To the Editor: From their recent study of 110construction insulators. Bourbeau and colleagues conclude that asbestos-related pleural abnormality is associated with impaired lung function (1). The authors' definition of pleural abnormality includes not only discretepleural plaques but also pleural thickening visible on the lateral chest wall in the posterior-anterior chest radiograph without occlusion of the costophrenic angle. However. according to the 1980 International Labour Office (ILO) classification of chest radiographs (2) isolated chest wall thickening is a distinct abnormality. We and others have found it to be associated with restrictions to lung expansion independent of discrete plaques. filling of costophrenic angles. or parenchymal change (3). Thus, if our interpretation of the authors' analysis is correct, they have not excluded the presence of IW diffuse pleural thickening as the sole explanation for their findings. Wehope that they will clarify the situation as. up until now. isolated discrete plaques appear not to have been incriminated as a cause for asbestos-related respiratory impairment. It would be a pity if these plaques were now wrongly incriminated on the basis of a terminologic ambiguity. J. E. CorES. D.M., ER.C.P. B. KING. M.B.• CH.B. Division of Environmental & Occupational Medicine University of Newcastle Upon Tyne Newcastle upon Tyne, UK 1. Bourbeau J, Ernst P, Chrome J, Armstrong B, Becklake MR. The relationship between respiratory impairment and asbestos-related pleural abnormality in an active work force. Am Rev Respir Dis 1990; 142:837-42. 2. International Labour Office. Guidelines for the use of ILO international classification of radiographs of pneumocomioses. Revised 1980 revision. Geneva: ILO, 1980. Occupational Safety and Health Series No. 22. 3. Cotes JE. King B. Relationship of lung function to radiographic reading (ILO) in patients with asbestos related lung disease.Thorax 1988; 43:777-83.

From the Authors: We would like to take this opportunity to answer the letter by Drs. Cotes and King concerning our article which recently appeared in your journal (1). As pointed out, we did not differentiate between isolated pleural plaques and diffuse pleural thickening along the lateral chest wall even if this distinction is made within the IW classification. We do not believe such a distinction is warranted for two reasons. First. trained readers using the classification are unable to distinguish discrete, pleural plaques from diffuse thickening not affecting the costophrenic angle in a repeatable manner (2). Second. diffuse pleural thickening in the absence of blunting of the costophrenic angle most likely represents confluent pleural plaques without visceral pleural involvement (3) and we therefore believe it is more appropriate to consider this abnormality together with discrete pleural plaques. Our primary message was the importance to lung function of diffuse pleural thickening whose presence was attested to by costophrenic angle blunting. The small deficits related to pleural change along the lateral chest wall may have been caused by discrete or confluent pleural plaques. or even by the unusual occurrence

of diffuse pleural thickening without costophrenic angle blunting. We do not believe it possible to distinguish these three pathologies using the posterior-anterior chest radiograph. Weconsider this distinction by the IW classification to be inappropriate and hope it will be changed in the next revision. PIERRE ERNST. M.D. Pulmonary Research Laboratory Department of Epidemiology and Biostatistics McGill University Montreal, PQ, Canada

1. Bourbeau J, Ernst P, Chrome J, Armstrong B, Becklake MR. The relationship between respiratory impairment and asbestos-related pleural abnormality in an active work force. Am Rev Respir Dis 1990; 142:837-42. 2. Bourbeau J, Ernst P. Between and within reader variability in the assessment of pleural abnormality using the ILO 1980 international classification of pneumoconioses. Am J Ind Med 1988; 14:537-43. 3. McLoud TC, Woods BO, Carrington CB, Epler GR, Gaensler EA. Diffuse pleural thickening in an asbestos-exposed population: prevalence and causes. AJR Am J Roentgenol 1985; 144: 9-


