The Pulmonary Circulation

As described in Chapter 1, the pulmonary circulation receives the entire output of the right ventricle. Its high-density capillary network surrounds the lung alveoli, allowing the O₂-poor blood from the pulmonary arteries to exchange CO₂ for O₂. The pulmonary veins return highly oxygenated blood to the left atrium. The pulmonary circulation contains about 800 mL of blood in recumbent subjects, falling to about 450 mL during quiet standing.

Mean pulmonary arterial pressure is ∼15 mmHg, and left atrial pressure is ∼5 mmHg. The right ventricle is able to drive its entire output through the pulmonary circulation utilizing a pressure head of only 10 mmHg because the resistance of the pulmonary circulation is only 10–15% that of the systemic circulation. This arises because the vessels of the pulmonary microcirculation are short and of relatively wide bore, with little resting tone. They are also very numerous, so that their total cross-section is similar to that of the systemic circulation. The walls of both arteries and veins are thin and distensible, and contain comparatively little smooth muscle.

The low pressure within the pulmonary circulation means that regional perfusion of the lungs in the upright position is greatly affected by gravity (Figure 26a). The extravascular pressure throughout the lungs is similar to the alveolar pressure (∼0 mmHg). However, the intravascular pressure is low in the lung apices, which are above the heart, and high in the lung bases, which are below the heart. Pulmonary vessels in the lung apices therefore collapse during diastole, causing intermittent flow. Conversely, vessels in the bases of the lungs are perfused throughout the cardiac cycle, and are distended. A small increase in pulmonary arterial pressure during exercise is sufficient to open up apical capillaries, allowing more O₂ uptake by the blood.

The low hydrostatic pressure in pulmonary capillaries (mean of 7–10 mmHg) does not lead to net fluid resorption, because it is balanced by a low extravascular hydrostatic pressure and an unusually high interstitial plasma protein oncotic pressure (∼18 mmHg). The lung capillaries therefore produce a small net flow of lymph, which is drained by an extensive pulmonary lymphatic network. During left ventricular failure or mitral stenosis, however, the increased left atrial pressure backs up into the pulmonary circulation, increasing fluid filtration and leading to pulmonary oedema.

Neither the sympathetic nervous system nor myogenic/metabolic autoregulation have much of a role in regulating pulmonary vascular resistance or flow. However, the pulmonary vasculature is well supplied with sympathetic nerves. When stimulated, these decrease the compliance of the vessels, limiting the pulmonary blood volume so that more blood is available to the systemic circulation.

The most important mechanism regulating pulmonary vascular tone is hypoxic pulmonary vasoconstriction (HPV), a process by which pulmonary vessels constrict in response to alveolar hypoxia. This unique mechanism (systemic vessels typically dilate

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