TO ACUTE HYPOXIA

C.J. Lambertsen, R. Gelfand, and E. Hopkin
Environmental Biomedical Stress Data Center, Institute for Environmental Medicine, University of Pennsylvania,
Philadelphia, PA. 19104-6068

Closed atmospheres in compartments of space vehicles or stations contain controlled levels of oxygen, and inert gas
and metabolically produced carbon dioxide. The present program has related to potential situations involving
accidental or purposeful (e.g. emergency) reduction of O2 content or ambient pressure in short or extended space
missions (4, 2). It is known that addition of carbon dioxide to a severely hypoxic inspired gas can prevent or delay
loss of consciousness (11, 5, 7). The purposes of the present program have been to obtain measurements defining
rates and degrees of major physiologic alterations induced by moderate abrupt inspiratory hypoxia, and the
physiologic alleviations of systemic acute hypoxia provided when systemic hypocapnia is prevented by addition of
carbon dioxide to the inspired gas.

The scope of studies comparing effects of hypoxia alone and with prevention of hypoxic hypocapnia has included
correlated measurements of dynamic changes in pulmonary ventilation, middle cerebral artery blood flow velocity,
arterial blood hemoglobin oxygen saturation, cardiac rate and output, and end-tidal CO2 and O2 partial pressures.
Related effects on specific mental functions were derived from brief stable state exposures (10). The slowly
developing multiple physiologic adaptations which occur during prolonged exposure to hypoxia (acclimatization)
(9,1) are relevant to but were not part of this study of acute responses to abrupt hypoxic exposures.

Studies were performed on groups of normal male subjects, semi-recumbent at rest and with cyclic leg ergometer.
Subjects were familiarized with instrumentation, but not informed of specific timing or changes in composition of
inspired gases. Measurements included: for pulmonary ventilation (Pneumotachygraph); for cardiac rate and output
(Impedence Cardiography); for middle cerebral artery blood flow velocity (Transcranial Doppler Flowmeter); for
arterial blood hemoglobin saturation (Pulse Oximeter); for end-tidal alveolar gas (Infra-red CO2 Analyzer and
Zirconia electrochemical cell O2 Analyzer); for mental function (multiple test types, including Arithmetic Tests of
Multiplication and Division). Physiologic data for dynamic states of effect and recovery on simultaneously
measured functions were stored at The Environmental Biomedical Stress Data Center for subsequent correlation
analyses and modeling.

The Graphic Summary of results represented by the sequence of Figures 1 to 9 describes patterns of related mental,
respiratory, oxygenation, and cardiovascular functions inherent in the acute hypoxic stress, and their modifications
by prevention of the forms of arterial and tissue hypocapnia associated with inspiratory hypoxia. Four % inspired
CO2 largely accomplished this aim, in both rest and moderate exercise states.

         Mental Function. The composite physiologic experiments series were preceded by measurements of mental
performance, to establish a degree of inspiratory hypoxia alone which would produce a distinct decrease in a
definable mental ability (10). Statistically significant reduction of performance test scores (Composite of Choice
Reaction Time, Visual Digit Span, Mathematical Operations, Time Reproduction) occurred during acute exposures
to 10% inspired O2 at 1 ATA at rest, but not while breathing 12% O2 (Figure 2). This reduction of test score was not
exaggerated by sequential periods of physical (leg) exercise at 50 Watts and at 100 Watts intensity (10). In a
separate series of subjects the reduction of arithmetic performance test scores by hypoxia was prevented by
including 4% CO2 with the 10% O2 in N2 inspired gas mixture (12).

        CO2 - Hypoxia Physiologic Interactions. Purposes of integration have included quantitative modeling of the
acute physiologic adaptations produced by two degrees of hypoxic inspiratory O2 concentration (10%, 12%) at 1

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ATA, at Rest and in graded Physical Work ( Figure 1). Each hypoxic situation included hypoxia alone and with
addition of 4% inspiratory CO2 to prevent hypocapnia and provide rapid stabilization of arterial hemoglobin
saturation. The effects of hypoxia and the natural consequent development of hypocapnia have direct relation to
normal neurogenic respiratory and cardiovascular control functions, and their influences on the internal systemic
oxygen and carbon dioxide environments (3, 6, 9). The correction of systemic hypocapnia is accompanied by an
increased pulmonary respiration which simultaneously provides improvement in arterial, systemic and brain
oxygenation (8) and sustains composite mental and physical performance in a stable degree of tolerable atmospheric

         The sequence of attached Figures 3 to 9 was obtained on the same subjects during the same respiratory
exposures to inspiratory hypoxia, with or without associated increase of inspiratory CO2. Details of individual
subject responses are retained in accessible form within the Environmental Biomedical Stress Data Center for
applications to predictive modeling, and as a base for investigations of other closed atmospheric systems and
durations of exposures. (Supported by NASA Grants NAG5-6200 and NAG5-4274.)

Dual purposes include: (a) Long term accessible incorporation, within the Environmental Biomedical Stress Data
Center, of dynamic and stable state responses of individuals and subject groups to acute inspiratory atmospheric
hypoxia, with and without modulation by low degrees of inspired carbon dioxide concentration. (b) Use of related
assets of Environmental Biomedical Stress Data Center for generating predictive relations of inspired CO2 and
exercise-generated CO2 as brain and arterial blood oxygenation, in sustained (multi-week) exposures to combined
hypoxic and hypercapneic atmospheres.

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10.            Gelfand, R., C.J. Lambertsen, and B. Youdelman. Mental performance at rest and in exercise with inspired O2
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               (Abstract). Undersea and Hyperbaric Med. 24(S): 18, 1997.
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