Effects of Posture on Alveolar‐Arterial CO₂ and O₂ Differences and on Alveolar Dead Space in Man

Abstract

BJURSTEDT, H., C. M. HESSER, G. LILJESTRAND and G. MATELL. Effects of posture on alveolar-arterial CO, and 0, differences and on alveolar dead space in man. Acta physiol. scand. 1962. 54. 65-82. -The increase in ventilation and lowering of the end-tidal Pco, after changing from the supine to the standing position were observed to be associated with a significant rise in the arterial to end-tidal CO, tension difference (average + 2.1 mm Hg) in addition to an increased effective alveolar to arterial 0, tension difference (+ 4.8 mm Hg). All dead spaces increased, the alveolar dead space (= the physiological minus the anatomical dead space) on an average by 28 ml. Assuming an unchanged distribution of ventilation this can be expressed as corresponding to 6 per cent of the alveoli being unperfused. A lowering of the alveolar Pco2 during standing is thus in part due to an increased arterial to end-tidal GO, tension difference. The end result is also influenced by a certain metabolic acidosis (average decrease in BHCO,B, 7 0.6 mM/l), in addition to peripheral retention of CO,. The Eff. VA/VE ratio decreased in all subjects, indicating a decline in the respiratory gas exchange efficiency by an average of 6 per cent. The changes observed may be explained as a consequence of the influence of gravityon the blood flow and its distribution not only in the systemic but also in the pulmonary circulation. Already in 1914 LILJESTRAND a n d WOLLIN showed that the alveolar CO, tension in m a n is lower during motionless standing than in the supine position. These authors had also confirmed a n d extended the old observation that assuming the up-right position calls forth a n increase in the pulmonary ventilation (cf. LILJESTRAND and WOLLIN 1913). Both the lowered alveolar 5-623015. Acta physiol. scand. Vol. 54. 65 66 H. BJURSTEDT ET A L .C:O, tension and the increase in pulmonary ventilation have been confirmed in numerous investigations (d. The mechanisms underlying the fall in the alveolar (20, and the increase in pulmonary ventilation after changing from the supine to the standing position are not fully understood. T h e former effect cannot be explained xilelj-b y an increased blowing off of CO, b y the hyperventilation, since the amount of C 0 2 eliminated during several minutes of motionless standing does not exceed the 0, uptake, as demonstrated b y HITCHCOCK and FER-GUSON as well as by RAHS and AXENT. These authors referred the lowered alveolar Pc:p2 during standing to impaired CO, elimination from the lungs, caused by the decrease in cardiac output with a concomitant CO, retention in the tissues and in venous blood, especially in the lo\ver portion of the body.By using special tecliniqucs for the continuous and simultaneous recording of blood gas changes 011 the centrifuge, rather drastic changes in the pulmonary circulation and gas exchange have been observed, both in the dog ;BARK, BJVRSTEDT and COLERIDGE 1959) and in man (BARR 1961 a). I n the espcriments to be reported beloiv, using similar techniques on the tilt-tabl...

Effects of Pulmonary Vascular Congestion on Postural Changes in the Perfusion and Filling of the Pulmonary Vascular Bed*

“…Furthermore, the ratio VD/VT increased in the normal group, whereas it did not in the hypertensive group. It would seem, therefore, that the difference in VD response to tilting in these two groups is related to pulmonary hypertension and is quite compatible with the suggestion made by Riley and co-workers (25) and by Bjurstedt and co-workers (26).…”

“…Severinghaus and Stupfel (33) have examined the problem of a-A CO2 gradients and alveolar dead space in detail, and in general they relate a-A CO2 gradient and alveolar dead space to changes in distribution of lung perfusion. Bjurstedt and co-workers (26) and Matell (34) found that the arterial-end-tidal CO2 gradient of normal upright men averaged 2 to 3 mm Hg. In the present study, the a-A CO2 gradient was 3.9 ± 1.5 mm Hg, and alveolar dead space was 64 ± 33 ml in a group of normal men upright on a bicycle saddle with their legs dangling (Table V).…”

Cerebral Autoregulatory Responses to Head-Up Tilt in Normal Subjects and Patients With Recurrent Vasovagal Syncope

“…6 -12 Arterial, end-tidal, and transcutaneous CO 2 levels have also been shown to fall significantly in normal subjects immediately after head-up tilt, [12][13][14][15][16] and Cencetti et al 12 showed a significant link between the declines in CBFV and CO 2 after head-up tilt. Despite the fall in CBFV during orthostatic stress, its effect on dynamic CA is unclear, with both intact 17,18 and impaired 19 CA being reported in normal subjects.…”

Cerebral blood flow during orthostasis: role of arterial CO2

“…These data suggest that factors in addition to a reduction in PaCO 2 play a role in the CBF response to orthostatic stress. transcranial Doppler; cerebral vasoconstriction; head-up tilt IT HAS BEEN WIDELY NOTED that orthostatic stress in humans decreases end-tidal PCO 2 (PET CO 2 ) or arterial PCO 2 (Pa CO 2 ) (1,4,17,27,36,38,41). Because Pa CO 2 is known to be critical in control of cerebral blood flow (CBF) (30), decreased Pa CO 2 during tilt could play a role in orthostatic intolerance through inappropriate cerebral vasoconstriction.…”