μ-PIV for the Analysis of Flow Fields near a Propagating Air-Liquid Interface

In a healthy lung, the inside surface of respiratory airways is coated with a thin film of lipids and proteins called lung surfactants (LS) which dynamically alter the surface tension and stabilize airways and reduce the work of breathing. Certain clinical events, such as gastric content aspiration, pneumonia, near-drowning, toxic gas inhalation, or chest/lung trauma will trigger lung surfactant “inactivation”. This inactivation is caused by the presence of LS inhibitors, including a variety of water-soluble and surface-active serum protein substances, such as albumin, fibrinogen, and IgG that are normally absent from the airway. These can leak through the capillary membrane from the damaged cells, causing LS to lose its ability to lower surface tension necessary for the lung function (Zasadzinski et al. 2010). Mechanical ventilation is inarguably a necessary life-sustaining form of medical intervention at this stage. However, since the leaked proteins inactivate the lung surfactants, the air-liquid interface exerts a wider range of excessive, irregular mechanical stresses and strains on the delicate and highly-sensitive tissues that make up the airways and alveoli of the lung, resulting ventilator-induced lung injury (VILI). This progressive failure will eventually cause more complex pathological conditions such as Acute Lung Injury (ALI) or Acute Respiratory Distress Syndrome (ARDS). Likewise surfactant deficiency, a hallmark of Respiratory Distress Syndrome of premature infants, leads to large interfacial stress that can damage airways and alveoli during an infant’s first breaths which clears amniotic fluid from the airways is it introduces air to the deep lung and alveoli.