Does extracorporeal membrane oxygenation attenuate hypoxic pulmonary vasoconstriction in a porcine model of global alveolar hypoxia?

Abstract

During severe respiratory failure, hypoxic pulmonary vasoconstriction (HPV) is partly suppressed, but may still play a role in increasing pulmonary vascular resistance (PVR). Experimental studies suggest that the degree of HPV during severe respiratory failure is dependent on pulmonary oxygen tension (PvO₂ ). Therefore, it has been suggested that increasing PvO₂ by veno-venous extracorporeal membrane oxygenation (V-V ECMO) would adequately reduce PVR in V-V ECMO patients. Whether increased PvO₂ by V-V ECMO decreases PVR in global alveolar hypoxia. Nine landrace pigs were ventilated with a mixture of oxygen and nitrogen. After 15 minutes of stable ventilation and hemodynamics, the animals were cannulated for V-V ECMO. Starting with alveolar normoxia, the fraction of inspiratory oxygen (F_I O₂ ) was stepwise reduced to establish different degrees of alveolar hypoxia. PvO₂ was increased by V-V ECMO. V-V ECMO decreased PVR (from 5.5 [4.5-7.1] to 3.4 [2.6-3.9] mm Hg L^-1  min, P = .006) (median (interquartile range),) during ventilation with F_I O₂ of 0.15. At lower F_I O₂ , PVR increased; at F_I O₂ 0.10 to 4.9 [4.2-7.0], P = .036, at F_I O₂ 0.05 to 6.0 [4.3-8.6], P = .002, and at F_I O₂ 0 to 5.4 [3.5 - 7.0] mm Hg L^-1  min, P = .05. The effect of increased PvO₂ by V-V ECMO on PVR depended highly on the degree of alveolar hypoxia. Our results partly explain why V-V ECMO does not always reduce right ventricular afterload at severe alveolar hypoxia.