Chest
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Review Practice Guideline
Pulmonary Rehabilitation: Joint ACCP/AACVPR Evidence-Based Clinical Practice Guidelines.
Pulmonary rehabilitation has become a standard of care for patients with chronic lung diseases. This document provides a systematic, evidence-based review of the pulmonary rehabilitation literature that updates the 1997 guidelines published by the American College of Chest Physicians (ACCP) and the American Association of Cardiovascular and Pulmonary Rehabilitation. ⋯ There is substantial new evidence that pulmonary rehabilitation is beneficial for patients with COPD and other chronic lung diseases. Several areas of research provide opportunities for future research that can advance the field and make rehabilitative treatment available to many more eligible patients in need.
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Transfusion practice has been under great scrutiny over the last 2 decades. The examination of transfusion risks and benefits have been particularly important in the critically ill patient population. This review will examine some of the important controversies still surrounding the use of RBC transfusion in the critically ill patient.
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Randomized Controlled Trial Comparative Study
Fixed and autoadjusting continuous positive airway pressure treatments are not similar in reducing cardiovascular risk factors in patients with obstructive sleep apnea.
A strong association between obstructive sleep apnea (OSA) and the risk for cardiovascular and cerebrovascular diseases has been reported. Continuous positive airway pressure (CPAP) is the first-line therapy for OSA, able not only to reduce daytime sleepiness but also to improve cardiovascular and metabolic outcomes. Autoadjusting CPAP (APAP), an alternative treatment to CPAP, can reduce OSA symptoms while increasing long-term CPAP compliance without the high costs of CPAP titration. However, no data are available on the effects of APAP on cardiovascular risk factors ⋯ Our results suggest that CPAP and APAP, despite significant effects on OSA indexes and symptoms, do not improve cardiovascular risk factors in the same fashion.
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Observational studies of patients receiving prolonged mechanical ventilation and other forms of critical care support have determined acquired neuromuscular disorders to be extremely common. Early studies used electrophysiologic investigations to diagnose critical illness polyneuropathy (CIP) and muscle biopsy to confirm critical illness myopathy (CIM). More recent approaches seek to obviate these invasive techniques and build on a standardized bedside neuromuscular examination to identify patients with acquired weakness syndromes. ⋯ In addition, a strong association appears to exist between acquired weakness and protracted ventilator dependence, an important determinant of ICU length of stay. Multivariate analysis has identified several risk factors associated with increased incidence for ICU-acquired weakness, including severe systemic inflammation, medications (specifically, corticosteroids and neuromuscular blocking agents), glycemic control, and immobility. We advocate an approach to this common syndrome that identifies risk factors early in the hope of minimizing their impact.
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Smoking is one of the major lifestyle factors influencing the health of human beings. Life-long cigarette smokers have a higher prevalence of common diseases such as atherosclerosis and COPD with significant systemic impact. The present review evaluates current knowledge concerning possible pathways through which cigarette smoking can affect human health, with special focus on extrapulmonary effects. ⋯ Furthermore, rheologic, coagulation and endothelial function markers like hematocrit, blood and/or plasma viscosity, fibrin d-dimer, circulating adhesion molecules (intracellular adhesion molecule-1, selectins), tissue plasminogen activator antigen, and plasminogen activator inhibitor type I are altered in chronic cigarette smokers. Although most of smoking-induced changes are reversible after quitting, some inflammatory mediators like CRP are still significantly raised in ex-smokers up to 10 to 20 years after quitting, suggesting ongoing low-grade inflammatory response persisting in former smokers. New longitudinal epidemiologic and genetic studies are required to evaluate the role of smoking itself and possible gene/environment interplay in initiation and development of smoking-induced common diseases affecting humans.