To the Editor: We read with great interest the article by Wilcox and colleagues (1) about respiratory muscle function during obstructive sleep apnea. The results certainly bring new insights concerning inspiratory muscle function during non-rapid eye movement (NREM) sleep obstructive apnea. From gastric pressure and abdominal movement recording. the authors conclude that abdominal musclesare recruited in expiration during obstructive apnea in NREM sleep. The concern of the authors about limited previous data on expiratory muscle function during obstructive apnea gained our attention. Wewould like to remind the authors of our own contribution in abdominal muscle activity during sleep apnea syndrome in children, published in 1989. We have previously reported abdominal muscle expiratory electromyographic (EMG) activity in children with obstructive sleep apnea during NREM and rapid eye movement (REM) sleep (2). Our results showed marked differences in abdominal muscle recruitment in REM sleep as compared with NREM sleep in each child. During NREM sleep a progressive increase in abdominal muscle expiratory EMG activity was consistently recorded during the course of each obstructive apnea. On the contrary. "phasic" REM sleep obstructive apneas were characterized by a total absence of abdominal muscle expiratory EMG activity. Apnea termination in each child was associated with arousal and abdominal muscle expiratory EMG activity independent of the preceding sleep state. In addition. nonapneic breathing with snoring was associated with the presence of expiratory abdominal muscle EMG dischargesonly during NREM sleep (Stages 3 and 4). Our finding of major differences between NREM and REM sleep can be explained by the postural muscles (e.g.• abdominal muscles) inhibition characteristic of REM sleep. In agreement with Wilcox and colleagues (1). we speculated that the absence of abdominal muscle expiratory activity may partly explain more severe obstructive apneas, as it has been repeatedly reported in patients during REM sleep. 1197



Assistant Professor Department of Pediatrics Faculty of Medicine University of Sherbrooke Sherbrooke, Quebec, Canada CLAUDE GAULTIER, M.D., PH.D.

Professor of Physiology Physiology Laboratory Hopital Antoine Beclere Clamart, France 1. Wilcox PG, Pare PO, Road JO, Fleetham JA. Respiratory muscle function during obstructive sleep apnea. Am Rev Respir Dis 1990; 142:533-9. 2. Praud JP, O'Allest AM, Nedelcoux H, Curzi-Oascalova L, Guilleminault C, Gaultier C. Sleep-related abdominal muscle behavior during partial or complete obstructed breathing in prepubertal children. Pediatr Res 1989; 26:347-50.

From the Authors: We thank Dr. Praud and colleagues for bringing to our attention their contribution on abdominal muscle activity during sleep apnea (1), which was published after the original submission of our article on respiratory muscle function during obstructive sleep apnea (2). Increased upper airway resistance in NREM sleep has been previously shown to increase both inspiratory and expiratory muscle actfvity in patients without sleep apnea (3). In a recent article, Sanci and coworkers (4) also have demonstrated that abdominal muscle activity progressively increases during obstructive sleep apnea in NREM sleep. Progressive recruitment of expiratory muscles, particularly the abdominal muscles during the expiratory phase of obstructive apnea in NREM sleep, would cause diaphragm lengthening and optimize diaphragmatic function during inspiration when ventilation resumes at apnea termination. JOHN A. FLEETHAM, ER.C.P. (C)

Division of Respiratory Medicine Department of Medicine University Hospital (UBC) Vancouver, BC, Canada 1. Praud JP, O'Allest AM, Nedelcoux H, Curzi-Oascalova L, Guilleminault C, Gaultier C. Sleep-related abdominal muscle behavior during partial or complete obstructive breathing in prepubertal children. Pediatr Res 1989; 26:347-50. 2. Wilcox PG, Pare PO, Road JO, Fleetham JA. Respiratory muscle function during obstructive sleep apnea. Am Rev Respir Dis 1990; 142:533-9. 3. Skatrud J, Dempsey J, Badr S, Begle R. Effort of airway impedance on CO 2 retention and respiratory muscle activity during NREM sleep. J Appl Physiol 1988; 65:1676-85. 4. Sanci S, Cibella F, Marrone 0, Bellia V, Bonsignore G. Abdominal muscle activity in obstructive sleep apnoeas. Eur Respir J 1990; 3:526-8.


