Stephen H. Loring

Patients on high inspired O₂ concentrations are at risk of atelectasis, a problem that has been quantitatively assessed using analysis of V̇_A/Q̇ equations. This approach ignores the potential of the elastic properties of the lung to support gas exchange through "apneic" oxygenation in units with no tidal ventilation, and is based on an error in the conservation of mass equations. To fill this gap, we correct the error and compare the pressure drops associated with apneic gas exchange with the pressure differences that can be supported by lung recoil. We analyze a worst case scenario: a small test unit in the Weibel Model A tree structure with zero tidal ventilation, 100% inspired O₂, the rest of the lung being normally ventilated tidally. We first computed the gas flux to the (unventilated) test unit and estimated the associated pressure drops. We then computed the difference in local gas pressure relative to the surrounding lung that would cause the unit to collapse. We compared these two, and finally computed the degree of airway narrowing that would change the stable (apneic gas exchange) regime to the unstable regime leading to collapse. We find that except under extreme conditions of loss of airway caliber exceeding roughly 90%, lung recoil is sufficient to maintain oxygenation through convective transport alone. We further argue that the fundamental V̇_A/Q̇ equations are invalid in these circumstances, and that the issue of atelectasis in low V̇_A/Q̇ will require modifications to account for this additional mode of gas exchange.

Recent studies applying the principles of respiratory mechanics to respiratory disease have used inconsistent and mutually exclusive definitions of the term “transpulmonary pressure.” By the traditional definition, transpulmonary pressure is the pressure across the whole lung, including the intrapulmonary airways, (i.e., the pressure difference between the opening to the pulmonary airway and the pleural surface). However, more recently transpulmonary pressure has also been defined as the pressure across only the lung tissue (i.e., the pressure difference between the alveolar space and the pleural surface), traditionally known as the “elastic recoil pressure of the lung.” Multiple definitions of the same term, and failure to recognize their underlying assumptions, have led to different interpretations of lung physiology and conclusions about appropriate therapy for patients. It is our view that many current controversies in the physiological interpretation of disease are caused by the lack of consistency in the definitions of these common physiological terms. In this article, we discuss the historical uses of these terms and recent misconceptions that may have resulted when these terms were confused. These misconceptions include assertions that normal pleural pressure must be negative (subatmospheric) and that a pressure in the pleural space may not be substantially positive when a subject is relaxed with an open airway. We urge specificity and uniformity when using physiological terms to define the physical state of the lungs, the chest wall, and the integrated respiratory system.

The human pharyngeal airway during sleep is conventionally modeled as a Starling resistor. However, inspiratory flow often decreases with increasing effort (negative effort dependence, NED) rather than remaining fixed as predicted by the Starling resistor model. In this study, we tested a major prediction of the Starling resistor model—that the resistance of the airway upstream from the site of collapse remains fixed during flow limitation. During flow limitation in 24 patients with sleep apnea, resistance at several points along the pharyngeal airway was measured using a pressure catheter with multiple sensors. Resistance between the nose and the site of collapse (the upstream segment) was measured before and after the onset of flow limitation to determine whether the upstream dimensions remained fixed (as predicted by the Starling resistor model) or narrowed (a violation of the Starling resistor model). The upstream resistance from early to mid inspiration increased considerably during flow limitation (by 35 ± 41 cmH₂O·liter⁻¹·s⁻¹, P < 0.001). However, there was a wide range of variability between patients, and the increase in upstream resistance was strongly correlated with the amount of NED ( r = 0.75, P < 0.001). Therefore, patients with little NED exhibited little upstream narrowing (consistent with the Starling model), and patients with large NED exhibited large upstream narrowing (inconsistent with the Starling model). These findings support the idea that there is not a single model of pharyngeal collapse, but rather that different mechanisms may dominate in different patients. These differences could potentially be exploited for treatment selection.

Pneumoperitoneum for laparoscopic surgery is known to stiffen the chest wall and respiratory system, but its effects on resting pleural pressure in humans are unknown. We hypothesized that pneumoperitoneum would raise abdominal pressure, push the diaphragm into the thorax, raise pleural pressure, and squeeze the lung, which would become stiffer at low volumes as in severe obesity. Nineteen predominantly obese laparoscopic patients without pulmonary disease were studied supine (level), under neuromuscular blockade, before and after insufflation of CO₂to a gas pressure of 20 cmH₂O. Esophageal pressure (Pes) and airway pressure (Pao) were measured to estimate pleural pressure and transpulmonary pressure (Pl = Pao − Pes). Changes in relaxation volume (Vrel, at Pao = 0) were estimated from changes in expiratory reserve volume, the volume extracted between Vrel, and the volume at Pao = −25 cmH₂O. Inflation pressure-volume (Pao-Vl) curves from Vrel were assessed for evidence of lung compression due to high Pl. Respiratory mechanics were measured during ventilation with a positive end-expiratory pressure of 0 and 7 cmH₂O. Pneumoperitoneum stiffened the chest wall and the respiratory system (increased elastance), but did not stiffen the lung, and positive end-expiratory pressure reduced Ecw during pneumoperitoneum. Contrary to our expectations, pneumoperitoneum at Vrel did not significantly change Pes [8.7 (3.4) to 7.6 (3.2) cmH₂O; means (SD)] or expiratory reserve volume [183 (142) to 155 (114) ml]. The inflation Pao-Vl curve above Vrel did not show evidence of increased lung compression with pneumoperitoneum. These results in predominantly obese subjects can be explained by the inspiratory effects of abdominal pressure on the rib cage.

Steady-state and transient variations in frictional force observed in tribological experiments of mesothelial tissues sliding in lubricant were analyzed with a mathematical model to test the hypothesis that such phenomena are manifestations of elastohydrodynamic lubrication and, importantly, do not require physical contact between the sliding surfaces. The model incorporates three phenomena characteristic of elastohydrodynamic lubrication: thinning of the liquid layer between sliding surfaces under a normal load (“squeeze-out”), thickening of the liquid layer due to hydrodynamic pumping, and smoothing of the elastic surfaces caused by hydrodynamic pressure gradients. Observations in soft mesothelial tissues sliding in lubricant showed variations in steady state friction with velocity, load, and lubricant viscosity. In non-steady sliding, the decay rate of frictional transients at the start of rotation varied with velocity, the amplitudes of these transients varied with the preceding periods without rotation, and frictional force varied during sinusoidal sliding. Model simulations were qualitatively similar to experimental results, supporting these mechanisms. Higher lubricant viscosity increased lubricating layer thickness and lowered friction at low speeds and increased friction at high speeds, supporting hydrodynamic pumping. We conclude that the frictional variations seen with sliding mesothelial tissues are consistent with elastohydrodynamic lubrication without contact between the sliding surfaces.