Respiratory consequences of obesity and diabetes

Abstract

Introduction: While sustained hyperglicemia affects the smooth muscle tone and the elastin-collagen network, the effect of diabetes mellitus on the function and structure of the airways and the lung parenchyma has not been char¬acterized, and the confounding influence of obesity has not been elucidated. Objective: To reveal the separate and additive roles of diabetes mellitus and obesity on the respiratory function. Method: Non-obese mechanically ventilated patients were categorized as control non-diabetic (n = 80) and diabetic (n = 35) groups. Obese patients with (n = 33) or without (n = 47) associated diabetes were also enrolled. Forced oscillation technique was applied to measure airway resistance (Raw), tissue damping (G), and tissue elastance (H). Capnography was utilized to determine phase 3 slopes and ventilation dead space parameters. Arterial and central venous blood samples were analyzed to assess intrapulmonary shunt fraction (Qs/Qt) and the lung oxygenation in-dex (PaO2/FiO2). Results: Diabetes without obesity increased the Raw (7.4 ± 5 cmH2O.s/l vs. 3.0 ± 1.7 cmH2O.s/l), G (11.3 ± 4.9 cmH2O/l vs. 6.2 ± 2.4 cmH2O/l), and H (32.3 ± 12.0 cmH2O/l vs. 25.1 ± 6.9 cmH2O/l, (p<0.001 for all), com¬pared with the corresponding control groups. Capnographic phase 3 slope was increased in diabetes without signifi¬ cant changes in PaO2/FiO2 or Qs/Qt. While similar detrimental changes in respiratory mechanics and alveolar het¬erogeneity were observed in obese patients without diabetes, these alterations also compromised gas exchange. Conclusion: The intrinsic mechanical abnormalities in the airways and lung tissue induced by diabetes are counterbal¬anced by hypoxic pulmonary vasoconstriction, thereby maintaining intrapulmonary shunt fraction and oxygenation ability of the lungs.