ECMO induces the activation of many infl ammatory pathways. Some are directly acti- vated by the contact-phase reaction to foreign surfaces, while others are triggered by TF release and thrombin generation. From this point of view, ECMO is a perfect model for understanding the complex interaction between infl ammation and coagulation [ 50 ].
Contact with foreign surfaces activates the complement system through the alter- native pathway, with the release of the anaphylatoxins C3a (alternative pathway) and C5a (terminal pathway) [ 51 ]. Activated complement factors induce the synthe- sis of cytokines, belonging to both the subgroups of proinfl ammatory (interleukin-6 and interleukin-8, tumor necrosis factor-α) and anti-infl ammatory (interleukin-10) cytokines [ 52 – 54 ]. Proinfl ammatory cytokines are involved in increased vascular permeability and endothelial dysfunction. Another infl ammatory mechanism involves endotoxins. Bacterial lipopolysaccharide is released by gram-negative bac- teria and induces TNF-α release by the macrophages [ 55 ] and interleukin-6 release by endothelial cells [ 56 ]. During ECMO, like in CPB, endotoxins may be released mainly due to bacterial translocation from a poorly perfused gut mucosa [ 57 , 58 ].
Endotoxins activate circulating monocytes, which in turn release cytokines and blood-borne TF, subsequently activating the coagulation cascade. In turn, the acti- vation of thrombin generation promotes infl ammation, leading to a vicious circle.
As for the hemostatic activation, and even to a greater degree, biocompatible surfaces are associated with a blunting of the complement activation, neutrophil activation, and cytokines release [ 2 – 6 ].
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ECMO for Circulatory Support
F. Sangalli et al. (eds.), ECMO-Extracorporeal Life Support in Adults, 93 DOI 10.1007/978-88-470-5427-1_8, © Springer-Verlag Italia 2014
The end point of any mechanical circulatory support (MCS) is to restore adequacy of perfusion in order to prevent organ damage or to restore normal organ function when damage is already commenced. Reduction of left ventricular end-diastolic pressure, cardiac wall tension, and pulmonary congestion, together with a modula- tion of the neurohormonal response to acute and chronic heart failure, like endoge- nous catecholamine, renin-angiotensin system, ANP, and cytokine release, are all aims of mechanical circulatory support.
Myocardial recovery from reversible acute cardiogenic shock or cardiac “reverse remodeling” in chronic heart failure is what we ultimately would like to achieve in our patients. When this is not possible, but recovery of organ dysfunction has been reached, MCS offers other options: bridge to transplant, bridge to bridge, or destina- tion therapy. These end points, in particular destination therapy, can be obtained with left ventricular assist devices (L-VAD). While L-VAD is a one-ventricle sup- port system and requires a normally functioning right ventricle, extracorporeal life support (ECLS) is a bi-ventricular and respiratory support, acting as a heart and lung bypass, thus reproducing the complete cardiopulmonary bypass (CPB) adopted for open-heart surgery.
ECLS, or more commonly ECMO (extracorporeal membrane oxygenation), is nowadays widely used to support the patient’s respiratory system or both circulatory and respiratory systems in life-threatening clinical conditions. The ECLS concept is
M. G. Mondino , MD • F. Milazzo , MD • R. Paino , MD
Department of Cardio-Thoracic-Vascular Anaesthesia and Intensive Care , Ospedale Niguarda Ca’Garnda , Piazza Ospedale Maggiore 3 , Milan 20162 , Italy e-mail: michelegiovanni.mondino@ospedaleniguarda.it, michelemondino@gmail.com;
fi lippo.mlazzo@ospedaleniguarda.it; roberto.paino@ospedaleniguarda.it R. Fumagalli , MD (*)
Department of Anaesthesia and Intensive Care , Ospedale Niguarda Ca’Granda , Piazza Ospedale Maggiore 3 , Milan 20162 , Italy
Dipartimento di Scienza della Salute , Università Milano Bicocca , Milan , Italy e-mail: roberto.fumagalli@unimib.it, roberto.fumagalli@ospedaleniguarda.it
Interactions with Normal Circulation 8
Michele G. Mondino , Filippo Milazzo , Roberto Paino , and Roberto Fumagalli
quite straightforward: venous blood is drained from the body into the artifi cial lung and pumped back into the patient’s circulatory system.
The relative simplicity of this circuit though can modify patients’ physiology in different ways. In fact, once the patient starts to be supported by ECMO, depending on the type and location of cannulas and according to the underlying clinical conditions, different hemodynamic changes are foreseeable. When blood exiting the artifi cial lung returns into the patient’s venous system, we talk about venovenous ECMO (VV ECMO), and our system is indeed in series with the patient’s cardio- pulmonary physiology. When the blood leaving our circuit is returned into the patient’s artery, we are talking about venoarterial ECMO (VA ECMO), which is instead parallel. These basic concepts together with the abnormal physiology of the patient needing extracorporeal support must be taken into account when consider- ing the physiology of extracorporeal circulation.
We will look at VA and VV ECMO separately, to analyze how these can impact on circulatory and respiratory systems, and the possible complications that can arise.