The pulmonary circulation

Key points

Pulmonary blood flow approximates to cardiac output and can increase several-fold with little change in pulmonary arterial pressure.
Passive distension and recruitment of closed pulmonary capillaries, particularly in the upper zones of the lung, allow pulmonary vascular resistance to fall as blood flow increases.
Active control of pulmonary vascular resistance has only a minor role in controlling pulmonary vascular resistance and involves intrinsic responses in vascular smooth muscle, modulated by numerous neural and humoral factors.
Hypoxic pulmonary vasoconstriction of pulmonary arterioles is a fundamental difference from the systemic circulation, although the mechanism of this response to hypoxia remains uncertain.

The evolution of warm-blooded animals led to a 10-fold increase in oxygen requirements, which may only be achieved through having a pulmonary circulation almost completely separate from the systemic circulation (page 302).

Pulmonary blood flow

The flow of blood through the pulmonary circulation is approximately equal to the flow through the whole of the systemic circulation. It therefore varies from approximately 6 L.min ⁻¹ under resting conditions to as much as 25 L.min ⁻¹ during strenuous exercise. It is remarkable that such an increase can normally be achieved with minimal increase in pressure. Pulmonary vascular pressures and vascular resistance are much less than those of the systemic circulation. Consequently the pulmonary circulation has only limited ability to control the regional distribution of blood flow within the lungs, and is affected by gravity, which results in overperfusion of dependent regions of the lungs. Maldistribution of the pulmonary blood flow has important consequences for gaseous exchange, and these are considered in Chapter 7 .

In fact, the relationship between the inflow and outflow of the pulmonary circulation is much more complicated ( Fig. 6.1 ). The lungs receive a significant quantity of blood from the bronchial arteries, which usually arise from the arch of the aorta. Blood from the bronchial circulation returns to the heart in two ways. From a plexus around the hilum, blood from the pleurohilar part of the bronchial circulation returns to the superior vena cava via the azygos veins, and this fraction (about one-third) may thus be regarded as normal systemic flow, neither arising from nor returning to the pulmonary circulation. However, another fraction of the bronchial circulation, distributed more peripherally in the lung, passes through postcapillary anastomoses to join the pulmonary veins, constituting an admixture of venous blood with the oxygenated blood from the alveolar capillary networks.

• Fig. 6.1, Schema of bronchopulmonary anastomoses and other forms of venous admixture in a normal subject. Part of the bronchial circulation returns venous blood to the systemic venous system, while another part returns venous blood to the pulmonary veins constituting venous admixture. Other forms of venous admixture are the Thebesian circulation of the left heart and flow through atelectatic parts of the lungs. It is clear from this diagram why the output of the left heart must be slightly greater than that of the right heart.

The situation may be further complicated by blood flow through precapillary anastomoses from the bronchial arteries to the pulmonary arteries. These communications (so-called Sperr arteries ) have muscular walls, and are thought to act as sluice gates, opening when increased pulmonary blood flow is required. Their functional significance in normal subjects is unknown, but in diseased lungs flow through these anastomoses may be crucial. For example, in situations involving pulmonary oligaemia (e.g., pulmonary artery stenosis, pulmonary embolism) blood from the bronchial arteries will flow through the anastomoses to supplement pulmonary arterial flow. It should be noted that a Blalock–Taussig shunt operation achieves the same purpose for palliation of patients with cyanotic congenital heart disease.

Pulmonary blood volume

As a first approximation the right heart pumps blood into the pulmonary circulation, and the left heart pumps away the blood that returns from the lungs. Therefore provided that the output of the two sides is the same, the pulmonary blood volume will remain constant. However, very small differences in the outputs of the two sides must result in large changes in pulmonary blood volume if they are maintained for more than a few beats.

Factors influencing pulmonary blood volume

Posture

Change from the supine to the erect position decreases the pulmonary blood volume by almost one-third, which is about the same as the corresponding change in cardiac output. Both changes result from pooling of blood in dependent parts of the systemic circulation.

