Researchers are studying pulmonary gas exchange in various physiological and pathological states using animal models. In one experiment, the partial pressure of oxygen (PO₂) in the upper airways is determined to be 150 mm Hg while breathing ambient air at rest. Analysis of the respiratory gases in a particular lung segment reveals the following: Which of the following best explains these respiratory gas findings?

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11ec160b_3ce4_9f6d_9249_f13e984157fe_MD0001_00 Under normal conditions, the PO₂ of inspired ambient air is approximately 160 mm Hg. This value decreases to approximately 150 mm Hg in the trachea due to the partial pressure of water vapor. Normal alveolar PO₂ is 104 mm Hg, which lies between the tracheal (150 mm Hg) and systemic venous blood (40 mm Hg) PO₂ concentrations. Likewise, normal alveolar PCO₂ is 40 mm Hg, also between its respective tracheal (0 mm Hg) and systemic venous blood concentrations (45 mm Hg). Transfer of O₂ and CO₂ between the blood and the alveoli depends on both perfusion and diffusion. Under normal resting conditions, diffusion of O₂ and CO₂ is a quick process, with blood needing to traverse only one-third of the total pulmonary capillary length to completely equilibrate. In this setting, gas exchange is perfusion-limited (ie, diffusion is fast enough that the total gas exchange depends only on the amount of blood supplied to the alveoli). Diffusion-limited gas exchange takes place when diffusion across the alveolar membrane is relatively slow enough to become the major limitation to gas exchange. This can occur with exercise (due to extremely high perfusion volumes that the diffusion rate cannot keep up with) or with pathologic conditions that disrupt the alveolar membrane (eg, pulmonary fibrosis, emphysema) and slow diffusion. CO₂ diffuses 20 times faster than O₂, even when the alveolar membrane is somewhat disrupted; therefore, alveolar and capillary CO₂ concentrations typically fully equilibrate while alveolar and capillary O₂ concentrations do not. In this experiment, there is a large PO₂ gradient between the alveoli (104 mm Hg) and the pulmonary venous blood (70 mm Hg) but pulmonary venous PCO₂ is normal (40 mm Hg), indicating incomplete gas exchange most likely due to diffusion impairment. (Choice A) Bronchopulmonary shunting describes the normal small drop in PO₂ and small increase in PCO₂ that occurs due to the pulmonary veins receiving deoxygenated blood from the bronchial circulation. However, this normally only results in about a 4 mm Hg drop in PO₂ within the pulmonary veins. (Choice C) In normal alveolar ventilation and perfusion, the alveolar and pulmonary capillary PO₂ rapidly reach equilibrium at 104 mm Hg. (Choice D) Intrapulmonary shunting can occur when the alveoli fill with fluid (eg, pneumonia, pulmonary edema) or collapse (eg, atelectasis) and alveolar ventilation is essentially zero. This patient's alveolar PO₂ of 104 mm Hg is not consistent with shunting (alveolar PO₂ equilibrates with venous blood at 40 mm Hg when ventilation is zero). (Choice E) Poor alveolar ventilation (ie, hypoventilation) does not affect gas exchange between the alveoli and the blood; therefore, no O₂ gradient is created. Educational objective: Gas exchange between the alveoli and pulmonary capillary blood depends on both perfusion and diffusion. The exchange of O₂ and CO₂ in a normal individual at rest is perfusion-limited, so alveolar and capillary partial pressures are equal. Situations in which O₂ exchange becomes diffusion-limited (eg, emphysema, pulmonary fibrosis) cause a large gradient between alveolar and capillary PO₂; PCO₂ is less affected due to the greater diffusing capacity of CO₂. __________ References: A simple model to demonstrate perfusion and diffusion limitation of gases. (http://www.ncbi.nlm.nih.gov/pubmed/23209018)

Researchers Are Studying Pulmonary Gas Exchange in Various Physiological and Pathological