Interfacial Rheology and Breathing*

The dependence of the Laplace pressure, ΔP = 2γ/R, on alveolar radius, R, means that interconnected alveoli are metastable if γ is constant. However, while not generally appreciated in the medical literature, but well known in the foam and emulsion stability literature, the dynamic resistance of an interfacial film to compression can reverse the Laplace instability. The dilatational modulus, ε=A∂γ/∂A , relates the change in surface tension, γ, to the change in molecular area, A, as the interface is compressed at frequency, ω (ranging from 1-20 radians/second for normal breathing). If the dilatational modulus is large enough, the resistance to interfacial compression can overcome the Laplace pressure so that the gas pressure in the alveolus no longer increases with decreasing radius. For (2ε-γ) > 0, the Laplace pressure decreases with decreasing radius and increases with increasing radius, which reverses the Laplace instability, thereby stabilizing the alveoli against collapse. Under normal conditions, lung surfactant generates conditions such that (2ε-γ) > 0, and the lung remains stable. However, during Acute Respiratory Distress Syndrome, trauma or disease leads to a dramatic increase in the concentration of albumin and lysophosphatidylcholine, soluble surface-active molecules that compete for the interface with lung surfactant. Using a newly designed capillary microtensiometer, we have found that increasing concentrations of lysophosphatidylcholines, a product of the inflammation induced degradation of phospholipids, causes the dilatational modulus to decrease as ω decreases, resulting in (2ε-γ) < 0, creating conditions that induce the Laplace instability. This suggests a mechanism underlying ARDS which kills 50,000 people each year with no known cure. Increasing the breathing frequency or decreasing the lysophosphatidylcholine concentration can increase the dilatational modulus and may restore proper lung function in ARDS.