Accurate dilution of a small blood volume with a carbon monoxide-saturated solution allows measurement of the whole blood O2 concentration as an increase in O2 tension in the solution. We have improved the method by simplifying both equipment and procedure. We also suggest an additional step in which the mixture is acidified, thereby allowing the measurement of CO2 concentration in the same solution with a CO2 electrode. The accuracy of both the O2 and CO2 determinations compares favorably with that obtained with other micromethods.
To measure a lung volume that is not directly accessible, one often follows dilution of a single-gas tracer, present initially only in the lung or in a rebreathing bag. The final volume available to the tracer is assumed to be the sum of the two initial components. Since O2 is taken up and CO2 is eliminated during the few breaths required for mixing, the total volume changes. The error in lung volume due to this volume change can exceed 10%. In this paper we 1) present theoretical and experimental data to demonstrate the effect of CO2 and O2 exchange, 2) introduce a general equation, based on N2 and Ar, which allows one to circumvent the problems created by these fluxes, and 3) show the pitfall of the back-extrapolation approach for a single tracer.
Changes in the speed with which equilibrium between alveolar gas and capillary blood is approached along the course of the pulmonary capillary are analyzed graphically. Inflections do not occur in the curve of blood oxygen content vs. time but may occur in the curve of blood oxygen tension vs. time. Such inflections depend on the rate of change of the alveolar-capillary tension gradient in relation to the rate of change of the slope of the oxyhemoglobin dissociation curve. Three graphic methods for estimating the mean alveolar-capillary diffusion gradient are presented. Submitted on August 8, 1956
An increased urinary-alveolar PN2 difference was demonstrated in normal, full-term infants during time first 6 days of life. This uADN2 results only from regions of the lungs with a low VA/Q and is not affected by true venous admixture, a diffusion barrier, or the presence of atelectasis. The mean aADN2 of 25 mm Hg on the first day of life was comparable to the N2 difference found in patients with severe emphysema. The mean PN2 difference decreased gradually and by time sixth day was approximately 10 mm. The histologic signs of amniotic detritus in the lungs of virtually all new-born infants dying of non-respiratory causes on the first day of life and the subsequent lower incidence of these materials in the lungs of infants dying during the first week suggests the possibility of partial obstruction and low VA/Q in some regions of the lung. The temporary increase in uADN2, which was found in some cases may indicate that atelectatic areas may open at different times.
Abstract : The USAF Military Airlift Command is charged with air evacuation of injured and ill patients in times of war and peace. In recent years the types of patients eligible for transport have expanded to include those with illnesses or injuries that require full-time mechanical support of respiratory functions with closed-system positive-pressure mechanical ventilators. The clinical condition of some patients meets the criteria of the Adult Respiratory Distress Syndrome, which is characterized by low pulmonary compliance and poor gas exchange. Respiratory support of such patients in a sea-level environment may require a combination of high-pressure mechanical ventilation and high inspired oxygen tensions. During air evacuation, these patients are routinely exposed to cabin pressures equivalent to 8,000 ft standard atmosphere (564 torr); and during rapid cabin decompression, to pressures equivalent to 40,000 ft standard atmosphere (141 torr). Concern that such environmental situations will exhaust already strained machine and physiological reserves, with potential damage to transported patients, has prompted this evaluation of the effects of altitude on the mechanical performance of ventilators and the functioning of already damaged physiological gas-exchange systems.
The fourth and last volume of the Handbook of Physiology section on the respiratory system deals with the ultimate goal of the system, gas exchange. To fulfill this role the lung cyclically expands and contracts and the alveoli are perfused; the regulatory function is geared to optimize the exchange of oxygen and carbon dioxide. Like other areas of respiratory physiology, the study of gas exchange has made giant strides since the first edition of the Handbook was published. Much of what was written then remains important and serves as a basis for the more recent developments. Consequently, like all good reviews, this volume includes “something old and something new, something borrowed and something true.” Although logic and didactic practice dictate the chapter order, from the description of basic physical principles to their application under both normal and unusual conditions, some changes in representation have been introduced. For example, the fundamental gas laws, instead of following the usual cut-and-dried presentation, are developed in their historical context. By its nature a book written by many specialists dealing with overlapping topics must contain some duplication. Although the goal was to minimize repetition, we deemed it more important to maintain the integrity and continuity of each chapter and did not request the authors to cripple their contributions by deleting all that was to be found elsewhere. Finally, progress in science often results from divergence of opinion and controversy. The authors are complimented for giving both sides of the argument whenever possible and excused for occasionally allowing their biases to show. With a mixture of pride and relief we present this book, hoping that it will serve its public as well as the first edition has for so many years. Leon E. Farhi S. Marsh Tenney
