The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology
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Mechanical ventilation (MV) has been indicated in the treatment of acute respiratory failure (ARF) if conservative treatment fails. Invasive MV is associated to a variety of complications. The recent innovations of noninvasive methods of MV (NMV) avoid the complications of invasive MV, whilst ensuring a similar degree of efficacy. ⋯ This in turn has several advantages in terms of avoiding complications of invasive MV, reducing the length of stay in ICU and probably the number of ICU readmissions. Side effects of NMV seem less severe than those induced by invasive MV. In conclusion in selected patients a trial of noninvasive mechanical ventilation, as an adjunct to medical therapy, should be instituted at an early stage of ARF episodes before severe acidosis ensures, to avoid ET intubation.
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Laënnec invented the stethoscope in 1816 and published a treatise on auscultation in 1819. We then had to wait until the 1950s to observe development of modern devices and methods of recording and signal-processing, which allowed objective studies of lung sounds in time and frequency fields. Tracheobronchial sounds generated by ventilation originate in the upper airways, the frequency content of these sounds has led to extensive research. ⋯ Clearly, further studies need to be performed in order to elucidate the true mechanisms involved in generating vesicular lung sounds, the redistribution of intrapulmonary gas or vibrations caused by the stretching of lung tissue. The devices developed are already useful for monitoring the state of patients in intensive care. Sooner or later, real time analysis and automated diagnosis will become available.
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Cough is due to activation of sensory receptors in the larynx and lower respiratory tract, sending impulses to the brainstem. The central organization of cough is poorly understood. The afferent pathways for cough are from receptors in and under the epithelium of the airways. ⋯ The central connections of the C-fibre receptors inhibit cough. Thus, the sensitivity of the cough reflex and its pattern of response is due to a complex interaction between C-fibre receptors and rapidly adapting receptors, with peripheral and central nervous interactions. How these mechanisms apply to clinical cough in patients is at present poorly understood, but is beginning to be clarified.
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Airflow limitation has two well-defined components, increased resistance, which is found predominantly in the small airways, and loss of elastic recoil. Small airways contribute to the increased resistance to flow by the narrowing of the airway lumen. Morphometric studies have shown that smokers have increased epithelial abnormalities, cellular inflammatory infiltrates in the airway wall, increased muscle and fibrosis, when compared with nonsmokers. ⋯ Furthermore, in PLE, airflow limitation is correlated with loss of recoil but not with abnormalities in the small airways. We believe that the mechanisms involved in the pathogenesis of the two types of emphysema in smokers are different; an airborne mechanism for CLE, possibly related to airway hyperresponsiveness, and a bloodborne mechanism for PLE, which may be related to dysfunction of alpha 1-antiproteases. We conclude that the separation of smokers based on their emphysema type is essential if we are to understand the pathogenesis of chronic obstructive pulmonary disease (COPD) in these subjects.
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An L-arginine-dependent pathway, metabolising L-arginine to citrulline and nitrogen oxides, has been described in many cell types in different species, including man. Two subtypes of this nitric oxide synthase have been reported: a constitutive enzyme type, releasing nitric oxide after stimulation, is typically found in endothelial and neural cells; another subtype can be induced in macrophages after cytokine treatment. This review summarizes the literature on the known and proposed roles of this L-arginine-dependent nitric oxide production in different pulmonary processes. ⋯ The details of the role and distribution of nitric oxide synthase in the (human) lung and airways are not yet completely understood. Nitric oxide is believed to play a role in various pulmonary physiological processes, such as bronchodilation and the cytotoxic action of certain cells. The modulation of nitric oxide release will therefore, most probably lead to application of novel therapies in diseases such as asthma and inflammatory pulmonary diseases.