and SVV were unable to predict fluid responsiveness after IAH induction. Future studies should take into consideration these findings when exploring relationships between dynamic preload indicators and fluid responsiveness during IAH. © 2015 Díaz et al.