Pulmonary circulation physiology

The pulmonary circulation is a low-resistance, low-impedance, highly compliant and therefore high-capacitance vascular bed. It is highly dependent upon the performance of the two ventricles it connects, and because the capillaries of the pulmonary circulation run within the walls of the alveoli, the resistance of the pulmonary vasculature depends upon airway (and pleural) pressures. It is poorly equipped for self-regulation, unlike the coronary or cerebral circulation. At any time, a given stroke volume ejected from the RV is proportioned into a pass-through component that returns to the LV, and a stored component that remains temporarily within the pulmonary vasculature. The capacitance of the pulmonary circulation is approximately 400-500 ml, or about a tenth of the circulating blood volume. The pulmonary capillary blood volume is about 100-200 ml, and circulation time is about 0.75 sec.

The blood flow through the lungs is equal to the alveolar ventilation, and both occur in a phasic manner, but the rates are different (respiratory rate is much slower than heart rate). Therefore matching of blood flow to ventilation occurs on a regional basis by means of a system of hypoxic vasoconstriction, in that vessels in poorly ventilated, hypoxic areas of the lung are vasoconstricted so as not to waste blood flow to those poorly gas exchanging areas. This is fundamentally different from the systemic circulation where arterioles dilate in areas of hypoxemia and poor oxygenation.

Pulmonary vascular resistance is defined by the equation: R= Ppa-Pla/ Q, where Ppa-Pla is the difference of mean pressures between the pulmonary artery and the left atrium respectively, and Q is the pulmonary blood flow in L/min. Normal R is 0.1mmHg/L/min (or 100 dynes/sec.cm5)

Changes in PVR can be either active or passive. Active changes refer to changes in arterial tone mediated by the sympathetic nerves or hypoxic vasoconstriction (see below), whereas passive changes are alterations of caliber or pressure resulting from changes in lung volumes, gravitational effects and recruitment.

Changes in the structure of the pulmonary vessels, or so-called remodeling, can also change PVR, and therefore, the pressure in the circulation. For example, the fetal vessels are thicker and more muscularized than adults and failure of this muscularization to regress in the neonatal period causes persistent pulmonary hypertension. Similarly, unlike the yak, which is native to high altitudes, humans living at high altitude have muscularized vessels and therefore higher PVR, and higher pulmonary arterial pressures for a given cardiac output. Thus at 4540m with an ambient P02 of 80 mmHg, the mean PA pressure is about 28 mmHg in healthy humans, twice that of persons at sea level (about 12 mmHg), with the same cardiac output.