JOAO BATISTA BORGES SOBRINHO DORINI
Projetos de Pesquisa
Unidades Organizacionais
LIM/09 - Laboratório de Pneumologia, Hospital das Clínicas, Faculdade de Medicina
4 resultados
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- How large is the lung recruitability in early acute respiratory distress syndrome: a prospective case series of patients monitored by computed tomography(2012) MATOS, Gustavo F. J. de; STANZANI, Fabiana; PASSOS, Rogerio H.; FONTANA, Mauricio F.; ALBALADEJO, Renata; CASERTA, Raquel E.; SANTOS, Durval C. B.; BORGES, Joao Batista; AMATO, Marcelo B. P.; BARBAS, Carmen S. V.Introduction: The benefits of higher positive end expiratory pressure (PEEP) in patients with acute respiratory distress syndrome (ARDS) have been modest, but few studies have fully tested the ""open-lung hypothesis"". This hypothesis states that most of the collapsed lung tissue observed in ARDS can be reversed at an acceptable clinical cost, potentially resulting in better lung protection, but requiring more intensive maneuvers. The short-/middle-term efficacy of a maximum recruitment strategy (MRS) was recently described in a small physiological study. The present study extends those results, describing a case-series of non-selected patients with early, severe ARDS submitted to MRS and followed until hospital discharge or death. Methods: MRS guided by thoracic computed tomography (CT) included two parts: a recruitment phase to calculate opening pressures (incremental steps under pressure-controlled ventilation up to maximum inspiratory pressures of 60 cmH(2)O, at constant driving-pressures of 15 cmH(2)O); and a PEEP titration phase (decremental PEEP steps from 25 to 10 cmH2O) used to estimate the minimum PEEP to keep lungs open. During all steps, we calculated the size of the non-aerated (-100 to +100 HU) compartment and the recruitability of the lungs (the percent mass of collapsed tissue re-aerated from baseline to maximum PEEP). Results: A total of 51 severe ARDS patients, with a mean age of 50.7 years (84% primary ARDS) was studied. The opening plateau-pressure was 59.6 (+/- 5.9 cmH(2)O), and the mean PEEP titrated after MRS was 24.6 (+/- 2.9 cmH(2)O). Mean PaO2/FiO(2) ratio increased from 125 (+/- 43) to 300 (+/- 103; P < 0.0001) after MRS and was sustained above 300 throughout seven days. Non-aerated parenchyma decreased significantly from 53.6% (interquartile range (IQR): 42.5 to 62.4) to 12.7% (IQR: 4.9 to 24.2) (P < 0.0001) after MRS. The potentially recruitable lung was estimated at 45% (IQR: 25 to 53). We did not observe major barotrauma or significant clinical complications associated with the maneuver. Conclusions: MRS could efficiently reverse hypoxemia and most of the collapsed lung tissue during the course of ARDS, compatible with a high lung recruitability in non-selected patients with early, severe ARDS. This strategy should be tested in a prospective randomized clinical trial.
- Electrical impedance tomography in acute respiratory distress syndrome(2018) BACHMANN, M. Consuelo; MORAIS, Caio; BUGEDO, Guillermo; BRUHN, Alejandro; MORALES, Arturo; BORGES, Joao B.; COSTA, Eduardo; RETAMAL, JaimeAcute respiratory distress syndrome (ARDS) is a clinical entity that acutely affects the lung parenchyma, and is characterized by diffuse alveolar damage and increased pulmonary vascular permeability. Currently, computed tomography (CT) is commonly used for classifying and prognosticating ARDS. However, performing this examination in critically ill patients is complex, due to the need to transfer these patients to the CT room. Fortunately, new technologies have been developed that allow the monitoring of patients at the bedside. Electrical impedance tomography (EIT) is a monitoring tool that allows one to evaluate at the bedside the distribution of pulmonary ventilation continuously, in real time, and which has proven to be useful in optimizing mechanical ventilation parameters in critically ill patients. Several clinical applications of EIT have been developed during the last years and the technique has been generating increasing interest among researchers. However, among clinicians, there is still a lack of knowledge regarding the technical principles of EIT and potential applications in ARDS patients. The aim of this review is to present the characteristics, technical concepts, and clinical applications of EIT, which may allow better monitoring of lung function during ARDS.
