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Background and Objective: The COVID-19 pandemic magnified the importance of gas exchange abnormalities in early respiratory failure. Pulse oximetry (SpO2) has not been universally effective for clinical decision-making, possibly because of limitations. The alveolar gas monitor (AGM100) adds exhaled gas tensions to SpO2 to calculate the oxygen deficit (OD). The OD parallels the alveolar-to-arterial oxygen difference (AaDO2) in outpatients with cardiopulmonary disease. We hypothesized that the OD would discriminate between COVID-19 patients who require hospital admission and those who are discharged home, as well as predict need for supplemental oxygen during the index hospitalization. Methods: Patients presenting with dyspnea and COVID-19 were enrolled with informed consent and had OD measured using the AGM100. The OD was then compared between admitted and discharged patients and between patients who required supplemental oxygen and those who did not. The OD was also compared to SpO2 for each of these outcomes using receiver operating characteristic (ROC) curves. Results: Thirty patients were COVID-19 positive and had complete AGM100 data. The mean OD was significantly (p = 0.025) higher among those admitted 50.0 ± 20.6 (mean ± SD) vs. discharged 27.0 ± 14.3 (mean ± SD). The OD was also significantly (p < 0.0001) higher among those requiring supplemental oxygen 60.1 ± 12.9 (mean ± SD) vs. those remaining on room air 25.2 ± 11.9 (mean ± SD). ROC curves for the OD demonstrated very good and excellent sensitivity for predicting hospital admission and supplemental oxygen administration, respectively. The OD performed better than an SpO2 threshold of <94%. Conclusions: The AGM100 is a novel, noninvasive way of measuring impaired gas exchange for clinically important endpoints in COVID-19. [ABSTRACT FROM AUTHOR]

Compare and contrast strategies remain common pedagogical practices within physiological education. With the support of an American Physiological Society Teaching Career Enhancement Award, we have developed a junior- or senior-level undergraduate curriculum for exercise physiology that compares and contrasts the physiological adaptations of chronic terrestrial exercise (TEx) and microgravity ([mu]G). We used a series of peer-reviewed publications to demonstrate that many of the physiological adaptations to TEx and [mu]G are opposite. For example, TEx typically improves cardiovascular function and orthostatic tolerance, whereas [mu]G can lead to declines in both. TEx leads to muscle hypertrophy, and [mu]G elicits muscle atrophy. TEx increases bone mineral density and red blood cell mass, whereas [mu]G decreases bone mineral density and red blood cell mass. Importantly, exercise during spaceflight remains a crucial countermeasure to limit some of these adverse physiological adaptations to [mu]G. This curriculum develops critical thinking skills by dissecting peer-reviewed articles and discussing the strengths and weaknesses associated with simulated and actual [mu]G studies. Moreover, the curriculum includes studies on both animals and humans, providing a strong translational component to the curriculum. In summary, we have developed a novel space physiology curriculum delivered during the final weeks of an exercise physiology course in which students gain critical new knowledge that reinforces key concepts presented throughout the semester.

The mechanics of breathing has always been a difficult topic for some medical and graduate students. The subject is very quantitative and contains a number of concepts that some students have trouble with, including physical principles such as pressure, flow, volume, resistance, elasticity, and compliance. Apparently, present-day students find the subject more difficult than students of 20 years ago. A possible reason for this is that the teaching of elementary physics in high school and college is now given less emphasis, whereas other topics, such as molecular biology, receive a great deal of attention. Another factor may be that many of us grew up building radios and other such devices, whereas modern students tend to plug in an electronic unit with little idea of its function. Some examples of misconceptions of present-day students who have taken our course are given. To help the weaker students, we now include a primer at the beginning of our handout for the course that covers simple physical principles. Examples of some of the most difficult concepts for students are given. (Contains 17 figures.)

A complete course of respiratory physiology suitable for first-year medical and graduate students has been placed on the Web for our own students and for other educational institutions. There are several reasons for doing this. The first is that the modern-day student uses a variety of options for acquiring knowledge. These include attending lectures, reading texts, iPod downloads, and surfing the internet. This Web-based course is another option that may be preferable for some students. A second reason is that it is becoming increasingly difficult for some medical schools to find faculty members who are willing and able to teach the principles of respiratory physiology. This is a potentially serious problem because a sound knowledge of respiratory physiology will always be necessary for the intelligent practice of medicine. Schools with limited faculty may find it useful to use these Web-based lectures followed by a discussion session with students. Another reason is that some schools have moved away from systematic lectures to case-based discussions, with the possibility that students will not be exposed to some of the principles of respiratory physiology. The hope is that this comprehensive course of lectures will help students to assimilate this important material as the medical school curriculum continues to expand at a rapid rate. (Contains 1 table.)

