| Literature DB >> 33624260 |
Anthony R Prisco1, Jazmin Aguado-Sierra2, Constantine Butakoff3, Mariano Vazquez2, Guillaume Houzeaux2, Beatriz Eguzkitza2, Jason A Bartos1, Demetris Yannopoulos1, Ganesh Raveendran1, Mikayle Holm4,5, Tinen Iles5, Claudius Mahr6, Paul A Iaizzo7.
Abstract
Venous-arterial extracorporeal membrane oxygenation (VA-ECMO) treatment for acute cardiogenic shock in patients who also have acute lung injury predisposes development of a serious complication called "north-south syndrome" (NSS) which causes cerebral hypoxia. NSS is poorly characterized and hemodynamic studies have focused on cerebral perfusion ignoring the heart. We hypothesized in NSS the heart would be more likely to receive hypoxemic blood than the brain due to the proximity of the coronary arteries to the aortic annulus. To test this, we conducted a computational fluid dynamics simulation of blood flow in a human supported by VA-ECMO. Simulations quantified the fraction of blood at each aortic branching vessel originating from residual native cardiac output versus VA-ECMO. As residual cardiac function was increased, simulations demonstrated myocardial hypoxia would develop prior to cerebral hypoxia. These results illustrate the conditions where NSS will develop and the relative cardiac function that will lead to organ-specific hypoxia. Illustration of the impact of north-south syndrome on organ-specific oxygen delivery. Patients on VA-ECMO have two sources of blood flow, one from the VA-ECMO circuit and one from the residual cardiac function. When there is no residual cardiac function, all organs are perfused with oxygenated blood. As myocardial recovery progresses, blood supply from the two sources will begin to mix resulting in non-homogeneous mixing and differential oxygenation based upon the anatomical site of branching vessels.Entities:
Keywords: Acute respiratory distress syndrome; Computational fluid dynamics; North-south syndrome; VA-ECMO
Mesh:
Year: 2021 PMID: 33624260 PMCID: PMC7901681 DOI: 10.1007/s12265-021-10110-2
Source DB: PubMed Journal: J Cardiovasc Transl Res ISSN: 1937-5387 Impact factor: 3.216