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Low flow veno-venous extracorporeal CO2 removal for acute hypercapnic respiratory failure.
Minerva Anestesiologica 2017 August
BACKGROUND: Ventilation with low tidal volume and airway pressure results in a survival benefit in ARDS patients. Previous research suggests that avoiding mechanical ventilation altogether may be beneficial in some cases of respiratory failure. Our hypothesis was that low flow veno-venous extracorporeal CO2 removal (ECCO2R) enables maintenance of a lung protective ventilation strategy or awake spontaneous ventilation despite severe hypercapnic respiratory failure (HRF).
METHODS: Twenty patients with HRF were investigated while mechanically ventilated (N.=14) or breathing spontaneously close to respiratory exhaustion (N.=6). Low flow ECCO2R was performed using a hemoperfusion device with a polypropylene gas-exchanger.
RESULTS: Causes of HRF were severe ARDS (N.=11), COPD (N.=4), chronic lung transplant rejection (N.=3) and cystic fibrosis (N.=2). During the first 8h of ECCO2R, PaCO2 decreased from 10.6 (9.3-12.9) to 7.9 (7.3-9.3) kPa (P<0.001) and pH increased from 7.23 (7.09-7.40) to 7.36 (7.27-7.41) (P<0.05). Thereafter, steady state was achieved while maintaining lung protective tidal volume (4.7 (3.8-6.5) mL/kg) and peak ventilator pressure (28 (27-30) mbar at 24 h). During the first 48 h, thrombocyte count decreased by 52% (P<0.01), Fibrinogen by 38% (P<0.05). Intubation could be avoided in all spontaneously breathing patients. In 4/6 high blood flow extracorporeal circulation was required due to increased oxygen demand. 6/14 mechanically ventilated patients recovered from respiratory support.
CONCLUSIONS: Our results suggest that in mechanically ventilated patients with HRF, low flow ECCO2R supports the maintenance of lung protective tidal volume and peak ventilator pressure. In selected awake patients with acute HRF, it may be a novel treatment approach to avoid mechanical ventilation, hence preventing ventilator- and sedation-associated morbidity and mortality.
METHODS: Twenty patients with HRF were investigated while mechanically ventilated (N.=14) or breathing spontaneously close to respiratory exhaustion (N.=6). Low flow ECCO2R was performed using a hemoperfusion device with a polypropylene gas-exchanger.
RESULTS: Causes of HRF were severe ARDS (N.=11), COPD (N.=4), chronic lung transplant rejection (N.=3) and cystic fibrosis (N.=2). During the first 8h of ECCO2R, PaCO2 decreased from 10.6 (9.3-12.9) to 7.9 (7.3-9.3) kPa (P<0.001) and pH increased from 7.23 (7.09-7.40) to 7.36 (7.27-7.41) (P<0.05). Thereafter, steady state was achieved while maintaining lung protective tidal volume (4.7 (3.8-6.5) mL/kg) and peak ventilator pressure (28 (27-30) mbar at 24 h). During the first 48 h, thrombocyte count decreased by 52% (P<0.01), Fibrinogen by 38% (P<0.05). Intubation could be avoided in all spontaneously breathing patients. In 4/6 high blood flow extracorporeal circulation was required due to increased oxygen demand. 6/14 mechanically ventilated patients recovered from respiratory support.
CONCLUSIONS: Our results suggest that in mechanically ventilated patients with HRF, low flow ECCO2R supports the maintenance of lung protective tidal volume and peak ventilator pressure. In selected awake patients with acute HRF, it may be a novel treatment approach to avoid mechanical ventilation, hence preventing ventilator- and sedation-associated morbidity and mortality.
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