Data on extracorporeal life support (ECLS) use and survival submitted to the Extracorporeal Life Support Organization's data registry from the inception of the registry in 1989 through July 1, 2016, are summarized in this report. The registry contained information on 78,397 ECLS patients with 58% survival to hospital discharge. Extracorporeal life support use and centers providing ECLS have increased worldwide. Extracorporeal life support use in the support of adults with respiratory and cardiac failure represented the largest growth in the recent time period. Extracorporeal life support indications are expanding, and it is increasingly being used to support cardiopulmonary resuscitation in children and adults. Adverse events during the course of ECLS are common and underscore the need for skilled ECLS management and appropriately trained ECLS personnel and teams.

Disclaimer: ECMO has, and will certainly continue, to play a role in the management of COVID-19 patients. It should be emphasized that this initial guidance is based on the current best evidence for ECMO use during this pandemic. Guidance documents addressing additional portions of ECMO care are currently being assembled for rapid publication and distribution to ECMO centers worldwide.

Extracorporeal life support (ECLS) was developed more than 50 years ago, initially with venoarterial and subsequently with venovenous configurations. As the technique of ECLS significantly improved and newer skills developed, complexity in terminology and advances in cannula design led to some misunderstanding of and inconsistency in definitions, both in clinical practice and in scientific research. This document is a consensus of multispecialty international representatives of the Extracorporeal Life Support Organization, including the North America, Latin America, EuroELSO, South West Asia and Africa, and Asia-Pacific chapters, imparting a global perspective on ECLS. The goal is to provide a consistent and unambiguous nomenclature for ECLS and to overcome the inconsistent use of abbreviations for ECLS cannulation. Secondary benefits are ease of multicenter collaboration in research, improved registry data quality, and clear communication among practitioners and researchers in the field.

Abstract-Our previous studies have demonstrated that inhaled nitric oxide (NO) decreases nitric oxide synthase (NOS) activity in vivo and that this inhibition is associated with rebound pulmonary hypertension upon acute withdrawal of inhaled NO. We have also demonstrated that inhaled NO elevates plasma endothelin-1 (ET-1) levels and that pretreatment with PD156707, an ETA receptor antagonist, blocks the rebound hypertension. The objectives of this study were to further elucidate the role of ET-1 in the rebound pulmonary hypertension upon acute withdrawal of inhaled NO. Inhaled NO (40 ppm) delivered to thirteen 4-week-old lambs decreased NOS activity by 36.2% in control lambs (PϽ0.05), whereas NOS activity was preserved in PD156707-treated lambs. When primary cultures of pulmonary artery smooth muscle cells were exposed to ET-1, superoxide production increased by 33% (PϽ0.05). This increase was blocked by a preincubation with PD156707. Furthermore, cotreatment of cells with ET-1 and NO increased peroxynitrite levels by 26% (PϽ0.05), whereas preincubation of purified human endothelial nitric oxide synthase (eNOS) protein with peroxynitrite generated a nitrated enzyme with 50% activity relative to control (PϽ0.05). Western blot analysis of peripheral lung extracts obtained after 24 hours of inhaled NO revealed a 90% reduction in 3-nitrotyrosine residues (PϽ0.05) in PD156707-treated lambs. The nitration of eNOS was also reduced by 40% in PD156707-treated lambs (PϽ0.05). These data suggest that the reduction of NOS activity associated with inhaled NO therapy may involve ETA receptor-mediated superoxide production. ETA receptor antagonists may prevent rebound pulmonary hypertension by protecting endogenous eNOS activity during inhaled NO therapy. Key Words: nitric oxide Ⅲ rebound pulmonary hypertension Ⅲ receptor blockade Ⅲ superoxide Ⅲ peroxynitrite I nhaled nitric oxide (NO) is a selective, potent pulmonary vasodilator that is currently used as an adjunct therapy for a number of pulmonary vasculature disease states. 1 However, a number of studies have observed an acute and potentially life-threatening increase in pulmonary vascular resistance (PVR) upon acute withdrawal of inhaled NO. In children with congenital heart disease, this is manifested by an increase in PVR that may compromise cardiac output. 2,3 In newborns with persistent pulmonary hypertension, this is manifested by a sudden decrease in systemic arterial oxygen saturation. 4 This rebound pulmonary hypertension can occur after only hours of therapy and is independent of the initial response; patients with no initial pulmonary vasodilatory response can have life-threatening pulmonary vasoconstriction upon withdrawal. These manifestations of acute NO withdrawal suggest that inhaled NO may alter endogenous endothelial function, but its mechanisms are unclear.In vitro and in vivo studies indicate that exogenous NO decreases endothelial nitric oxide synthase (eNOS) activity, an effect mediated, in part, by superoxide production. 5,6 eNOS is responsible for ...