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We report the case of a patient that had undergone a left pneumonectomy during which a double-lumen tube was used and an undetected right bronchial laceration occurred. After diagnosis the patient underwent a second operation to repair the tear. The role of high-frequency percussive ventilation in enabling adequate gas exchange during the bronchial repair is described and discussed.

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High-frequency percussive ventilation (HFPV) has been proved useful in patients with acute respiratory distress syndrome. However, its physiological mechanisms are still poorly understood. The aim of this work is to evaluate the effects of mechanical loading on the tidal volume and lung washout during HFPV. For this purpose a single-compartment mechanical lung simulator, which allows the combination of three elastic and four resistive loads (E and R, respectively), underwent HFPV with constant ventilator settings. With increasing E and decreasing R the tidal volume/cumulative oscillated gas volume ratio fell, while the duration of end-inspiratory plateau/inspiratory time increased. Indeed, an inverse linear relationship was found between these two ratios. Peak and mean pressure in the model decreased linearly with increasing pulsatile volume, the latter to a lesser extent. In conclusion, elastic or resistive loading modulates the mechanical characteristics of the HFPV device but in such a way that washout volume and time allowed for diffusive ventilation vary agonistically.

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High-frequency percussive ventilation (HFPV) has proved its unique efficacy in the treatment of acute respiratory distress, when conventional mechanical ventilation (CMV) has demonstrated a limited response. We analysed flow (V(dot)), volume (V) and airway pressure (Paw) during ventilation of a single-compartment mechanical lung simulator, in which resistance (R) and elastance (E) values were modified, while maintaining the selected ventilatory settings of the HFPV device. These signals reveal the physical effect of the imposed loads on the output of the ventilatory device, secondary to constant (millisecond by millisecond) alterations in pulmonary dynamics. V(dot), V and Paw values depended fundamentally on the value of R, but their shapes were modified by R and E. Although peak Paw increased 70.3% in relation to control value, mean Paw augmented solely 36.5% under the same circumstances (maximum of 9.4 cm H2O). Finally, a mechanism for washing gas out of the lung was suggested.

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In recent years, the usefulness of high frequency ventilation (HFV) has been clinically reassessed as an alternative to conventional mechanical ventilation (CMV). HFV has often been combined with or in some cases even completely replaced CMV in the attempt to reduce iatrogenic injury. High frequency percussive ventilation (HFPV) is a specific mode of HFV that has been successfully applied in the treatment of acute respiratory failure after smoke inhalation; it has also been more widely used in pediatric than in adult patients. This article gives an introduction to and a description of the basic principles of HFPV, a mode of ventilation which we found particularly versatile and reliable in our preliminary clinical experience with the maneuver.

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Treatment of acute respiratory failure is still a hot issue in intensive care everyday practice: in the last few years high frequency ventilation techniques have been employed as a therapy for adult respiratory distress syndrome (ARDS) and acute respiratory failure (ARF). We applied high frequency percussive ventilation (HFPV) to 3 patients affected by ARDS or ARF, who did not improve after 24 hours of conventional mechanical ventilation (CMV). All our patient underwent 12 hours of HFPV, and showed an improvement of both respiratory exchange and radiological imaging. Even if the pathogenesis of ARF was quite different, in all patient we registered a good response and no complications.

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Viscoelasticity represents an important component of respiratory mechanics, being responsible, in some cases, for most of the pressure dissipated during breathing. Hitherto the methods available for determining the viscoelastic properties have been simplified, but are still time-demanding and depend on a great deal of calculation. In this study, a simple means of determining respiratory viscoelastic properties during mechanical ventilation was introduced. The viscoelastic constants of the respiratory system, modelled as a Maxwell body, were studied in 17 normal subjects and seven patients with acute lung injury (ALI) using two end-inspiratory occlusions; one with a short inspiratory time (tI) to determine the elastic component of viscoelasticity and the other with a long tI to assess the resistive component of viscoelasticity. The results were reproducible and similar to those provided by the previously described multiple-breath method (MB). The mean+/-SD viscoelastic resistance was 5.31+/-1.50 cm H2O x L(-1) x s with the proposed method and 5.71+/-1.87 cm H2O x L(-1) x s with the MB method in normal subjects, and 8.93+/-2.82 cm H2O x L(-1) x s and 10.36+/-3.13 cm H2O x L(-1), respectively in ALI patients. The mean+/-SD viscoelastic elastance was 3.92+/-0.84 cm H2O x L(-1) and 4.94+/-1.01 cm H2O x L(-1) in normal subjects and 7.08+/-2.01 cm H2O x L(-1) and 8.21+/-1.16 cm H2O x L(-1) in ALI patients, respectively. The mean+/-SD viscoelastic time constant was 1.36+/-0.24 s and 1.17+/-0.34 s in normal subjects and 1.26+/-0.35 s and 1.24+/-0.23 in ALI patients, respectively. The method was easy to perform and applicable at the bedside in clinical routine.

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In order to explain the time dependency of resistance and elastance of the respiratory system, a linear viscoelastic model (Maxwell body) has been proposed. In this model the maximal viscoelastic pressure (Pvisc.max) developed within the tissues of the lung and chest wall at the end of a constant-flow (V') inflation of a given time (tI) is given by: Pvisc,max = R2V'(1-e(-tI/tau2), where R2 and tau2 are, respectively, the resistance and time constant of the Maxwell body. After rapid airway occlusion at t1, tracheal pressure (Ptr) decays according to the following function: Ptr(t) = Pvisc(t) + Prs,st = Pvisc,max(etocc/tau2)+ Prs,st, where tocc/is time after occlusion and Prs,st is static re-coil pressure of the respiratory system. By fitting Ptr after occlusion to this equation, tau2 and Pvisc,max are obtained. Using these values, together with the V' and tI pertaining to the constant-flow inflation preceding the occlusion, R2 can be calculated from the former equation. Thus, from a single breath, the constants tau2, R2 and E2 (R2/tau2) can be obtained. This method was used in 10 normal anaesthetized, paralysed, mechanically ventilated subjects and six patients with acute lung injury. The results were reproducible in repeated tests and similar to those obtained from the same subjects and patients with the time-consuming isoflow, multiple-breath method described previously.

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The paper reports the results of 80 cases of vulvar dystrophy and 11 cases of burning vulva. The Authors put forward a protocol for therapy which also aims to provide the basis for a comparative study of this pathology about which little is known from a clinical and research point of view.

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