Adaptive Support Ventilation May Deliver Unwanted Respiratory Rate–Tidal Volume Combinations in Patients with Acute Lung Injury Ventilated According to an Open Lung Concept

2011 ◽  
Vol 114 (5) ◽  
pp. 1138-1143 ◽  
Author(s):  
Dave A. Dongelmans ◽  
Frederique Paulus ◽  
Denise P. Veelo ◽  
Jan M. Binnekade ◽  
Margreeth B. Vroom ◽  
...  
Keyword(s):  
Body Weight ◽  
Respiratory Rate ◽  
Predicted Body Weight ◽  
Adaptive Support Ventilation ◽  
Support Ventilation ◽  
Controlled Ventilation ◽  
Open Lung ◽  
Pressure Controlled Ventilation ◽  
Adaptive Support ◽  
Pressure Controlled

Background With adaptive support ventilation, respiratory rate and tidal volume (V(T)) are a function of the Otis least work of breathing formula. We hypothesized that adaptive support ventilation in an open lung ventilator strategy would deliver higher V(T)s to patients with acute lung injury. Methods Patients with acute lung injury were ventilated according to a local guideline advising the use of lower V(T) (6-8 ml/kg predicted body weight), high concentrations of positive end-expiratory pressure, and recruitment maneuvers. Ventilation parameters were recorded when the ventilator was switched to adaptive support ventilation, and after recruitment maneuvers. If V(T) increased more than 8 ml/kg predicted body weight, airway pressure was limited to correct for the rise of V(T). Results Ten patients with a mean (±SD) Pao(2)/Fio(2) of 171 ± 86 mmHg were included. After a switch from pressure-controlled ventilation to adaptive support ventilation, respiratory rate declined (from 31 ± 5 to 21 ± 6 breaths/min; difference = 10 breaths/min, 95% CI 3-17 breaths/min, P = 0.008) and V(T) increased (from 6.5 ± 0.8 to 9.0 ± 1.6 ml/kg predicted body weight; difference = 2.5 ml, 95% CI 0.4-4.6 ml/kg predicted body weight, P = 0.02). Pressure limitation corrected for the rise of V(T), but minute ventilation declined, forcing the user to switch back to pressure-controlled ventilation. Conclusions Adaptive support ventilation, compared with pressure-controlled ventilation in an open lung strategy setting, delivers a lower respiratory rate-higher V(T) combination. Pressure limitation does correct for the rise of V(T), but leads to a decline in minute ventilation.

scholarly journals Assessment of Fluid Responsiveness After Tidal Volume Challenge During Pressure-Controlled Ventilation Volume Guaranteed: An observational study

2020 ◽  
Author(s):  
Yu Jiang ◽  
Lingling Jiang ◽  
Jun Hu ◽  
Ye Zhang
Keyword(s):  
Body Weight ◽  
Tidal Volume ◽  
Fluid Responsiveness ◽  
Transient Increase ◽  
Anesthesia Induction ◽  
Predicted Body Weight ◽  
Controlled Ventilation ◽  
Pressure Controlled Ventilation ◽  
Pressure Controlled ◽  
Volume Challenge

