The influence of posture on the pulmonary blood volume and the alveolar gas tensions

Abstract

In a recent series of papers Main has dealt with the problem of the fall in the tension of the carbon dioxide in the alveolar air which occurs on the assumption of the erect postur,e. In 1937 he suggested that it was due to an increase in pulmonaiy ventilation. Hitchcock & Ferguson [1938] disagreed with this and pointed out that the phenomenon took place without an increase in ventilation of the lungs. In two of the latter's subjects there was both a fall in the pulmonary ventilation and in the alveolar C02 tension on standing. In 1941 Main defended himself by applying a different interpretation to the term 'over-ventilation'. He pointed out that if the pulmonary ventilation was reduced, and at the same time the volume of blood circulating in the lungs was less, this latter volume could be over-ventilated with a consequent fall in CO2 tension. That Main was, however, mainly concerned with ventilation and the factors affecting this, and not with circulatory phenomena, can be judged from the theme of his papers. In 1940, his opening sentence is: 'The cause of the overventilation in the erect posture is unknown', and he proceeds to investigate whether the fall in pressure within the carotid sinus which occurs on standing is responsible for the increase in breathing. He gives vasopressor drugs to see whether the pressure changes they produce will influence alveolar CO2 tension by their effect on pulmonary vent-ilation. He concludes that the respiratory stimulant is a 'relative cerebral anaemia'. These views are similar to those expressed by Turner [1927], who states that the very moderate increases in respiratory activity which occur on standing can be very easily explained as the result of carotid sinus reflexes and diminished cerebral circulation.The alteration in vital capacity which was pointed out by Hill [1895] has been brought forward as a factor influencing respiration. Bohr [1907] agrees that the vital capacity increases on standing, and Brunton [1908] points out that since the diaphragm has to raise and lower the viscera when one is recumbent, but merely to move them horizontally when upright, this is the key to the limitations which posture places on breathing. Christie & Beams [1922] found from the average of 290 normal subjects that the vital capacity decreases by

Changes in alveolar carbon dioxide tension by night and during sleep

“…Such a spontaneous rhythm might be responsible for some of the changes ascribed to sleep. Others may be ascribable to posture, since recumbency (Mackay, 1943) leads to a rise in alveolar C02 tension.…”

Changes in Capacity of the Leg Veins Studied by a Simple Counter‐pressure Technique

“…Further, any emotional disturbances would be expected to lessen with repetition of the test, out in fact the expiratory shift did not change with repeated suit inflation. The symptomatic response was remarkably slight even when the suit was inflated with the subjects in the head-down position; there was no evidence of the " marked sense of suffocation " described by MacKay [1943] following the release of tourniquets around the lower limbs. A change of pulmonary compliance would also affect expiratory reserve.…”

Respiratory responses to the inhalation of oxygen at atmospheric pressure in normal subjects and in cases of congenital heart disease*

“…If the hyperventilation with oxygen can be explained in terms of a local accumulation of carbon dioxide in the tissues of the respiratory centre, as has been suggested by Lambertsen et al (1953), a fall in alveolar carbon dioxide concentration would be expected. MacKay (1943) has suggested that a change in pulmonary flow can also alter alveolar carbon dioxide concentration independently of changes in ventilation. There is some evidence that oxygen brings about a small reduction in cardiac output (Whitehorn, Edelmann & Hitchcock, 1946;Dripps & Comroe, 1947), but it seems unlikely that relative over-ventilation persists for more than the immediate period of adjustment in pulmonary flow.…”