Systemic vascular tone

Because the systemic circulation has much greater vasomotor activity than the pulmonary circulation, an overall increase in vascular tone will tend to squeeze blood from the systemic into the pulmonary circulation. This may result from the release of endogenous catecholamines, administration of vasoconstrictor drugs or passive compression of the body in a G-suit. The magnitude of the resulting volume shift will depend on many factors such as position, overall blood volume and activity of the numerous humoral and nervous mechanisms controlling pulmonary vascular tone at the time (see later). Conversely, it seems likely that pulmonary blood volume would be diminished when systemic tone is diminished, for example during sepsis or with regional anaesthesia when systemic vascular resistance is decreased.

Pulmonary vascular pressures

Pulmonary arterial pressure is only about one-sixth of systemic arterial pressure, although the capillary and venous pressures are not greatly different for the two circulations ( Fig. 6.2 ). Thus there is only a small pressure drop along the pulmonary arterioles, and therefore a reduced potential for active regulation of the distribution of the pulmonary blood flow. This also explains why there is little damping of the arterial pressure wave, and the pulmonary capillary blood flow is markedly pulsatile.

• Fig. 6.2, Comparison of typical mean pressure gradients along the systemic and pulmonary circulations (mean pressures relative to atmosphere).

Consideration of pulmonary vascular pressures carries a special difficulty in the selection of the reference pressure. Systemic pressures are customarily measured with reference to ambient atmospheric pressure, but this is not always appropriate when considering the pulmonary arterial pressure, which is relatively small in comparison with the intrathoracic and pulmonary venous pressures. This may be important in two circumstances. First, the extravascular (intrathoracic) pressure may have a major influence on the intravascular pressure and should be considered. Second, the driving pressure through the pulmonary circulation may be markedly influenced by the pulmonary venous pressure, which must be considered when measuring pulmonary vascular resistance. We must therefore distinguish between pressures within the pulmonary circulation expressed in the three different forms listed in the following paragraphs. Measurement techniques may be adapted to indicate these pressures directly ( Fig. 6.3 ).

• Fig. 6.3, Normal values for pressures in the pulmonary circulation relative to atmospheric pressure (cmH 2 O). Systolic and diastolic pressures are shown for the right ventricle and pulmonary trunk, and mean pressures elsewhere. Note the effect of gravity on pressures at different levels in the lung fields. Three different connected manometers are shown to indicate driving pressure, intravascular pressure and transmural pressure.

Intravascular pressure is the pressure at any point in the circulation relative to atmosphere. This is the customary way of expressing pressures in the systemic circulation, and is also the commonest method of indicating pulmonary vascular pressures.

Transmural pressure is the difference in pressure between the inside of a vessel and the tissue surrounding the vessel. In the case of the larger pulmonary vessels, the outside pressure is the intrathoracic pressure (commonly measured as the oesophageal pressure, as shown in Fig. 6.3 ). This method should be used to exclude the physical effect of major changes in intrathoracic pressure.

Driving pressure is the difference in pressure between one point in the circulation and another point downstream. The driving pressure of the pulmonary circulation as a whole is the pressure difference between pulmonary artery and left atrium. This is the pressure that overcomes the flow resistance and should be used for determination of vascular resistance.

These differences are far from solely academic. For example, an increase in intrathoracic pressure because of positive pressure ventilation will increase the pulmonary arterial intravascular pressure, but will also similarly increase pulmonary venous intravascular pressure; therefore driving pressure (and therefore flow) remains unchanged. Similarly, if the primary problem is a raised left atrial pressure, blood will ‘back up’ through the pulmonary circulation, and pulmonary arterial intravascular pressure will also be raised, but the driving pressure will again not be increased. Therefore for assessing pulmonary blood flow (and so resistance) driving pressure is the correct measurement, but this requires pulmonary venous (left atrial) pressure to be recorded, which is difficult to achieve (page 85). Pulmonary arterial intravascular pressure is usually measured, and the value must therefore be interpreted with caution.