West JB. Comparative physiology of the pulmonary blood-gas barrier: the unique avian solution. Am J Physiol Regul Integr Comp Physiol 297: R1625-R1634, 2009. First published September 30, 2009; doi: 10.1152/ajpregu.00459.2009.--Two opposing selective pressures have shaped the evolution of the structure of the blood-gas barrier in air breathing vertebrates. The first pressure, which has been recognized for 100 years, is to facilitate diffusive gas exchange. This requires the barrier to be extremely thin and have a large area. The second pressure, which has only recently been appreciated, is to maintain the mechanical integrity of the barrier in the face of its extreme thinness. The most important tensile stress comes from the pressure within the pulmonary capillaries, which results in a hoop stress. The strength of the barrier can be attributed to the type IV collagen in the extracellular matrix. In addition, the stress is minimized in mammals and birds by complete separation of the pulmonary and systemic circulations. Remarkably, the avian barrier is about 2.5 times thinner than that in mammals and also is much more uniform in thickness. These advantages for gas exchange come about because the avian pulmonary capillaries are unique among air breathers in being mechanically supported externally in addition to the strength that comes from the structure of their walls. This external support comes from epithelial plates that are part of the air capillaries, and the support is available because the terminal air spaces in the avian lung are extremely small due to the flow-through nature of ventilation in contrast to the reciprocating pattern in mammals. evolution; pulmonary circulation; gas exchange; type IV collagen; wall stress; stress failure; respiratory physiology doi: 10.1152/ajpregu.00459.2009.

The gas exchanging region in the avian lung, although proportionally smaller than that of the mammalian lung, efficiently manages respiration to meet the high energetic requirements of flapping flight. Gas exchange in the bird lung is enhanced, in part, by an extremely thin blood-gas barrier (BGB). We measured the arithmetic mean thickness of the different components (endothelium, interstitium, and epithelium) of the BGB in the domestic chicken lung and compared the results with three mammals. Morphometric analysis showed that the total BGB of the chicken lung was significantly thinner than that of the rabbit, dog, and horse (54, 66, and 70% thinner, respectively) and that all layers of the BGB were significantly thinner in the chicken compared with the mammals. The interstitial layer was strikingly thin in the chicken lung (~86% thinner than the dog and horse, and 75% thinner than rabbit) which is a paradox because the strength of the BGB is believed to come from the interstitium. In addition, the thickness of the interstitium was remarkably uniform, unlike the mammalian interstitium. The uniformity of the interstitial layer in the chicken is attributable to a lack of the supportive type I collagen cable that is found in mammalian alveolar lungs. We propose that the surrounding air capillaries provide additional structural support for the pulmonary capillaries in the bird lung, thus allowing the barrier to be both very thin and extremely uniform. The net result is to improve gas exchanging efficiency. capillary stress failure; lung morphology; bird respiratory physiology; air capillary; extracellular matrix; interstitium

I. Introduction II. Design of the Blood-Gas Barrier for Gas Exchange A. Flux of oxygen across the blood-gas barrier, biophysical factors and quantitative considerations B. Comparative observations on the structure [...]

The pulmonary blood-gas barrier is an extraordinary structure because of its extreme thinness, immense strength, and enormous area. The essential components of the barrier were determined early in evolution and have been highly conserved. For example, the barriers of the African, Australian, and South American lungfish that date from as much as 400 million years ago have essentially the same structure as in the modern mammal or bird. In the evolution of vertebrates from bony fishes through amphibia, reptiles, and ultimately mammals and birds, changes in the pulmonary circulation occurred to limit the stresses in the blood-gas barrier. Only in mammals and birds is there a complete separation of the pulmonary and systemic circulations, which is essential to protect the extremely thin barrier from the necessary high-vascular pressures. To provide the blood-gas barrier with its required strength, evolution has exploited the high ultimate tensile strength of type IV collagen in basement membrane. Nevertheless, stress failure of the barrier occurs under physiological conditions in galloping Thoroughbred racehorses and also apparently in elite human athletes at maximal exercise. The human blood-gas barrier maintains its integrity during all but the most extreme physiological conditions. However, many pathological conditions cause stress failure. The structure of the blood-gas barrier is apparently continually regulated in response to wall stress, and this regulation is essential to maintain the extreme thinness but adequate strength. The mechanisms of this regulation remain to be elucidated and constitute one of the fundamental problems in lung biology. vertebrate evolution; stress failure; type IV collagen; exercise-induced pulmonary hemorrhage; lung overinflation; pulmonary circulation

