Premium
Does extracorporeal membrane oxygenation attenuate hypoxic pulmonary vasoconstriction in a porcine model of global alveolar hypoxia?
Author(s) -
Holzgraefe Bernhard,
Larsson Anders,
Eksborg Staffan,
Kalzén Håkan
Publication year - 2020
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/aas.13588
Subject(s) - hypoxic pulmonary vasoconstriction , medicine , extracorporeal membrane oxygenation , interquartile range , hypoxia (environmental) , oxygenation , anesthesia , membrane oxygenator , vascular resistance , respiratory failure , vasoconstriction , cardiology , hemodynamics , oxygen , chemistry , organic chemistry
Background 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 (PvO 2 ). Therefore, it has been suggested that increasing PvO 2 by veno‐venous extracorporeal membrane oxygenation (V‐V ECMO) would adequately reduce PVR in V‐V ECMO patients. Objective Whether increased PvO 2 by V‐V ECMO decreases PVR in global alveolar hypoxia. Methods 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 O 2 ) was stepwise reduced to establish different degrees of alveolar hypoxia. PvO 2 was increased by V‐V ECMO. Results 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 O 2 of 0.15. At lower F I O 2 , PVR increased; at F I O 2 0.10 to 4.9 [4.2‐7.0], P = .036, at F I O 2 0.05 to 6.0 [4.3‐8.6], P = .002, and at F I O 2 0 to 5.4 [3.5 ‐ 7.0] mm Hg L −1 min, P = .05. Conclusions The effect of increased PvO 2 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.