Changes in alveolar and arterial gas tensions as related to altitude and age

Abstract

In the summer of 1962 at the White Mountain Research Station the early phases of altitude acclimatization were studied in six of the surviving eight members of the 1935 expedition to the Chilean Andes; they were from 58 to 71 years of age. Alveolar and arterial Po2 and Pco2 were determined for each man a few hours after arrival at 3,093 m and at 3,800 and 4,343 m over the next few days. The effects of age were superimposed on the classical responses to high altitude. The arterial and alveolar Pco2 values showed no significant gradient; the alveolar Pco2 was found to be lower for a given altitude than 27 years before. For example, their average alveolar Pco2 at 4,700 m in 1935 was 27.7 mm Hg as opposed to 25.1 mm Hg at 4,343 m in 1962. The case of Hall was exceptional: his alveolar Pco2 ranged from 21 to 24 mm Hg regardless of altitude for his sojourn of 22 days. In 1935 these six men had a mean A-a Po2 gradient of +3.0 mm Hg at 4,700 m, while in 1962 the gradient over the three altitudes was +12.4 mm Hg. These findings would likely be explained partially by age changes in the pulmonary ventilation-perfusion ratio. acclimatization; pulmonary ventilation-perfusion ratio; alveolar-arterial Po2 and Pco2 gradients; alveolar hyperventilation; aging and altitude Submitted on February 19, 1963

Diagnostic value of serum angiotensin converting enzyme activity in lung diseases.

“…Increased closure of the dependent small airways in the tidal volume range, with a subsequent fall in the oxygen tension of these alveoli, is a wellknown concomitant of increasing age (Terman and Newton, 1964;Holland et al, 1968).…”

Arterial Oxygen Tension in Relation to Age in Healthy Subjects

“…[14] T h e fa c to rs resp o n sib le fo r th is sy s te m a tic decline of a rte ria l o x y gen te n sio n w ith in c re a sin g age are n o t y e t fully e lu c id a te d , th o u g h som e c o n sid e ra tio n s can be m a d e : a rte ria l h y p o x a e m ia is n o to rio u sly cau sed b y a lv e o la r h y p o v e n tila tio n or by an e x ag g eratio n of th e (r = -0 . fa c to rs resp o n sib le in y o u n g su b je c ts for an a lv e o la r-a rte ria l oxygen g ra d ie n t. E x p e rim e n ta l d a ta to su p p o rt the p resen ce o f an alv eo lar h y p o v e n tila tio n in th e ag ed are la c k in g [9] while an in c re a sin g alv eo la r-a rte ria l 0 2 te n sio n d ifference w ith age has been d e m o n s tra te d [3,13,27,29,17].…”

The impact of age on cerebral perfusion, oxygenation and metabolism during exercise in humans

“…Indeed, the provision of supplemental CO 2 during high intensity exercise in young healthy participants, in order to prevent the hyperventilation-mediated fall in P aCO 2 and maintain the partial pressure of end-tidal CO 2 (P ETCO 2 ) at 50 mmHg, increases MCA V mean by ß40% and cerebral oxygenation by ß15% (Subudhi et al 2011). Some studies have observed that elderly individuals have a reduced P aCO 2 and P ETCO 2 (Terman & Newton, 1964;Fisher et al 2013;Flück et al 2014). To assess influence of the age-related reduction in P aCO 2 on the cerebral circulatory responses to exercise, Flück et al (2014) administered supplemental CO 2 to the inspired air (when P aCO 2 dropped below 40 mmHg) in order to prevent a hyperventilation-mediated reduction in P aCO 2 during incremental exhaustive leg cycling in healthy young and older individuals.…”

“…). Some studies have observed that elderly individuals have a reduced and (Terman & Newton, ; Fisher et al . ; Flück et al .…”