Introduction

Veno-venous ECMO allows gas exchange and is used to support failing lungs. The cardiovascular system remains intact, and the heart continues to pump the blood around the patient’s body.

A simplified view of veno-venous ECMO is that the blood is taken from and returned to the venous system. If the blood is circulated through a functioning oxygenator, gas exchange will happen. If there is no oxygenator (or no gas flow through the oxygenator), the blood will just return in the same state as it drained (perhaps a bit cooler if no heat exchanger is in place). The whole-blood volume (including the proportion that went through the ECMO circuit) is pumped by the heart through the lungs and circulation.

Veno-venous ECMO is usually instituted in the context of severe acute respiratory failure. It supports oxygenation and CO₂ removal and allows the implementation of safer ventilation strategies. This is inaccurately referred to as ‘protective’ ventilation (any positive-pressure ventilation is deemed to cause damage to the lung) and could be called the ‘least-damaging lung ventilation’.

Veno-venous ECMO can be continued for as long as appropriate; investigations are directed at confirming the underlying diagnosis and ensuring specific therapy is administered.

Patients supported with veno-venous ECMO frequently have additional non-pulmonary organ failure and require a high level of critical care support (e.g. acute renal failure).

The day-to-day management of patients on veno-venous ECMO includes all that is common to critically ill patients plus some specific elements. This chapter describes those specific elements.

Locally agreed protocols for the care of ECMO patients should be incorporated into training.

Monitoring of the patient on veno-venous ECMO has been described in Chapter 4.

Stabilization on veno-venous ECMO

Insertion of ECMO cannulas should ideally take place in an operating room. A variety of configurations can be used. It is often striking how rapidly ventilation and other support can be modified after veno-venous ECMO support has been started.

Lung ventilation can be adapted immediately after veno-venous ECMO has been established. The aim is to institute a less-damaging mechanical ventilation with lower levels of pressure. Multiple publications are available, but most clinicians would agree to aim for a standard setting (Table 8.1). Veno-venous ECMO circuits are very efficient at exchanging CO₂. While unproven, it makes sense to decrease the patient PaCO₂ progressively to avoid extreme vasoactive responses. This can easily be achieved by initiating veno-venous ECMO with a low gas sweep through the oxygenator (e..g 2 L/min) that is progressively increased (e.g. within the first hour). A low gas sweep will usually not affect oxygenation as transfer of O₂ will be limited by other factors (as long as the delivered fraction of O₂ in the sweep gas is 100%). In veno-venous ECMO, the inspired fraction of O₂ in the sweep gas should always be 100%. As explained in previous chapters, oxygenation in patients supported with veno-venous ECMO is dependent on the blood flow in the circuit in relation to the patient’s cardiac output.

Inotropes and other vasoactive drugs will often have been increased to very high levels to maintain some haemodynamic stability in critically ill patients awaiting veno-venous ECMO (often wrongly interpreted as a reason to consider veno-arterial support). This is often exacerbated by high airway and intrathoracic pressure, low O₂ levels, high doses of sedative agents, high CO₂ and profound acidosis. The rate of infusion of these drugs can (and should) very often be decreased rapidly.

Red blood cell transfusion is advocated by some, as the O₂ content in the blood will be limited and extra red blood cells will increase the O₂-carrying capacity. Others advocate the use of restrictive transfusion policies identical to those used in other critically ill patients. Justification for a liberal transfusion strategy is that veno-venous ECMO rarely increases the PaO₂ to normal physiological levels. In the absence of a guarantee that a PaO₂ as low as 6 kPa is acceptable, many clinicians will transfuse in the early stages of support. The increased oncotic pressure offered by red blood cell transfusion may be added benefit in critically ill patients in whom the systemic inflammatory response is increased by the use of an ECMO circuit.

If the PaO₂ remains low despite optimal blood flow through the ECMO circuit, it can be presumed that the issue is either inadequate flow for body weight (especially in patients in excess of 100 kg) or high cardiac output leading to a small proportion of circulating blood going through the ECMO circuit. Solutions to this problem include: (1) the insertion of an additional drainage cannula to increase flow through the ECMO circuit as long as the return cannula can accommodate the increase in flow and pressure; and (2) measures to decrease O₂ consumption (such as cooling the core temperature using the heater/cooler in the ECMO circuit to modify the patient’s body temperature) or actions to reduce the cardiac output (β-blockers are sometimes used to achieve this, but questions remain on the overall physiological impact this may have). (Note that double-lumen cannulas have an optimized return lumen size for the drainage lumen size, and that adding an extra cannula to improve flow will have only a limited effect.)

If the venous blood is highly desaturated, a second oxygenator may be incorporated into the circuit. While this is difficult to model, this definitely increases the transit time for blood in each oxygenator, and post-oxygenator PaO₂ will be higher.

After stabilization, the patient can now undergo multiple non-invasive tests to determine the cause and remedy the insult that led to respiratory failure.