The maintenance of the adequate tissue oxygen supply–demand balance is fundamental in the critically ill patients on ECMO. The conduct of the extracorporeal mechanical device should provide an optimal tissue perfusion throughout the management of the different pathophysiological variables encountered during the ECMO assistance.

The SvO₂, measured in the main pulmonary artery with the Swan-Ganz catheter, has been largely recognized as a good indicator of the global tissue perfusion provided by both the patient’s cardiac performance and the extracorporeal assistance. According to the Fick principle, SvO₂ value results from the combination of five major variables (Fig. 32.1):

where SaO ₂ arterial, O ₂ saturation, CI cardiac index, PO O₂ affinity, Hb oxyhaemoglobin content.

SvO₂ does not always correspond to the effective tissue O₂ tension (PvO₂) that depends on the position on the oxyhaemoglobin dissociation curve. During ECMO the continuous variation of either the haemodynamic parameters or the haemoglobin content and the arterial blood oxygenation makes the trend of the SvO₂ values a better indicator than an absolute value of mixed venous oxygen saturation of the matching between the oxygen delivery (DO₂) and the oxygen consumption (VO₂) [9]. As it is clearly showed by the Fick equation, the variation of any of the determinants of the SvO₂ can lead to significant changes of the SvO₂ values during its continuous monitoring. Because the relationships among the five components of the equation are mathematically different and it is uncommon that only one of the variables changes independently from the others in a clinical contest, a “normal” value of SvO₂ is quite difficult to define; it has been demonstrated that a SvO₂ range between 60 and 80 % suggests an appropriate peripheral perfusion.

Although the measurement of the SvO₂ during ECMO generally correctly reflects the effectiveness of the tissue perfusion, sometimes SvO₂ value could not adequately indicate the global perfusion.

Although the SvO₂ expresses the match between DO₂ and VO₂, the value of the SvO₂ calculated in the main pulmonary artery could not reflect the eventual regional distribution of the blood flow and the different perfusion of the different body districts. It should be considered that during VA ECMO, low coronary and/or cerebral flow can occur because of a certain degree of deoxygenated and oxygenated blood mixture at level of the descending thoracic aorta.

Patients submitted to VV ECMO do not generally present cardiac function impairment, since severe respiratory dysfunction requiring extracorporeal support because of being a nonresponder to the conventional therapy can occur in patients with chronic pulmonary hypertension and right heart decompensation. Therefore, cardiac dysfunction can coexist with respiratory failure even when a cardiocirculatory support is not required. Because VV ECMO do not provide circulatory support, it has generally few effects on the systemic haemodynamic. This is not always true because it should be considered that the high blood flow in the pulmonary artery would increase the pulmonary vascular resistances (PVR) with consequent increase of the right ventricle (RV) afterload that can lead to RV failure. For this reason the patients in VV ECMO require an advanced haemodynamic monitoring too.

VV ECMO supports the respiratory function providing an adequate arterial oxygenation and CO₂ removal. The adequate monitoring during VV ECMO should be focused on the effectiveness of the respiratory support provided by both the extracorporeal help and the patient’s breathing [10]. The arterial oxygen saturation and the SvO₂ are the best indicators of the respiratory profile. According to the guidelines, the respiratory support provided by the VV ECMO is considered adequate when the SaO₂ >80 % and SvO₂ >70 % [11]. As reported by some recent literature, low tissue oxygenation and low perfusion are associated with worse outcome. For this reason higher values of SaO_2: could be required in patients under VV ECMO to maintain an adequate organ perfusion [5]. In VV ECMO the arterial oxygenation strictly depends on the blood flow, so the higher is the flow through the circuit, the better is the oxygenation. Conversely, because the CO₂ is highly diffusive, low blood flows are generally sufficient to provide decarboxylation. Blood gases can be easily measured by blood samples obtained from the patient’s arterial line.

Hypoxaemia, and consequently low SvO₂, can frequently occur in VV ECMO because of different mechanisms. One of them is the recirculation. Recirculation is an unavoidable effect of the VV ECMO depending on the aspiration back into the extracorporeal circuit of a variable portion of the oxygenated blood previously infused in the right atrium (RA) [12]. This phenomena is strictly correlated to the physical characteristic of the venous cannula and to the position of the proximal and distal lumen on the same cannula [13, 14]. The main effect of the recirculation is that the blood in the RA can be poorly oxygenated and the oxygen delivery can be decreased, leading to global and/or regional hypoperfusion. For the presence of the recirculation, the value of the mixed venous saturation measured at the venous line of the ECMO circuit is not always appropriate. SvO₂ should be directly measured in the pulmonary artery by the Swan-Ganz catheter which can be considered a better indicator of the global perfusion. Another significant cause of hypoxaemia during VV ECMO is the mixture between the oxygenated blood coming from the circulatory support and the low oxygenated blood running from the patient’s venae cavae. In the RA the blood oxygen content decreases, and the tissue oxygenation is lower than that required.