Posted by James

Our data show that in chronically stable hypercapnic patients with COPD, NPV reduces respiratory muscle activity (EMG), slightly increases muscle strength (MIP and МЕР), and improves arterial blood gas values (Pa02 and PaCOa). These changes were coincident with significant increases in Ti, Vt, and Ti/Ttot and a decrease in RF.
In patients with COPD, increase in airway resistance and lung hyperinflation enhance the energy demand of the respiratory muscles; furthermore, the hypoxemia reduces the available energy supply and it is known that if energy demands are greater than supplies, the muscle will eventually fatigue.
In this study, both study group (A) and control group (B) exhibited hyperinflation (FRC) and airway obstruction (FEV^, a markedly low inspiratory (MIP) and expiratory (МЕР) muscle force, and chronic hypercapnia and hypoxia; so, consistently with the accumulating evidence that respiratory muscle fatigue and development of hypercapnia are closely related, we think that both groups A and В were in a situation of respiratory muscle fatigue. In this situation and particularly in hyperinflated patients with COPD, rapid and shallow breathing has also been observed and it has been related to afferents arising from vagal pulmonary endings. More recently, a decrease in both Vt and Ti with constant Vt/Ti and increase in RF have been interpreted as a compensatory mechanism by which overloaded or fatigued respiratory muscles contract at optimal length without substantially changing their geometry. Such a mechanism theoretically postpones more severe fatigue, but the increase in PaCOz is an unescapable consequence.
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Posted by James
Functional data of the three groups were summarized in Table 1. As shown, the study group (A) and the control group (B) exhibited similar VC, FRC, FEVi, and FEV/VC ratio, MIP and МЕР, and Pa02, and PaCOz; these values being significantly different compared with the mean value of the normal control group (C group). Breathing characteristics (Table 2) were also similar in groups A and В but, compared with group C, both groups A and В exhibited a significantly lower Vt (p<0.01) and Ti (p<0.01) and a greater RF (p<0.01 and p<0.05, respectively) and lower Ttot (p<0.01 and p<0.05, respectively) and Ti/ Ttot (p<0.05 for both comparisons). The Vt/Ti was slightly greater in patients, but this difference was not significant; similarly, Ve did not significantly differ among the three groups. In addition, in groups A and В both EMGd (p<0.01) and EMGint (p<0.01) were significantly higher than in normal subjects.
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Posted by James
Subjects
Eleven hospitalized patients, nine men and two women, were studied after the nature of the experimental technique and the purpose of the investigation had been fully explained to them. Patients were defined as suffering from COPD according to the American Thoracic Society (ATS) criteria. All patients were free of active cardiovascular disease. An age-matched group of six normal subjects (mean±SD age, 62.0±8.7 years) was also included as a control.
Functional Evaluation
Routine spirometry obtained with subjects in a seated position and arterial blood gas values were measured as previously described. The normal values for lung volumes are those proposed by European Community for Coal and Steel. Maximal static inspiratory and expiratory pressures (MIP and МЕР) at functional residual capacity (FRC) and total lung capacity (TLC), respectively, against an obstructed mouthpiece, with a small leak to minimize oral pressure artifacts, were measured using a differential pressure transducer (Statham SC 1001). Subjects performed maximal inspiratory and expiratory efforts and were instructed to maintain maximal pressures for at least 1 s. The mean of three reproducible and satisfactory measurements was calculated.
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Posted by James

To the last years, several studies have been devoted to investigating the role of respiratory muscle function in the development of hypercapnia in patients with COPD. Some of these studies have reported that in acutely ill patients, diaphragmatic muscle fatigue is associated with increase in PaC02, decrease in maximal inspiratory pressure (MIP), and increase in respiratory frequency (RF) along with a decrease in tidal volume (Vt). Similar ventilatory response, observed in patients with stable COPD during loaded breathing, has been interpreted as probably due to poor inspiratory muscle function. In this connection, Roussos has recently hypothesized that in patients with COPD, the rapid and shallow breathing accompanying chronic hypercapnia may stem from afferents arising from overloaded or fatigued respiratory muscles.
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Posted by James

To our knowledge, this case is the first report of bilateral post-traumatic paramediastinal lung cysts. Furthermore, it illustrates several characteristic features of this condition. All patients have a history of blunt chest trauma, which may be minor. Over 80 percent are 30 years of age or less, with no previous pulmonary complaints. Many patients present with hemoptysis, chest pain, cough, and dyspnea. There may be a low-grade fever with mild leukocytosis.
A number of factors have been implicated as important mechanisms of injury. Initially, a blunt force applied to the chest wall results in compression and high pressures within the underlying pulmonary parenchyma. This may lead to the rupture of small bronchi, causing the surrounding alveoli to burst. Air can then enter between the layers of the pulmonary ligament. Rupture of capillaries around the lacerated alveoli then leads to accumulation of blood within the newly formed air space. A closed glottis may play a role in producing high intrathoracic pressure from chest compression. The bursting process may involve any area of either lung, although the apices are usually spared. An alternative theory proposes that a blow to the chest wall creates a concussive wave, leading to shearing stresses which exceed the elasticity of the pulmonary tissue. Still another proposal notes that increased intrathoracic pressure may be followed by negative pressure due to elastic recoil after compression. This might produce bursting followed by shearing forces, leading to parenchymal lacerations, and escape of air and fluid into the lung.
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Posted by James
Case Report
The patient was a 25-year-old white man with a history of intravenous drug abuse, bisexual behavior, HIV antibody-positive status, a perirectal abscess, hepatitis B, and recurrent lower- extremity staphylococcal infections, who presented to University Medical Center after a motorcycle accident. An emergency-room, portable chest roentgenogram was initially interpreted as revealing no gross abnormality (Fig 1). The patient was treated for chin lacerations and discharged the next day. Four days later, he was readmitted with cough, hemoptysis, pleuritic chest pain, and low- grade fever. Read the rest of this entry »
Posted by James
Unilateral post-traumatic and paramediastinal lung cysts are uncommon and usually do not require treatment. Nevertheless, recognition of a traumatic lung cyst is important, since misdiagnosis may lead to unnecessary surgery. This report describes a patient whose bilateral post-traumatic paramediastinal lung cysts were mistaken for hemi- diaphragmatic hernias. Read the rest of this entry »