Ventilatory drive in chronic pulmonary emphysema

A. P. Fishman, P. Samet, André Cournand

Research output: Contribution to journalArticle

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Abstract

1. 1. The studies reported in this paper confirm the well documented observation that some patients with chronic pulmonary emphysema manifest an abnormally small increase in minute ventilation when CO2 is added to inspired air. This diminished ventilatory response, despite a considerable increase in arterial Pco2, is characteristic of patients with chronic pulmonary emphysema who also have chronic CO2 retention. 2. 2. The mechanism underlying the abnormal ventilatory response in these patients appears to be a selective depression of the respiratory center to the stimulus of increased arterial blood PCO2 and/or hydrogen ion concentration, since responsiveness to other stimuli such as exercise is well maintained. Restriction in the ventilatory capacity of the chest bellows is not the limiting factor to increase in minute ventilation during CO2 breathing in patients with emphysema and CO2 retention; by way of contrast, this restriction may suffice to limit the ventilatory response to the CO2 stimulus in some patients with emphysema but without CO2 retention. 3. 3. The poor ventilatory response to the CO2 stimulus is generally not reversible in patients with CO2 retention of long duration even though the arterial blood PCO2 and alkali reserve may be restored toward normal levels as a result of prolonged administration of the carbonic anhydrase inhibitor, diamox. 4. 4. In addition to its action in decreasing the alkali reserve, diamox also reduces the arterial blood PCO2. The mechanism of this action is not established. 5. 5. The relief or aggravation of hypoxemia within the physiologic range has little effect on the ventilatory response to inspired CO2 in patients with emphysema and CO2 retention. This suggests that the hypoxic stimulus is rather weak; however, as is well known, breathing pure O2 consistently depresses the ventilatory response. The contrast between these observations emphasizes the importance of distinguishing between the physiologic and pharmacologic levels of O2 tension in the blood. 6. 6. The therapeutic implications of these observations, in patients with chronic pulmonary emphysema, are threefold. First, a distinction must be made between the effect of reduced ventilatory drive, and considerable restriction in ventilatory capacity in limiting minute ventilation. Second, attention must be focused on the means for prevention and prompt relief of CO2 retention. The role of diamox and of mechanical hyperventilation in the various stages of the disease has been described in this connection. Finally, by mobilizing large stores of Co2 from the body, continuous diamox therapy in patients with prolonged CO2 retention may restore mental alertness and a sense of well-being and diminish the threat of CO2 narcosis.

Original languageEnglish
Pages (from-to)533-548
Number of pages16
JournalThe American Journal of Medicine
Volume19
Issue number4
StatePublished - Oct 1 1955

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Pulmonary Emphysema
Acetazolamide
Emphysema
Ventilation
Alkalies
Respiration
Respiratory Center
Carbonic Anhydrase Inhibitors
Stupor
Hyperventilation
Thorax
Air
Observation
Exercise

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Fishman, A. P., Samet, P., & Cournand, A. (1955). Ventilatory drive in chronic pulmonary emphysema. The American Journal of Medicine, 19(4), 533-548.

Ventilatory drive in chronic pulmonary emphysema. / Fishman, A. P.; Samet, P.; Cournand, André.

In: The American Journal of Medicine, Vol. 19, No. 4, 01.10.1955, p. 533-548.

Research output: Contribution to journalArticle

Fishman, AP, Samet, P & Cournand, A 1955, 'Ventilatory drive in chronic pulmonary emphysema', The American Journal of Medicine, vol. 19, no. 4, pp. 533-548.
Fishman AP, Samet P, Cournand A. Ventilatory drive in chronic pulmonary emphysema. The American Journal of Medicine. 1955 Oct 1;19(4):533-548.
Fishman, A. P. ; Samet, P. ; Cournand, André. / Ventilatory drive in chronic pulmonary emphysema. In: The American Journal of Medicine. 1955 ; Vol. 19, No. 4. pp. 533-548.
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