Abstract Background: The reliability of pulse pressure variation (PPV) and stroke volume variation (SVV) to predict fluid responsiveness have not previously been established when using pressure-controlled ventilation-volume guaranteed (PCV-VG) mode. We hypothesized that with a transient increase in tidal volume from 6 to 8 mL/kg of predicted body weight (PBW), which we reference as the “tidal volume challenge (TVC)”, the changes to PPV and SVV will be an indicator of fluid responsiveness.Methods: The patients were first ventilated with a tidal volume of (Vt) 6 mL/kg of predicted body weight (PBW) using PCV-VG. Following intravenous anesthesia induction, PPV6 and SVV6 were recorded, then the TVC was performed, which increased Vt from 6 mL/kg to 8 mL/kg PBW for 1 minute and PPV8 and SVV8 were recorded again. The changes in value of PPV and SVV (ΔPPV6-8 and ΔSVV6-8) were calculated after TVC. Following the minute of TVC, the tidal volume was returned to 6 ml/kg PBW for the fluid challenge (FC), a colloid infusion of 6ml/kg PBW for 20 minutes. Patients were classified as responders if there was an increase in cardiac index (CI) of more than 15% after FC, otherwise the patients were identified as non-responders. Eligible patients were divided into groups of responders or non-responders.Results: 37 patients were classified as responders and 44 were non-responders. PPV6 and SVV6 could not predict the fluid responsiveness, while PPV8 and SVV8 could predict the fluid responsiveness when using PCV-VG mode. The changes in value of PPV and SVV after TVC (ΔPPV6-8 and ΔSVV6-8) identified true fluid responders with the highest sensitivity and specificity in the above variables, which predicted fluid responsiveness with the area under the receiver operating characteristic curves (AUCs) (95% CIs) being 0.96 (0.93-1.00) and 0.98 (0.96-1.00), respectively. No significant difference was found when comparing the AUCs of ΔPPV6-8 and ΔSVV6-8 (P > 0.05). Linear correlation was represented between the change value of CI after FC and the change value of SVV or PPV after TVC (r = 0.68; P < 0.0001 and r = 0.77; P < 0.0001, respectively).Conclusions: A transient increase in tidal volume, which we reference as the “tidal volume challenge (TVC)” could enhance the predictive value of PPV and SVV for the evaluation of fluid responsiveness in patients under ventilation with PCV-VG.Trial registration: Chinese Clinical Trial Registry (ChiCTR2000028995). Prospectively registered on 11 January 2020. http://www.medresman.org.

scholarly journals Pressure-Controlled Ventilation-Volume Guaranteed Mode Combined with an Open-Lung Approach Improves Lung Mechanics, Oxygenation Parameters, and the Inflammatory Response during One-Lung Ventilation: A Randomized Controlled Trial

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Jianli Li ◽  
Baogui Cai ◽  
Dongdong Yu ◽  
Meinv Liu ◽  
Xiaoqian Wu ◽  
...  
Keyword(s):  
Lung Ventilation ◽  
Protective Ventilation ◽  
Lung Mechanics ◽  
Lung Protective Ventilation ◽  
One Lung Ventilation ◽  
Controlled Ventilation ◽  
Open Lung ◽  
Pressure Controlled Ventilation ◽  
Pressure Controlled ◽  
Open Lung Approach

We evaluated the effectiveness of pressure-controlled ventilation-volume guaranteed (PCV-VG) mode combined with open-lung approach (OLA) in patients during one-lung ventilation (OLV). First, 176 patients undergoing thoracoscopic surgery were allocated randomly to four groups: PCV+OLA (45 cases, PCV-VG mode plus OLA involving application of individualized positive end-expiratory pressure (PEEP) after a recruitment maneuver), PCV (44 cases, PCV-VG mode plus standard lung-protective ventilation with fixed PEEP of 5 cmH2O), VCV+OLA (45 cases, volume-controlled ventilation (VCV) plus OLA), and VCV (42 cases, VCV plus standard lung-protective ventilation). Mean airway pressure (Pmean), dynamic compliance (Cdyn), PaO2/FiO2 ratio, intrapulmonary shunt ratio (Qs/Qt), dead space fraction (VD/VT), and plasma concentration of neutrophil elastase were obtained to assess the effects of four lung-protective ventilation strategies. At 45 min after OLV, the median (interquartile range (IQR)) Pmean was higher in the PCV+OLA group (13.00 (12.00, 13.00) cmH2O) and the VCV+OLA group (12.00 (12.00, 14.00) cmH2O) than in the PCV group (11.00 (10.00, 12.00) cmH2O) and the VCV group (11.00 (10.00, 12.00) cmH2O) (P<0.05); the median (IQR) Cdyn was higher in the PCV+OLA group (27.00 (24.00, 32.00) mL/cmH2O) and the VCV+OLA group (27.00 (22.00, 30.00) mL/cmH2O) than in the PCV group (23.00 (21.00, 25.00) mL/cmH2O) and the VCV group (20.00 (18.75, 21.00) mL/cmH2O) (P<0.05); the median (IQR) Qs/Qt in the PCV+OLA group (0.17 (0.16, 0.19)) was significantly lower than that in the PCV group (0.19 (0.18, 0.20)) and the VCV group (0.19 (0.17, 0.20)) (P<0.05); VD/VT was lower in the PCV+OLA group (0.18±0.05) and the VCV+OLA group (0.19±0.07) than in the PCV group (0.21±0.07) and the VCV group (0.22±0.06) (P<0.05). The concentration of neutrophil elastase was lower in the PCV+OLA group than in the PCV, VCV+OLA, and VCV groups at total-lung ventilation 10 min after OLV (162.47±25.71, 198.58±41.99, 200.84±22.17, and 286.95±21.10 ng/mL, resp.) (P<0.05). In conclusion, PCV-VG mode combined with an OLA strategy leads to favorable effects upon lung mechanics, oxygenation parameters, and the inflammatory response during OLV.

