Chest
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Septic cardiomyopathy is a key feature of sepsis-associated cardiovascular failure. Despite the lack of consistent diagnostic criteria, patients typically exhibit ventricular dilatation, reduced ventricular contractility, and/or both right and left ventricular dysfunction with a reduced response to volume infusion. ⋯ Because there are no specific/causal therapeutics for the treatment of septic cardiomyopathy, the current guidelines for the treatment of septic shock represent the cornerstone of septic cardiomyopathy therapy. This review provides an up-to-date overview of the current understanding of the pathophysiology, summarizes the evidence of currently available diagnostic tools and treatment options, and highlights the importance of further urgently needed studies aimed at improving diagnosis and investigating novel therapeutic targets for septic cardiomyopathy.
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A 58-year-old postmenopausal woman presented to her primary care physician with lower back pain. She denied respiratory symptoms. ⋯ She denied a history of smoking, alcohol use, or recreational drug use. A review of systems was otherwise negative.
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Individuals living with spinal cord injury or disease (SCI/D) are at increased risk for sleep-disordered breathing (SDB), with a prevalence that is three- to fourfold higher than the general population. The main features of SDB, including intermittent hypoxemia and sleep fragmentation, have been linked to adverse cardiovascular outcomes including nocturnal hypertension in patients with SCI/D. ⋯ Despite the strong association between SDB and SCI/D, access to diagnosis and management remains limited. This review explores the role of SCI/D in the pathogenesis of SDB, poor sleep quality, the barriers in diagnosing and managing SDB in SCI/D, and the alternative approaches and future directions in the treatment of SDB, such as novel pharmacologic and nonpharmacologic treatments.
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Developing an effective treatment for COPD, and especially pulmonary emphysema, will require an understanding of how fundamental changes at the molecular level affect the macroscopic structure of the lung. Currently, there is no accepted model that encompasses the biochemical and mechanical processes responsible for pulmonary airspace enlargement. We propose that pulmonary emphysematous changes may be more accurately described as an emergent phenomenon, involving alterations at the molecular level that eventually reach a critical structural threshold where uneven mechanical forces produce alveolar wall rupture, accompanied by advanced clinical signs of COPD. The coupling of emergent morphologic changes with biomarkers to detect the process, and counteract it therapeutically, represents a practical approach to the disease.
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The prevalence of lung conditions, such as COPD and pulmonary fibrosis, and lung infections, such as pneumonia, increases sharply with age. The physiologic, cellular, and immunologic changes that occur during aging contribute to the development of lung disease. ⋯ Individuals with good lung function live longer, healthier lives, although the mechanisms by which this scenario occurs are not understood. The present article reviews changes in the aging lung that facilitate development of disease and the evidence supporting the idea that robust lung function reduces the risk of developing chronic inflammatory conditions that occur with age.