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

Abstract 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.