Qiuhua Chen

Pulmonary acute respiratory distress syndrome: positive end-expiratory pressure titration needs stress index

BACKGROUND The heterogeneity of lung injury in pulmonary acute respiratory distress syndrome (ARDS) may have contributed to the greater response of hyperinflated area with positive end-expiratory pressure (PEEP). PEEP titrated by stress index can reduce the risk of alveolar hyperinflation in patients with pulmonary ARDS. The authors sought to investigate the effects of PEEP titrated by stress index on lung recruitment and protection after recruitment maneuver (RM) in pulmonary ARDS patients. MATERIALS AND METHODS Thirty patients with pulmonary ARDS were enrolled. After RM, PEEP was randomly set according to stress index, oxygenation, static pulmonary compliance (Cst), or lower inflection point (LIP) + 2 cmH2O strategies. Recruitment volume, gas exchange, respiratory mechanics, and hemodynamic parameters were collected. RESULTS PEEP titrated by stress index (15.1 ± 1.8 cmH2O) was similar to the levels titrated by oxygenation (14.5 ± 2.9 cmH2O), higher than that titrated by Cst (11.3 ± 2.5 cmH2O) and LIP (12.9 ± 1.6 cmH2O) (P < 0.05). Compared with baseline, PaO2/FiO2 and recruitment volume were significantly improved after PEEP titration with the four strategies (P < 0.05). PaO2/FiO2 and recruitment volume were similar when using PEEP titrated by stress index and oxygenation but higher than that titrated by Cst and LIP. Compared with baseline, lung compliance increased significantly when PEEP determined by Cst, but there was no difference of Cst in these four strategies. There was no influence of PEEP titration with the four strategies on hemodynamic parameters. CONCLUSIONS PEEP titration by stress index might be more beneficial for pulmonary ARDS patients after RM.

Optimization of positive end-expiratory pressure by volumetric capnography variables in lavage-induced acute lung injury.

Background: In the acute respiratory distress syndrome (ARDS), lung-protective ventilation strategies combine the delivery of small tidal volumes (V<smlcap>T</smlcap>) with sufficient positive end-expiratory pressure (PEEP). However, an optimal approach guiding the setting of PEEP has not been defined. Monitoring volumetric capnography is useful to detect changes in lung aeration. Objectives: The aim of this study was to determine whether volumetric capnography may be a useful method to determine the optimal PEEP in ARDS. Methods: In 8 lung-lavaged piglets, PEEP was reduced from 20 to 4 cm H₂O in steps of 4 cm H₂O every 10 min followed by full lung recruitment. Volumetric capnography, respiratory mechanics, blood gas analysis, hemodynamic data and whole-lung computed tomography scans were obtained at each PEEP level. Results: After lung recruitment, end-expiratory lung volume progressively decreased from 1,160 ± 273 ml at PEEP 20 cm H₂O to 314 ± 86 ml at PEEP 4 cm H₂O. The ratio of alveolar dead space (V<smlcap>D</smlcap>_alv) to alveolar V<smlcap>T</smlcap> (V<smlcap>T</smlcap>_alv) and the phase III slope of volumetric capnography (S_III) reached a minimum at PEEP 16 cm H₂O. At this PEEP level, overaerated lung regions were significantly reduced, nonaerated lung regions did not increase, and partial pressure of oxygen in arterial blood/fraction of inspired oxygen (P/F) and static respiratory system compliance (Crs) reached a maximum. At PEEP levels <16 cm H₂O, nonaerated lung regions significantly increased, P/F and Crs deteriorated, and V<smlcap>D</smlcap>_alv/V<smlcap>T</smlcap>_alv and S_III began to increase. Conclusions: In this surfactant-depleted model, PEEP at the lowest V<smlcap>D</smlcap>_alv/V<smlcap>T</smlcap>_alv and S_III allows an optimal balance between lung overinflation and collapse. Hence, volumetric capnography is a useful bedside approach to identify the optimal PEEP.

Higher frequency ventilation attenuates lung injury during high-frequency oscillatory ventilation in sheep models of acute respiratory distress syndrome.

Background:High-frequency oscillatory ventilation (HFOV) at higher frequencies minimizes the tidal volume. However, whether increased frequencies during HFOV can reduce ventilator-induced lung injury remains unknown. Methods:After the induction of acute respiratory distress syndrome in the model by repeated lavages, 24 adult sheep were randomly divided into four groups (n = 6): three HFOV groups (3, 6, and 9 Hz) and one conventional mechanical ventilation (CMV) group. Standard lung recruitments were performed in all groups until optimal alveolar recruitment was reached. After lung recruitment, the optimal mean airway pressure or positive end-expiratory pressure was determined with decremental pressure titration, 2 cm H2O every 10 min. Animals were ventilated for 4 h. Results:After lung recruitment, sustained improvements in gas exchange and compliance were observed in all groups. Compared with the HFOV-3 Hz and CMV groups, the transpulmonary pressure and tidal volumes were statistically significantly lower in the HFOV-9 Hz group. The lung injury scores and wet/dry weight ratios were significantly reduced in the HFOV-9 Hz group compared with the HFOV-3 Hz and CMV groups. Expression of interleukin-1&bgr; and interleukin-6 in the lung tissue, decreased significantly in the HFOV-9 Hz group compared with the HFOV-3 Hz and CMV groups. Malondialdehyde expression and myeloperoxidase activity in lung tissues in the HFOV-9 Hz group decreased significantly, compared with the HFOV-3 Hz and CMV groups. Conclusion:The use of HFOV at 9 Hz minimizes lung stress and tidal volumes, resulting in less lung injury and reduced levels of inflammatory mediators compared with the HFOV-3 Hz and CMV conditions.