We read with great interest the articles by Corbridge and colleagues (1) and by Parker and coworkers (2). Both studies deal with the pathogenesis of high airway pressure/high lung volume ventilation-induced pulmonary edema. The stimulating paper by Corbridge and colleagues confirms the findings of Webb and Tierney (3) who showed that, for a given level of peak airway pressure, positive endexpiratory pressure (PEEP) reduced pulmonary edema. Webb and Tierney speculated that by inactivating surfactant, high airway pressure ventilation promoted an hydrostatic type edema and that by preserving surfactant, PEEP reduced the amount of edema (4, 5). Corbridge and coworkers take up the same explanation. However, we and others have demonstrated that this edema was accompanied

by permeability alterations (2, 6-8) that were underlied by ultrastructural alterations (6, 7) and that PEEP, in addition to decreasing edema, also reduced the importance of epithelial alterations (7). The reasoning of Corbridge and colleagues on the hydrostatic nature of this edema is based on the increase in the ratio of wet lung weight to body weight (WW/BW) in the large tidal volume (Vrj-low PEEP group when compared with the small Vr-high PEEP group, whereas there was no significant difference between groups in the ratio of dry weight to body weight (DW/BW), which reflects increased permeability (6, 7,9). We do not agree with this reasoning because of methodologic uncertainty. Indeed, the researchers did not make any correction for intrapulmonary blood, a fact that can explain the wide scattering of their data. It is highly desirable to make such a correction before drawing firm conclusions from the moderate difference in WW/BW between groups (P = 0.041), which could be due to differences in blood trapping. The same pitfall also might explain the lack of difference in DW/BW between groups. It would be possible to partially dismiss the error because of uncertainty of blood remaining in lungs by calculating the ratio of WW/DW, which has nevertheless been considered less reliable than blood-free parameters (10). It would be interesting to know whether this ratio would differ with respect to the ventilatory mode. In addition, the absence of increase in DW/BW in their large VT-IowPEEP group cannot be considered as attesting to the hydrostatic nature of high-volume ventilation edema because, according to the solute flow equation (11), when lung microvasculature is injured (as was the case after HCI, in their experiments) an increase in fluid filtration would increase the amount of extravasated protein. We are in complete agreement with Corbridge and coworkers when they point out that high' VT ventilation may be detrimental to lungs, but we would like to add a word of caution about their conclusions on the better mode of ventilation. We believe it would be excessive to consider that overinflation-induced lung injury does not occur with low VT. Indeed, we have shown that a permeability type edema was present in animals ventilated with PEEP and moderately elevated VT(7), and also occurred with normal VTventilation together with a markedly increased functional residual capacity (12). The report by Parker and colleagues clearly demonstrates that increased microvascular pressure participates in the genesis of highvolume ventilation edema. Nevertheless, we, cannot fully agree with their contention that "a major portion of the edema formed during high-pressure ventilation was hydrostatic in nature" and wonder whether they underestimated the actual magnitude of the alteration of permeability induced by lung distension. Indeed, the protein reflection coefficient was estimated 1 to 2 h after cessation of high airway pressure ventilation. Therefore, there exists some possibility that the observed value did not reflect the actual one during ventilation because microvascular permeability may return to a normal level after cessation of overinflation (13). Our concern arises from our observation of a highly significant relationship between the amount of water and protein in the extravasated fluid during lung distension injury. The slope of this relationship was consistent with the outpouring of pure plasma from lung vasculature during high-volume ventilation (7). Because Parker and coworkers have measured both extravascular lung water and blood-free dry lung weights, we would be interested to know whether they found the same relationship as we did. Finally, pulmonary edema after lung overinflation could result from the additive effects of both a severe permeability alteration and of hydrostatic enhancement of transvascular escape because of (1) depletion/inactivation of surfactant (4, 5), (2) a decreased perimicrovascular pressure of extraalveolar vessels during lung inflation (14, 15), and (3) an increase in intravascular pressure as shown by Parker and colleagues. These additive effects could explain the fulminating course of such edema. DIDIER DREYFUSS, M.D. GEORGES SAUMON, M.D.

Xavier Bichat Faculty of Medicine University of Paris Paris, France

Respiratory muscle function during obstructive sleep apnea.

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