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Extracorporeal Carbon Dioxide Removal
Objectives
This chapter will:
- 1.
Explain the physiology of CO 2 removal during extracorporeal support.
- 2.
Describe potential clinical applications of extracorporeal CO 2 removal systems (ECCO 2 R) support therapy in patients with acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD) as well as in those with acute kidney injury requiring renal replacement therapy.
Mechanical ventilation (MV) is a lifesaving treatment delivered to patients who suffer of a wide spectrum of respiratory failure. However, several concerns have emerged about its limits and iatrogenic potential. Extracorporeal life support (ECLS) techniques complement MV in several circumstances: (1) to correct life-threatening hypoxemia in patients with acute respiratory distress syndrome (ARDS) when all conventional therapies have failed; (2) to minimize the risk of ventilator-induced lung injury (VILI), allowing an “ultra-protective” ventilation strategy with very low tidal volume; and (3) to prevent the risk of endotracheal intubation when noninvasive mechanical ventilation is failing. To accomplish these putative indications, ECLS techniques range from the full-support devices called extracorporeal membrane oxygenation (ECMO, blood flow ≥ 3 L/min), which ensures full oxygenation and carbon dioxide (CO 2 ) clearance with minimal need of MV, to minimally invasive extracorporeal CO 2 removal systems (ECCO 2 R, blood flow 0.4–1 L/min), which remove CO 2 without any effect on oxygenation. The objectives of this chapter are to review fundamental concepts of CO 2 handling during ECCO 2 R and provide current evidences of its application in patients with ARDS, chronic obstructive pulmonary disease (COPD), and acute kidney injury (AKI) requiring renal replacement therapy.
From Renal to Respiratory Dialysis (Historical Perspective)
Since the late 1970s, hypoxia and hypoventilation were described as usual respiratory adverse events that occurred during hemodialysis. The reduction in arterial partial pressure of CO 2 (PaCO 2 ) was considered the leading mechanism of these alterations, and the acetate buffer that was used conventionally at that time in dialysis circuits was identified as the primum movens of this physiologic disturbance. In fact, decrease of PaCO 2 resulted from the corresponding reduction of HCO 3 − in exchange for acetate. When bicarbonate dialysate was used, hypopnea and hypoxia were not detected. In those years, Kolobow and Gattinoni attempted to take advantage of this adverse effect and designed a modified venovenous ECMO circuit (blood flow of around 1 L/min) to reduce minute ventilation and consequently the risk of lung overdistension in patients with severe ARDS. Moreover, at that time full ECMO with high blood flow rates failed to demonstrate any improvement in survival of these patients because of ventilation strategy that did not prevent VILI and major bleeding complications.
Carbon Dioxide Physiology
Carbon dioxide is produced in mitochondria as the end product of the aerobic metabolism and in blood combines with free water (H 2 O) to form carbonic acid (H 2 CO 3 ); this reaction is catalyzed in red blood cells (RBC) and on pulmonary capillaries membranes by carbonic anhydrase, which is not present in plasma. At physiologic pH ranges, 96% of carbonic acid is dissociated in bicarbonate ion (HCO 3 − ) and hydrogen ion (H + ).
Five percent of the total CO 2 is conveyed in physical solution, following Henry's solubility law, stating that the mass of a dissolved gas is proportional to its partial pressure. The remaining fraction of CO 2 binds to carbamino compounds to their free amine group (R-NH 2 ). Among these, hemoglobin (Hb) is the most efficient CO 2 carrier, in particular in its reduced, nonoxygenated form.
In the healthy adult subject at rest, the amount of CO 2 production by systemic metabolism (VCO 2 ) is about 200 mL/min, which can increase to a value of 30% higher in pathologic conditions. The concentration of CO 2 in arterial blood is about 48 mL/dL (at a PaCO 2 of 40 mm Hg), and the same in mixed venous blood is 52 mL/dL (at a PvCO 2 of 46 mm Hg). Consequently, an ideal ECCO 2 R device may be able theoretically to remove up to 250 mL/min of CO 2 with a low blood flow of 500 mL/min.
In fact, ECCO 2 R systems are able only to remove the amount of the dissolved CO 2 from blood, and in the membrane lung the input partial pressure of CO 2 is directly proportional to CO 2 removal. However, as has been mentioned already, only a small amount of CO 2 is dissolved in blood. Finding a way to increase free CO 2 entering the membrane lung is a hot topic for the actual research in the field. In animal models, the acidification of blood entering the membrane lung with lactic acid demonstrated to be effective in increasing the CO 2 removal capacity of a low-flow ECCO 2 R device, but the impact on ventilation was limited to a rise in energy expenditure resulting from lactic acid infusion. In another animal model, Zanella et al. proposed an appealing approach to enhance the inlet CO 2 concentration by blood acidification using an electrodialysis cell and thus avoiding the undesired effects related to the addition of an acid solution to the blood. Bicarbonate ion and dissolved CO 2 are in equilibrium in blood, and changes in acid-base status can promote the conversion of one form in the other one. Electrodialysis can enhance PaCO 2 in blood before entering the membrane lung through the application of an electrical current to solutions separated by ion-exchange membranes into an acid and a base chamber. In the acid chamber, Cl − ions combine with H + thus reducing pH; on the contrary, in the base chamber OH − ions derived from hydrolysis compensate for Cl − loss and create an alkaline milieu. Blood in the circuit therefore is acidified with this net exchange of HCO 3 − for Cl − , and CO 2 extraction is increased about two times more compared with standard ECCO 2 R efficiency.
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