Surgery – Respiratory method or device – Means for supplying respiratory gas under positive pressure
Patent
1996-01-31
1998-02-03
Millin, Vincent
Surgery
Respiratory method or device
Means for supplying respiratory gas under positive pressure
12820421, 12820418, A61M 1600
Patent
active
057133492
DESCRIPTION:
BRIEF SUMMARY
FIELD OF THE INVENTION
The invention relates to a device and corresponding method for controlling delivery of fluid to a dispensing apparatus.
A device as aforedescribed is used in a number of fields such as, for example, the medical field and the invention has particular, but not exclusive, application to the medical field wherein the device is used for controlling drug delivery to a nebuliser, face mask or any other dispensing apparatus and in particular respiratory dispensing apparatus.
BACKGROUND TO THE INVENTION
It is well known to use a nebuliser or face mask to deliver therapeutic drugs to the respiratory system. This is usually for the purpose of treating diseases such as asthma. In addition therapeutic agents may be administered by intubation. This method is typically used for treating ARDS (Adult Respiratory Distress Syndrome).
The use of the invention as a means of treating individuals suffering from ARDS will now be described, but it is not intended that the invention should be limited to such use.
ARDS may sometimes result from direct injury to the lungs (for example, from aspiration of gastric contents, pneumonia, or inhalation of a toxic substance); ARDS may also be caused by a systemic disorder (such as Sepsis) or alternatively by a drug reaction. Occasionally, multiple factors are involved. The syndrome develops in as many 150,000 Americans annually. Since ARDS was first described, the mortality rate among patients has remained relatively constant at about 50%. However, the usual cause of death has changed from hypoxia to multi-organ dysfunction. Therapy is supportive, consisting primarily of mechanical ventilation and positive end-expiratory pressure to decrease hypoxemia.
It has recently become clear that the mechanical abnormalities associated with ARDS are not homogeneously distributed throughout the lungs. The lungs are functionally small and in essence, a patients' lungs can be divided into areas that are infiltrated, consolidated, or collapsed (and thus poorly aerated and poorly compliant) and regions that have nearly normal levels of compliance and ventilation. In the early stages of ARDS, these regions are not fixed; even simple actions, such as moving from a supine to a prone position, can alter the location of aerated and non-aerated regions. As the disease progresses, these regions become increasingly fixed.
In healthy lungs, blood is shunted away from poorly aerated regions. In lungs affected by ARDS, poorly aerated regions continue to be perfused. A substantial mis-match between ventilation and profusion may develop leading to hypoxemia. The immediate (but not the sole) cause of poor aeration is pulmonary odema due to a generalised defect in capillary-membrane permeability. This defect may cause simultaneous dysfunction of other organs as well. Although it is incompletely understood, the capillary defect is believed to be produced by an array of inflammatory mediators, including cytokines, complement, and arachidonate metabolites. These mediators damage the endothelium and allow fluid and proteins to leak across it. In the early stages of ARDS odema is confined to the interstitium; later, however, it may enter the alveoli.
Additional physiological effects of these mediators include vasoconstriction and platelet aggregation, both of which may decrease blood flow to aerated regions of the lungs. Neutrophil-derived proteases and oxygen radicals may damage lung tissue directly. Abnormalities of surfactant may also develop. In the later stages of ARDS, fibrosis may occur. Clinically, these changes are manifested as increases in pulmonary-artery pressure and pulmonary vascular resistance. This creates a therapeutic dilemma. If systemic vasodilators are administered to decrease pulmonary vascular resistance, the likelihood that hypotension will develop is increased.
Similarly, the use of mechanical ventilation and positive end-expiratory pressure may sometimes increase the alveolar injury associated with ARDS by causing hyperinflation in compliant regions of the lungs. Thus, it
REFERENCES:
patent: 4648395 (1987-03-01), Sato et al.
Deane, Jr. William J.
Millin Vincent
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