**2. Pathophysiological rationale for ECCO2R**

Both in asthma and COPD exacerbations, diffuse narrowing of the airways results in profound physiologic consequences. Airway narrowing prevents the lungs from completely emptying ("air trapping") due to resistance to expiratory flow and bronchial closure at higher than average lung volumes. Air trapping results in dynamic hyperinflation (DHI) [7] which is the excessive increase in end-expiratory lung volume above the relaxation volume of the respiratory system, generating intrinsic positive end-expiratory pressure (auto-PEEP) [8]. As a result, the patient breathes at higher total lung volumes, depending on increased residual volume [9] which reduces tidal ventilation. The net effect is that the work of breathing increases significantly. The diaphragm, intercostal muscles, and even the abdominal muscles are overloaded causing respiratory muscle fatigue and dyspnea.

Pharmacotherapy with bronchodilators and systemic corticosteroids are the cornerstones of medical therapy, designed to reduce this pathophysiological airflow obstruction and improve symptoms.

Patients suffering from a combination of persistent or worsening hypercapnia, respiratory muscle fatigue, and a decline in mental status require mechanical ventilation (MV) along with lung-protective ventilator strategies (e.g., low-tidal-volume ventilation, relatively short inspiratory time and longer expiratory times) [10, 11].

The goal of mechanical ventilation is to provide adequate gas exchange while waiting for airflow obstruction to respond to bronchodilator therapy. However, mechanical ventilation may aggravate alveolar hyperinflation by worsening DHI, which may lead to worsened hypercapnia, barotrauma, and alveolar rupture leading to pneumothorax and further hemodynamic deterioration [12].

Furthermore, during mechanical ventilation, these patients receive sedatives or neuromuscular blockade to facilitate ventilatory support [13]. Sedation and paralysis preclude mobilization, promoting muscular deconditioning and potentially contributing to the long-term cognitive sequelae of critical illness [14].

**93**

*Extracorporeal Carbon Dioxide Removal for the Exacerbation of Chronic Hypercapnic…*

as extracorporeal membrane oxygenation are entertained as a possible salvage

During exacerbation relieving the native lung from at least part of the CO2 elimination with ECCO2R could potentially improve the acid–base balance, reduce patient's work of breathing with a consequent reduction in respiratory rate and ventilatory drive, and lower alveolar ventilation. The application of ECCO2R may allow lower tidal volumes and respiratory rate, resulting in the extension of the expiratory time, suiting better the high expiratory time constant of the respiratory system with expiratory flow limitation. By these physiological mechanisms, ECCO2R can counteract the vicious circle of dynamic hyperinflation and its detrimental respiratory and cardiovascular consequences. The derived beneficial effects on respiratory mechanics, ventilatory muscle efficiency, work of breathing, and cardiovascular function may improve gas exchanges and relieve dyspnea, thus potentially preventing NIV failure or facilitate weaning from IMV, and, also by rapidly decreasing and weaning off sedation, reduce the rates of delirium, reduce feeding problems, and allow social contacts with friends and family, as well as allow sufficient physio-

When conventional therapeutic options are not successful, novel therapies such

ECCO2R is designed to remove carbon dioxide (CO2) and, unlike extracorporeal

The device consists of a drainage cannula placed in a large central vein or artery, a membrane lung, and a return cannula into the venous system (**Figure 1**). Blood is pumped through the membrane lung, and CO2 is removed by diffusion. A flowing gas known as "sweep gas" containing little or no CO2 runs along the other side of the membrane, ensuring a diffusion gradient from blood to another side, allowing

In contrast to ECMO, where the need for oxygenation requires high blood flow rates, ECCO2R allows much lower blood flow rates, a result of significant differences in CO2 and oxygen (O2) kinetics. Almost all the O2 in blood is carried by hemoglobin, which displays sigmoidal saturation kinetics. Assuming normal hemoglobin and venous O2, each liter of venous blood can only carry an extra 40–60 ml of O2 before the hemoglobin is fully saturated. Blood flows of 5–7 L/min are therefore required to supply enough O2 for an average adult. Conversely, most CO2 is transported as dissolved bicarbonate, displaying linear kinetics without saturation. Considering that 1 L of blood is transported around 500 mL of CO2, a perfectly efficient system flow of 0.5 L/min would be enough to remove all of the CO2 produced [1, 15, 16]. Also, CO2 diffuses more readily than O2 across extracorporeal membranes because of higher solubility. However, in practice, ECCO2R is usually able to remove up to 25% of carbon dioxide production given the limitations of blood flow, blood CO2 content, hemoglobin, and membrane efficiency [17].

In the veno-venous configuration, blood is drawn from a central vein by a draining cannula, using a centrifugal or roller pump to generate flow across the membrane. CO2 diffuses into the "sweep gas" and is returned into the venous circulation (**Figure 1A**). Single site cannulation is possible using a double lumen cannula. This approach allows low flow through the use of smaller cannulas (15–19F), commonly introduced via the right internal jugular vein. The setup is very similar to renal

membrane oxygen (ECMO), does not provide significant oxygenation.

*DOI: http://dx.doi.org/10.5772/intechopen.84936*

therapy to reduce myopathy and critical care illness [14].

**3. ECCO2R technical aspects and principle**

therapeutic modality.

CO2 removal.

**3.1 VV-ECCO2R**

*Extracorporeal Carbon Dioxide Removal for the Exacerbation of Chronic Hypercapnic… DOI: http://dx.doi.org/10.5772/intechopen.84936*

When conventional therapeutic options are not successful, novel therapies such as extracorporeal membrane oxygenation are entertained as a possible salvage therapeutic modality.

During exacerbation relieving the native lung from at least part of the CO2 elimination with ECCO2R could potentially improve the acid–base balance, reduce patient's work of breathing with a consequent reduction in respiratory rate and ventilatory drive, and lower alveolar ventilation. The application of ECCO2R may allow lower tidal volumes and respiratory rate, resulting in the extension of the expiratory time, suiting better the high expiratory time constant of the respiratory system with expiratory flow limitation. By these physiological mechanisms, ECCO2R can counteract the vicious circle of dynamic hyperinflation and its detrimental respiratory and cardiovascular consequences. The derived beneficial effects on respiratory mechanics, ventilatory muscle efficiency, work of breathing, and cardiovascular function may improve gas exchanges and relieve dyspnea, thus potentially preventing NIV failure or facilitate weaning from IMV, and, also by rapidly decreasing and weaning off sedation, reduce the rates of delirium, reduce feeding problems, and allow social contacts with friends and family, as well as allow sufficient physiotherapy to reduce myopathy and critical care illness [14].
