MECHANICAL VENTILATION IN ACUTE LUNG INJURY AND ACUTE RESPIRATORY DISTRESS SYNDROME

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)¹³ occur in diseases such as sepsis and severe pneumonia49, 69 that cause diffuse inflammation in the pulmonary parenchyma. Increased pulmonary vascular permeability leads to extravasation of protein-rich fluid into the pulmonary interstitium, small bronchioles, and alveolar airspaces.¹³³ Injury to type II pneumocytes decreases surfactant production, and existing surfactant is inactivated by plasma proteins that leak into small airways and alveoli.87, 124, 133, 137 With inadequate surfactant function, increased surface tension at air–fluid interfaces causes diffuse microatelectasis.⁵⁴ Other airspaces fill with fluid, inflammatory cells, and debris and are therefore unavailable for ventilation and gas exchange. Hypoxemia therefore occurs primarily from arteriovenous shunt.³⁶ Some aerated lung regions are poorly ventilated because their regional compliances are reduced or their airway resistances are elevated from regional inflammation and interstitial fluid extravasation. These “low ventilation-perfusion (V/Q)” units may contribute further to hypoxemia. Other lung units may be overventilated if their airspace compliances are relatively high or their regional blood flows are reduced by microthrombi and capillary obliteration.83, 133 Such “high V/Q” units cause high deadspace and elevated ventilation requirements in ALI and ARDS patients. In milder cases, hypoxemia may be corrected with increased fractional inspiration of oxygen (F io₂) and spontaneous increases in minute ventilation are sufficient to maintain normal arterial partial pressure of carbon dioxide (Pa co₂). In more severe cases, mechanical ventilation is necessary to ensure adequate gas exchange and prevent death from severe hypoxemia and hypercapnia.