Absence of apnœa after forced breathing

Abstract

As is well known, forced breathing is usually followed by a period of apncea of more or less duration, depending upon the extent to which the forced breathing has been performed. It has, incidentally, been noted that in some subjects forced breathing is not followed by apncea; but so far as we know no case has been thoroughly studied in which forced breathing is not followed by apncea. This paper will be devoted to the detailed study of niy own case, as I present the apparently anomalous phenomenon, not merely of the absence of apncea, but even of a natural hyperpnoea succeeding forced breathing.Volumetric tracing of a forced breathing experiment. Fig. 1 is a tracing by means of the body plethysmograph described by Haldane and Priestley2, and represenits with a high degree of accuracy the volume of air breathed. It will be noted that immediately followirg the period of forced breathing there is an interval of about half a minute in which there is a natural hyperpncea nearly twice the volume of the normal respiration. Subsequent to this natural hyperpnoea the tracing shows that the respiration diminishes in volume below that of the normal period. This diminution, though distinct, is obviously comparatively small; more accurate determinations will be considered later.Normal reaction to an increase of 0O2. To determine whether or not I reacted in the usual way to an increase of CO2 I entered an air chamber in which the CO2 percentage was progressively increased. With the door of the chamber open I determined my normal alveolar 1 My sincerest thanks are due to Dr Haldane who has directed this research; to Dr Douglas who has rendered valuable aid; to Dr Florence Buchanan who was kind enough to investigate the heart-rate by photographing records with the capillary electrometer; and to Mr Barcrof t of Cambridge under whose direction the determinations of the dissociation curves were made. 2 This Journal, xxxii. p. 225. 1905.

Hyperventilation in Arteriolar Hypertension

“…Vincent and Cameron (2) in 1915 showed that hyperventilation in the human subject with normal blood pressure was associated with a rapid and considerable fall in blood pressure. This work confirmed earlier observations by Hill and Flack (3) and by Boothby (4). Collier, Densham, and Wells (5) found no effects of hyperventilation on the blood pressure of most of their human subjects with normal blood pressures.…”

Ventilation volume as a stimulus to spontaneous ventilation after prolonged artificial ventilation

“…The involuntary continuation of overventilation after less than 2 hr of voluntary active overventilation has been described by Boothby (1912) in himself, and by Mills (1946) in six normal subjects. Boothby's explanation was that the lowered arterial pCO2 caused cerebral vasoconstriction, that this caused the pCO2 of the 'respiratory centre' to rise from inadequate perfusion, and that the high intracellular pCO2 provided the stimulus for continued overventilation.…”

Post-hyperventilation apnoea in patients with brain damage

“…Haldane and Priestley (1905) and Douglas and Haldane (1909) demonstrated by a series of experiments, mainly on themselves, that a period of apnoea followed hyperventilation; they attributed this interruption of breathing to a lowering of the carbon dioxide tension (PCO2) in the respiratory centre to a value below the threshold for activity. Boothby (1912) failed to confirm the phenomenon, while Mills (1946) demonstrated hyperpnoea after forced breathing in 25 out of 35 subjects studied, and complete absence of apnoea in 12 of 16 subjects in a further study (personal communication). Fink (1961) likewise could not elicit post-hyperventilation apnoea in 13 normal conscious subjects; he suggested that maintenance of normal respiratory rhythm in the wakeful state is due to a non-chemical stimulus which acts in the absence of metabolic stimuli and can be damped by sleep, anaesthesia, sedation, or neurological dysfunction.…”