RESUMO
BACKGROUND: Variable ventilation recruits alveoli in atelectatic lungs, but it is unknown how it compares with conventional recruitment manoeuvres. OBJECTIVES: To test whether mechanical ventilation with variable tidal volumes and conventional recruitment manoeuvres have comparable effects on lung function. DESIGN: Randomised crossover study. SETTING: University hospital research facility. ANIMALS: Eleven juvenile mechanically ventilated pigs with atelectasis created by saline lung lavage. INTERVENTIONS: Lung recruitment was performed using two strategies, both with an individualised optimal positive-end expiratory pressure (PEEP) associated with the best respiratory system elastance during a decremental PEEP trial: conventional recruitment manoeuvres (stepwise increase of PEEP) in pressure-controlled mode) followed by 50âmin of volume-controlled ventilation (VCV) with constant tidal volume, and variable ventilation, consisting of 50âmin of VCV with random variation in tidal volume. MAIN OUTCOME MEASURES: Before and 50âmin after each recruitment manoeuvre strategy, lung aeration was assessed by computed tomography, and relative lung perfusion and ventilation (0%â=âdorsal, 100%â=âventral) were determined by electrical impedance tomography. RESULTS: After 50âmin, variable ventilation and stepwise recruitment manoeuvres decreased the relative mass of poorly and nonaerated lung tissue (percent lung mass: 35.3â±â6.2 versus 34.2â±â6.6, P â=â0.303); reduced poorly aerated lung mass compared with baseline (-3.5â±â4.0%, P â=â0.016, and -5.2â±â2.8%, P â<â0.001, respectively), and reduced nonaerated lung mass compared with baseline (-7.2â±â2.5%, P â<â0.001; and -4.7â±â2.8%, P â<â0.001 respectively), while the distribution of relative perfusion was barely affected (variable ventilation: -0.8â±â1.1%, P â=â0.044; stepwise recruitment manoeuvres: -0.4â±â0.9%, P â=â0.167). Compared with baseline, variable ventilation and stepwise recruitment manoeuvres increased Pa O 2 (172â±â85mmHg, P â=â0.001; and 213â±â73âmmHg, P â<â0.001, respectively), reduced Pa CO 2 (-9.6â±â8.1âmmHg, P â=â0.003; and -6.7â±â4.6âmmHg, P â<â0.001, respectively), and decreased elastance (-11.4â±â6.3âcmH 2 O, P â<â0.001; and -14.1â±â3.3âcmH 2 O, P â<â0.001, respectively). Mean arterial pressure decreased during stepwise recruitment manoeuvres (-24â±â8âmmHg, P â=â0.006), but not variable ventilation. CONCLUSION: In this model of lung atelectasis, variable ventilation and stepwise recruitment manoeuvres effectively recruited lungs, but only variable ventilation did not adversely affect haemodynamics. TRIAL REGISTRATION: This study was registered and approved by Landesdirektion Dresden, Germany (DD24-5131/354/64).
Assuntos
Pulmão , Atelectasia Pulmonar , Suínos , Animais , Pulmão/diagnóstico por imagem , Atelectasia Pulmonar/terapia , Respiração Artificial/métodos , Respiração com Pressão Positiva/métodos , Modelos TeóricosRESUMO
OBJECTIVES: To determine the impact of positive end-expiratory pressure during mechanical ventilation with and without spontaneous breathing activity on regional lung inflammation in experimental nonsevere acute respiratory distress syndrome. DESIGN: Laboratory investigation. SETTING: University hospital research facility. SUBJECTS: Twenty-four pigs (28.1-58.2 kg). INTERVENTIONS: In anesthetized animals, intrapleural pressure sensors were placed thoracoscopically in ventral, dorsal, and caudal regions of the left hemithorax. Lung injury was induced with saline lung lavage followed by injurious ventilation in supine position. During airway pressure release ventilation with low tidal volumes, positive end-expiratory pressure was set 4 cm H2O above the level to reach a positive transpulmonary pressure in caudal regions at end-expiration (best-positive end-expiratory pressure). Animals were randomly assigned to one of four groups (n = 6/group; 12 hr): 1) no spontaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory pressure - 4 cm H2O, 2) no spontaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory pressure + 4 cm H2O, 3) spontaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory pressure + 4 cm H2O, 4) spontaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory pressure - 4 cm H2O. MEASUREMENTS AND MAIN RESULTS: Global lung inflammation assessed by specific [F]fluorodeoxyglucose uptake rate (median [25-75% percentiles], min) was decreased with higher compared with lower positive end-expiratory pressure both without spontaneous breathing activity (0.029 [0.027-0.030] vs 0.044 [0.041-0.065]; p = 0.004) and with spontaneous breathing activity (0.032 [0.028-0.043] vs 0.057 [0.042-0.075]; p = 0.016). Spontaneous breathing activity did not increase global lung inflammation. Lung inflammation in dorsal regions correlated with transpulmonary driving pressure from spontaneous breathing at lower (r = 0.850; p = 0.032) but not higher positive end-expiratory pressure (r = 0.018; p = 0.972). Higher positive end-expiratory pressure resulted in a more homogeneous distribution of aeration and regional transpulmonary pressures at end-expiration along the ventral-dorsal gradient, as well as a shift of the perfusion center toward dependent zones in the presence of spontaneous breathing activity. CONCLUSIONS: In experimental mild-to-moderate acute respiratory distress syndrome, positive end-expiratory pressure levels that stabilize dependent lung regions reduce global lung inflammation during mechanical ventilation, independent from spontaneous breathing activity.
Assuntos
Pneumonia/terapia , Respiração com Pressão Positiva/métodos , Síndrome do Desconforto Respiratório/terapia , Mecânica Respiratória/fisiologia , Animais , Modelos Animais de Doenças , Feminino , Masculino , SuínosRESUMO
Aneurysmal subarachnoid hemorrhage (aSAH) often causes cardiopulmonary dysfunction. Therapeutic strategies can be guided by standard (invasive arterial/central venous pressure measurements, fluid balance assessment), and/or advanced (pulse index continuous cardiac output, pulse dye densitometry, pulmonary artery catheterization) hemodynamic monitoring. We conducted a systematic review and meta-analysis of the literature to determine whether standard compared with advanced hemodynamic monitoring can improve patient management and clinical outcomes after aSAH. A literature search was performed for articles published between January 1, 2000 and January 1, 2019. Studies involving aSAH patients admitted to the intensive care unit and subjected to any type of hemodynamic monitoring were included. A total of 14 studies were selected for the qualitative synthesis and 3 randomized controlled trials, comparing standard versus advanced hemodynamic monitoring, for meta-analysis. The incidence of delayed cerebral ischemia was lower in the advanced compared with standard hemodynamic monitoring group (relative risk [RR]=0.71, 95% confidence interval [CI]=0.52-0.99; P=0.044), but there were no differences in neurological outcome (RR=0.83, 95% CI=0.64-1.06; P=0.14), pulmonary edema onset (RR=0.44, 95% CI=0.05-3.92; P=0.46), or fluid intake (mean difference=-169 mL; 95% CI=-1463 to 1126 mL; P=0.8) between the 2 groups. In summary, this systematic review and meta-analysis found only low-quality evidence to support the use of advanced hemodynamic monitoring in selected aSAH patients. Because of the small number and low quality of studies available for inclusion in the review, further studies are required to investigate the impact of standard and advanced hemodynamic monitoring-guided management on aSAH outcomes.