Raphaël Giraud1,2,3, Carlo Banfi4,5,6,7, Benjamin Assouline8,6,7, Amandine De Charrière8,6,7, Maurizio Cecconi9,10, Karim Bendjelid8,6,7. 1. Intensive Care Unit, Geneva University Hospitals, 4, Rue Gabrielle Perret-Gentil, 1205, Geneva, Switzerland. Raphael.Giraud@hcuge.ch. 2. Faculty of Medicine, University of Geneva, Geneva, Switzerland. Raphael.Giraud@hcuge.ch. 3. Geneva Hemodynamic Research Group, Geneva, Switzerland. Raphael.Giraud@hcuge.ch. 4. University of Milan, Gruppo Ospedaliero San Donato, Milan, Italy. 5. Department of Cardio-Thoracic Surgery, Istituto Clinico Sant'Ambrogio, Milan, Italy. 6. Faculty of Medicine, University of Geneva, Geneva, Switzerland. 7. Geneva Hemodynamic Research Group, Geneva, Switzerland. 8. Intensive Care Unit, Geneva University Hospitals, 4, Rue Gabrielle Perret-Gentil, 1205, Geneva, Switzerland. 9. Humanitas Clinical and Research Center, IRCCS, via Manzoni 56, Rozzano, Italy. 10. Department of Biomedical Sciences, Humanitas University, via Rita Levi Montalcini, Pieve Emanuele, 20090, Milan, Italy.
Abstract
BACKGROUND: Chronic obstructive pulmonary disease (COPD) exacerbation and protective mechanical ventilation of acute respiratory distress syndrome (ARDS) patients induce hypercapnic respiratory acidosis. MAIN TEXT: Extracorporeal carbon dioxide removal (ECCO2R) aims to eliminate blood CO2 to fight against the adverse effects of hypercapnia and related acidosis. Hypercapnia has deleterious extrapulmonary consequences, particularly for the brain. In addition, in the lung, hypercapnia leads to: lower pH, pulmonary vasoconstriction, increases in right ventricular afterload, acute cor pulmonale. Moreover, hypercapnic acidosis may further damage the lungs by increasing both nitric oxide production and inflammation and altering alveolar epithelial cells. During an exacerbation of COPD, relieving the native lungs of at least a portion of the CO2 could potentially reduce the patient's respiratory work, Instead of mechanically increasing alveolar ventilation with MV in an already hyperinflated lung to increase CO2 removal, the use of ECCO2R may allow a decrease in respiratory volume and respiratory rate, resulting in improvement of lung mechanic. Thus, the use of ECCO2R may prevent noninvasive ventilation failure and allow intubated patients to be weaned off mechanical ventilation. In ARDS patients, ECCO2R may be used to promote an ultraprotective ventilation in allowing to lower tidal volume, plateau (Pplat) and driving pressures, parameters that have identified as a major risk factors for mortality. However, although ECCO2R appears to be effective in improving gas exchange and possibly in reducing the rate of endotracheal intubation and allowing more protective ventilation, its use may have pulmonary and hemodynamic consequences and may be associated with complications. CONCLUSION: In selected patients, ECCO2R may be a promising adjunctive therapeutic strategy for the management of patients with severe COPD exacerbation and for the establishment of protective or ultraprotective ventilation in patients with ARDS without prognosis-threatening hypoxemia.
BACKGROUND: Chronic obstructive pulmonary disease (COPD) exacerbation and protective mechanical ventilation of acute respiratory distress syndrome (ARDS) patients induce hypercapnic respiratory acidosis. MAIN TEXT: Extracorporeal carbon dioxide removal (ECCO2R) aims to eliminate blood CO2 to fight against the adverse effects of hypercapnia and related acidosis. Hypercapnia has deleterious extrapulmonary consequences, particularly for the brain. In addition, in the lung, hypercapnia leads to: lower pH, pulmonary vasoconstriction, increases in right ventricular afterload, acute cor pulmonale. Moreover, hypercapnic acidosis may further damage the lungs by increasing both nitric oxide production and inflammation and altering alveolar epithelial cells. During an exacerbation of COPD, relieving the native lungs of at least a portion of the CO2 could potentially reduce the patient's respiratory work, Instead of mechanically increasing alveolar ventilation with MV in an already hyperinflated lung to increase CO2 removal, the use of ECCO2R may allow a decrease in respiratory volume and respiratory rate, resulting in improvement of lung mechanic. Thus, the use of ECCO2R may prevent noninvasive ventilation failure and allow intubated patients to be weaned off mechanical ventilation. In ARDS patients, ECCO2R may be used to promote an ultraprotective ventilation in allowing to lower tidal volume, plateau (Pplat) and driving pressures, parameters that have identified as a major risk factors for mortality. However, although ECCO2R appears to be effective in improving gas exchange and possibly in reducing the rate of endotracheal intubation and allowing more protective ventilation, its use may have pulmonary and hemodynamic consequences and may be associated with complications. CONCLUSION: In selected patients, ECCO2R may be a promising adjunctive therapeutic strategy for the management of patients with severe COPD exacerbation and for the establishment of protective or ultraprotective ventilation in patients with ARDS without prognosis-threatening hypoxemia.
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