Document zdVx3jrwoKNyGYXQwEam5Z0Gm
tmlustrial Hygiene Digest
August, 1967
two I vo -1 t'ad electrocardiograms have been processed using only one third of a small computer system's capacity. There are 8 references.
7 j7 Measurement of Pilot Fatigue. F.S. Preston. Trans. Soc. Occ. Med. Jj_7, 52-56 (April, 1967).
The subject of fatigue in airline pilots is discussed with particular regard to the operational problems of the industry. So far no reliable means of assessing pilot fatigue in quantitative terms has been found, although much work has been carried out by researchers in many count ries. There is no short-cut to safety in aviation and the assessment of pilot fatigue and the prevention of errors in flight by pilots can only be achieved by study of all the factors affecting skill and mental performance. The reduction of flying accidents due to human error in the air and on the ground can only be achieved by the utilization of knowledge from the biological and engineering sciences and further active research programs. There are 15 references.
-- Author's summary
7 38 Use of Ultrasound to Measure Left Ventricular Stroke Volume. H. Feigenbaum, A. Zaky, and W.K. Nasser, Circulation 25. 1 092-1 099 (June, 1967).
A technique was developed whereby left ventricular stroke volume could be measured with
diagnostic ultrasound. This technique utilized an ultrasound measure of left ventricular dia
meter and a measure of the amount of motion exhibited by a portion of the left ventricle near
the mitral ring. The formula used to calculate left ventricular stroke volume was based on
the hypothesis that left ventricular Wall motion was proportional to left ventricular stroke
volume and inversely proportional to left ventricular volume or diameter. Ultrasound stroke
volume measurements were obtained simultaneously with Fick stroke volume determinations on
16 patients with no mitral or aortic insufficiency. The correlation between the two methods
of measuring stroke volume was excellent (r=0..973, p<0. 001). When the regression equation
was used to predict stroke volume from the ultrasound measurements, the results were within
11 ml. or + 15% of the Fick stroke volume.
-- J. Am. Med. Assn. References b Reviews
739 Inner Ear Pathology of Sudden Deafness. D. D. Beal, W.G. Hemenway, andJ.R. Lindsay. Arch. Otolaryngol. 8J, 591 -598 (June, 1967).
Two cases are presented of rapidly developing unilateral deafness in adults. One was associated with an upper respiratory infection probably viral in nature. The histopathology characteristic ally corresponded in type with previously documented cases of maternal rubella, mumps, and measles although differing in degree. As in the previously reported cases, the portal of entry to the inner ear has most probably been the tria vascularia during viremia.
-- J. Am. Med. Assn. References & Reviews
740 Eye Burns Caused by Tear Gas. D. K. Hoffmann. Brit. J. Ophthalmol. _51_, 265-268 (April, 1967).
A short description is given of the experience gained in treating almost 50 cases of ocular in
juries caused by tear gas weapons. The clinical course of the burns is characteristic. Treat
ment remains symptomatic until more is known about the chemical changes occurring in the tis
sues, caused by infiltrated substances. The visual acuity achieved after treatment may vary
from almost perfect vision to perception of light, depending on the distance of the shot and the
amount of infiltrated substance.
-- J. Am. Med. Assn. References b Reviews
741 The Mechanisms of Some Structural Alterations of the Lung Caused by Environmental Health. Paul Gross, M. D. Arch. Environmental Health 14, 883-891 (June, 1967). (Reprints available from IHF).
The basic structure of the lung, the alveolar wall, is composed of two embryologically different tissues, the capillary network, which is derived from the mesoderm; and the alveolar mem brane, an entodermal derivative. Each of these components reacts in a specific manner to inhaled environmental irritants. In general, the alveolar capillary responds to an irritant that is sufficiently aggressive to penetrate the protective alveolar membrane. This response con sists of pulmonary edema or of acute pneumonia or both. The alveolar membrane responds also to irritants that are less aggressive. Structural alterations produced by irritation of the alveolar membrane consist of thickening of alveolar walla by proliferation of alveolar cells and the elaboration of a precollagenous argyrophilic supporting stroma. This proliferated tissue is avascular and may extend into air spaces to a degree that may result in their occlusion.
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