Evolution of Diaphragm Thickness Under Veno-arterial ECMO

Diaphragm, Extracorporeal Membrane Oxygenation Complication

diaphragm, ECMO, ICU

The main objective is to evaluate the evolution of the thickness of the diaphragm (during the first week of treatment) by VA ECMO in the resuscitation patients. The comprehension of the mechanisms involved in the diaphragm ailment will identify modifiable factors that lead to muscle degradation and thus to the deterioration of patients' prognosis.

The evolution of diaphragm muscle thickness is described in human resuscitation under mechanical ventilation, but the incidence, causes and functional impact have not been studied in patients undergoing cardiopulmonary bypass ECMO (extra-corporeal membrane oxygenation) veno-arterial (VA). More generally, the muscular mechanisms of dyspnea in cases of acute cardiac dysfunction are not known. The evolution of the diaphragmatic thickness in intensive care has been described during prolonged stay in intensive care and from the initial phase of septic status. It is associated with dyspnea, weaning delay of mechanical ventilation and impact on patient outcomes. The atrophy of the diaphragm muscle is related to both loss of function and loss of muscle performance. The same is true for hypertrophy that is caused by overuse of the muscle and also causes loss of function. Decreased cardiac muscle performance may require both cardiac assistance and respiratory assistance. Cardiac and respiratory dysfunction may complicate withdrawal of respiratory assistance and extracorporeal circulatory support devices. These two supports, respiratory and circulatory support, make it possible to mitigate the insufficiency of the systemic flow, the oxygenation and the purification of the CO2. Respiratory assistance is known to influence the diaphragmatic function. The role of muscle pump function in the weaning process of the ECMO, however, remains largely unknown. Ultrasound is used in the patient's bed in daily practice to measure cardiac function, the study of vessels but also the diaphragm muscle. It allows to study the trophicity of the diaphragm and these efforts via its contraction. The hypothesis that there is muscular involvement of the diaphragm in this measurable condition by ultrasound method can be formulated. No study has systematically explored the existence of diaphragmatic atrophy under VA ECMO. The influence of cardiac and respiratory assistance is not known. The purpose of this study is to provide a description of the diaphragm physiology of patients treated with VA ECMO. It is to evaluate the evolution of the trophicity of the diaphragm muscle in intensive care. Secondly, to evaluate the factors that influence it at the time of weaning. In this study it's planed to include a cohort of patients with a longitudinal evaluation of the thickness of the diaphragm during a cardiogenic shock under ECMO, and an evaluation of the influence of ECMO parameters and ventilation on the diaphragm.

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