couple of generations ago, almost all American children and youths took large amounts of codliver oil, whereas no~ owing to advances in science, they are given pure vitamin D mostly in enriched milk, without the antiplatelet facto!: Too much science? We must also reflect that when the Roman Catholic Church relaxed its rule on the eating offish on Friday, it did the public health a disservice. Too much liberalizing of religious customs? In any case, the contrast between the way the cholesterol problem and the fish oil problem is being handled is notable. REFERENCES 1 Keys A, Menotti A, Aravanis C, Blackburn H, Djordevic BS, Buzina R, et ale The seven countries study: 2,289 deaths in 15 years. Prev Med 1984; 13:141-54 2 Bottiger LE, Carlson LA. Risk factors for death for males and females. Acta Moo Scand 1982; 211:437-42 3 Wei JY, Bulkley BH. Myocardial infarction before age 36 years in
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women: predominance of apparent nonatherosclerotic events. Am Heart J 1982; 104:561-66 Ulvenstam G, Bergstrand R, Johansson S, Vedin A, Wtlhelmsson C, Wedel H, et ale Prognostic value of cholesterol levels after myocardial infarction. Prev Med 1984; 13:355-66 Kramer JR, Kitazume H, Proudfit WL, Matsuda Y, Williams GW, Sones FM. Progression and regression of coronary atherosclerosis: relation to risk factors. Am Heart J 1983; 105:134-44 ten Kate ~ Boman H, Daiger S~ Motulsky AG. Increased frequency of coronary heart disease in relatives of wives of myocardial infarct survivors: assortive mating for lifestyle and risk factors? Am J Cardioll984; 53:399-403 Mitchell JRA. What constitutes evidence on the dietary prevention of coronary heart disease? Cosy beliefs or harsh facts? Int J Cardiol 1984; 5:287-98 Phillips GB. Hyperestrogenemia, diet, and disorders ofwestern societies. Am J Med 1985; 78:363-66 Krombout 0, Bosscheiter EB, Courlander C de L. The inverse relation between fish consumption and 2O-year mortality from coronary heart disease. N Eng} J Med 1985; 312:1205-09 O'Dea K, Sinclair AJ. Increased proportion ofarachOOonic acid in plasma lipids after two weeks on a diet of tropical seafood. J Clin Nutr 1982; 36:868-72
Some Neglected Aspects of Respiratory Function In Pleural Effusions The Diaphragmatic Arch Mark D. Altschule, M.D. *
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etween breaths, the diaphragm, pulled up by the nonnal negative intrapleural pressure, assumes a domed shape. Its attachments are all peripheral. When the diaphragm contracts it becomes flat and loses its dome, thereby pulling in air through the nasopharynx and large aitways. At the end of inspiration, it relaxes and, under the influence of the lung parenchyma, is pulled back into its domed shape. These changes are best seen in lateral roentgenographic views of the chest. Loss of the domed shape, owing to loss of pulmonary elasticity or any other factol; seriously impairs nonnal breathing and increases the activity of the other respiratory muscles. The effects of pleural effusions depend not only on the amount of the fluid but also on the presence or absence of extensive pulmonary parenchymal lesions. Nonnally, the measurements of pulmonary function vary so much that defining the effects of hydrothorax is difficult. Physical and roentgenographic examination are both inaccurate since the amount of free fluid present is always larger than expected, unless the fluid is encapsulated. If a radiopaque liquid lipid substance is introduced into the pleural space it will Hoat to the top, thereby defining the upper limit of the effusion. Studied in this way, the effusion is always higher than expected. Egophony is the most accurate physical sign of fluid level, but it is not always present. Mediastinal shift is an accurate roentgenographic sign oflarge pleural effusions, but is absent with smaller effusions. A pleural effusion of moderate or large size causes an increase in peripheral venous pressure, but not necessarily above nonnal limits. This pre-cardiac phenomenon is not *Francis A. Countway Medical Library, Harvard Medical School, Boston. Reprint requests: Dr. Altschule, Haroard Medical School, Boston 02115.
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accompanied by a fall in cardiac output. The amount ofrise of the latter during exercise may, however, be limited. The effects of hydrothorax on respiratory function are usually surprisingly small, although the presence of the fluid causes atelectasis as revealed by a decrease in functional residual (subtidal) air volume in the lungs. This is unlikely to cause dyspnea or arterial hypoxemia at rest, but it may cause respiratory discomfort on exertion. The reason for the common absence ofarterial hypoxemia at rest is well-known. Air in the lungs (functional residual air) is oxygenated by mixing with inspired ail: The ratio of effective inspired air (tidal air minus dead-space volume x respiratory rate) to functional residual air must be 2:1 or higher to cause effective air mixture in the lungs and prevent arterial blood hypoxia. Accordingly when respiration is made shallow by the presence of an effusion, the simultaneous production of atelectasis keeps the ratio at about 2:1 so that mixing in the remaining functional lung is adequate. However; atelectasis limits the expansibility of the lungs and may produce dyspnea on exertion. When thoracocentesis is perfonned, atelectasis is not immediately abolished; re-expansion may take as long as several weeks. The immediate effect of thoracocentesis is to restore the nonnal diaphragmatic arch, thereby making respiration more efficient despite the persistence of atelectasis. There may also be some decrease in venous pressure, followed by diuresis if peripheral edema is also present. It is a clinical fact that when a small pleural effusion causes dyspnea, and a small thoracocentesis (400 to 500 ml) gives relief: there must also be extensive parenchymal pulmonary disease. REFERENCE
1 Altschule MD, Zamcheck N. The effects of pleural effusion on circulation and respiration in man. J Clin Invest 1944; 23:325-31 Crtticallssues in Clinical care (AlaI1c D. AIt1Ichule)