PURPOSE: Our aim was to compare adaptive support ventilation with and without closed loop control by end tidal CO2 (ASVCO2, ASV) with pressure (PC) and volume control ventilation (VC) during simulated clinical scenarios [normal lungs (N), COPD, ARDS, brain injury (BI)]. METHODS: A lung model was used to simulate representative compliance (mL/cmH2O): resistance (cmH2O/L/s) combinations, 45:5 for N and BI, 60:7.7 for COPD, 15:7.7 and 35:7.7 for ARDS. Two levels of PEEP (cmH2O) were used for each scenario, 12/16 for ARDS, and 5/10 for others. The CO2 productions of 2, 3, 4 and 5 mL/kg predicted body weight/min were simulated. Tidal volume was set to 6 mL/kg during VC and PC. Outcomes of interest were end tidal CO2 (etCO2) and plateau pressure (P Plat). RESULTS: EtCO2 levels in N and BI and COPD were similar for all modes. In ARDS, etCO2 was higher in ASVCO2 than in other modes (p < 0.001). Under all mechanical conditions ASVCO2 revealed a narrower range of etCO2. P Plat was similar for all modes in all scenarios but ARDS where P Plat in ASV and ASVCO2 were lower than in VC (p = 0.001). When P Plat was ≥ 28 cmH2O, P plat in ASV and ASVCO2 were lower than in VC and PC (p = 0.024). CONCLUSION: All modes performed similarly in most cases. Minor differences observed were in favor of the closed loop modes. Overall, ASVCO2 maintained tighter CO2 control. The ASVCO2 had the greatest impact during ARDS allowing etCO2 to increase and protecting against hypocapnia evident with other modes while ensuring lower P plat and tidal volumes.
PURPOSE: Our aim was to compare adaptive support ventilation with and without closed loop control by end tidal CO2 (ASVCO2, ASV) with pressure (PC) and volume control ventilation (VC) during simulated clinical scenarios [normal lungs (N), COPD, ARDS, brain injury (BI)]. METHODS: A lung model was used to simulate representative compliance (mL/cmH2O): resistance (cmH2O/L/s) combinations, 45:5 for N and BI, 60:7.7 for COPD, 15:7.7 and 35:7.7 for ARDS. Two levels of PEEP (cmH2O) were used for each scenario, 12/16 for ARDS, and 5/10 for others. The CO2 productions of 2, 3, 4 and 5 mL/kg predicted body weight/min were simulated. Tidal volume was set to 6 mL/kg during VC and PC. Outcomes of interest were end tidal CO2 (etCO2) and plateau pressure (P Plat). RESULTS:EtCO2 levels in N and BI and COPD were similar for all modes. In ARDS, etCO2 was higher in ASVCO2 than in other modes (p < 0.001). Under all mechanical conditions ASVCO2 revealed a narrower range of etCO2. P Plat was similar for all modes in all scenarios but ARDS where P Plat in ASV and ASVCO2 were lower than in VC (p = 0.001). When P Plat was ≥ 28 cmH2O, P plat in ASV and ASVCO2 were lower than in VC and PC (p = 0.024). CONCLUSION: All modes performed similarly in most cases. Minor differences observed were in favor of the closed loop modes. Overall, ASVCO2 maintained tighter CO2 control. The ASVCO2 had the greatest impact during ARDS allowing etCO2 to increase and protecting against hypocapnia evident with other modes while ensuring lower P plat and tidal volumes.
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