The pulmonary capillaries of neonatal lungs are potentially vulnerable to stress failure because of the complex changes in the pulmonary circulation that occur at birth. We studied the ultrastructure of the blood-gas barrier (BGB) in premature and 1-day-old rabbit lungs and compared it with the ultrastructure of adult lungs. Normal gestation of rabbits is 30 days. After extensive pilot measurements, three premature (27 days gestation) and three newborn (1 day old) rabbit lungs were perfusion-fixed at arterial, venous, and airway pressures of 25, 0, and 10 cm[H.sub.2]O, respectively, and the measurements were compared with those of three adult lungs. The thickness of the capillary endothelium, alveolar epithelium, and interstitium of the BGB was measured at right angles to the barrier at random points. A striking finding was the large number of measurements of the interstitial thickness in 1-day-old lungs that were very thin (0-0.1 [micro]m). The percentages of occurrence of very thin interstitium in premature, 1-day-old, and adult lungs were 35.3 [+ or -] 9.4, 71.7 [+ or -] 5.2, and 43.0 [+ or -] 2.6, respectively (P < 0.02 for 1 day old vs. premature and adult). Given the previously found relationship between stress failure and interstitial thickness, this large proportion of very thin interstitial layers in the capillaries of 1-day-old lungs is a reasonable explanation for their previously demonstrated vulnerability to stress failure. lung morphology; capillary stress; stress failure; pulmonary edema; pulmonary hemorrhage

The pulmonary capillaries of neonatal lungs are potentially vulnerable to stress failure because of the complex changes in the pulmonary circulation that occur at birth. We perfusion fixed the lungs from nine anesthetized newborn rabbits at capillary transmural pressures ([P.sub.tm]) of 5 [+ or -] 5, 10 [+ or -] 5, and 15 [+ or -] 5 cm[H.sub.2]O. Normal microscopic appearances were seen at [P.sub.tm] values of 5 [+ or -] 5 and 10 [+ or -] 5 cm[H.sub.2]O, but massive airway edema was observed in lungs perfused at a [P.sub.tm] of 15 [+ or -] 5 cm[H.sub.2]O. Consistent with this, no disruptions of the alveolar epithelium were observed at [P.sub.tm] values of 5 [+ or -] 5 cm[H.sub.2]O, but mean values of 0.11 and 1.22 breaks/mm epithelium were found at [P.sub.tm] of 10 [+ or -] 5 and 15 [+ or -] 5 cm[H.sub.2]O, respectively (P < 0.05 for 5 [+ or -] 5 vs. 15 [+ or -] 5 cm[H.sub.2]O). These pressures are in striking contrast to those in the adult rabbit in which, by a similar procedure, a [P.sub.tm] of 52.5 cm[H.sub.2]O, is required before stress failure is consistently seen. We conclude that stress failure of pulmonary capillaries in newborn rabbit lungs can occur at [P.sub.tm] values of less than one-third of those that are required in adult lungs. neonatal lung; lung morphometry; capillary wall stress; stress failure

