Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo
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Monaldi Arch Chest Dis · Oct 1999
ReviewPhysiological changes during severe airflow obstruction in chronic obstructive pulmonary disease.
Chronic expiratory flow limitation and hyperinflation are the mechanical hallmarks of chronic obstructive pulmonary disease (COPD). Although carbon dioxide retention is dependent on the severity of airflow limitation, there is considerable variability in the relationships between arterial carbon dioxide tension (Pa,CO2) and forced expiratory volume in one second (FEV1) or total lung resistance (RL). In stable COPD patients with severe airflow obstruction, shallow breathing and inspiratory muscle weakness are the main factors associated with CO2 retention. ⋯ During acute bronchoconstriction, COPD patients with severe airflow obstruction recruited the rib cage inspiratory muscles proportionally more than the diaphragm. The associated recruitment of abdominal muscles results in a reduction in abdominal volume at end-expiration and contributes to a significant extent to PEEPi. Dynamic hyperinflation can be overestimated during chronic and acute airway obstruction if abdominal muscle function is not evaluated.
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Intrapleural instillation of fibrinolytic agents has been shown, in a number of studies, to be an effective and safe mode of treatment in complicated parapneumonic effusions and empyema, minimizing the need for surgical intervention. Streptokinase and urokinase are the fibrinolytics used, but the technique of instillation is not yet standardized. The usual dose of streptokinase is 250,000 IU, 100,000 IU for urokinase. ⋯ Generally, fibrinolytics are more successful if used early in the process of pleural infection (in complicated parapneumonic effusions rather than in empyemas). Adverse reactions are rare, of the allergic type and more frequent for streptokinase. Urokinase is safer but more expensive.
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Monaldi Arch Chest Dis · Apr 1999
ReviewPulmonary hypertension in acute respiratory distress syndrome.
A mild degree of pulmonary hypertension is commonly observed in patients with acute respiratory distress syndrome (ARDS). Vasoconstriction plays a dominant role in increasing the mean closing pressure of the pulmonary vascular bed. Pulmonary hypertension increases right ventricular afterload, but right ventricular failure rarely occurs in patients with ARDS. ⋯ Consequently, generalized pulmonary vasodilation by intravenous vasodilators aggravates arterial hypoxaemia. Conversely, selective administration of vasodilators, such as inhaled nitric oxide, in well-ventilated lung units improves gas exchange by diverting pulmonary blood flow to better oxygenated regions. However, preliminary results from large prospective randomized controlled trials indicate that inhaled nitric oxide does not reduce mortality nor the duration of mechanical ventilation in patients with ARDS.
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This paper reviews respiratory muscle performance in patients suffering from congestive heart failure. Respiratory muscle dysfunction is well documented in these patients, and is thoroughly discussed. The mechanisms underlying its development and the potential consequences are also presented.