1. Atelectasis

2. 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

3. 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.

4. 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.

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

6. 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

7. 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

8. 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