12: Anatomic and physiologic aspects of the pulmonary vasculature

OUTLINE

Anatomy, 165

Physiology, 166

Pulmonary Vascular Resistance, 166

Distribution of Pulmonary Blood Flow, 168

Pulmonary Vascular Response to Hypoxia, 169

Other Aspects of Pulmonary Vascular Physiology, 170

The pulmonary vasculature is responsible for transporting deoxygenated blood to the alveoli and then carrying freshly oxygenated blood back to the left atrium and ventricle for pumping through the aorta to the systemic arterial circulation. Although the pulmonary circulation is often called the “lesser circulation,” the lungs are the only organ system that receives the entire cardiac output. This extensive system of pulmonary vessels is susceptible to a variety of disease processes, ranging from those that primarily affect the vasculature to those that are either secondary to airway or pulmonary parenchymal disease or due to the transport of material that is foreign to the pulmonary vessels, including blood clots.

Before diseases of the pulmonary vasculature are considered in Chapters 13 and 14, this chapter discusses a few of the general anatomic and physiologic aspects of the pulmonary vessels. Included in the discussion on physiology are several topics relating to the hemodynamics of the pulmonary circulation, as well as a brief consideration of some nonrespiratory metabolic functions of the pulmonary circulation.

Anatomy

In contrast to the systemic arteries, which carry blood from the left ventricle to the rest of the body, the pulmonary arteries, which carry blood from the right ventricle into the lungs, are relatively low-pressure, thin-walled vessels. Under normal circumstances, the mean pressure within the main pulmonary arteries is approximately 15 mm Hg, roughly one-sixth of the pressure in the aorta. The pulmonary trunk, which carries the outflow from the right ventricle, divides almost immediately into the right and left main pulmonary arteries, which subsequently divide into smaller branches. Throughout these progressive divisions, the pulmonary arteries and their branches travel with companion airways, closely following the course of the progressively dividing bronchial tree. By the time the vessels are considered arterioles, the

outer diameter is less than approximately 0.1 mm. An important feature of the smaller pulmonary arteries is the presence of smooth muscle within the walls, which permits a vasoconstrictive response to various stimuli, particularly hypoxia, resulting in preferential routing of perfusion to well-ventilated lung units.

(See Chapter 1 for discussion of mismatch.)

The pulmonary capillaries form an extensive network of communicating channels coursing through alveolar walls. Rather than being described as a series of separate vessels, the capillary system can be viewed as a continuous meshwork or sheet bounded by alveolar walls on each side and interrupted by “posts” of connective tissue, akin to the appearance of an underground parking garage. The capillaries are in close proximity to alveolar gas, separated only by alveolar epithelial cells and a small amount of interstitium present in some regions of the alveolar wall (see Figs. 8.1 and 8.2). Overall, the capillary surface area is approximately 125 m2 and represents approximately 85% of the available alveolar surface area. The architecture of this capillary system is extraordinarily well suited to the requirements of gas exchange, inasmuch as it contains an enormous effective surface area of contact between pulmonary capillaries and alveolar gas.

The pulmonary veins, which are responsible for transporting oxygenated blood from the pulmonary capillaries to the left atrium, progressively combine into larger vessels until four major pulmonary veins enter the left atrium. Unlike the pulmonary arteries and their branches, the pulmonary venous system does not follow the course of the corresponding bronchial structures until the level of the hila.

The bronchial arteries, which are part of the systemic circulation, provide nutrient blood flow to a variety of nonalveolar structures, such as the bronchi and the visceral pleural surface. There is significant variability in the anatomy of the bronchial circulation. Generally, a single bronchial artery of variable origin (upper right intercostal, right subclavian, or internal mammary artery) supplies the right lung. Two bronchial arteries, usually arising from the thoracic aorta, supply the left lung. Venous blood from the large extrapulmonary airways drains via bronchial veins into the azygos vein and eventually into the right atrium. In contrast, venous blood from intrapulmonary airways drains into the pulmonary venous system emptying into the left atrium. This blood leaving the intrapulmonary airways and draining back to the left atrium never enters the pulmonary capillary bed and thus provides a small amount of anatomic shunting of deoxygenated blood into the systemic arterial circulation.

An extensive network of lymphatic channels is also located primarily within the connective tissue sheaths around small vessels and airways. Although these channels do not generally course through the interstitial tissue of the alveolar walls, they are in sufficiently close proximity to be effective at removing liquid and some solutes that constantly pass into the interstitium of the alveolar wall.

Physiology

Pulmonary vascular resistance

Although the pulmonary circulation handles the same cardiac output from the right ventricle as the systemic circulation handles from the left ventricle, the former operates under much lower pressures and has substantially less resistance to flow than the latter. The systolic and diastolic pressures in the pulmonary artery are normally approximately 25 and 10 mm Hg, respectively, in contrast to 120 and 80 mm Hg in the systemic arteries. The pulmonary vascular resistance (PVR) can be calculated according to Eq. 12.1:

The change or drop in pressure across the pulmonary circuit is the mean pulmonary artery (mPA)

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pressure minus the mean left atrial (mLA) pressure, and the flow is the cardiac output (Eq. 12.2). Thus:

Left atrial pressure is difficult to measure directly. However, a special catheter called a pulmonary artery balloon occlusion catheter or Swan-Ganz catheter is clinically used for indirect left atrial pressure measurements (Fig. 12.1). This catheter is inserted into a large vein (usually the internal jugular vein in the neck or the femoral vein in the groin) and passed through the right heart into a pulmonary artery. The catheter tip is equipped with a small soft balloon that, when inflated, lodges in a segmental pulmonary artery and temporarily blocks flow to the segment, creating a static, minimally compressible column of blood between the catheter and the left atrium. After a short period of equilibration, because there is no blood flow passing the catheter tip, the pressure measured at the tip of the catheter reflects the pressure “downstream” in the pulmonary veins and left atrium.

pulmonary vessels receive no blood flow, but they are capable of carrying part of the pulmonary blood flow should the pressure increase. In addition, because pulmonary vessels have relatively thin walls, they are distensible and can enlarge their diameter under increased pressure to accommodate additional blood flow. With a means for increasing the total cross-sectional area of the pulmonary vasculature on demand, the pulmonary circulation is capable of lowering its resistance when the need for increased flow arises.

