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THE APNŒIC PAUSE
Author(s) -
Milroy T. H.
Publication year - 1913
Publication title -
quarterly journal of experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0370-2901
DOI - 10.1113/expphysiol.1913.sp000146
Subject(s) - ventilation (architecture) , chemistry , carbonic acid , distension , oxygen , anesthesia , respiration , respiratory system , lung , medicine , anatomy , mechanical engineering , organic chemistry , engineering
(1) Alterations in the rate or degree of distension of the pulmonary alveoli when the amount of ventilation is constant does not affect the duration of the apnœic pause in any constant direction, but a repetition of ventilation periods tends to prolong the pause. (2) Removal of the vagal control does not interfere with the production of the apnœic pause. (3) Any rise in the CO 2 content of the air used for ventilation shortens the apnœic pause, and any increase in the carbonic acid content of the gas mixture used to distend the lung after pulmonary ventilation with air shortens the period. With increasing CO 2 content of these gas mixtures, irrespective of the amount of oxygen, the apnœic pause proportionately decreases. Rich oxygen‐holding mixtures in the absence of carbonic acid prolong the pause. (4) Injection of small quantities of acid solutions directly into the carotid during the pause leads to respiratory movements of an exaggerated type, as does also injection into the central end of the carotid. Injections into the external jugular vein are much less effective. (5) With the excitation of such respirations during the pause there is associated an increased passage out of carbonic acid from pulmonary blood to air. (6) These effects are produced after removal of the vagal control, but the excitability of the centre under such conditions seems to be diminished. (7) The passage of CO 2 from alveolar gas mixtures to blood or from blood to alveoli seems to depend entirely upon the difference of the pressure of that gas in the blood and air in the alveoli. (8) It seems most probable that the effective stimulus of the respiratory centre rendered quiescent by over‐ventilation is a rise in the carbonic acid concentration in that centre, whether brought about by the normal rise in carbonic acid formation during the pause, with its associated rise in the Ch', or primarily to a rise in the Ch' from the formation of acid products of incomplete oxidation giving rise secondarily to an increase in the free CO 2 tension.