PHYL 422 Review Questions
Set 6
Modified from Shumaker and Hlastala’s Textbooks
1. What might happen to the vertical gradient in blood flow in an individual in outer space under zero-gravity conditions?
2. If the left main pulmonary artery were transiently occluded and cardiac output remained unchanged (thus diverting all blood flow through the
right lung), would the pulmonary artery pressure approximately double?
3. Describe the influence of gravity on the distribution of pulmonary blood flow. Include an explanation of the four-zone model. Are there any
recent experiments that question the validity of this model?
4. If the pulmonary artery pressure were reduced in a patient who had haemorrhaged, how might this influence the three zones of the lung?
5. What happens to fluid that leaks from the pulmonary capillaries into the lung interstitial space?
6. What are the different consequences of lung interstitial edema and alveolar edema for lung gas exchange?
7. Why does the pulmonary vascular resistance increase at high lung volumes?
8. What effect might exposure to high altitude have on the pulmonary arterial pressure?
9. Describe how ventilation with positive end-expired pressure (which increases lung volume throughout the ventilatory cycle) would influence
pulmonary vascular resistance and pulmonary arterial pressure.
Answers
1. In the absence of gravity, the distribution of blood flow from the top to the bottom of the lung should become more uniform.
2. No. Any increase in the pulmonary arterial pressure will recruit and distend vessels in the right lung, tending to reduce their resistance.
Pressure may increase but should not double.
3. It has been thought that gravity influences the distribution of pulmonary blood flow via an influence on pulmonary vascular pressures. The
four-zone model assumes that vascular pressures increase lower in the lung because of the weight of blood above. It also assumes that the
vascular pressure decreases higher in the lung, changing in proportion to height up the lung as determined by density of blood. In zone 1,
alveolar pressure exceeds both arterial and venous pressure compressing the alveolar capillaries, resulting in zero blood flow. In zone 2, arterial
pressure exceeds alveolar pressure, which exceeds venous pressure. Pulmonary blood flow increases with descent into zone 2. In zone 3, both
arterial and venous pressures exceed alveolar pressure, causing all capillaries to be open. The result should be a decreasing flow with
increasing height within the lungs. Measurements of blood flow to small regions of the lung demonstrate a decreasing flow with ascent up the
lung but a great amount of heterogeneity within any isogravitational plane; thus the argument can be made that gravity has little influence on
pulmonary blood flow distribution.
4. A sufficient decrease in mean pulmonary arterial pressure could cause zone I regions to appear at the uppermost regions of the lung. A
decrease in pulmonary venous pressure could also convert zone III regions into zone II regions.
5. Most fluid that leaves the vascular space is eventually returned to the circulation through the lymphatic system. But if this system is
overwhelmed, there can be interstitial edema and in severe cases alveolar edema.
6. Interstitial edema has less of an influence on lung gas exchange because it does not significantly interfere with gas transfer between alveolar
gas and pulmonary capillary blood. By contrast, in alveolar edema the flooded alveoli cannot participate in gas exchange yet still receive blood
flow.
7. Stretch and distortion of alveolar septal walls causes an increase in the resistance of alveolar vessels, including alveolar capillaries.
8. Exposure to high altitude causes the alveolar oxygen tension to decrease. This can cause acute hypoxic pulmonary vasoconstriction in all
lung regions, causing an increase in pulmonary arterial pressure. This effect is reversed on return to sea level.
9. Positive end-expiratory pressure increases mean alveolar pressure, which in turn increases pulmonary capillary resistance and, hence,
pulmonary vascular resistance and pulmonary artery pressure.