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The effects of cardiac output and pulmonary arterial hypertension on volumetric capnography derived-variables during normoxia and hypoxia

Mosing, Martina ; Kutter, Annette ; Iff, Samuel ; Raszplewicz, Joanna ; Mauch, Jacqueline ; Bohm, Stephan ; Tusman, Gerardo

In: Journal of Clinical Monitoring and Computing, 2015, vol. 29, no. 1, p. 187-196

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    Title
    • The effects of cardiac output and pulmonary arterial hypertension on volumetric capnography derived-variables during normoxia and hypoxia
    Author
    • Mosing, Martina. Division of Anaesthesiology, Equine Department, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 260, 8057, Zurich, Switzerland
    • Kutter, Annette. Division of Anaesthesiology, Equine Department, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 260, 8057, Zurich, Switzerland
    • Iff, Samuel. CTU Bern, University of Bern, Finkenhubelweg 11, 3012, Bern, Switzerland
    • Raszplewicz, Joanna. Division of Anaesthesiology, Equine Department, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 260, 8057, Zurich, Switzerland
    • Mauch, Jacqueline. Department of Anesthesiology, Kantonsspital Luzern, Spitalstrasse, 6000, Lucerne, Switzerland
    • Bohm, Stephan. Swisstom AG, Schulstrasse 1, 7302, Landquart, Switzerland
    • Tusman, Gerardo. Department of Anesthesiology, Hospital Privado de Comunidad, Mar del Plata, Argentina
    Document Type
    • Postprint
    Language
    • English
    Published in
    • Journal of Clinical Monitoring and Computing, 2015, vol. 29, no. 1, p. 187-196. Springer Netherlands
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:332218
    Summary
    The aim of this study was to test the effect of cardiac output (CO) and pulmonary artery hypertension (PHT) on volumetric capnography (VCap) derived-variables. Nine pigs were mechanically ventilated using fixed ventilatory settings. Two steps of PHT were induced by IV infusion of a thromboxane analogue: PHT25 [mean pulmonary arterial pressure (MPAP) of 25mmHg] and PHT40 (MPAP of 40mmHg). CO was increased by 50% from baseline (COup) with an infusion of dobutamine ≥5μgkg−1min−1 and decreased by 40% from baseline (COdown) infusing sodium nitroglycerine ≥30μgkg−1min−1 plus esmolol 500μgkg−1min−1. Another state of PHT and COdown was induced by severe hypoxemia (FiO2 0.07). Invasive hemodynamic data and VCap were recorded and compared before and after each step using a mixed random effects model. Compared to baseline, the normalized slope of phase III (SnIII) increased by 32% in PHT25 and by 22% in PHT40. SnIII decreased non-significantly by 4% with COdown. A combination of PHT and COdown associated with severe hypoxemia increased SnIII by 28% compared to baseline. The elimination of CO2 per breath decreased by 7% in PHT40 and by 12% in COdown but increased only slightly with COup. Dead space variables did not change significantly along the protocol. At constant ventilation and body metabolism, pulmonary artery hypertension and decreases in CO had the biggest effects on the SnIII of the volumetric capnogram and on the elimination of CO2.