Abstract
Gas exchange is the primary function of the lung. The basic process is the transfer of oxygen (O2) from the inspired air to the bloodstream and the transport of carbon dioxide (CO2) produced by metabolism out of the body via the expired gas. The three main structural considerations at play to facilitate this function are (1) the system of airways and the mechanical actions of the chest wall and respiratory muscles to move gas in and out of the lung; (2) the provision of a blood-gas interface which is very thin and has a very large surface area to promote the passive flow of O2 and CO2, driven only by partial pressure differences between alveolar gas and pulmonary capillary blood; and (3) the provision of a pulmonary vasculature sufficient both to perfuse the very large surface area of the blood-gas interface and to accommodate the full cardiac output with relatively low resistance.
Gas exchange also occurs in the tissues throughout the body by passive transfer. Oxygen is transported to tissues by passive transfer from arterial blood, and CO2 is transported from tissues to venous blood by passive transfer to venous blood. The main transport mechanism for O2 in the blood is by binding of O2 with hemoglobin (Hb) in the red blood cells. There is minimal O2 dissolved in plasma. The three mechanisms for transport of CO2 in the blood are (1) dissolving in plasma, (2) forming dissociated bicarbonate ions (HCO3−), and (3) binding with Hb.
Several factors affect gas exchange including the rates of lung ventilation and perfusion, the matching of ventilation to perfusion within the lung, Hb levels, alveolar O2 partial pressure, metabolic demand, exercise, and pathological changes.
The most common tests for assessing gas exchange are the single-breath uptake of carbon monoxide (CO) by the lung (called DLCO or diffusing capacity in North America and called TLCO or transfer factor in Europe), the analysis of arterial blood gases (ABG), and the measurement of oxygen saturation of Hb using pulse oximetry (SpO2). These measurements are very useful in the diagnosis and management of various lung diseases.
This chapter will describe the pathways for gas exchange, factors affecting gas exchange, measurements of gas exchange, and the interpretation of such measurements.
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Appendix
Appendix
The MIGET is based on the physical principles governing inert gas elimination by the lungs. When an inert gas in solution is infused into systemic veins, the proportion of gas eliminated by ventilation from a lung unit depends only on the solubility of the gas and the V̇A/Q̇ ratio of that unit. The relationship is given by the following equation:
where Pc′ and \( \mathrm{P}\overline{\mathrm{v}} \) are the partial pressures of the gas in end-capillary blood and mixed venous blood, respectively, and λ is the blood-gas partition coefficient. The ratio of Pc′ over \( \mathrm{P}\overline{\mathrm{v}} \) is known as the retention.
To obtain the V̇A/Q̇ distribution of the lung, a saline solution containing low concentrations of six inert gases of different solubility (sulfur hexafluoride [SF6], ethane, cyclopropane, isoflurane, diethyl ether, and acetone) is infused slowly into a peripheral vein until a steady state is reached. The inert gas concentrations in the arterial, mixed venous, and expired gas samples are collected and analyzed. Retention and excretion values for the inert gases are graphed against their solubility in blood. With a 50-compartment model, the retention-solubility plots can be transformed to obtain the distribution of V̇A/Q̇ ratios in the lung. A lung containing shunt units (V̇A/Q̇ = 0) shows increased retention of the least-soluble gas, SF6. Conversely, a lung having large amounts of ventilation-to-lung units with very high V̇A/Q̇ ratios and dead space (V̇A/Q̇ = infinity) shows increased retention of the high-solubility gases (such as ether and acetone).
In healthy subjects, the distributions for both ventilation and blood flow (dispersion) are narrow and span only one log of V̇A/Q̇ ratios. Essentially, no ventilation or blood flow occurs outside the range of approximately 0.3–3.0 on the V̇A/Q̇ ratio scale, and no significant intrapulmonary shunt is detected. With aging, the dispersion of ventilation and perfusion increases. In older subjects, as much as 10% of the total blood flow may go to lung units with V̇A/Q̇ values of less than 0.1, but still no shunt is detected. The increased low V̇A/Q̇ regions adequately explain the decreased Pao2 and increased \( {\mathrm{P}}_{\left(\mathrm{A}-\mathrm{a}\right){\mathrm{O}}_2} \) difference with aging. The cause of such age-related V̇A/Q̇ mismatch often is attributed to degenerative processes in the small airways with aging.
Various abnormal patterns of V̇A/Q̇ distributions measured by the MIGET method adequately explain gas exchange abnormalities in diseased lungs. For example, Fig. 5.6 shows the distribution of V̇A/Q̇ ratios from an individual with chronic obstructive lung disease. The V̇A/Q̇ distribution is bimodal, and large amounts of ventilation go to lung units with extremely high V̇A/Q̇ ratios. This V̇A/Q̇ pattern can be seen in individuals with predominant emphysema (Fig. 5.6, top). Presumably the high V̇A/Q̇ regions represent lung units in which many capillaries have been destroyed by the emphysematous process. In some patients, there are regions of low V̇A/Q̇ (Fig. 5.6, middle), as is commonly seen in patients with predominant chronic bronchitis. Finally, some patients have combinations of both high and low V̇A/Q̇ units (Fig. 5.6, bottom). Note that the main modes of V̇A and Q̇ in the middle and the bottom graphs center on units with V̇A/Q̇ ratio greater than 1 (high V̇A/Q̇ units).
Distribution of V̇A/Q̇ ratios in different patients with COPD, illustrating predominant emphysema, with high V̇A/Q̇ units (top), predominant chronic bronchitis, with low V̇A/Q̇ units (middle), and a mixture of both high and low V̇A/Q̇ units (bottom). (Reproduced with permission from Springer)
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Graham, B.L., MacIntyre, N., Huang, Y.C. (2018). Gas Exchange. In: Kaminsky, D., Irvin, C. (eds) Pulmonary Function Testing. Respiratory Medicine. Humana Press, Cham. https://doi.org/10.1007/978-3-319-94159-2_5
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DOI: https://doi.org/10.1007/978-3-319-94159-2_5
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