Indication for Cardiac ECMO

Cardiac (VA) ECMO may be indicated in patients with cardiogenic shock (impaired cardiac output resulting in end-organ dysfunction) that is refractory to maximal conventional therapy with inotropic drugs and less invasive mechanical support, for example intra-aortic balloon counterpulsation. Common causes of such cardiogenic shock are included in Table 23.1.

Concomitant respiratory failure is not an absolute requirement for considering cardiac ECMO over alternative mechanical circulatory support devices. There have been no randomised controlled trials in adults that have compared VA ECMO against isolated ventricular support with a temporary ventricular assist device (VAD). However, the coexistence of respiratory indications such as severe refractory hypoxia, hypercapnic respiratory failure or symptomatic pulmonary hypertension is certainly persuasive in deciding to pursue cardiac ECMO instead of other circulatory support techniques. The advantages of ECMO over alternative mechanical circulatory support devices such as ventricular assist devices (VAD) include the rapidity of insertion, the ability to support biventricular failure at high flow rates and the potential to support patients with concomitant lung injury when required.

More recently, cardiac ECMO has also been used to restore circulation during cardiac arrest refractory to standard resuscitative management (termed ‘extracorporeal cardiopulmonary resuscitation’ (eCPR)). This may be beneficial when a witnessed arrest occurs in hospital, especially if the patient is in an intensive care or cardiac catheter laboratory setting and ECMO can be instituted rapidly. Evidence suggests that outcome is best with resuscitation periods of less than 30 minutes although there are case reports of survival with far longer arrests.

Contraindications for Cardiac ECMO

Deciding to commence ECMO is a major decision and ideally it should be multidisciplinary with involvement of cardiology (and respiratory) physicians, cardiothoracic surgeons and specialist intensivists. The difficulty is that the patient is often deteriorating rapidly in cardiogenic shock with an uncertain diagnosis and prognosis at the time the decision needs to be made. A delay in restoring blood pressure and flow can result in irrecoverable multiorgan failure despite adequate ECMO flow. In many cases in critically ill patients, at the time of cannulation it is uncertain whether organ function is recoverable and support is expectant. Cardiac ECMO is not a long-term therapy and should only be considered in patients with anticipated early recovery, or as a bridge to heart transplantation or implantation of a long-term VAD. Cardiac ECMO is therefore contraindicated in patients with irrecoverable cardiac failure who will not be candidates for transplantation or VAD implantation and in patients with established multiorgan failure.

The following are considered relative contraindications to cardiac ECMO: the presence of severe aortic regurgitation, aortic dissection, contraindications to therapeutic anticoagulation (such as active bleeding, a haemorrhagic intracranial event), pre-existent multiorgan failure and patients who have already been mechanically ventilated for >10–14 days.

Although there are no absolute guidelines on the indications and contraindications for cardiac ECMO, the Extracorporeal Life Support Organisation (ELSO) and the European Extracorporeal Life Support (ECLS) Working Group have published recommendations for the use of ECMO in critically ill patients.

Circuit Design and Considerations

The ECMO circuit is similar for VV and VA use and consists of vascular access cannulae, a pump, an oxygenator, a temperature control system, monitors and access points.

The vascular access cannulae and circuit tubing are made of a plastic, which therefore necessitates therapeutic anticoagulation to prevent activation of the clotting cascade and thrombosis of the circuit. Heparin bonding of the material aims to reduce this activation. Most commonly anticoagulation is with unfractionated heparin, although there are reports of utilising newer agents such as bivilirudin and argatroban in the context of antithrombin III deficiency and heparin induced thrombocytopenia. Efforts are focused on developing a truly biocompatible plastic, which will obviate the need for anticoagulation which is responsible for a significant proportion of ECMO complications.

Blood flow through the circuit is driven by an external pump. Two types exist: simple roller-pumps and constrained vortex centrifugal pumps.

ECMO oxygenators are usually polymethylpentene hollow-fibre devices, and modern devices have low resistance. Carbon dioxide is readily extracted via gradient-mediated mechanisms whilst the addition of oxygen is slower due to its reduced solubility and diffusion characteristics. An air/oxygen blender is used to achieve the desired FiO₂ and titrated based on arterial blood gases.

Cannulation Strategies

Peripheral Cannulation

Vascular access cannulae can be placed centrally, as for CPB, or peripherally to establish VA ECMO (Figure 23.1). They can be inserted by surgical cut-down under direct vision or percutaneously using the Seldinger technique under ultrasound guidance. The most common configuration in adults is placement of the venous drainage cannula in the femoral vein and reperfusion cannula into the femoral artery. The axillary/subclavian artery can also be utilised as an alternative arterial return vessel. Another strategy, commonly used in paediatric and neonatal ECMO, is the internal jugular vein–common carotid artery cannulation.

Each strategy has important considerations.

Figure 23.1 Peripheral ECMO. The blood is drained from a large vein, typically IVC, using femoral access. It is then pumped through an oxygenator and returned to the patient into the femoral artery in a retrograde fashion. A reperfusion line from the inflow cannula is inserted into the distal femoral artery to provide distal limb perfusion. Diagram drawn by Anna Valchanova.

