Institute for Continuing Education

Surfactants in Respiratory Care

Course Objectives

Upon successful completion of this module, you will be able to:

• Describe the biochemical composition of pulmonary surfactant, including the role of dipalmitoylphosphatidylcholine (DPPC) and the four surfactant proteins (SP-A, SP-B, SP-C, and SP-D).
• Explain how the type II pneumocyte synthesizes, stores, secretes, and recycles surfactant, and trace the surfactant life cycle from lamellar body to surface film.
• Apply Laplace’s law to explain how surfactant lowers surface tension and stabilizes alveoli of differing size against collapse.
• Interpret the static pressure–volume curve of the lung, including hysteresis and the effect of surfactant on compliance and the work of breathing.
• Relate the timing of fetal surfactant production to gestational age and interpret the lecithin–sphingomyelin (L/S) ratio and other markers of fetal lung maturity.
• Explain the rationale, timing, and effects of antenatal corticosteroid therapy on fetal lung maturation.
• Analyze the pathophysiology of neonatal respiratory distress syndrome (hyaline membrane disease) as the prototypical surfactant-deficiency state.
• Differentiate primary surfactant deficiency from secondary surfactant inactivation in meconium aspiration, ARDS, and pneumonia.
• Compare the available surfactant replacement agents—animal-derived (beractant, calfactant, poractant alfa) versus synthetic—by source, composition, and dosing.
• Distinguish prophylactic from rescue surfactant strategies and describe the administration techniques ranging from INSURE to the less-invasive LISA/MIST and aerosolized approaches.
• Describe the respiratory therapist’s responsibilities before, during, and after surfactant administration, including preparation, positioning, and ventilator and CPAP management.
• Recognize and respond to the common transient complications of surfactant administration, including bradycardia, desaturation, reflux, and endotracheal tube obstruction.
• Evaluate why surfactant replacement transformed the outcome of neonatal RDS yet has produced disappointing results in adult ARDS.

Course Information

In the 1920s the importance of surface tension in pulmonary physiology was first realized. However, it was not until the 1950s that surfactant was first described, when it was found that material obtained from alveolar washes could significantly reduce surface tension on dynamic film compression. Soon after these early reports, it was speculated that a deficiency of pulmonary surfactant may play an important role in the pathophysiology of various pulmonary conditions. Following these reports there has been an explosion of information on surfactant composition, metabolism, biophysical, and physiological activity. This has led to a better understanding of surfactant deficient and dysfunctional disease states, and the potential therapeutic benefits of surfactant replacement therapy.

The major role of surfactant is to allow large variations in surface tension during lung expansion and deflation. This action promotes alveolar stability, reduces atelectasis, decreases edema formation and minimizes the work of respiration. These physiological functions are dependent on the biophysical properties of surfactant which include: rapid adsorption to the air-liquid interface, respreadability after compression, and the ability to alter surface tension during dynamic compression and expansion.