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Department of Medicine, Queen's University, Kingston, Ontario, Canada
Correspondence and requests for reprints should be addressed to Denis E. O'Donnell, Professor of Medicine and Physiology, Division of Respiratory and Critical Care Medicine, Respiratory Investigation Unit, Department of Medicine Queen's University, 102 Stuart Street Kingston, ON, K7L 2V6 Canada. E-mail: odonnell{at}post.queensu.ca
The following articles are based on presentations given during a seminar entitled "Hyperinflation: A Critical Target in COPD" at the 100th International Conference of the American Thoracic Society, held in Orlando, Florida in May 2004. Hyperinflation is a very exciting topic in chronic obstructive pulmonary disease (COPD) because, as detailed in the following articles, it is something that we can address in clinical practice. By treating hyperinflation in COPD, we can help our patients.
Hyperinflation in COPD is not a new idea. In 1837, the Irish physician William Stokes, whose name is given to Stokes–Adams attack and Cheyne–Stokes respiration, published a textbook entitled "A Treatise on the Diagnosis and Treatment of Diseases of the Chest" (1). In the section on emphysema, he wrote the following:
I shall describe a sign which promises to be of the greatest importance in diagnosis. By making the [emphysematous] patient perform a number of forced inspirations rapidly...the repetition of the inspiratory efforts cause such an accumulation of air in the diseased portion of the lung as ultimately to nearly prevent its further expansion. The results of this experiment are easily explained by referring to difficulty of expiration which occurs in this disease.
Stokes clearly described the phenomenon we now term air trapping or dynamic lung hyperinflation. He realized over 167 years ago that patients with expiratory difficulty as a result of emphysema experienced serious inspiratory difficulty, as a result of the rapid accumulation of air that occurred in the lungs when ventilation suddenly increased. While static lung hyperinflation has been recognized as a hallmark characteristic of emphysema for many years, we have only recently come to realize the potentially negative consequences of acute dynamic hyperinflation in all patients with COPD—even in those with early disease.
This early clinical observation of hyperinflation by Stokes was seemingly forgotten for many years. Forced expiratory volume in 1 second (FEV1), without regard for hyperinflation, became the primary outcome measure in clinical trials, and the exclusive target for COPD interventions. This has resulted in some therapeutic nihilism and has also led us to neglect to measure the effects of drugs and other interventions on lung hyperinflation. Renewed interest in hyperinflation has been inspired by the discovery that parameters of hyperinflation correlate better with patient-centered health outcomes than does FEV1 (2). Hence, targeting hyperinflation can make a difference to the patient.
In the following articles we revisit the topic of hyperinflation, examining the interactions of abnormal lung mechanics, dyspnea and activity limitation in COPD, and how these can be successfully manipulated by a number of modern therapeutic interventions.
FOOTNOTES
Conflict of Interest Statement: D.E.O. acted as Principal Investigator for two Multi-National Trials. Queen's University received $376,137 between 2001 and 2004 for this. An additional single site, mechanistic study with Prof. O'Donnell (PI) was financed to the amount of $83,260, which was received by Research Services, Queen's University, Kingston, Ontario, Canada. Prof. O'Donnell is a member of the speaker's bureau for Boehringer Ingelheim and Pfizer and has received research grants from these companies.
REFERENCES
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