The American review of respiratory disease
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Am. Rev. Respir. Dis. · Nov 1984
Comparative StudyTracheal mucus clearance in high-frequency oscillation. II: Chest wall versus mouth oscillation.
We compared the tracheal mucus clearance rate (TMCR) in anesthetized dogs during spontaneous breathing (SB), ventilation by high-frequency oscillation at the airway opening (HFO/AO), and ventilation by high-frequency oscillation of the chest wall (HFO/CW). The HFO/AO was carried out by using a piston pump with a high impedance transverse flow at the proximal end of the endotracheal tube; HFO/CW was effected by creating rapid pressure oscillations in an air-filled cuff wrapped around the lower thorax of the animal, causing small tidal volumes at the mouth. The TMCR was measured by observing the rate of displacement of a charcoal marker in the lower trachea; a fiberoptic bronchoscope was used to deposit the marker before each experiment and to relocate it after a 5-min run. ⋯ At 13 Hz with an oscillatory tidal volume (VTO) of 1.5 ml/kg, mean TMCR was 240% of control with HFO/CW (p less than 0.001) and 76% of control with HFO/AO (NS). During HFO/AO at 20 Hz and a VTO of 3 ml/kg, mean TMCR was 97% of control. We conclude that high-frequency ventilation by rapid chest wall compression enhances tracheal mucus clearance when compared with spontaneous breathing, whereas high-frequency oscillation at the mouth does not.
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A variety of central nervous system (CNS) insults may be complicated by the acute development of pulmonary edema. This occurrence has been termed neurogenic pulmonary edema (NPE), and experimental models have clearly shown that CNS insults may cause pulmonary edema. Unfortunately, the pathophysiologic aspects of this response are not clearly understood. ⋯ The mediating factor for a permeability defect is not clear. The implications of these findings are that NPE may be caused by either permeability abnormalities or hydrostatic insults, may present clinically in a variety of ways, and may require different approaches to treatment. Our understanding of the CNS sites that might mediate NPE is not sophisticated enough, at present, to define the neural mechanisms involved in the pathogenesis of NPE.