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A log‐normal distribution of (A) ventilation per unit volume and (B) blood flow per unit volume with less dispersion and (C) how these are combined to give a log‐normal distribution of ventilation‐perfusion ratios. From Reference .

Figure 2.

Typical example of a log‐normal distribution of ventilation‐perfusion ratio as used in this analysis. In this case, the log standard deviation of ventilation (or blood flow) per unit volume is equal to 1.5. From References and .

Figure 3.

Acute effect of imposing ventilation‐perfusion inequality on a homogeneous lung. All variables were held constant except the oxygen uptake and carbon dioxide output. Note that the reduction of carbon dioxide transfer is almost as great as that of oxygen. From Reference and .

Figure 4.

Effects of increasing ventilation‐perfusion ratio inequality on gas exchange in a lung model in which oxygen uptake and carbon dioxide output are maintained at 300 and 240 ml·min^{−1}, respectively (steady‐state conditions). Note the rapid fall in the Po_{2} of arterial and mixed venous blood and the corresponding increases in Pco_{2}. From References and .

Figure 5.

(A) The effects of increasing total ventilation on the Po_{2} and Pco_{2} of arterial blood for different degrees of ventilation‐perfusion inequality. The log standard deviation of the distribution is shown on each line. (B) The results for Po_{2} and Pco_{2} of mixed venous blood. From References and . The normal ventilation is shown by the arrow.

Figure 6.

(A) The effects of increasing total blood flow on the Po_{2} and Pco_{2} of arterial blood. (B) The changes in the Po_{2} and Pco_{2} of mixed venous blood. From References and .

Figure 7.

(A) The effects of increasing the inspired Po_{2} on the arterial Po_{2}. Note that the arterial Po_{2} remains very low even for high inspired oxygen concentrations when the degree of ventilation‐perfusion inequality is severe. (B) The alveolar‐arterial Po_{2} difference plotted against the alveolar Po_{2} for different degrees of ventilation‐perfusion inequality. At the relatively moderate standard deviation of 0.8, the alveolar‐arterial difference is still very high when the alveolar Po_{2} is 600 mmHg. From References and .

Figure 8.

Gas exchange behavior of a bimodal distribution of ventilation‐perfusion ratios where the abnormal mode is centered on a very high ventilation‐perfusion ratio (type A). See text for details.

Figure 9.

Same as Figure except that the abnormal mode is centered on a very low ventilation‐perfusion ratio (type B). Both Figures and are from Wagner (personal communication).

Figure 10.

Conceptual stages in the changes of pulmonary gas exchange that occur after imposing ventilation‐perfusion inequality on a homogeneous lung. See text for details. From Reference .

Figure 11.

Diagram showing why the very nonlinear oxygen dissociation curve interferes with the uptake of oxygen in a lung with ventilation‐perfusion inequality. From Reference .

Figure 12.

(A) The effects of increasing ventilation on the arterial Po_{2} and Pco_{2} when the oxygen dissociation curve is made linear (cf. Figure ). This emphasizes how the normal nonlinear dissociation curve prevents the return of the arterial Po_{2} to normal in the presence of ventilation‐perfusion inequality even when the ventilation is greatly raised. (B) The effects on the Po_{2} and Pco_{2} of mixed venous blood. From References and .

Figure 13.

Example of a distribution of ventilation‐perfusion ratios in a young, normal subject as measured with the multiple inert gas infusion technique . Note that the distribution appears to be log normal with a small dispersion. The log standard deviation is about 0.3. From Reference .

Figure 14.

An example of the distribution of ventilation‐perfusion ratios in a patient with chronic obstructive pulmonary disease with type A presentation. Note the bimodal distribution and the large amount of ventilation going to lung units with an abnormally high ventilation‐perfusion ratio. From Reference .

Figure 15.

An example of the distribution of ventilation‐perfusion ratios in a patient with chronic obstructive pulmonary disease with type B presentation. Note again the bimodal distribution, but this time, there is a large amount of blood flow going to lung units with an abnormally low ventilation‐perfusion ratio. From Reference .

Figure 1.