- THAM reduces CO2-associated increase in pulmonary vascular resistance - an experimental study in lung-injured piglets(2015) HOSTMAN, Staffan; BORGES, Joao Batista; SUAREZ-SIPMANN, Fernando; AHLGREN, Kerstin M.; ENGSTROM, Joakim; HEDENSTIERNA, Goran; LARSSON, AndersIntroduction: Low tidal volume (VT) ventilation is recommended in patients with acute respiratory distress syndrome (ARDS). This may increase arterial carbon dioxide tension (PaCO2), decrease pH, and augment pulmonary vascular resistance (PVR). We hypothesized that Tris(hydroxymethyl) aminomethane (THAM), a pure proton acceptor, would dampen these effects, preventing the increase in PVR. Methods: A one-hit injury ARDS model was established by repeated lung lavages in 18 piglets. After ventilation with V-T of 6 ml/kg to maintain normocapnia, VT was reduced to 3 ml/kg to induce hypercapnia. Six animals received THAM for 1 h, six for 3 h, and six serving as controls received no THAM. In all, the experiment continued for 6 h. The THAM dosage was calculated to normalize pH and exhibit a lasting effect. Gas exchange, pulmonary, and systemic hemodynamics were tracked. Inflammatory markers were obtained at the end of the experiment. Results: In the controls, the decrease in VT from 6 to 3 ml/kg increased PaCO2 from 6.0 +/- 0.5 to 13.8 +/- 1.5 kPa and lowered pH from 7.40 +/- 0.01 to 7.12 +/- 0.06, whereas base excess (BE) remained stable at 2.7 +/- 2.3 mEq/L to 3.4 +/- 3.2 mEq/L. In the THAM groups, PaCO2 decreased and pH increased above 7.4 during the infusions. After discontinuing the infusions, PaCO2 increased above the corresponding level of the controls (15.2 +/- 1.7 kPa and 22.6 +/- 3.3 kPa for 1-h and 3-h THAM infusions, respectively). Despite a marked increase in BE (13.8 +/- 3.5 and 31.2 +/- 2.2 for 1-h and 3-h THAM infusions, respectively), pH became similar to the corresponding levels of the controls. PVR was lower in the THAM groups (at 6 h, 329 +/- 77 dyn.s/m(5) and 255 +/- 43 dyn.s/m(5) in the 1-h and 3-h groups, respectively, compared with 450 +/- 141 dyn.s/m(5) in the controls), as were pulmonary arterial pressures. Conclusions: The pH in the THAM groups was similar to pH in the controls at 6 h, despite a marked increase in BE. This was due to an increase in PaCO2 after stopping the THAM infusion, possibly by intracellular release of CO2. Pulmonary arterial pressure and PVR were lower in the THAM-treated animals, indicating that THAM may be an option to reduce PVR in acute hypercapnia.
- Non-lobar atelectasis generates inflammation and structural alveolar injury in the surrounding healthy tissue during mechanical ventilation(2014) RETAMAL, Jaime; BERGAMINI, Bruno Curty; CARVALHO, Alysson R.; BOZZA, Fernando A.; BORZONE, Gisella; BORGES, Joao Batista; LARSSON, Anders; HEDENSTIERNA, Goeran; BUGEDO, Guillermo; BRUHN, AlejandroIntroduction: When alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation. Methods: A total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with FIO2 = 1.0, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (V-T) = 10 ml/kg and positive end-expiratory pressure (PEEP) = 3 cmH(2)O (V(T)10/PEEP3); and 2) V-T=20 ml/kg and PEEP = 0 cmH2O (V(T)20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n = 12); tissue cytokines (n = 12); and micro-computed tomography (microCT; n = 2). An additional six, non-ventilated, healthy animals were used as controls. Results: Atelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm(3). There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the V(T)20/ZEEP than VT10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1 beta and cytokine-induced neutrophil chemoattractant-1 between regions. Conclusions: The present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue.