In patients with acute respiratory distress syndrome (ARDS), inflammation of the pulmonary circulation causes increased vascular permeability. Protein-rich fluid leaks from the blood into the pulmonary interstitium and alveolar airspaces (1). Surfactant production by type II pneumocytes is reduced, and existing surfactant is inactivated by extravasated plasma proteins (Chap. XX). Increased weight of the edematous lungs causes compression atelectasis, mainly in dependent areas. Surface tension rises at air/fluid interfaces, causing atelectasis of substantial portions of the pulmonary parenchyma (2), (Chap. XX). Intrapulmonary shunt caused by noncardiogenic edema and diffuse atelectasis may exceed 40% (3), causing life-threatening impairments of arterial oxygenation (hypoxemic respiratory failure). The reduction in aerated lung volume and increased surface tension cause lung compliance to decrease. Airway resistance may also be increased by edema of bronchial mucosa and excessive airway secretions (4). Lower lung compliance and higher airway resistance increase the work of breathing per unit of ventilation. Some relatively unaffected lung units become overventilated because ventilation is preferentially distributed to the aerated zones, whereas the more diseased lung units are less accessible for tidal ventilation. Other lung units have excessive ventilation relative to perfusion because small blood vessels become occluded by inflammation and microthrombi or compressed by high airway pressures. These “high VQ” units contribute further to increased physiological deadspace, which may exceed 60% of total ventilation (3, 5). Increased metabolic demands from acute illness further increase requirements for ventilation. In many patients, the increased work of breathing and requirements for ventilation cannot be sustained with spontaneous respiratory efforts.
|Original language||English (US)|
|Title of host publication||Acute Respiratory Distress Syndrome|
|Number of pages||37|
|State||Published - Jan 1 2003|
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