The efficiency of pulmonary gas exchange has long been assessed using the alveolar-arterial difference in PO2, the A-aDO2, a construct developed by Richard Riley ~70years ago. However, this measurement is invasive (requiring an arterial blood sample), time consuming, expensive, uncomfortable for the patients, and as such not ideal for serial measurements. Recent advances in the technology now provide for portable and rapidly responding measurement of the PO2 and PCO2 in expired gas, which combined with the well-established measurement of arterial oxygen saturation via pulse oximetry (SpO2) make practical a non-invasive surrogate measurement of the A-aDO2, the oxygen deficit. The oxygen deficit is the difference between the end-tidal PO2 and the calculated arterial PO2 derived from the SpO2 and taking into account the PCO2, also measured from end-tidal gas. The oxygen deficit shares the underlying basis of the measurement of gas exchange efficiency that the A-aDO2 uses, and thus the two measurements are well-correlated (r 2~0.72). Studies have shown that the new approach is sensitive and can detect the age-related decline in gas exchange efficiency associated with healthy aging. In patients with lung disease the oxygen deficit is greatly elevated compared to normal subjects. The portable and non-invasive nature of the approach suggests potential uses in first responders, in military applications, and in underserved areas. Further, the completely non-invasive and rapid nature of the measurement makes it ideally suited to serial measurements of acutely ill patients including those with COVID-19, allowing patients to be closely monitored if required. [ABSTRACT FROM AUTHOR]

Weightlessness appears to alter some aspects of lung function but not enough to cause serious effects. This was the conclusion of a study of 8 members of the Spacelab, which is carried in the payload bay of the space shuttle. While they were in the Spacelab, the astronauts used machines to measure various aspects of lung function. The lung surface area where gas exchange takes place increased as did the output of the heart. The lung was more uniformly ventilated than it is under gravity. Many of the changes confirmed that the lungs are sensitive to gravity., The lung is exquisitely sensitive to gravity, and so d is of interest to know how its function is altered in the weightlessness of space. Studies on National Aeronautics nautics and Space Administration (NASA) Spacelabs during the last 4 years have provided the first comprehensive data on the extensive changes in pulmonary function that occur in sustained microgravity. Measurements of pulmonary function were made on astronauts during space shuttle flights lasting 9 and 14 days and were compared with extensive ground-based measurements before and after the flights. Compared with preflight measurements, cardiac output increased by 18% during space flight, and stroke volume increased by 46%. Paradoxically, the increase in stroke volume occurred in the face of reductions in central venous pressure and circulating blood volume. Diffusing capacity increased by 28% and the increase in the diffusing capacity of the alveolar membrane was unexpectedly large based on findings in normal gravity. The change in the alveolar membrane may reflect the effects of uniform filling of the pulmonary capillary bed. Distributions of blood flow and ventilation throughout the lung were more uniform in space, but some unevenness remained, indicating the importance of nongravitational factors. A surprising finding was that airway closing volume was approximately the same in microgravity and in normal gravity, emphasizing the importance of mechanical properties of the airways in determining whether they close. Residual volume was unexpectedly reduced by 18%, in microgravity, possibly because of uniform alveolar expansion. The findings indicate that pulmonary function is greatly altered in microgravity, but none of the changes observed so far will apparently limit long-term space flight. in addition, the data help to clarify how gravity affects pulmonary function in the normal gravity environment on Earth. JAMA 1997;277:1957-1961

West, John B. High altitude limits of living things. High Alt Med Biol. 22:342–345, 2021.—The tolerance of animals to high altitude is generally limited by the low partial pressure of oxygen (PO2) in the air. Plant growth at high altitude is also limited but by different mechanisms. This article is a brief survey of the limiting factors of all living things. By a curious coincidence, the highest point on earth, that is Mt. Everest at 8,848 m, appears to be right at the limit of human tolerance to hypoxia. The altitude of the highest permanent human habitation, that is a town, is 5,100 m. This altitude is partly determined by the hypoxia, but also by economic factors. For other terrestrial mammals, birds, and insects, the highest altitudes for permanent habitation apparently belong to field mice (Phyllotis xanthopygus rupestris) and jumping spiders (Euophrys omnisuperstes) at about 6,700 m. Birds have been known to fly as high as 11,000 m although how much they are elevated by atmospheric updrafts is not clear. The record for animals for survival in extreme hypoxia is arguably held by the primitive invertebrate, the tardigrade (Hypsibius dujardini). This has been shown to tolerate the hard vacuum of space where the PO2 is essentially zero for many days. Less is known about the tolerance of plants to extreme altitude. However, vascular plants have been collected at >6,000 m in the Himalayas, and moss grows even higher. Lichens are very tolerant of severe hypoxia. There is evidence that global warming is increasing the highest altitudes at which plants can survive. [ABSTRACT FROM AUTHOR]

