Amplitude-modulated Ventilation: Conclusions
We have modeled the pressure response to a deep lung inflation as that caused by an impulse change in volume, and have defined the compliance as V(t)/P(t) following the impulse input. This is equivalent to the time derivative of the system step response. This simplified model predicts that lung compliance as a function of time should change with time constants on the order of those measured for tissue strip and surface film relaxation. Although we have not solved for the values of the individual model parameters, it is clear that since the dynamics of both normal and LPS-treated strips and surface films were similar and had time constants an order of magnitude shorter than the dominant time constant observed in the intact damaged lung, this simplified approach is inadequate to explain the difference in the Cdyn response observed between the two treatment groups in the intact animal lung. sildenafil citrate pink
Several possible explanations exist for the failure of the model to adequately explain the intact lung response in the damaged lung. Our attempt to describe tissue and surface film dynamics in terms of a linear viscoelastic model may be inadequate, especially in the case of the surface films, which demonstrate plastoelastic characteristics (volume dependent elastic and dissipative behavior). The model fails to incorporate the time constants involved with surface film flows across the alveolar surface. Furthermore, there is no attempt to incorporate a dynamic expression for parenchymal collapse and reopening once a stability limit is reached. Our decision to neglect inertial and viscous terms in extending the static equilibrium equations to a dynamic problem may be incorrect. Lastly, the model may be adequate for predicting stability in the normal lung but not be acceptable in the damaged lung where a continuum approach may no longer be valid.
Amplitude modulated ventilation, administered as intermittent deep breaths to guinea pigs with experimental ALI, resulted in an increase in lung compliance which lasted many respiratory cycles. The response was greater in magnitude and longer lasting than that observed in control animals. Viscoelastic dynamic responses of parenchymal tissue strips and surfactant film preparations from damaged and control animals used in a microstructural model of alveolar stability failed to adequately predict the time responses observed in the intact lung. We are currently developing a more detailed dynamic model of alveolar microstructure which we hope will allow us to better understand how AMV may work, and how we can plan rationale strategies for improving alveolar stability and overall lung function in ALI without promoting damage in previously intact regions of the lung.
Category: Respiratory Symptoms
Tags: gas exchanging, lung compliance, lung inflation, lung tissue, parenchyma, transpulmonary pressure