Surfactant and lung function following cardiac surgery

Cardio-pulmonary bypass (CPB) is associated with prolonged mechanical ventilation (PMV) in the intensive care unit (ICU),1 and an increase in morbidity and mortality.2 Surfactant dysfunction could result in atelectasis and contribute to PMV.3 However, it is unclear whether cessation of mechanical ventilation, with resultant atelectasis, and the use of a foreign bypass circuit during CPB, would affect the concentration of surfactant constituents and whether this, in turn, is associated with PMV. Pulmonary surfactant, which increases lung compliance and opposes atelectasis by reducing alveolar surface tension,4 is produced in the lung by alveolar type II cells. It is comprised of 10% protein4, predominantly the surfactant proteins A, B, C & D, and 90% phospholipid, which can be separated into large surfactant aggregates (LA) and small surfactant aggregates (SA).5 LA, the metabolic precursors to SA, are the greatest contributors to reduction of surface tension.5 In models of acute lung injury, LA are disproportionately converted to SA, resulting in an increased SA:LA ratio.6 This depletion of LA stores is associated with decreased lung compliance and function.6 Normal surfactant functioning and production is an important contributor to decreasing atelectasis and the need for PMV.7 Intra-operative atelectasis, accompanied by inflammation in the alveoli, has been associated with reduced intra-operative gas exchange, and the need for PMV.8 During CPB, ventilation is often ceased allowing the lungs to collapse to functional residual capacity (FRC) for prolonged periods. In addition, exposure of patient blood to the foreign bypass circuit may result in the systemic inflammatory response syndrome (SIRS), which is also a significant contributing factor to surfactant concentration and activity, and therefore atelectasis.9 The purposes of this study are to examine the effect of CPB during cardiac surgery on surfactant composition and whether changes are associated with decreased respiratory function and prolongation of mechanical ventilation in these patients. Specifically, we aimed to examine the effect of both cessation of mechanical ventilation and the effects of the bypass circuit (extracorporeal circulation) on the above factors. Respiratory function was assessed by using the post-operative ratio of the partial pressure of oxygen in arterial blood (PaO2) to the fraction of inspired oxygen (FiO2) and the length of mechanical ventilation. We hypothesized that CPB would be associated with an increase in SA concentration, and thereby an increase in the SA:LA ratio among cardiac surgery patients, compared to patients undergoing cardiac surgery without CPB, and that this change in surfactant composition would be associated with more prolonged mechanical ventilation in the CPB group.