Respiratory Mechanics and Surfactant in the Acute Respiratory Distress Syndrome

Abstract

1. Although abnormalities in pulmonary surfactant were initially implicated in the pathogenesis of the acute respiratory distress syndrome (ARDS) 30 years ago, most subsequent research has focused on mediators of the parenchymal acute lung injury (ALI) and the associated increase in alveolocapillary permeability. 2. Surfactant is essential for normal breathing and the severity of ALI correlates with surfactant dysfunction and abnormalities in surfactant composition; however, no relationship has been shown with respiratory system compliance. In neonates and most animal models, respiratory system compliance will directly reflect the elastic properties of the lung. However, the greater vertical height of the chest wall in adults, in combination with the increase in lung density due to ALI, results in dependent collapse of alveoli. Because simple, global measurement of compliance is strongly influenced by the volume of aerated lung, alternative measures of respiratory mechanics may reflect surfactant dysfunction. 3. Using a dynamic, volume-dependent model of respiratory mechanics to indirectly reflect this heterogeneous inflation, we have found direct relationships with surfactant composition in patients with ARDS. A failure of surfactant to increase surface tension in large alveoli may also explain why lung overdistension occurs at relatively low pressures. Furthermore, surfactant dysfunction will exaggerate heterogeneous lung inflation, augmenting regional overinflation, and is essential for ALI secondary to repetitive opening and closing of alveoli during tidal ventilation. 4. Ventilation-induced ALI has also been shown to result in massive increases in pro-inflammatory cytokines within the lung. Because ALI itself fails to compartmentalize cytokines, with spillover into the systemic circulation resulting in distant organ dysfunction, surfactant dysfunction may have widespread implications.

Genetics of Acute Respiratory Distress Syndrome: Challenges, Approaches, Surfactant Proteins as Candidate Genes

“…In summary, in ARDS, given the fact that abnormalities in oxygenation, pulmonary mechanics, and inflammatory processes are critical in the development of ARDS, 47,86 pulmonary surfactant and its individual components may be key in our understanding of disease pathogenesis because of their role in normal lung func-tion, innate host defense, and inflammatory processes in the lungs. Moreover, given the genetic variability of SP-A and SP-B [60][61][62]87 and their functional roles, it is possible that these serve as markers to identify disease subgroups (see Fig.…”

Acute Respiratory Failure after Administration of Hydrogen Peroxide as an Emetic in a Cat

“…The initial differential diagnosis included pulmonary edema (noncardiogenic or cardiogenic) and pneumonia. Based on the history, clinical signs, laboratory results, and thoracic radiography, H 2 O 2 aspiration with consequent noncardiogenic lung edema/pneumonia was suspected [8–11].…”

Positive pressure ventilation: what is the real cost?

“…29 Surfactant dysfunction changes compliance and exaggerates heterogeneous lung inflation necessitating ventilation patterns which may cause further damage. 11 30 69 123 Surfactant has a role in the immune defences of the lung. The lung provides more than 50 m 2 of contact across a fine membrane and is therefore a potential site for invasion.…”