Alexander von Humboldt (1769–1859) was one of the most distinguished German scientists of the late 18th and early 19th centuries. His fame came chiefly from his extensive explorations in South America and his eminence as a plant naturalist. He attempted to climb the inactive volcano Chimborazo in Ecuador, which was thought to be the highest mountain in the world at the time, and he reached an altitude of about 5,543 m, which was a record height for humans. During the climb, he had typical symptoms of acute mountain sickness, which he correctly attributed to the low level of oxygen, and he was apparently the first person to make this connection. His ability as a naturalist enabled him to recognize the effect of high altitude on the distribution of plants, and by comparing his observations on Chimborazo with those in the European Alps and elsewhere, he inferred that the deleterious effects of high altitude were universal. During his return trip to Europe, he called on President Thomas Jefferson in Washington, where he was given a warm reception, and discussed conservation issues. He then returned to Paris, where he produced 29 volumes over a period of 31 years describing his travels. Here the effects of high altitude on the distribution of plants compared with animals are briefly reviewed. Following Humboldt’s death in 1859, there was extensive coverage of his contributions, but curiously, his fame has diminished over the years, and inexplicably, he now has a lower profile in North America. [ABSTRACT FROM AUTHOR]

As earthlings, we take the oxygen in the air that we breathe for granted. Few people realize that this easy access to oxygen makes us unique in the whole universe. Nowhere else in our planetary system or in distant stars has stable oxygen ever been detected. However, the present plentiful supply of oxygen in our atmosphere was not always there. Long after the Earth was formed some 4.5 billion years ago, the PO2 in the atmosphere was near zero, and it remained so for millions of years. But about 2 billion years ago, the PO2 dramatically increased to as high as 200 mmHg during the Great Oxygen Event, due to the activity of microorganisms, the cyanobacteria. Subsequently, the oxygen level fell to the intermediate values that we have today. Here, we also look to the future, for example, the next 50 years. This period will be special because it will include the beginnings of human space exploration, initially to the Moon and Mars. Neither of these has atmospheric oxygen. Nevertheless, plans to visit and live on both of these are developing rapidly. We consider the fascinating problems of how to ensure that sufficient oxygen will be available for the groups of people. Although it is interesting to discuss these issues now, we can expect that major advances will be made in the next few years. [ABSTRACT FROM AUTHOR]

When using a new noninvasive method for measuring the efficiency of pulmonary gas exchange, a key measurement is the oxygen deficit, defined as the difference between the end-tidal alveolar PO2 and the calculated arterial PO2. The end-tidal PO2 is measured using a rapid gas analyzer, and the arterial PO2 is derived from pulse oximetry after allowing for the effect of the PCO2 on the oxygen affinity of hemoglobin. In the present report we show that the values of end-tidal PO2 and PCO2 are highly reproducible, providing a solid foundation for the measurement of the oxygen deficit. We compare the oxygen deficit with the classical ideal alveolar-arterial PO2 difference (A-aDO2) as originally proposed by Riley, and now extensively used in clinical practice. This assumes Riley’s criteria for ideal alveolar gas, namely no ventilation-perfusion inequality, the same PCO2 as arterial blood, and the same respiratory exchange ratio as the whole lung. It transpires that, in normal subjects, the end-tidal PO2 is essentially the same as the ideal value. This conclusion is consistent with the very small oxygen deficit that we have reported in young normal subjects, the significantly higher values seen in older normal subjects, and the much larger values in patients with lung disease. We conclude that this noninvasive measurement of the efficiency of pulmonary exchange is identical in many respects to that based on the ideal alveolar PO2, but that it is easier to obtain. [ABSTRACT FROM AUTHOR]

When using a new noninvasive method for measuring the efficiency of pulmonary gas exchange, a key measurement is the oxygen deficit, defined as the difference between the end-tidal alveolar PO2 and the calculated arterial PO2. The end-tidal PO2 is measured using a rapid gas analyzer, and the arterial PO2 is derived from pulse oximetry after allowing for the effect of the PCO2 on the oxygen affinity of hemoglobin. In the present report we show that the values of end-tidal PO2 and PCO2 are highly reproducible, providing a solid foundation for the measurement of the oxygen deficit. We compare the oxygen deficit with the classical ideal alveolar-arterial PO2 difference (A-aDO2) as originally proposed by Riley, and now extensively used in clinical practice. This assumes Riley’s criteria for ideal alveolar gas, namely no ventilation-perfusion inequality, the same PCO2 as arterial blood, and the same respiratory exchange ratio as the whole lung. It transpires that, in normal subjects, the end-tidal PO2 is essentially the same as the ideal value. This conclusion is consistent with the very small oxygen deficit that we have reported in young normal subjects, the significantly higher values seen in older normal subjects, and the much larger values in patients with lung disease. We conclude that this noninvasive measurement of the efficiency of pulmonary exchange is identical in many respects to that based on the ideal alveolar PO2, but that it is easier to obtain. [ABSTRACT FROM AUTHOR]

