The adsorption of lung surfactant to an air-water interface is strongly inhibited by the competitive adsorption of albumin and other surface active serum proteins, and is likely the explanation of surfactant inactivation in Acute Respiratory Distress Syndrome (ARDS). In vitro, lung surfactant adsorption to the interface is restored by the addition of hydrophilic non-adsorbing polymers and increased mono and divalent salts, suggesting a promising therapy for ARDS. The different approaches can be explained and quantified using classic colloidal science such as the Smolukowski analysis of colloid stability. This paper will primarily address the mechanism by which chitosan, a highly cationic biopolymer, enhances lung surfactant adsorption to the air-water interface. Chitsoan reverses albumin induced surfactant inhibition at significantly lower concentrations (0.01 mg/mL) than non-ionic polymers (10 mg/mL) though its effect is surprisingly muted by increasing the concentration greater than tenfold. Fluorescence and confocal microscopy images of the interface show distinct changes in morphology between albumin and surfactant-covered regions offering a visual confirmation of surfactant adsorption to the interface. We will compare these results to the depletion attraction generated by non-ionic polymers and the electrostatic effects generated by mono and divalent salts which have both been shown previously to enhance surfactant adsorption.