Pulmonary edema is known to induce a rapid and shallow breathing pattern. However, its effects on the level and pattern of distribution of motor activity to the respiratory muscles is unclear. In the present study we evaluated the effect of
oleic acid induced
pulmonary edema on the electrical activity of the inspiratory muscles (costal and crural diaphragm and parasternal and external intercostal muscles) in the dog, and related it to the transdiaphragmatic pressure and ventilatory parameters over the course of CO2 rebreathing.
Pulmonary edema, reflected by a 7.1 +/- 0.6 wet to dry ratio, decreased lung compliance by 57%, increased pulmonary shunt to 35%, and was associated with a rapid and shallow breathing pattern. When compared at equal levels of PCO2 during CO2 rebreathing before and during
edema, ventilation and mean inspiratory flow were increased only at lower levels of
hypercapnia and their responses to increasing levels of PCO2 were significantly diminished during
edema. Transdiaphragmatic pressures were elevated during
edema as compared to control values. The rate of rise of the electrical activity of all inspiratory muscles increased significantly during
edema at all levels of PCO2. Peak activity, however, remained unchanged, due to shortening of the inspiratory duration. The EMG responses to progressive
hypercapnia were not affected by
edema.
Pulmonary edema did not change the pattern of breathing and neural output to the inspiratory muscles in vagotomized dogs. We conclude that stimulation of pulmonary proprioreceptors during
edema increases neural output to all inspiratory muscles. The neural response to
hypercapnia is not altered by
edema, and is additive to the vagal input. The ventilatory response to CO2 is blunted during severe
edema, due to alterations in lung mechanics.