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  • Title: [Effect of lung strain on breathing mechanics in dogs with acute respiratory distress syndrome].
    Author: Liu Q, Guo Y, Shan M, Lan C, Chen R.
    Journal: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue; 2018 Sep; 30(9):872-876. PubMed ID: 30309414.
    Abstract:
    OBJECTIVE: To explore the effect of lung strain on breathing mechanics in dogs with acute respiratory distress syndrome (ARDS). METHODS: Twenty-four healthy male Beagle dogs were recruited to reproduce medium ARDS models with venous injection of 0.18 mL/kg oleic acid, and they were randomly assigned to five groups with random numbers table method. In lung protective ventilation (LPV) group (n = 4), the ventilation was supported for 24 hours with tidal volume (VT) at 6-8 mL/kg, and in lung strain 1.0, 1.5, 2.0, 2.5 groups (S1.0, S1.5, S2.0, S2.5 groups), the VT was calculated from lung strain, the volume recruitment by positive end expiratory pressure (VPEEP) and functional residual capacity (FRC). Five groups were given mechanical ventilation for 24 hours or until reaching the end point of the experiment [when the dosage of norepinephrine was higher than 1.4 μg×kg-1×min-1, the blood pressure was still lower than 60 mmHg (1 mmHg = 0.133 kPa) for more than 30 minutes, which was regarded as the end point of the experiment]. Static lung compliance (Cst), airway plateau pressure (Pplat) and lung stress during the experiment were recorded. Linear regression analysis was used to fit the regression equations of lung strain and Cst descending rate, Pplat and lung stress for analyzing their relationships. RESULTS: The VT of group LPV was (7.1±0.5) mL/kg. With the increase of lung strain, VT was gradually increased. VT of group S1.0 [(7.3±1.8) mL/kg] was similar to group LPV. VT of groups S1.5, S2.0, S2.5 was significantly higher than that of group LPV (mL/kg: 13.3±5.5, 18.7±5.4, 20.1±7.4 vs. 7.1±0.5, all P < 0.05). Moreover, under the same lung strain, the difference in VT among individuals was large. The Cst of each group was decreased significantly at the end of the experiment as compared with that before model reproduction. With the increase of lung strain, the rate of Cst descending was increased, Cst dropped more significantly in groups S2.0 and S2.5 than that in groups S1.0 and S1.5 [(48.0±15.0)%, (54.4±9.5)% vs. (25.9±13.7)%, (38.6±8.1)%, all P < 0.05]. Pplat and pulmonary stress at model reproduction in all groups were significantly higher than those before model reproduction, and they increased with the prolongation of ventilation time. Pplat and lung stress at 4 hours of ventilation in group S1.5 were significantly higher than those in group LPV [Pplat (cmH2O, 1 cmH2O = 0.098 kPa): 26.2±2.3 vs. 20.2±4.2, lung stress (cmH2O): 20.5±2.0 vs. 16.6±2.5, both P < 0.05], and they increased with lung strain increasing till to the end of experiment. It was shown by correlation analysis that lung strain was positively related with Cst descending rate, Pplat and lung stress at 4 hours of ventilation (r value was 0.716, 0.660, 0.539, respectively, all P < 0.05), which indicated a strong linear correlation. It was shown by fitting linear regression analysis that when lung strain increased by 1, Cst descending rate increased by 19.0% [95% confidence interval (95%CI) = 14.6-23.3, P = 0.000], Pplat increased by 10.8 cmH2O (95%CI = 7.9-13.7, P = 0.002), and the lung stress increased by 7.4 cmH2O (95%CI = 4.7-10.2, P = 0.002). CONCLUSIONS: In animal ARDS models, the larger the lung strain, the higher the Pplat and lung stress during mechanical ventilation, VT originated for lung strain 2.0 and 2.5 may further reduce Cst in ARDS models, when lung strain over 1.5, Pplat and lung stress increased significantly, which exceeded the safe range of LPV (35 cmH2O and 25 cmH2O, respectively), and further aggravated ventilator induced lung injury (VILI).
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