The oxygen deficit (OD) is the difference between the end-tidal alveolar Po2 and the calculated Po2 of arterial blood based on measured oxygen saturation that acts as a proxy for the alveolar-arterial Po2 difference. Previous work has shown that the alveolar gas meter (AGM100) can measure pulmonary gas exchange, via the OD, in patients with a history of lung disease and in normal subjects breathing 12.5% O2. The present study measured how the OD varied at different values of inspired O2. Healthy subjects were split by age (young 22–31; n = 23; older 42–90; n = 13). Across all inspired O2 levels (12.5, 15, 17.5, and 21%), the OD was higher in the older cohort 10.6 ± 1.0 mmHg compared with the young −0.4 ± 0.6 mmHg (P < 0.0001, using repeated measures ANOVA), the difference being significant at all O2 levels (all P < 0.0001). The OD difference between age groups and its variance was greater at higher O2 values (age × O2 interaction; P = 0.002). The decrease in OD with lower values of inspired O2 in both cohorts is consistent with the increased accuracy of the calculated arterial Po2 based on the O2-Hb dissociation curve and with the expected decrease in the alveolar-arterial Po2 difference due to a lower arterial saturation. The persisting higher OD seen in older subjects, irrespective of the inspired O2, shows that the measurement of OD remains sensitive to mild gas exchange impairment, even when breathing 21% O2. [ABSTRACT FROM AUTHOR]

Fritz Rohrer (1888–1926) has a special place in the history of respiratory physiology for two reasons. The first is that he laid the foundations of modern pulmonary mechanics in the early 1900s. For example, his seminal paper on pulmonary dynamics, that is, the pressure-flow relationships in the airways, was published in 1915 in one of the top journals in the field. It included extensive measurements of airway dimensions in postmortem human lungs and a sophisticated analysis of the modes of airflow. This was closely followed by a very original analysis of lung statics, which included studies of airway pressures at normal, maximal, and minimal lung volumes in relaxed normal volunteers, and was published in 1916. Remarkably, both papers were essentially ignored at the time. Fortunately, in 1925 he was able to summarize his major findings in a chapter in an important handbook of physiology. However, he tragically died from pulmonary tuberculosis in the following year at the early age of 37. The second reason for his importance in the history of pulmonary mechanics is that inexplicably his very innovative research was essentially ignored for about 30 years. It was not until the 1940s that his work was rediscovered, although not in time to save investigators from duplicating his very original studies. Possible reasons why his work was ignored for so long are discussed. Even today it is not easy to recover some important features of his career, and some aspects of his very original research are still almost unknown. [ABSTRACT FROM AUTHOR]

The efficiency of pulmonary gas exchange is often assessed by the ideal alveolar-arterial partial pressure difference (A-aDO2). Through a combination of pulse oximetry and rapidly responding gas analyzers to measure the partial pressures of O2 and CO2 in expired gas, one can measure the oxygen deficit. Defined as the difference between the measured alveolar PO2 and the arterial PO2 calculated from SpO2, the oxygen deficit is a substitute for the alveolar-arterial PO2 difference. The oxygen deficit is physiologically reasonable in that it increases with age in healthy subjects and is well correlated with the A-aDO2. To calculate arterial PO2 from saturation, the saturation should be below the very flat upper part of the O2-Hb dissociation curve; good estimates can be made provided the arterial O2 saturation is below ~95%. Since saturations at or above 95% imply reasonably well-maintained gas exchange efficiency, this limitation is of only minor concern. Calculations show that it is necessary to take into account the change in PO2 at a saturation of 50% of the O2-Hb dissociation curve based on the measured alveolar PCO2. As the measurement is designed to be noninvasive, determination of any base excess is not practical, but calculations show that the effect of assuming a zero base excess is modest, with a similar small effect from an abnormal body temperature. Taken together, these results show that a noninvasive assessment of pulmonary gas exchange efficiency can be obtained from subjects with below-normal arterial O2 saturations through a combination of expired O2 and CO2 measurements and SpO2 made during quiet breathing. NEW & NOTEWORTHY The details and limitations of a noninvasive measurement of pulmonary gas exchange efficiency, the oxygen deficit, are described. The oxygen deficit, calculated from expired gas measurements made during quiet breathing coupled with pulse oximetry, is a good surrogate measurement of the ideal alveolar-arterial PO2 difference and does not require arterial blood gas sampling. [ABSTRACT FROM AUTHOR]

