Pathophysiology of pulmonary edema.
ABSTRACT Pulmonary edema is a frequent and common cause of death in patients in critical care settings. It is seen as a complication of myocardial infarcts, hypertension, pneumonia, smoke inhalation, and high-altitude pulmonary edema. Pulmonary edema occurs when there are alterations in Starling forces and capillary permeability, opposition to lymphatic flow in the lungs, decreased plasma oncotic pressure, central nervous system lesions, and following some types of strenuous exercise. Pulmonary edema presents initially with crackles, wheezing, and dry cough and progresses to tachypnea, dyspnea, orthopnea, pink frothy sputum, and cyanosis. Treatment involves supportive therapy, reduction in blood volume, and oxygen therapy.
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ABSTRACT: Pulmonary physiologists have documented many transient changes in the lung and the respiratory system during and following exercise, including the incomplete oxygen saturation of arterial blood in some subjects, possibly due to transient pulmonary oedema. The large increase in pulmonary arterial pressure during exercise, leading to either increased pulmonary capillary leakage and/or pulmonary capillary stress failure, is likely to be responsible for any increase in extravascular lung water during exercise. The purpose of this article is to summarise the studies to date that have specifically examined lung water following exercise. A limited number of studies have been completed with the specific purpose of identifying pulmonary oedema following exercise or a similar intervention. Of these, approximately 50% have observed a positive change and the remaining have provided results that are either inconclusive or show no change in extravascular lung water. While it is difficult to draw a firm conclusion from these studies, we believe that pulmonary oedema does occur in some humans following exercise. As such, this is a phenomenon of significance to pulmonary and exercise physiologists. This possibility warrants further study in the area with more precise measurement tools than has previously been undertaken.Sports Medicine 02/2006; 36(6):501-12. DOI:10.2165/00007256-200636060-00004
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ABSTRACT: The morphogenic opiate pentapeptide leucine-enkephalin (lenk) in a hydrated dimyristoylphosphatidylcholine (DMPC) bilayer is studied using NMR spectroscopy and molecular dynamics simulation. Contrary to the frequent assumption that the peptide attains a single fixed conformation in the presence of membranes, we find that the lenk molecule is flexible, switching between specific bent conformations. The constraints to the orientation of the aromatic rings that are identified by the NMR experiment are found by the MD simulation to be related to the depth of the peptide in the bilayer. The motion of the N-H vectors of the peptide bonds with respect to the magnetic field direction as observed by MD largely explain the magnitude of the observed residual dipolar coupling (RDC), which are much reduced over the static (15)N-(1)H coupling. The measured RDCs are nevertheless significantly larger than the predicted ones, possibly due the absence of long-time motions in the simulations. The conformational behavior of lenk at the DMPC surface is compared to that in the aqueous solution, both in the neutral and in the zwitterionic forms.Journal of the American Chemical Society 02/2006; 128(1):159-70. DOI:10.1021/ja054785q
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ABSTRACT: We tested the hypothesis that intense short duration hypoxic exercise would result in an increase in extravascular lung water (EVLW), as evidenced by an increase in lung density. Using computed tomography (CT), baseline lung density was obtained in eight highly trained male cyclists (mean +/- SD: age = 28 +/- 8 years; height = 180 +/- 9 cm; mass = 71.6 +/- 8.2 kg; VO2max= 65.0 +/- 5.2 ml kg min(-1)). Subjects then completed an intense hypoxic exercise challenge on a cycle ergometer and metabolic data, HR and %S(p)O2 were recorded throughout. While breathing 15% O2, subjects performed five 3 km cycling intervals (mean power, 286 +/- 20 W; HR = 91 +/- 4% HRmax) separated by 5 min of recovery. From a resting hypoxic S(p)O2 of 92 +/- 4%, subjects further desaturated during exercise to 76 +/- 3%. CT scans were repeated 76 +/- 10 min (range 63-88 min) following the completion of exercise. There was no change in lung density from pre (0.18 +/- 0.02 g ml(-1)) to post-exercise (0.18 +/- 0.04 g ml(-1)). The substantial reduction in S(p)O2 may be explained by a number of potential mechanisms, including decreased pulmonary diffusion capacity, alveolar hypoventilation, reduced red cell transit time, ventilation/perfusion inequality or a temperature and pH induced rightward-shift in the oxyhaemoglobin dissociation curve. Alternatively, the integrity of the blood gas barrier may have been disrupted without any measurable increase in lung density.Arbeitsphysiologie 05/2007; 99(6):623-31. DOI:10.1007/s00421-006-0388-1