title: Collateral ventilation.
abstract: Ventilation may bypass obstructed airways through collateral channels, including interalveolar pores of Kohn, bronchiole-alveolar communications of Lambert, and interbronchiolar pathways of Martin. Resistance through these channels, like resistance through small airways, increases with decreasing lung volume and with hypocapnia. But whereas the distention of collateral channels and small airways by a variety of factors is similar, the efficiency of ventilation through collateral channels is less than the efficiency through airways. Gas inspired through collateral channels is contaminated with alveolar gas from surrounding lung so that the dead space for collateral ventilation is increased. When one part of the lung ventilates out of phase with the surrounding lung, pulmonary interdependence promotes more homogeneous ventilation. In the presence of airways obstruction, interdependence may be a primary factor governing the rate of collateral ventilation. In man, collateral ventilation is unimportant in normal lungs. However, with disease, it may be critical in producing or compensating for abnormalities. For example, the long time constant for collateral ventilation in the middle lobe may be responsible for atelectasis, which results in the middle lobe syndrome. On the other hand, the short time constant for collateral ventilation in emphysema may be essential for the distribution of ventilation beyond obstructed airways.
mesh_terms: D000403:Airway Resistance; D000818:Animals; D001980:Bronchi / Q000033:anatomy & histology; D002245:Carbon Dioxide / Q000502:physiology; D004285:Dogs; D004548:Elasticity; D006801:Humans; D008168:Lung / Q000033:anatomy & histology* / Q000502:physiology; D008170:Lung Compliance; D011650:Pulmonary Alveoli / Q000033:anatomy & histology; D011653:Pulmonary Diffusing Capacity; D012123:Pulmonary Ventilation
chemical_list: D002245:Carbon Dioxide