Relative partial photoionization cross-sections and angular distribution parameters, β, have been measured for the first, I+(3P2)←I(2P3/2), and fourth, I+(1D2)←I(2P3/2), (5p)-1 photoelectron (PE) bands of atomic iodine, by performing angle-resolved constant-ionic-state (CIS) measurements on these PE bands in the photon energy range 11.0–23.0 eV. Three Rydberg series, two ns and one nd series, which converge to the I+ 3P1 limit at 11.33 eV and four Rydberg series, two ns and two nd series, which converge to the I+ 1D2 limit at 12.15 eV were observed in the first PE band CIS spectra. The fourth band CIS spectrum showed structure in the 12.9–14.1eV photon energy range, which is also seen in the first band CIS spectra. This structure arises from excitation to ns and nd Rydberg states that are parts of series converging to the I+ 1S0 limit we reported on earlier, as well as 5s→5p excitations in the photon energy range 17.5–22.5 eV. These atomic iodine CIS spectra show reasonably good agreement with the equivalent spectra obtained for atomic bromine. The β-plots for the first PE band recorded up to the I+ 3P1 and I+ 1D2 limits only show resonances corresponding to some of the 5p→nd excitations observed in the first band CIS spectra scanned to the I+ 1D2 limit (12.15 eV). These plots are interpreted in terms of an angular momentum transfer model with the positive values of β obtained on resonances corresponding to parity allowed jt=1 and 3 channels and the off-resonance negative β values corresponding to parity unfavored channels, where jt is the quantum number for angular momentum transfer between the molecule, and the ion and photoelectron. The β-plots recorded for iodine are significantly different from those obtained for atomic bromine. Comparison of the experimental CIS spectra and β-plots with available theoretical results highlights the need for higher level calculations which include factors such as configuration interaction in the initial and final states, relativistic effects including spin-orbit interaction, and autoionization via resonant Rydberg states. [ABSTRACT FROM AUTHOR]

Relative partial photoionization cross sections and angular distribution parameters β have been measured for the first and fourth (5p)-1 photoelectron (PE) bands of atomic iodine by performing angle-resolved constant-ionic-state (CIS) measurements on these PE bands between the 1D2 and 1S0 (5p)-1 ionic thresholds in the photon energy region of 12.9–14.1 eV. Rydberg series arising from the 5p→ns and 5p→nd excitations are observed in both the first PE band, I+(3P2)←I(2P3/2), and the fourth PE band, I+(1D2)←I(2P3/2), CIS spectra. For each Rydberg state, the resonance energy, quantum defect, linewidth, line shape, and photoelectron angular distribution parameter β have been determined. For the β-plots for each PE band, only resonances corresponding to 5p→nd excitations are observed; no resonances were seen at photon energies corresponding to the 5p→ns resonances in the CIS spectra. The β-plots are interpreted in terms of the parity unfavored channel with jt=4 being the major contributor at the 5p→nd resonance positions, where jt is the quantum number for angular momentum transferred between the molecule, and the ion and photoelectron. Comparison of the results obtained with those published for bromine shows reasonably good agreement for the CIS spectra but poor agreement for the β-plots. It appears that parity unfavored channels are playing a greater role in the valence (np)-1 ionization of atomic iodine than in the corresponding ionization of atomic bromine. [ABSTRACT FROM AUTHOR]

The angle-resolved photoelectron (PE) spectroscopy technique is employed to study the properties of the reactive intermediate IF and I atoms. The contributions from atomic iodine are shown to be more intense in the threshold photoelectron (TPE) spectra, as compared to the PE spectra.