Dear Editor,

We congratulate Sklar et al. for their systematic review of extracorporeal carbon dioxide removal (ECCO2R) in patients with chronic obstructive pulmonary disease (COPD) [1]. We would like to complete the discussion of the review in the light of recent preliminary data obtained to study the effects of ECCO2R in COPD patients under invasive mechanical ventilation (IMV) [2]. We discuss herein the physiological mechanisms by which ECCO2R could exert beneficial clinical effects in these patients.

In the adult respiratory distress syndrome ECCO2R permits one to counteract hypercapnia that results from lung protective ventilation. However, in spontaneously breathing COPD patients with severe acute exacerbations ECCO2R could exert additional benefits by sparing a significant amount of work of breathing (WOB). Reduction in WOB may also directly contribute to minimize CO2 production (VCO2) by reducing respiratory muscle energy expenditure.

We obtained measurements in two acutely exacerbated COPD patients (61 and 88 years old) during the weaning process of IMV. Both patients were treated with ECCO2R (Hemolung, Alung Technologies, Pittsburgh, USA) shortly after intubation with the main goals of controlling hypercapnia, diminishing hyperinflation, and promoting a rapid weaning process. By measuring VCO2 on the respirator (Engström Carestation, GE Healthcare) with and without ECCO2R, we had the unique opportunity to indirectly assess CO2 production related to respiratory muscle activity change. Data were obtained at low levels of pressure support (10 cmH2O) mimicking a spontaneous breathing trial (SBT). Inspiratory WOB was calculated as previously described, and based on simultaneous esophageal and gastric pressure measurements (Nutrivent catheter, Sidam, Mirandola, Italy) [3]. Data were obtained under ECCO2R at a sweep gas flow rate of 10 and 0 L/min after 1 h of stabilization. Main results are presented in Fig. 1: ECCO2R decreased both WOB (40 and 24 %) and PaCO2 (32 and 16 %). Total VCO2 (ventilator and extracorporeal) decreased during ECCO2R, probably related to the decrease in WOB which is a major determinant of the total VCO2 in decompensated spontaneously breathing COPD patients. The subsequent clinical course was uneventful.

Fig. 1
figure 1

Measurements and calculations obtained in two severe IMV COPD patients during the weaning process. Patients were ventilated under the pressure support mode at fixed low levels of assistance. Data were obtained under ECCO2R at a sweep gas flow rate of 10 L/min (ECCO2R+) and 0 L/min (ECCO2R−) after 1 h of stabilization. WOB inspiratory work of breathing, calculated using Campbell’s method, expressed in joules per liter of ventilation. VCO 2 vent respiratory CO2 elimination (equal to total CO2 elimination at a sweep gas flow rate of 0 L/min). VCO 2 tot total CO2 elimination (equal to respiratory plus extracorporeal CO2 eliminations)

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Our data indicate that ECCO2R is associated with a decreased WOB, at least in the specific context of our measurements. Similar results have been obtained by Pisani et al. during SBT [4]. It can be concluded that ECCO2R can limit the level of hypercapnia not only by direct removal of CO2 but also by sparing some level of respiratory muscle effort, as confirmed by our CO2 measurements.

Finally, Sklar et al. suggested that improvement in pH between 1 and 24 h after initiation of ECCO2R may be attributable to metabolic rather than to respiratory acidosis. On the basis of our measurements, however, we offer an alternative explanation to that provided by the authors. We speculate that an intracellular acidosis reduction within the respiratory muscle may also contribute to the reduction in metabolic acidosis [5].