Lung
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Noninvasive positive pressure ventilation (NPPV) has reemerged as an effective strategy for reducing morbidity and mortality associated with acute exacerbations of chronic obstructive pulmonary disease (COPD). During acute respiratory failure, dynamic hyperinflation, intrinsic PEEP, and increased airway resistance result in a mechanical workload that exceeds inspiratory muscle capacity. NPPV provides augmentation of alveolar ventilation and respiratory muscle rest. ⋯ NPPV performs better in COPD patients without significant comorbid illness. It should be initiated during COPD exacerbations if arterial pH is less than 7.35 or if the patient is severely distressed. Pressure support ventilation (10-20 cmH2O) via face mask is likely the optimal technique and, when successful, results in rapid clinical improvement.
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The symptom of breathlessness is an important outcome measure in the management of patients with chronic obstructive pulmonary disease (COPD). Clinical ratings of dyspnea and routine lung function are weakly related to each other. However, in the clinical setting breathlessness in COPD is encountered under conditions of increased respiratory effort, impeded respiratory muscle action, or functional weakness. ⋯ Our results demonstrate that the level of chronic exertional dyspnea in COPD increases as the ventilatory muscle derangement increases. The level of the relationships among dyspnea ratings and MVV and respiratory effort helps to explain some of the mechanisms of chronic dyspnea of COPD. These measures should be considered for therapeutic intervention to reduce dyspnea.
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Comparative Study
Evaluation of alveolar permeability and lung ventilation in patients with chronic renal failure using Tc-99m DTPA radioaerosol inhalation lung scintigraphy.
Lung ventilation (LV) and alveolar permeability (AP) were measured in 24 male chronic renal failure (CRF) patients on regular hemodialysis (HD). LV and AP were determined by Tc-99m DTPA aerosol inhalation lung scintigraphy using commercial lung radioaerosol delivery units. The equilibrium LV images were visually interpreted by two independent and experienced nuclear medicine physicians. ⋯ In addition, there was no significant correlation for k value and albumin level (r2 = 0.008) or for k value and HD duration (r2 = 0.228). In conclusion, CRF can predispose patients to LV change and AP damage. However, the degree of AP damage is not related to serum albumin level or HD duration.
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Models of pulmonary edema have been used to study the nuclear magnetic resonance (NMR) characteristics of lung water. Several investigators have measured changes in the relaxation times in the permeability type of pulmonary edema, but relatively few have measured relaxation times in the hydrostatic type of pulmonary edema. In this study we determined the characteristics of NMR relaxation times T1, T2 (Hahn spin-echo decay) and water content in acute hydrostatic pulmonary edema induced by noradrenaline administration in rats. ⋯ The increase in T2s was significantly correlated with an increase in water content, but the increase in the T2f value was not correlated with water content or with a change in T2s. The T2s component, which likely reflected changes in interstitial water, was more closely related than the T2f component to an increase in water content in hydrostatic pulmonary edema. Results suggested that regional changes in hydrostatic pulmonary edema may be evaluated by multicomponent T2 analysis.
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In recent years the alveolar macrophage has been found to play a central role in interstitial lung disease. Pulmonary histiocytosis X is characterized by infiltrating fibroblasts, mononuclear cells, and CD-1-positive Langerhans cells. Bronchoalveolar lavage (BAL) fluid displays an increase of CD-1-positive cells and a remarkable exaggeration of the total cell count with only slight changes in the differential cell count. ⋯ These findings are consistent with phenotypic changes of alveolar macrophages in other interstitial lung diseases such as sarcoidosis and idiopathic pulmonary fibrosis. Local proliferation and the fresh influx of blood monocytes seem to be responsible for the increase in immature and functionally activated alveolar macrophages. The increase in oxygen radical release and fibronectin production suggests an augmented tissue injuring and fibrosing capacity of alveolar macrophages in pulmonary histiocytosis X.