The Pulmonary Vasculature

Abstract

The pulmonary circulation is a low-pressure, low-resistance circuit whose primary function is to deliver deoxygenated blood to, and oxygenated blood from, the pulmonary capillary bed enabling gas exchange. The distribution of pulmonary blood flow is regulated by several factors including effects of vascular branching structure, large-scale forces related to gravity, and finer scale factors related to local control. Hypoxic pulmonary vasoconstriction is one such important regulatory mechanism. In the face of local hypoxia, vascular smooth muscle constriction of precapillary arterioles increases local resistance by up to 250%. This has the effect of diverting blood toward better oxygenated regions of the lung and optimizing ventilation-perfusion matching. However, in the face of global hypoxia, the net effect is an increase in pulmonary arterial pressure and vascular resistance. Pulmonary vascular resistance describes the flow-resistive properties of the pulmonary circulation and arises from both precapillary and postcapillary resistances. The pulmonary circulation is also distensible in response to an increase in transmural pressure and this distention, in addition to recruitment, moderates pulmonary arterial pressure and vascular resistance. This article reviews the physiology of the pulmonary vasculature and briefly discusses how this physiology is altered by common circumstances.

Fig. 1

Schematic diagram of gravitational relationships. The large red arrow indicates the direction of the gravitational vector, the black arrow perpendicular to the gravitational vector indicates the isogravitational direction, i.e., lung regions that are isogravitational are all in the same plane with respect to gravity. Gravitationally nondependent lung is the highest isogravitational plane under consideration whereas gravitationally dependent is lowest plane of consideration.

Fig. 2

A dichotomous branching model. The basic transformation is the dichotomous branching of each terminal element. The asymmetric branching of the terminal branch divides initial flow (F₀) into two fractions γ and 1 – γ that are distributed to the daughter branches, where γ = 0.5 would be equal distribution between daughter branches. Following a second iteration in which all terminal nodes branch again, blood flow is now distributed to four terminal branches. Numbers in blue show calculated flow to each branch based on F₀ of 6 L/min and a γ of 0.6 and show how even relatively minor asymmetry in flow in the initial branches can give rise to large differences after a relatively small number of iterations. (Modified from Glenny and Robertson.)

Fig. 3

Regional ventilation and perfusion scaled to the measured minute ventilation and cardiac output in prone posture. Data are from a microsphere study in mechanically ventilated pigs. Ventilation was measured by inhaled aerosolized fluorescent microspheres, and perfusion from injected fluorescent microspheres. These microspheres lodge in the small airways and capillaries proportional to ventilation and perfusion respectively and are quantified in approximately 1 cm cubes postmortem. Both ventilation and perfusion display regional clustering in which adjacent regions have similar flows. Note the strong spatial correlation in which regions that receive high ventilation receive high perfusion and regions that receive less ventilation receive less perfusion. (Reproduced with permission from Altemeier et al.)

Fig. 4

Calculation of fractal dimension from imaging data. The relative dispersion (standard deviation/mean) is calculated at the highest resolution of measurement. This calculation is repeated by dividing the lung into progressively larger blocks, i.e., lower resolution. The fractal dimension is 1-slope of the relationship of the plot of log relative dispersion versus log piece size.

Fig. 5

The Zone model of pulmonary perfusion. (A) Schematic diagram of the original experiment. Detectors (gray circles) are placed on the chest wall. Radiolabeled CO₂, used as a tracer gas, is inhaled and time–activity curves constructed during a breath hold. The CO₂, a soluble and perfusion-limited gas, is cleared proportional to regional blood flow. In nondependent lung, clearance of the isotope is delayed compared with dependent lung. These observations led to the development of the Zone model of pulmonary perfusion (B, C) that relates perfusion to the relationships between alveolar P_A, pulmonary arterial P_a, and pulmonary venous, P_v, pressure. In Zone I, when P_A is greater than both P_a and P_v, the capillary is collapsed and flow is zero. In Zone II the difference between P_A and P_a dictates flow, whereas in Zone III lung, the difference between P_a and P_v dictates flow since both are greater than alveolar pressure. Later, this model was modified to include a fourth Zone where perfusion was reduced with decreasing height. Zone IV was originally attributed to increased interstitial pressure increasing resistance in dependent lung vessels.

Fig. 6

Left: the relationship between alveolar PO₂ and the local ventilation–perfusion $\left({\dot{\text{V}}}_{\text{A}}/\dot{\text{Q}}\right)$ ratio in normoxia. Right: schematic representation of restoration of oxygenation by HPV in a lung unit. (1) When ventilation and perfusion are well matched, PO₂ is high (pink dot). (2) After ventilation is reduced to a lung region, in this case by partial airway obstruction, the ventilation–perfusion ratio decreases and PO₂ is reduced (dark blue dot). (3) Activation of HPV reduces local perfusion, matching ventilation and acting to restore the local ventilation–perfusion ratio towards baseline. This increases the alveolar PO₂ in the lung unit back to baseline (purple dot). HPV, hypoxic pulmonary vasoconstriction.

Fig. 7

Measurement of pulmonary vascular resistance (PVR). PVR is calculated from the inflow pressure, pulmonary artery pressure, P_a, the outflow pressure, left atrial pressure, P_la, and cardiac output, $\dot{\text{Q}}$ which is the flow rate. P_la is often estimated from pulmonary arterial occlusion pressure, P_aOP. This is measured via a catheter that is introduced into the pulmonary artery and manipulated distally in the pulmonary circulation where a balloon is inflated to occlude the vessel and prevent filling. P_aOP is measured distal to the balloon and reflects back pressure from the left atrium.

Fig. 8

Three forces acting on blood–gas barrier. Circumferential tension (T_tmp) is given by capillary transmural pressure X radius of curvature (r). In this example, alveolar pressure (P_alv) is atmospheric so that capillary transmural pressure is equal to capillary hydrostatic pressure (P_cap). Surface tension of alveolar lining layer (T_st) exerts an inward-acting force to support the capillary. Longitudinal tension in alveolar wall elements associated with inflation of lung (T_el) is presumably transmitted mainly by collagen fibers on the thick side of the capillary but may affect wall tension on the thin side, especially at high lung volumes. (Reproduced with permission from West et al.)

Fig. 9

The effect of mild exercise on the distribution of pulmonary blood flow. With exercise, blood flow is redistributed to the nondependent lung (left panel) and perfusion heterogeneity as measured by the relative dispersion is reduced (middle and right) even after accounting for the effect of gravity (right panel). (Modified with permission from Hall et al.)