Control system design for a Continuous Positive Airway Pressure ventilator.

Continuous Positive Airway Pressure (CPAP) ventilation remains a mainstay treatment for obstructive sleep apnea syndrome (OSAS). Good pressure stability and pressure reduction during exhalation are of major importance to ensure clinical efficacy and comfort of CPAP therapy. In this study an experimental CPAP ventilator was constructed using an application-specific CPAP blower/motor assembly and a microprocessor. To minimize pressure variations caused by spontaneous breathing as well as the uncomfortable feeling of exhaling against positive pressure, we developed a composite control approach including the feed forward compensator and feedback proportional-integral-derivative (PID) compensator to regulate the pressure delivered to OSAS patients. The Ziegler and Nichols method was used to tune PID controller parameters. And then we used a gas flow analyzer (VT PLUS HF) to test pressure curves, flow curves and pressure-volume loops for the proposed CPAP ventilator. The results showed that it met technical criteria for sleep apnea breathing therapy equipment. Finally, the study made a quantitative comparison of pressure stability between the experimental CPAP ventilator and commercially available CPAP devices.

An estimation of mechanical stress on alveolar walls during repetitive alveolar reopening and closure.

Alveolar overdistension and mechanical stresses generated by repetitive opening and closing of small airways and alveoli have been widely recognized as two primary mechanistic factors that may contribute to the development of ventilator-induced lung injury. A long-duration exposure of alveolar epithelial cells to even small, shear stresses could lead to the changes in cytoskeleton and the production of inflammatory mediators. In this paper, we have made an attempt to estimate in situ the magnitudes of mechanical stresses exerted on the alveolar walls during repetitive alveolar reopening by using a tape-peeling model of McEwan and Taylor (35). To this end, we first speculate the possible ranges of capillary number (Ca) ≡ µU/γ (a dimensionless combination of surface tension γ, fluid viscosity µ, and alveolar opening velocity U) during in vivo alveolar opening. Subsequent calculations show that increasing respiratory rate or inflation rate serves to increase the values of mechanical stresses. For a normal lung, the predicted maximum shear stresses are <15 dyn/cm(2) at all respiratory rates, whereas for a lung with elevated surface tension or viscosity, the maximum shear stress will notably increase, even at a slow respiratory rate. Similarly, the increased pressure gradients in the case of elevated surface or viscosity may lead to a pressure drop >300 dyn/cm(2) across a cell, possibly inducing epithelial hydraulic cracks. In addition, we have conceived of a geometrical model of alveolar opening to make a prediction of the positive end-expiratory pressure (PEEP) required to splint open a collapsed alveolus, which as shown by our results, covers a wide range of pressures, from several centimeters to dozens of centimeters of water, strongly depending on the underlying pulmonary conditions. The establishment of adequate regional ventilation-to-perfusion ratios may prevent recruited alveoli from reabsorption atelectasis and accordingly, reduce the required levels of PEEP. The present study and several recent animal experiments likewise suggest that a lung-protective ventilation strategy should not only include small tidal volume and plateau pressure limitations but also consider such cofactors as ventilation frequency and inflation rate.

A micromechanical model for estimating alveolar wall strain in mechanically ventilated edematous lungs.

To elucidate the micromechanics of pulmonary edema has been a significant medical concern, which is beneficial to better guide ventilator settings in clinical practice. In this paper, we present an adjoining two-alveoli model to quantitatively estimate strain and stress of alveolar walls in mechanically ventilated edematous lungs. The model takes into account the geometry of the alveolus, the effect of surface tension, the length-tension properties of parenchyma tissue, and the change in thickness of the alveolar wall. On the one hand, our model supports experimental findings (Perlman CE, Lederer DJ, Bhattacharya J. Am J Respir Cell Mol Biol 44: 34-39, 2011) that the presence of a liquid-filled alveolus protrudes into the neighboring air-filled alveolus with the shared septal strain amounting to a maximum value of 1.374 (corresponding to the maximum stress of 5.12 kPa) even at functional residual capacity; on the other hand, it further shows that the pattern of alveolar expansion appears heterogeneous or homogeneous, strongly depending on differences in air-liquid interface tension on alveolar segments. The proposed model is a preliminary step toward picturing a global topographical distribution of stress and strain on the scale of the lung as a whole to prevent ventilator-induced lung injury.