When cardiac output increases, recruitment and distention of pulmonary vessels decrease pulmonary vascular resistance and prevent a significant increase in pulmonary artery pressure.

Another factor that affects PVR is lung volume. In discussing the nature of this effect, it is useful to distinguish two categories of pulmonary vessels on the basis of their size and location. One category, called alveolar vessels, includes the capillary network coursing through alveolar walls. When alveoli are expanded and lung volume is raised, these vessels are compressed within the stretched alveolar walls, and their contribution to PVR increases. In contrast, when alveoli are emptied and lung volume is lowered, the resistance of these alveolar vessels decreases. The other category consists of the larger vessels called extra-alveolar vessels. They are not compressed by air-filled alveoli. The supporting structure that surrounds the walls of these vessels has attachments to alveolar walls, and the elastic recoil of the alveolar walls provides radial traction to keep these vessels open. This concept is similar to that discussed in Chapter 6 concerning the effect of alveolar wall attachments on airway diameter (see Fig. 6.6). When lung volume is increased, elastic recoil of the alveolar walls increases, the extra-alveolar vessels become larger, and their resistance decreases. When lung volume is decreased, elastic recoil of the alveolar walls decreases, extra-alveolar vessels narrow, and their resistance increases. This differential effect of lung volume on the resistance of alveolar versus extra-alveolar vessels is shown in Fig. 12.2. The total PVR is least at the normal resting expiratory position of the lung (i.e., at functional residual capacity).

The three-zone model for describing the determinants of pulmonary blood flow discussed in Chapter 1 actually is more complicated now that a zone 4 has been recognized. In this zone, which occupies the base of the lung at low lung volumes, blood flow progressively diminishes as the most dependent region of the lung is approached. To explain why a zone 4 exists, we must return to the concept of extra-alveolar pulmonary vessels. At the lung bases, the weight of the lung results in decreased alveolar volume, accompanied by distortion and compression of extra-alveolar vessels. As a result, the resistance of the extra-alveolar vessels considerably increases, the total vascular resistance in this zone increases, and blood flow diminishes.

The distribution of blood flow in the lung can be measured with radioactive isotopes. A perfusion scan is a particularly useful technique that involves intravenous injection of radiolabeled particles, specifically macroaggregates of albumin, that are of sufficient size to lodge in the pulmonary capillaries. An external counter over the lung records the distribution of lodged particles and, hence, the distribution of blood flow to the lung. This technique, when performed in the upright individual, not only confirms the expected gradient of blood flow in the lung but also detects regions of decreased or absent perfusion in disease states, such as pulmonary embolism (see Chapter 3).

Pulmonary vascular response to hypoxia

An important physiologic feature of the pulmonary circulation is its response to hypoxia. When alveoli in an area of lung contain gas with a low PO2, generally less than 60 to 70 mm Hg, the vessels supplying that region of lung undergo vasoconstriction. This response occurs primarily at the level of the small arteries or arterioles and serves as a protective mechanism by decreasing perfusion to poorly ventilated alveoli.

Hence, ventilation-perfusion mismatch is decreased, and blood flow to areas with a low ventilationperfusion ratio, from which hypoxemic blood would return to the left heart, is minimized. When localized regions of lung have a low PO2, the vasoconstrictive response also is localized. In these circumstances, the overall PVR does not significantly increase. However, with a more generalized decrease in PAO2, as in many forms of lung disease or in persons exposed to high altitude, pulmonary vasoconstriction is more generalized. In this circumstance, PVR and pulmonary artery pressure are both increased. What would be a protective response in the case of localized disease is thus detrimental in the case of generalized disease and widespread alveolar hypoxia.

Pulmonary vasoconstriction occurs in response to alveolar hypoxia. This protective mechanism reduces blood flow to poorly ventilated alveoli, minimizing ventilation-perfusion mismatch.

However, there is one setting in which such generalized pulmonary vasoconstriction in response to alveolar hypoxia is most beneficial: the fetus. In utero, the alveoli receive no aeration, making the entire lung hypoxic. The result is marked pulmonary vasoconstriction, which is accompanied by very high PVR and diversion of blood away from the lung. Blood preferentially flows through the foramen ovale from the right to the left atrium and through the ductus arteriosus from the pulmonary artery to the aorta. This allows the majority of the blood oxygenated by the placenta to go directly into the systemic circulation of the fetus, bypassing the nonaerated lungs.

At birth, when the first few breaths are taken, the lungs expand and oxygen flows into the alveoli. The PVR falls, allowing blood to flow into the lungs. The fall in PVR is due to both the reversal of diffuse hypoxic pulmonary vasoconstriction and the mechanical effects of the inflated lung helping to open previously compressed vessels. As a result of this pulmonary vasodilation (as well as constriction of the ductus arteriosus), right ventricular output passes through the lungs, where the blood is oxygenated. Interestingly, the hypoxic vasoconstriction that persists throughout adult life may be directly related to this