Respiratory consequences of obesity and diabetes

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 characterized, 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 index (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), compared with the corresponding control groups. Capnographic phase 3 slope was increased in diabetes without significant changes in PaO2/FiO2 or Qs/Qt. While similar detrimental changes in respiratory mechanics and alveolar heterogeneity 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 counterbalanced by hypoxic pulmonary vasoconstriction, thereby maintaining intrapulmonary shunt fraction and oxygenation ability of the lungs. Orv Hetil. 2022; 163(2): 63–73.