Albumin kinetics, intravascular fluid volume, and respiratory function in pigs ventilated at different levels of mechanical power following crystalloid vs. albumin infusion

Background: The rationale of albumin use lies in its potential to increase oncotic pressure and optimize tissue perfusion. Randomized trials have not demonstrated a survival benefit, and the effects of albumin on volemia remain unclear. This study investigates, in healthy pigs, the effects of a 48-h albumin infusion on intravascular fluid volume, albumin kinetics, and its impact on respiratory function. Methods: Thirty-nine healthy female pigs ventilated for 48 h were grouped according to mechanical power (high ~ 18 J/min vs. low ~ 6 J/min) and type of fluid (5% albumin solution vs. crystalloid), generating four experimental groups: MPLOW-Crystalloid; MPLOW-Albumin; MPHIGH-Crystalloid; and MPHIGH-Albumin. Results: Intravascular fluid volume was similar across groups (MPLOW-Crystalloid: 1.92 (± 0.38)L; MPHIGH-Crystalloid: 1.72 (± 0.40)L; MPLOW-Albumin: 1.86 (± 0.37)L; MPHIGH-Albumin: 2.10 (± 0.58)L; p 0.389). For the same mechanical power, the fraction of albumin lost from the plasma was higher in the albumin compared to the crystalloid groups (MPLOW-Albumin: 62 (± 13)% vs. MPLOW-Crystalloid: − 16 (± 66)%; and MPHIGH-Albumin: 58 (± 24)% vs. MPHIGH-Crystalloid: 29 (± 14)%; p < 0.001). Albumin groups showed greater ascites (MPLOW-Crystalloid: 261 (± 380)mL; MPHIGH-Crystalloid: 144 (± 148)mL; MPLOW-Albumin: 710 (± 664)mL; MPHIGH-Albumin: 685 (± 651)mL; p 0.034), and worse end-expiratory lung gas volume and elastance, despite comparable histological damage. Conclusions: In our cohort, prolonged albumin infusion did not lead to a difference in intravascular fluid volume, but it resulted in the loss of ~ 60% of the infused albumin and ascites development. Ascites was associated with lower end-expiratory lung gas volume and higher elastance, despite similar histological lung damage across the groups.