Another unique feature of the pulmonary circulation is the ability to decrease resistance when pulmonary arterial pressure rises, as seen with an increase in cardiac output. When pressure rises, there is a marked decrease in pulmonary vas cular resistance (Fig. 20.4). Similarly, increasing pulmonary venous pressure causes pulmonary vascular resistance to fall. These responses are very different from those of the systemic circulation, where an increase in perfusion pressure increases vascular resistance. Two local mechanisms in the pulmonary circulation are responsible (Fig. 20.5). The first mechanism is known as capillary recruitment. Under normal conditions, some capillaries are partially or completely closed in the top part of the lungs because of the low perfusion pressure. As blood flow increases, the pressure rises and these collapsed vessels are opened, lowering overall resistance. This process of opening capillaries is the primary mechanism for the fall in pulmonary vascular resistance when cardiac output increases. The second mechanism is capillary distension or widening of capillary segments, which occurs because the pulmonary capillaries are exceedingly thin and highly compliant.
The fall in pulmonary vascular resistance with increased cardiac output has two beneficial effects. It opposes the tendency of blood velocity to speed up with increased flow rate, maintaining adequate time for pulmonary capillary blood to take up oxygen and dispose of carbon dioxide. It also results in an increase in capillary surface area, which
Pressure profiles of the pulmonary and sys-"temic circulations. Unlike the systemic circulation, the pulmonary circulation is a low-pressure and low-resistance system. Pulmonary circulation is characterized as normally dilated, while the systemic circulation is characterized as normally constricted. Pressures are given in mm Hg; a bar over the number indicates mean pressure.
enhances the diffusion of oxygen into and carbon dioxide out of the pulmonary capillary blood.
Capillary recruitment and distension also have a protective function. High capillary pressure is a major threat to the lungs and can cause pulmonary edema, an abnormal accumulation of fluid, which can flood the alveoli and impair gas exchange. When cardiac output increases from a resting level of 5 L/min to 25 L/min with vigorous exercise, the decrease in pulmonary vascular resistance not only minimizes the load on the right heart but also keeps the capillary pressure low and prevents excess fluid from leaking out of the pulmonary capillaries.
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