Neuromechanical properties in obese patients during carbon dioxide rebreathing

doi:10.1016/0002-9343(83)91171-3

The American Journal of Medicine

Volume 75, Issue 1, July 1983, Pages 81-90

https://doi.org/10.1016/0002-9343(83)91171-3 Get rights and content

Abstract

During hypercapnia-induced hyperventilation, obese patients with a prior history of alveolar hypoventilation appear to have significantly more blunted ventilatory response than simply obese patients who never retained carbon dioxide. In addition, these patients with former obesity-hypoventilation syndrome have decreased neuromuscular responses as measured by way of the mouth occlusion technique when compared with either the patients with simple obesity or normal subjects. The patients with simple obesity appear to have augmented responses in comparison with normal subjects. Simple mechanical considerations and baseline breathing variables failed to distinguish the simple obesity group from the group with former obesity-hypoventilation syndrome. Thus, the decreased neuromuscular responsiveness to carbon dioxide (mouth-occlusion pressure/end-tidal carbon dioxide pressure) among the group with former obesity-hypoventilation syndrome when compared with that in the group with simple obesity is a consequence of a blunted neural (central) drive, and not due to any apparent worse mechanical limitations. The augmented mouth-occlusion pressure/end-tidal carbon dioxide pressure and increased integrated, rectified electromyographic signal of the diaphragm found in the group with simple obesity presumably reflect their attempt to maintain ventilatory homeostasis in the presence of severe respiratory loads. Neuromechanical coupling values, as reflected in the integrated electromyographic signal of the diaphragm versus transdiaphragmatic pressure and mouth-occlusion pressure versus mean inspiratory flow, are identical in the two groups. On the basis of these studies, it would appear that although mechanical loads put all obese patients at a disadvantage, the addition of an acute extra load on the respiratory system produces the obesity-hypoventilation syndrome in those obese persons who have truly blunted central hypercapnic responses.

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Obesity hypoventilation syndrome (OHS) is a complex disorder. Its clinical manifestations represent the sum of the various derangements induced by obesity. This chapter describes many of these derangements. Some of the phenomena discussed in this chapter have been observed in patients with OHS, and others were observed in patients with similar conditions or in animal models that simulate some of the salient features of OHS. Other chapters in this book discuss the evolution of OHS, the pathogenesis of severe sleep apnea in patients with obesity, and the cardiovascular, immune, and neurological changes seen in patients with OHS.
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^☆: This study was supported in part by the Medical Research Council of Canada and the Canadian Lung Association.

¹: From the Meakins-Christie Laboratories, Royal Victoria Hospital, McGill University and Notre Dame Hospital, University of Montreal, Montreal, Quebec, Canada.

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Clinical studyNeuromechanical properties in obese patients during carbon dioxide rebreathing☆

Abstract

Am J Med

Am J Med

Respir Physiol

Am J Med

Chest

Extreme obesity associated alveolar hypoventilation: a Pickwickian syndrome

Am J Med

The total work of breathing in normal and obese men

J Clin Invest

Effect of mass loading the respiratory system in man

J Appl Physiol

Pulmonary function in obese patients

J Clin Invest

New weight standards for men and women

Statistical bulletin

A clinical method for assessing the ventilatory response to carbon monoxide

Aust Ann Med

Improved technique for estimating pressure from esophageal balloons

J Appl Physiol

Influence of lung volume and electrode position on electromyography of the diaphragm

J Appl Physiol

Clinical study
Neuromechanical properties in obese patients during carbon dioxide rebreathing☆