scholarly journals Static and Dynamic Transpulmonary Driving Pressures Affect Lung and Diaphragm Injury during Pressure-controlled versus Pressure-support Ventilation in Experimental Mild Lung Injury in Rats

2020 ◽  
Vol 132 (2) ◽  
pp. 307-320 ◽  
Author(s):  
Eliete F. Pinto ◽  
Raquel S. Santos ◽  
Mariana A. Antunes ◽  
Ligia A. Maia ◽  
Gisele A. Padilha ◽  
...  
Keyword(s):  
Lung Injury ◽  
Pressure Support Ventilation ◽  
Pressure Support ◽  
Driving Pressure ◽  
Lung Damage ◽  
Inspiratory Time ◽  
Support Ventilation ◽  
Controlled Ventilation ◽  
Pressure Controlled Ventilation ◽  
Pressure Controlled

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Pressure-support ventilation may worsen lung damage due to increased dynamic transpulmonary driving pressure. The authors hypothesized that, at the same tidal volume (VT) and dynamic transpulmonary driving pressure, pressure-support and pressure-controlled ventilation would yield comparable lung damage in mild lung injury. Methods Male Wistar rats received endotoxin intratracheally and, after 24 h, were ventilated in pressure-support mode. Rats were then randomized to 2 h of pressure-controlled ventilation with VT, dynamic transpulmonary driving pressure, dynamic transpulmonary driving pressure, and inspiratory time similar to those of pressure-support ventilation. The primary outcome was the difference in dynamic transpulmonary driving pressure between pressure-support and pressure-controlled ventilation at similar VT; secondary outcomes were lung and diaphragm damage. Results At VT = 6 ml/kg, dynamic transpulmonary driving pressure was higher in pressure-support than pressure-controlled ventilation (12.0 ± 2.2 vs. 8.0 ± 1.8 cm H2O), whereas static transpulmonary driving pressure did not differ (6.7 ± 0.6 vs. 7.0 ± 0.3 cm H2O). Diffuse alveolar damage score and gene expression of markers associated with lung inflammation (interleukin-6), alveolar-stretch (amphiregulin), epithelial cell damage (club cell protein 16), and fibrogenesis (metalloproteinase-9 and type III procollagen), as well as diaphragm inflammation (tumor necrosis factor-α) and proteolysis (muscle RING-finger-1) were comparable between groups. At similar dynamic transpulmonary driving pressure, as well as dynamic transpulmonary driving pressure and inspiratory time, pressure-controlled ventilation increased VT, static transpulmonary driving pressure, diffuse alveolar damage score, and gene expression of markers of lung inflammation, alveolar stretch, fibrogenesis, diaphragm inflammation, and proteolysis compared to pressure-support ventilation. Conclusions In the mild lung injury model use herein, at the same VT, pressure-support compared to pressure-controlled ventilation did not affect biologic markers. However, pressure-support ventilation was associated with a major difference between static and dynamic transpulmonary driving pressure; when the same dynamic transpulmonary driving pressure and inspiratory time were used for pressure-controlled ventilation, greater lung and diaphragm injury occurred compared to pressure-support ventilation.

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