학술논문
Determinants of acute kidney injury during high-power mechanical ventilation: secondary analysis from experimental data.
Document Type
Academic Journal
Author
Gattarello S; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany. gattarello@gmail.com.; Lombardo F; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Romitti F; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; D'Albo R; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Velati M; Department of Anesthesia and Intensive Care Medicine Department, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy.; Fratti I; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Pozzi T; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Nicolardi R; Department of Anesthesia and Intensive Care Medicine Department, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy.; Fioccola A; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Busana M; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Collino F; Department of Anesthesia, Intensive Care and Emergency, 'Città Della Salute E Della Scienza' Hospital, Turin, Italy.; Herrmann P; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Camporota L; Department of Adult Critical Care, Guy's and St. Thomas' NHS Foundation Trust, London, UK.; Quintel M; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Department of Anesthesiology, Intensive Care and Emergency Medicine Donau-Isar-Klinikum Deggendorf, Deggendorf, Germany.; Moerer O; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Saager L; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Meissner K; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.; Gattinoni L; Department of Anesthesiology, University Medical Centre Göttingen, Göttingen, Germany.
Source
Publisher: Springer-Verlag, GmbH Country of Publication: Germany NLM ID: 101645149 Publication Model: Electronic Cited Medium: Print ISSN: 2197-425X (Print) Linking ISSN: 2197425X NLM ISO Abbreviation: Intensive Care Med Exp Subsets: PubMed not MEDLINE
Subject
Language
English
ISSN
2197-425X
Abstract
Background: The individual components of mechanical ventilation may have distinct effects on kidney perfusion and on the risk of developing acute kidney injury; we aimed to explore ventilatory predictors of acute kidney failure and the hemodynamic changes consequent to experimental high-power mechanical ventilation.
Methods: Secondary analysis of two animal studies focused on the outcomes of different mechanical power settings, including 78 pigs mechanically ventilated with high mechanical power for 48 h. The animals were categorized in four groups in accordance with the RIFLE criteria for acute kidney injury (AKI), using the end-experimental creatinine: (1) NO AKI: no increase in creatinine; (2) RIFLE 1-Risk: increase of creatinine of > 50%; (3) RIFLE 2-Injury: two-fold increase of creatinine; (4) RIFLE 3-Failure: three-fold increase of creatinine; RESULTS: The main ventilatory parameter associated with AKI was the positive end-expiratory pressure (PEEP) component of mechanical power. At 30 min from the initiation of high mechanical power ventilation, the heart rate and the pulmonary artery pressure progressively increased from group NO AKI to group RIFLE 3. At 48 h, the hemodynamic variables associated with AKI were the heart rate, cardiac output, mean perfusion pressure (the difference between mean arterial and central venous pressures) and central venous pressure. Linear regression and receiving operator characteristic analyses showed that PEEP-induced changes in mean perfusion pressure (mainly due to an increase in CVP) had the strongest association with AKI.
Conclusions: In an experimental setting of ventilation with high mechanical power, higher PEEP had the strongest association with AKI. The most likely physiological determinant of AKI was an increase of pleural pressure and CVP with reduced mean perfusion pressure. These changes resulted from PEEP per se and from increase in fluid administration to compensate for hemodynamic impairment consequent to high PEEP.
(© 2024. The Author(s).)
Methods: Secondary analysis of two animal studies focused on the outcomes of different mechanical power settings, including 78 pigs mechanically ventilated with high mechanical power for 48 h. The animals were categorized in four groups in accordance with the RIFLE criteria for acute kidney injury (AKI), using the end-experimental creatinine: (1) NO AKI: no increase in creatinine; (2) RIFLE 1-Risk: increase of creatinine of > 50%; (3) RIFLE 2-Injury: two-fold increase of creatinine; (4) RIFLE 3-Failure: three-fold increase of creatinine; RESULTS: The main ventilatory parameter associated with AKI was the positive end-expiratory pressure (PEEP) component of mechanical power. At 30 min from the initiation of high mechanical power ventilation, the heart rate and the pulmonary artery pressure progressively increased from group NO AKI to group RIFLE 3. At 48 h, the hemodynamic variables associated with AKI were the heart rate, cardiac output, mean perfusion pressure (the difference between mean arterial and central venous pressures) and central venous pressure. Linear regression and receiving operator characteristic analyses showed that PEEP-induced changes in mean perfusion pressure (mainly due to an increase in CVP) had the strongest association with AKI.
Conclusions: In an experimental setting of ventilation with high mechanical power, higher PEEP had the strongest association with AKI. The most likely physiological determinant of AKI was an increase of pleural pressure and CVP with reduced mean perfusion pressure. These changes resulted from PEEP per se and from increase in fluid administration to compensate for hemodynamic impairment consequent to high PEEP.
(© 2024. The Author(s).)