• Sarah Buehler, Sara Lozano-Zahonero, Steffen Wirth, Hanna Runck, Katharina Gamerdinger, Katharina Förster, Jörg Haberstroh, Josef Guttmann, and Stefan Schumann.
• 1Division of Experimental Anesthesiology, Department of Anesthesiology and Intensive Care Medicine, University Medical Center, Freiburg, Germany. 2Department of Cardiovascular Surgery, Heart Center, University of Freiburg, Freiburg, Germany. 3Experimental Surgery, CEMT-FR, University Medical Center Freiburg, Freiburg, Germany.
• Crit. Care Med. 2016 Jul 1; 44 (7): e502-8.

ObjectivesIn mechanical ventilation, normoventilation in terms of PCO2 can be achieved by titration of the respiratory rate and/or tidal volume. Although a linear relationship has been found between changes in respiratory rate and resulting changes in end-tidal cO2 (△PetCO2) as well as between changes in respiratory rate and equilibration time (teq) for mechanically ventilated patients without lung injury, it is unclear whether a similar relationship holds for acute lung injury or altered hemodynamics.DesignWe performed a prospective randomized controlled animal study of the change in PetCO2 with changes in respiratory rate in a lung-healthy, lung-injury, lung-healthy + altered hemodynamics, and lung-injury + altered hemodynamics pig model.SettingUniversity research laboratory.SubjectsTwenty mechanically ventilated pigs.InterventionsModerate lung injury was induced by injection of oleic acid in 10 randomly assigned pigs, and after the first round of measurements, cardiac output was increased by approximately 30% by constant administration of noradrenalin in both groups.Measurements And Main ResultsWe systematically increased and decreased changes in respiratory rate according to a set protocol: +2, -4, +6, -8, +10, -12, +14 breaths/min and awaited equilibration of Petco2. We found a linear relationship between changes in respiratory rate and △PetCO2 as well as between changes in respiratory rate and teq. A two-sample t test resulted in no significant differences between the lung injury and healthy control group before or after hemodynamic intervention. Furthermore, exponential extrapolation allowed prediction of the new PetCO2 equilibrium and teq after 5.7 ± 5.6 min.ConclusionsThe transition between PetCO2 equilibria after changes in respiratory rate might not be dependent on moderate lung injury or cardiac output but on the metabolic production or capacity of cO2 stores. Linear relationships previously found for lung-healthy patients and early prediction of PetCO2 equilibration could therefore also be used for the titration of respiratory rate on the PetCO2 for a wider range of pathologies by the physician or an automated ventilation system.

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