Abstract |
Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a life-saving technology that provides transient respiratory and circulatory support for patients with profound cardiogenic shock or refractory cardiac arrest. Among its potential complications, VA-ECMO may adversely affect lung function through various pathophysiological mechanisms. The interaction of blood components with the biomaterials of the extracorporeal membrane elicits a systemic inflammatory response which may increase pulmonary vascular permeability and promote the sequestration of polymorphonuclear neutrophils within the lung parenchyma. Also, VA-ECMO increases the afterload of the left ventricle (LV) through reverse flow within the thoracic aorta, resulting in increased LV filling pressure and pulmonary congestion. Furthermore, VA-ECMO may result in long-standing pulmonary hypoxia, due to partial shunting of the pulmonary circulation and to reduced pulsatile blood flow within the bronchial circulation. Ultimately, these different abnormalities may result in a state of persisting lung inflammation and fibrotic changes with concomitant functional impairment, which may compromise weaning from VA-ECMO and could possibly result in long-term lung dysfunction. This review presents the mechanisms of lung damage and dysfunction under VA-ECMO and discusses potential strategies to prevent and treat such alterations.
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Authors | Aurélien Roumy, Lucas Liaudet, Marco Rusca, Carlo Marcucci, Matthias Kirsch |
Journal | Critical care (London, England)
(Crit Care)
Vol. 24
Issue 1
Pg. 212
(05 11 2020)
ISSN: 1466-609X [Electronic] England |
PMID | 32393326
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Topics |
- Humans
- Extracorporeal Membrane Oxygenation
(adverse effects)
- Ischemia
(etiology, physiopathology)
- Parenchymal Tissue
(injuries, physiopathology)
- Respiratory Physiological Phenomena
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