Journal of Applied Physiology AJP: Lung Cellular and Molecular Physiology
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J Appl Physiol 107: 962-970, 2009. First published April 30, 2009; doi:10.1152/japplphysiol.00165.2009
8750-7587/09 $8.00
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REVIEW

HIGHLIGHTED TOPIC
The Respiratory Muscles in Chronic Obstructive Pulmonary Disease

Role of the respiratory muscles in acute respiratory failure of COPD: lessons from weaning failure

Martin J. Tobin,1 Franco Laghi,1 and Laurent Brochard2

1Division of Pulmonary and Critical Care Medicine, Edward Hines Jr. Veterans Affairs Hospital and Loyola University of Chicago Stritch School of Medicine, Hines, Illinois; and 2Medical ICU, AP-HP, Albert Chenevier-Henri Mondor Teaching Hospital, Paris 12 University, INSERM Unit 955, Créteil, France

Submitted 13 February 2009 ; accepted in final form 29 April 2009

ABSTRACT

It is problematic to withhold therapy in a patient with chronic obstructive pulmonary disease (COPD) who presents with acute respiratory failure so that detailed physiological measurements can be obtained. Accordingly, most information on respiratory muscle activity in patients experiencing acute respiratory failure has been acquired by studying patients who fail a trial of weaning after a period of mechanical ventilation. Such patients experience marked increases in inspiratory muscle load consequent to increases in resistance, elastance, and intrinsic positive end-expiratory pressure. Inspiratory muscle strength is reduced secondary to hyperinflation and possibly direct muscle damage and the release of inflammatory mediators. Most patients recruit both their sternomastoid and expiratory muscles, even though airflow limitation prevents the expiratory muscles from lowering lung volume. Even when acute hypercapnia is present, patients do not exhibit respiratory center depression; indeed, voluntary activation of the diaphragm, in absolute terms, is greater in hypercapnic patients than in normocapnic patients. Instead, the major mechanism of acute hypercapnia is the development of rapid shallow breathing. Despite the marked increase in mechanical load and decreased force-generating capacity of the inspiratory muscles, patients do not develop long-lasting muscle fatigue, at least over the period of a failed weaning trial. Although the disease originates within the lung parenchyma, much of the distress faced by patients with COPD, especially during acute respiratory failure, is caused by the burdens imposed on the respiratory muscles.

intrinsic positive end-expiratory pressure; load-capacity imbalance; work of breathing



Address for reprint requests and other correspondence: M. J. Tobin, Div. of Pulmonary and Critical Care Medicine, Edward Hines Jr. VA Hospital, 111N, 5th Ave. and Roosevelt Rd., Hines, IL 60141 (e-mail: mtobin2{at}lumc.edu)




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D. K. McKenzie, J. E. Butler, and S. C. Gandevia
Respiratory muscle function and activation in chronic obstructive pulmonary disease
J Appl Physiol, August 1, 2009; 107(2): 621 - 629.
[Abstract] [Full Text] [PDF]




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