A log‐normal distribution of (A) ventilation per unit volume and (B) blood flow per unit volume with less dispersion and (C) how these are combined to give a log‐normal distribution of ventilation‐perfusion ratios. From Reference .

Figure 2.

Typical example of a log‐normal distribution of ventilation‐perfusion ratio as used in this analysis. In this case, the log standard deviation of ventilation (or blood flow) per unit volume is equal to 1.5. From References and .

Figure 3.

Acute effect of imposing ventilation‐perfusion inequality on a homogeneous lung. All variables were held constant except the oxygen uptake and carbon dioxide output. Note that the reduction of carbon dioxide transfer is almost as great as that of oxygen. From Reference and .

Figure 4.

Effects of increasing ventilation‐perfusion ratio inequality on gas exchange in a lung model in which oxygen uptake and carbon dioxide output are maintained at 300 and 240 ml·min^{−1}, respectively (steady‐state conditions). Note the rapid fall in the Po_{2} of arterial and mixed venous blood and the corresponding increases in Pco_{2}. From References and .

Figure 5.

(A) The effects of increasing total ventilation on the Po_{2} and Pco_{2} of arterial blood for different degrees of ventilation‐perfusion inequality. The log standard deviation of the distribution is shown on each line. (B) The results for Po_{2} and Pco_{2} of mixed venous blood. From References and . The normal ventilation is shown by the arrow.

Figure 6.

(A) The effects of increasing total blood flow on the Po_{2} and Pco_{2} of arterial blood. (B) The changes in the Po_{2} and Pco_{2} of mixed venous blood. From References and .

Figure 7.

(A) The effects of increasing the inspired Po_{2} on the arterial Po_{2}. Note that the arterial Po_{2} remains very low even for high inspired oxygen concentrations when the degree of ventilation‐perfusion inequality is severe. (B) The alveolar‐arterial Po_{2} difference plotted against the alveolar Po_{2} for different degrees of ventilation‐perfusion inequality. At the relatively moderate standard deviation of 0.8, the alveolar‐arterial difference is still very high when the alveolar Po_{2} is 600 mmHg. From References and .

Figure 8.

Gas exchange behavior of a bimodal distribution of ventilation‐perfusion ratios where the abnormal mode is centered on a very high ventilation‐perfusion ratio (type A). See text for details.

Figure 9.

Same as Figure except that the abnormal mode is centered on a very low ventilation‐perfusion ratio (type B). Both Figures and are from Wagner (personal communication).

Figure 10.

Conceptual stages in the changes of pulmonary gas exchange that occur after imposing ventilation‐perfusion inequality on a homogeneous lung. See text for details. From Reference .

Figure 11.

Diagram showing why the very nonlinear oxygen dissociation curve interferes with the uptake of oxygen in a lung with ventilation‐perfusion inequality. From Reference .

Figure 12.

(A) The effects of increasing ventilation on the arterial Po_{2} and Pco_{2} when the oxygen dissociation curve is made linear (cf. Figure ). This emphasizes how the normal nonlinear dissociation curve prevents the return of the arterial Po_{2} to normal in the presence of ventilation‐perfusion inequality even when the ventilation is greatly raised. (B) The effects on the Po_{2} and Pco_{2} of mixed venous blood. From References and .

Figure 13.

Example of a distribution of ventilation‐perfusion ratios in a young, normal subject as measured with the multiple inert gas infusion technique . Note that the distribution appears to be log normal with a small dispersion. The log standard deviation is about 0.3. From Reference .

Figure 14.

An example of the distribution of ventilation‐perfusion ratios in a patient with chronic obstructive pulmonary disease with type A presentation. Note the bimodal distribution and the large amount of ventilation going to lung units with an abnormally high ventilation‐perfusion ratio. From Reference .

Figure 15.

An example of the distribution of ventilation‐perfusion ratios in a patient with chronic obstructive pulmonary disease with type B presentation. Note again the bimodal distribution, but this time, there is a large amount of blood flow going to lung units with an abnormally low ventilation‐perfusion ratio. From Reference .

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How to Cite

John B. West. Causes of and Compensations for Hypoxemia and Hypercapnia. Compr Physiol 2011, 1: 1541-1553. doi: 10.1002/cphy.c091007