Disturbance of Action Of Respiratory Muscles As A Contribution Cause of Dyspnea

Our plain-English summary of Disturbance of Action Of Respiratory Muscles As A Contribution Cause of Dyspnea, by A. Cournand, H.J. Brock, I. Rappaport, et al (1936).

The study

• Authors: A. Cournand, H.J. Brock, I. Rappaport, D.W. Richards JR
• Published: Archives of Internal Medicine (1936)
• Type of article: Journal article
• Our copy: from Johns-Manville's own medical library. The article is still under copyright, so we describe it here rather than post it.

In plain English

This article is not about asbestos. It is a physiology study of one man with pulmonary fibrosis and a history of pulmonary tuberculosis who was extremely short of breath (dyspneic) on slight exertion. For comparison, the authors also studied a second patient with pulmonary fibrosis who had low blood oxygen but little dyspnea, and a normal 27-year-old physician. Subjects stepped on a 20 cm step at two speeds while their breathing was recorded. Lung volumes were measured at rest, and arterial blood at rest and right after exercise. In the dyspneic patient, exercise caused no oxygen unsaturation of the arterial blood. His quiet breathing used mainly upper chest muscles, which stayed contracted during expiration, and his diaphragm moved at most 0.5 cm. During fast exercise his breaths were slowed and ventilation did not rise appreciably. After exercise, breathing became rapid and regular and dyspnea disappeared within two minutes. Repeating fast and slow exercise after epinephrine or atropine gave essentially the same results as without either drug. The authors concluded that his dyspnea was apparently due largely to hypertonic respiratory muscles and disturbed coordination between them.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Clinical physiology study of one patient (case study), compared with one other patient and one normal subject
• Who was studied: Three subjects in New York (Bellevue and Presbyterian Hospitals). The first was a man with pulmonary fibrosis and dyspnea whose pulmonary tuberculosis began in 1911; his age is unreadable in the scan. The second was A.C., a clerk aged 26 with advanced chronic pulmonary tuberculosis and arterial anoxemia, without dyspnea. The third was a physician aged 27 described as a normal subject. Experiments were carried out mainly in 1933.
• Exposure: No asbestos or other occupational exposure was studied. The experimental conditions were stepping exercise on a 20 cm step at about thirty-five steps a minute ('fast exercise', one minute) and about twenty steps a minute ('slow exercise', several minutes). In the dyspneic subject, the exercise was also repeated after injections of 1 mg epinephrine hydrochloride or 1 mg atropine sulfate.
• Main results:
  • In the dyspneic subject, the dyspnea that occurred with exercise was associated with no oxygen unsaturation of the arterial blood. Changes in blood acidity and carbon dioxide tension were small, and smaller than those in the anoxemic patient, who was scarcely made dyspneic.
  • In the dyspneic subject's quiet breathing, the upper chest (accessory) muscles predominated and the diaphragm's excursion reached at most 0.5 cm.
  • In the dyspneic subject, pleural pressure during quiet breathing oscillated from minus 8 to 0. The difference between deep inspiration and deep expiration averaged 14 cm. The authors took this as evidence that lung elasticity was moderately but not greatly impaired.
  • During the first minute of fast exercise, the dyspneic subject's breaths were slowed and total ventilation did not increase appreciably; at times it actually fell below the resting level. Aeration of the blood was nonetheless nearly adequate.
  • After exercise stopped, the dyspneic subject's breathing became rapid and regular and his sense of dyspnea disappeared in less than two minutes. His vital capacity, measured from thirty seconds to ten minutes after exercise, was 200 cc to 400 cc higher than before exercise.
  • Fast and slow exercise experiments in the dyspneic subject after epinephrine or atropine gave results essentially the same as those obtained without either drug.
  • Over several months of exercise experiments, the dyspneic subject's respiratory function and exercise tolerance improved. By the end, his breathing tracing was practically the same as the normal subject's.
• The authors' conclusion: The authors concluded that in this form of pulmonary fibrosis, dyspnea during mild exertion was apparently due in large part to a hypertonic state of the respiratory muscles and to a disturbance of the normal coordination between groups of them.
• Limitations the authors state:
  • The exercise was not of exactly the same degree for all three subjects, so quantitative comparisons between them could not be made.
  • The authors could not be certain that the unusual breathing behavior was connected with the disease in the patient's lungs.
  • The role of the other body muscles during the stepping exercise could hardly be deduced from these limited observations.
  • The authors stated there is no reason to suppose that a spastic muscular state is regularly of primary importance in the dyspnea of pulmonary fibrosis.
  • Attempts to measure the dyspneic subject's cardiac output at rest were unsuccessful.

Topics

Medical terms in this study, explained in our Lexicon: Dyspnea, Pulmonary Fibrosis, Diaphragm.

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