Chest
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Multicenter Study Comparative Study
Determinants of ICU care in the last month of life for Taiwanese cancer decedents, 2001 to 2006.
Use of the hospital ICU is rising rapidly for end-of-life care. The purpose of this population-based study was to determine the prevalence of ICU care in the last month of life of patients with cancer and the associations between ICU care and patient demographics, disease characteristics, physician specialty, hospital characteristics, and availability of health-care resources at the hospital and regional levels in Taiwan. ⋯ Slightly more than one-tenth of Taiwanese patients with cancer received ICU care in their last month of life. ICU use was strongly influenced by receiving care in hospitals and regions with abundant health-care resources. Resources should be devoted to ensure that ICU care at the end of life best meets patients' individual needs and interests.
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Vocal cord dysfunction (VCD) is a syndrome characterized by paroxysms of glottic obstruction due to true vocal cord adduction resulting in symptoms such as dyspnea and noisy breathing. Since first described as a distinct clinical entity in 1983, VCD has inadvertently become a collective term for a variety of clinical presentations due to glottic disorders. Despite an increased understanding of laryngeal function over the past 25 years, VCD remains a poorly understood and characterized entity. ⋯ VCD has been repeatedly misdiagnosed as asthma; however, the relationship between asthma and VCD is elusive. There are numerous case reports on VCD, but there is a paucity of prospective studies. Following an in-depth review of the medical literature, this article examines the available retrospective and prospective evidence to present an approach for evaluation of VCD including: (1) evaluation of factors associated with VCD, (2) differential diagnosis of movement disorders of the upper airway, and (3) clinical, spirometric, and endoscopic criteria for the diagnosis.
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The mechanisms and pathways of the sensation of dyspnea are incompletely understood, but recent studies have provided some clarification. Studies of patients with cord transection or polio, induced spinal anesthesia, or induced respiratory muscle paralysis indicate that activation of the respiratory muscles is not essential for the perception of dyspnea. Similarly, reflex chemostimulation by CO₂ causes dyspnea, even in the presence of respiratory muscle paralysis or cord transection, indicating that reflex chemoreceptor stimulation per se is dyspnogenic. ⋯ Brain imaging studies have provided information on central pathways subserving dyspnea: Dyspnea is associated with activation of the limbic system, especially the insular area. These findings permit a clearer understanding of the mechanisms of dyspnea: Afferent information from reflex stimulation of the peripheral sensors (chemoreceptors and/or vagal C fibers) is processed centrally in the limbic system and sensorimotor cortex and results in increased neural output to the respiratory muscles. A perturbation in the ventilatory response due to weakness, paralysis, or increased mechanical load generates afferent information from vagal receptors in the lungs (and possibly mechanoreceptors in the respiratory muscles) to the sensorimotor cortex and results in the sensation of dyspnea.
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Long-term therapy with the macrolide antibiotic erythromycin was shown to alter the clinical course of diffuse panbronchiolitis in the late 1980s. Since that time, macrolides have been found to have a large number of antiinflammatory properties in addition to being antimicrobials. These observations provided the rationale for many studies performed over the last decade to assess the usefulness of macrolides in other inflammatory airways diseases, such as cystic fibrosis, asthma, COPD, and bronchiolitis obliterans syndrome. This review summarizes the immunomodulatory properties of macrolides and the results of these recent studies demonstrating their potential for being disease-modifying agents.
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Case Reports
Long-term effects of epoprostenol on the pulmonary vasculature in idiopathic pulmonary arterial hypertension.
The current treatment of pulmonary arterial hypertension (PAH) uses vasodilator drugs. Although they improve symptoms associated with PAH, their chronic effects on the pulmonary vasculature and the right ventricle (RV) in humans remain unknown. We report the autopsy findings from a patient with idiopathic PAH treated with epoprostenol successfully for 18 years. ⋯ Although the long-term use of epoprostenol contributed to the patient's increased survival, it did not prevent progression of the underlying vascular disease. Remarkably, the RV was able to sustain a normal cardiac output in the face of advanced vascular pathology. The mechanisms by which the RV adapts to chronic PAH need further study.