Acid‑induced cell injury and death in lung epithelial cells is associated with the activation of mitogen‑activated protein kinases.

Gastric hydrochloric acid (HCl) has been regarded as a causative factor of acute lung injury (ALI). The activation of mitogen‑activated protein kinases (MAPKs) has been suggested to be a mechanism involved in the pathogenesis of ALI in vivo. However, the effects of HCl on MAPK activation in lung epithelial cells remain to be fully elucidated. Further investigation into the role of MAPK activation in acid‑induced cell injury and death is also needed. In the present study, BEAS‑2B cells were treated with HCl (pH 4.0 medium) for 5, 15 and 30 min, and the acidified medium was then removed. Cell viability and death were detected by MTT assay and trypan blue exclusion staining, respectively. The activation of MAPKs [c‑Jun N‑terminal kinase (JNK), p38 MAPK and extracellular signal‑regulated kinase (ERK) 1/2] was analyzed by western blot analysis. Cytotoxicity was assessed by lactate dehydrogenase (LDH) release, and IL‑8 levels in culture supernatants were measured by enzyme‑linked immunosorbent assay (ELISA). Cell apoptosis was detected as changes in the levels of capase‑3, Bad and fas by western blot analysis and the number of apoptotic cells by using Annexin V/propidium iodide (PI) staining. Following pre‑treatment with the JNK inhibitor II (10 µmol/l), the p38 inhibitor SB202190 (10 µmol/l) or the ERK inhibitor U0126 (10 µmol/l) for 30 min, BEAS‑2B cells were exposed to HCl for 30 min. Cell viability, cytotoxicity, IL‑8 levels and apoptosis were detected 4 h following acid stimulation. The viability of BEAS‑2B cells was inhibited and cell death was increased in the presence of HCl. HCl stimulation induced activation of MAPKs in a time‑dependent manner. HCl exposure increased the levels of IL‑8 and the release of LDH, and induced apoptosis in BEAS‑2B cells. JNK and p38 inhibitors increased cell viability and decreased cytotoxicity and cell apoptosis, while ERK inhibitor had no effect on cell viability, cytotoxicity or apoptosis. These results indicate that acid exposure induced epithelial cell injury and death. The activation of JNK and p38 is involved in HCl‑induced epithelial lung cell injury and death.

The Effect of Alveolar Dead Space on the Measurement of End-Expiratory Lung Volume by Modified Nitrogen Wash-Out/Wash-In in Lavage-Induced Lung Injury

BACKGROUND: The accuracy of end-expiratory lung volume measurement by the modified nitrogen wash-out/wash-in method (EELV-N2) depends on the precise determination of carbon dioxide elimination (V̇CO2), which is affected by alveolar dead space (VD-alv). The purpose of this study was to investigate the influence of VD-alv on EELV-N2. METHODS: Six piglets with lavage-induced acute lung injury were mechanically ventilated in a decremental PEEP trial that was reduced from 20 to 4 cm H2O in steps of 4 cm H2O every 10 min. EELV was measured by the modified EELV-N2 method and computed tomography scan (EELV-CT), volumetric capnography, blood gas measurements, and hemodynamic data were recorded at each PEEP level. The data were divided into higher and lower PEEP groups. RESULTS: During the decremental PEEP trial, EELV-N2 exhibited a high correlation (r2 = 0.86, P < .001) with EELV-CT, with a bias of −48.6 ± 150.7 mL (1 ± 18%). In the higher PEEP group, EELV-N2 was not correlated with EELV-CT, with a bias of –168.1 ± 171.5 mL (−14 ± 14%). However, in the lower PEEP group, EELV-N2 exhibited a high correlation (r2 = 0.86, P < .001) with EELV-CT, with a bias of 11.2 ± 97.2 mL (6 ± 17%). The measurement bias was negatively correlated with VD-alv (r2 = 0.44, P = .04) and V̇CO2 (r2 = 0.47, P = .03) in the higher PEEP group. CONCLUSIONS: In this surfactant-depleted model, EELV measurement by the modified EELV-N2 method reveals a systematic underestimation at high PEEP levels that is partly due to an increase in VD-alv.

Relationship between regional lung compliance and ventilation homogeneity in the supine and prone position.

The prone position (PP) improves ventilation homogeneity in acute respiratory distress syndrome. The aim of this study was to investigate whether the alleviation of ventilation inhomogeneity in PP was due to changes in regional lung compliance.