Physiological Basis of Extracorporeal Membrane Oxygenation and Extracorporeal Carbon Dioxide Removal in Respiratory Failure

Abstract

Extracorporeal life support (ECLS) for severe respiratory failure has seen an exponential growth in recent years. Extracorporeal membrane oxygenation (ECMO) and extracorporeal CO₂ removal (ECCO₂R) represent two modalities that can provide full or partial support of the native lung function, when mechanical ventilation is either unable to achieve sufficient gas exchange to meet metabolic demands, or when its intensity is considered injurious. While the use of ECMO has defined indications in clinical practice, ECCO₂R remains a promising technique, whose safety and efficacy are still being investigated. Understanding the physiological principles of gas exchange during respiratory ECLS and the interactions with native gas exchange and haemodynamics are essential for the safe applications of these techniques in clinical practice. In this review, we will present the physiological basis of gas exchange in ECMO and ECCO₂R, and the implications of their interaction with native lung function. We will also discuss the rationale for their use in clinical practice, their current advances, and future directions.

Keywords: acute respiratory distress syndrome (ARDS); chronic obstructive pulmonary disease (COPD); extracorporeal CO2 removal (ECCO2R); extracorporeal life support (ECLS); extracorporeal membrane oxygenation (ECMO).

Figure 1

ECLS modalities. Overview of the available extracorporeal support modalities and their role in the management of respiratory failure.

Figure 2

Schematic displays the oxygenation and decarboxylation of venous blood via the membrane lung. The VO₂ and VCO₂ are dependent on the content pre and post membrane and on the extracorporeal blood flow within the ECMO circuit.

Figure 3

Schematic overview of the determinants of arterial PaO₂. This is influenced by the degree of shunted deoxygenated blood from native lung, the ratio of ECBF to intrinsic cardiac output and amount of recirculation. Essentially, venous blood is divided into blood that is pumped through the ECMO membrane (ECBF) and an amount (Cardiac output minus ECBF) that bypasses the ECMO and mixes in the right atrium. Part of the ECBF (Qr) ‘recirculates’ back into the ECMO, decreasing the effective ECBF. Therefore, the effective ECBF (ECBFeff) is the difference between the ECBF and Qr. The oxygen content in the different compartments is illustrated.

Figure 4

ECMO initiation. The delivery of VV-ECMO optimises oxygenation and allows a reduction of mechanical power delivered to the lungs. ECMO produces venous hyperoxia which in turn reduces pulmonary vascular resistance and hypoxic pulmonary vasoconstriction. This improves right ventricular function and cardiac output. A consequence of this physiological change is a larger shunt fraction in the native lung and a lower ECBF/CO ratio, both resulting in a lower arterial oxygen tension. This is further compounded by “lung rest” strategies leading to progressive de-recruitment and alveolar hypoventilation. In order to maintain adequate oxygenation ECBF may need to be increased to re-balance this ratio.