Atelectasis

Atelectasis Atelectasis is of Greek origin and means lack of stretch Classified either by its pathophysiology or by the region and amount of lung involved Pathophysiologically can be divided into obstructive and nonobstructive causes

Atelectasis Obstructive (resorptive) atelectasis airway blockage Retained air then resorbed from non ventilated alveoli. Over time, the affected regions  airless The rate& extent of atelectasis depend upon the degree of collateral ventilation & the composition of inspired gas.

Atelectasis Collateral ventilation Greater between segments than between lobes. Lobar bronchus obstruction is more likely to produce lobar atelectasis than obstruction of a segmental bronchus Is provided via the pores of Kohn canals of Lambert, & fenestrations of Boren.  smaller bronchi obstruction can cause atelectasis only if these pathways are obliterated by an inflammatory process or by mucus.

Atelectasis Collateral ventilation Collateral ventilation is age-dependent Poorly developed in children Emphysematous lung have a larger collateral  longer time to collapse

Atelectasis Inspired Gas composition Faster atelectasis with higher FIO2 less nitrogen in alveolar space Nitrogen has a slow reabsorbtion rate because of minimal gradient between alveolar space & capillary blood

Atelectasis Non Obstructive Passive atelectasis  contact between the parietal and visceral pleurae is eliminated by a pleural effusion or pneumothorax Compressive atelectasis diminution in lung volume below the usual resting volume. chest wall, pleural, intraparenchymal masses loculated effusion

Atelectasis Non Obstructive Adhesive atelectasis  surfactant dysfunction Cicatrization atelectasis loss of volume as a result of severe parenchymal scarring. Replacement atelectasis  the alveoli of an entire lobe are filled by tumor, such as BAC