Visualization of airway obstruction in vivo during pulmonary vascular engorgement and edema

Although pulmonary vascular engorgement has often been hypothesized to decrease airway caliber, leading to airway obstruction in asthma, direct evidence for this hypothesis is lacking. In the present study, we used high- resolution computed tomography to directly measure the changes in the caliber and wall thickness of conducting airways after volume loading with normal saline (NS) and homologous blood. Five anesthetized dogs received 0.2 mg/kg of atropine followed by either three sequential fluid challenges of 50 ml/kg of NS or two sequential challenges of 25 ml/kg of blood. Several weeks later, the same dogs received the other fluid challenge. Volume loading with 150 ml/kg of NS decreased the average airway luminal area to 68 ± 3% (± SE) of baseline. Concomitantly, airway wall thickness increased to 150 ± 6% of baseline. Volume loading with 50 ml/kg of blood decreased the average airway luminal area to 81 ± 2% of baseline. Concomitantly, airway wall thickness increased to 108 ± 2% of baseline. Therefore, for comparable changes in pulmonary vascular pressure, an infusion of NS caused a significantly greater decrease in airway luminal area and a larger increase in airway wall thickness than an infusion of blood. This suggests that the presence of edema fluid in or immediately surrounding the airway wall acts to decrease the airway lumen. However, since the degree of airway narrowing was only moderate, even with a most extreme fluid load, it seems unlikely that airway wall thickening or edema could be a primary cause of conducting airway obstruction in patients with asthma or impaired left ventricular function. Unless the human airway can acutely absorb much larger volumes of interstitial water, obstructions severe enough to cause dyspnea would of necessity require active airway muscle contraction.