Studies on acidosis and dyspnea in renal and cardiac disease / Francis W. Peabody, Boston.

  • Peabody, Francis Weld, 1881-1927
Date:
1914
Catalogue details

Licence: In copyright

Credit: Studies on acidosis and dyspnea in renal and cardiac disease / Francis W. Peabody, Boston. Source: Wellcome Collection.

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    action by which this organ is enabled to separate acid from its com¬ bined base, excrete the acid and save the base to the body so that it may again combine with and neutralize acid. The lungs form the second excretory channel of importance, for by means of them carbon dioxid is excreted. Any tendency to the production of an acidosis in the body is immediately compensated for by an increase in respira¬ tion and a washing out of carbon dioxid. It seems probable that the kidney is the fundamental regulator of the reaction of the blood, but the lungs, acting more quickly in response to sudden calls, serve as the more delicate balance-wheel of the regulatory mechanism.5 The question of the regulation of respiration has, however, been fundamentally widened by the writings of the two Danish physiolo¬ gists, Hasselbalch and Lindhard, who have shown that there are two factors which must be considered. The first of these, and the one to which attention has hitherto been generally directed, is the nature or size of the stimulus to respiration. The second is the excitability of the respiratory center. This has been usually accepted as being a con¬ stant, and the possibility of its varying has been rather overlooked. To quote Hasselbalch’s own words:2 • The two factors, regulation of neutrality and excitability of the respiratory center, together govern the chemical regulation of respiration, and therefore the amount of the alveolar carbon dioxid tension is a function of the two factors, and cannot be regarded as a physiologic constant.”6 Hasselbalch states that a diminution in the carbon dioxid tension of the alveolar .air is thus not necessarily due to an increase of the acids in the blood, since this condition may be present when the respiratory center is hyperexcitable and responds to a hydrogen-ion concentration of the blood that is lower than normal. In such a case the threshold for the excitation of the center has become lowered, but the composition of the blood as far as acids other than carbon dioxid go may remain unchanged. That variations in the excitability of the respiratory center do actually occur has been shown. The excitability may be tested by the method of Lindhard7 in which the subject is given mixtures containing various percentages of carbon dioxid to breathe, and the increase in alveolar ventilation which results from a given increase in the inspired carbon dioxid is measured. Lindhard7 has shown that the excitability of the respiratory center varies inversely as the oxygen tension of the blood. The excitability 5. Campbell, Douglas, Haldane and Hobson: Jour. Physiol., 1913, xlvi, 301. 6. Die zwei Faktoren: Neutralitatsregulation und Reizbarkeit des Atem- zentrums beherrschen zusammen die chemische Atmungsregulation, so dass die Grosse der alveolaren C02—Spannung als Funktion der beiden Faktoren hervorgeht und nicht als physiologische Konstante betrachtet werden kann. 7. Lindhard: Jour. Physiol., 1911, xlii, 337.