Femoral Artery Cannulation

This is associated with two main complications:

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   1. With this strategy, oxygenated blood is pumped in a retrograde direction up the descending aorta and into the ascending aorta to perfuse the coronary arteries and cerebral vessels. However, this assumes that there is no residual left ventricular cardiac output. If there is native cardiac output with the aortic valve opening, there will be a ‘mixing zone’ where ejected native anterograde and reinfused retrograde blood meet (Figure 23.2). This can cause a problem if, in the context of respiratory failure, the blood exiting the left ventricle is deoxygenated. This situation is not infrequent when left ventricular failure is complicated by pulmonary oedema. As native cardiac function recovers and left ventricular ejection increases, if the mixing zone is within the descending aorta, the coronary and cerebral circulations may be exposed to deoxygenated blood. Monitoring of cerebral saturations and right radial artery blood gases can be indicative of this ‘differential cyanosis’ or Harlequin syndrome. Strategies to manage this complication include increasing ventilatory support in an attempt to improve oxygenation of the pulmonary venous blood, increasing the flow through the femoral arterial catheter with the aim of transferring the mixing zone to the ascending aorta, or placement of an additional reinfusion catheter into the internal jugular vein such that a proportion of the oxygenated blood is reinfused into the pulmonary circulation (increasing the saturation of antegrade ejected blood from the left ventricle). Alternatively, the femoral reinfusion cannula could be resited proximally to the subclavian, common carotid or ascending aorta.

Figure 23.2 Watershed phenomenon during venoarterial ECMO visualised by computed tomography. Antegrade blood flow (low contrast) from the heart competes with retrograde blood flow (high contrast) from the ECMO in the aorta, resulting in a watershed phenomenon (arrowhead). Here computed tomography of a patient with pulmonary embolism and reduced cardiac output demonstrates a rather proximal watershed, leading to perfusion of the right carotid artery with ‘heart blood’ (dark) and the left carotid artery with ‘ECMO blood’ (bright, arrows). Upper panel, sagittal oblique maximum intensity projection (MIP); middle panel, coronal oblique MIP; lower panel, transverse plane. From Napp et al. (2016).

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   2. The second complication of femoral arterial cannulation is ipsilateral ischaemic limb injury due to obstruction of distal femoral arterial blood flow that can lead to critical limb ischaemia necessitating fasciotomies or even amputation if not recognised. This can be avoided by placement of a small antegrade perfusion catheter into the superficial femoral artery distal to the ECMO cannula, to perfuse the leg.

Central Cannulation

Cardiac ECMO can also be instituted with central cannulation as for CPB (Figure 23.3). Central cannulation is performed by cardiothoracic surgeons via a median sternotomy. Larger catheters can be used which permit increased flow rates and maximal haemodynamic support with more certainty of the ECMO circuit taking over the whole of the patient’s circulation. This approach is most commonly used if a sternotomy has already been made, for example in patients with postcardiotomy cardiac failure following cardiac surgery or primary graft failure at transplantation. It is occasionally necessary in patients where peripheral access is not possible. There are also reports of this strategy being used in cases of severe sepsis, taking advantage of the greater haemodynamic support possible; however the requirement for sternotomy adds to the potential complications and morbidity in these patients. This approach necessarily involves a major surgical incision and therefore bleeding is the most frequent problem. Usually institution of anticoagulation is delayed 6–12 hours until bleeding is controlled.

Figure 23.3 (a) Central ECMO diagram: using open chest, the blood is drained via a cannula from a central vein (IVC or SVC) or right atrium. It is pumped through an oxygenator and returned through an arterial cannula into the ascending aorta. The chest can be left open for a short while, or the cannulae can be tunnelled under the skin and chest closed. Diagram drawn by Anna Valchanova. (b) A photograph of the outflow and inflow cannulae secured with spigots.

General Management of Patients on Cardiac ECMO

Patients supported by cardiac ECMO should be managed in an intensive care unit by multidisciplinary specialists. There are several important considerations that should be made when managing these patients, many of which are similar to patients supported by ‘respiratory’ (VV) ECMO.

The circulatory haemodynamics of patients must be closely monitored. ECMO support should be titrated to clinical targets, which may include:

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  Arterial oxygen saturations >90%

  
  
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  Venous oxygen saturations >70%

  
  
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  Adequate tissue perfusion, as judged by end-organ function and lactate levels.

In most cases there is some residual ventricular function, and it is beneficial for some pulsatility to continue. This allows emptying of the ventricles and less chance of distension and stasis. Low dose inotropic support is sometimes required to achieve ventricular ejection and aortic valve opening; the latter can be confirmed by echocardiography. In cases of severe left ventricular dysfunction with no effective contraction, peripheral cardiac ECMO can lead to overdistension of the left ventricle and left atrium, worsening pulmonary oedema. This can also lead to further myocardial injury. Serial echocardiography should be performed to monitor for this complication. If identified, several strategies have been described to facilitate decompression, including addition of a vent cannula via the left ventricular apex, or transseptal via the atrium, increasing inotropic support, further mechanical support such as Impella I or IABP, conversion to central ECMO or alternative support modalities such as a percutaneous VAD.

Anticoagulation must be monitored to prevent circuit thrombosis and embolism, which could be fatal. For patients receiving unfractionated heparin, an activated clotting time (ACT) of 180–210 seconds is recommended, which is lower than the >400 seconds recommended for CPB.

Lung protective ventilation is usually adopted to minimise barotrauma and volutrauma. Positive end expiratory pressure is applied to the lungs to maintain alveolar recruitment, but the ventilator is usually set to low tidal volumes, low inspiratory pressures and a low inspired oxygen fraction. Reduction in the ventilator support is often accompanied by increased venous return and cardiac output. This strategy is found to help prevent ventilator induced lung injury, oxygen toxicity and ventilator associated haemodynamic compromise. Indeed, prevention of further lung injury in these patients is one of the major advantages of cardiac ECMO. However, it is important to remember that in patients with improving ventricular function, more blood will be ejected from the right ventricle into the pulmonary circulation and increased ventilation will be necessary to prevent deoxygenated blood reaching the left atrium.

The most comprehensive guidelines on the management of patients on ECMO are published by ELSO. These provide guidance on the use of ECMO including training, resources and quality assurance. They are not intended to represent a standard of care, however, and practice described in the literature often differs in parts from this guidance.