Typical normal values for pressures within the pulmonary circulation are shown in Figure 6.3 .

Effect of intraalveolar pressure

Alteration of intraalveolar pressure causes changes in intrathoracic pressure according to the following relationship:

\begin{matrix} Intrathoracic pressure = \\ alveolar pressure − alveolar transmural pressure . \end{matrix}

$\begin{matrix} Intrathoracic pressure = \\ alveolar pressure − alveolar transmural pressure . \end{matrix}$

Alveolar transmural pressure is a function of lung volume (see Fig. 2.7 ), and when the lungs are passively inflated, the intrathoracic pressure will normally increase by rather less than half the inflation pressure. The increase will be even less if the lungs are stiff, and thus a low compliance protects the circulation from inflation pressure (page 391). Intravascular pressures are normally increased directly and instantaneously by the effects of changes in intrathoracic pressure, and this explains the initial rise in systemic arterial pressure during a Valsalva manoeuvre (page 389). It also explains the cyclical changes in pulmonary arterial pressure during spontaneous respiration, with pressures greater during expiration than during inspiration. Such changes would not be seen if transmural pressure was measured ( Fig. 6.3 ).

In addition to the immediate physical effect of an increase in intrathoracic pressure on intravascular pressures, there is a secondary physiological effect because of interference with venous return. This accounts for the secondary decline in systemic pressure seen in the Valsalva manoeuvre.

Pulmonary vascular resistance

Vascular resistance is an expression of the relationship between driving pressure and flow, as in the case of resistance to gas flow. It may be expressed in similar terms as follows:

\begin{matrix} Pulmonary vascular resistance \\ = \frac{pulmonary driving pressure}{cardiac output} . \end{matrix}

$\begin{matrix} Pulmonary vascular resistance \\ = \frac{pulmonary driving pressure}{cardiac output} . \end{matrix}$

There are, however, important caveats, and the concept of pulmonary vascular resistance is not a simple parallel to Ohm’s law, appropriate to laminar flow (page 28). First, the tubes through which the blood flows are not rigid, but tend to expand as flow is increased, particularly in the pulmonary circulation with its low vasomotor tone. Consequently the resistance tends to fall as flow increases, and the plot of pressure against flow rate is neither linear (see Fig. 3.2 ) nor curved with the concavity upwards (see Fig. 3.3 ), but curved with the concavity downwards. The second complication is that blood is a non-Newtonian fluid (because of the presence of the red blood cells), and its viscosity varies with the shear rate, which is a function of its linear velocity. For accurate measurement of pulmonary vascular resistance, corrections should be made for haematocrit at the time of measurement.

Vascular resistance in the lung

Although the relationship between flow and pressure in blood vessels is far removed from simple linearity, there is a widespread convention that pulmonary vascular resistance should be expressed in a form of the previous equation. This is directly analogous to electrical resistance, as though there were laminar flow of a Newtonian fluid through rigid pipes. It would, of course, be quite impractical in the clinical situation to measure pulmonary driving pressure at different values of cardiac output to determine the true nature of their relationship.

Vascular resistance is expressed in units derived from those used for expression of pressure and flow rate. Using conventional units, vascular resistance is usually expressed in units of mmHg per litre per minute. In absolute centimetre per gram per second units, vascular resistance is usually expressed in units of dynes per square centimetre per cubic centimetre per second (i.e., dyn.s.cm ⁻⁵ ). The appropriate SI units will probably be kPa.L ⁻¹ .min. Normal values for the pulmonary circulation in the various units are shown in Table 6.1 .

TABLE 6.1

Normal Values for the Pulmonary Circulation

	Driving Pressure	Pulmonary Blood Flow	Pulmonary Vascular Resistance
SI units	1.2 kPa	5 L.min ⁻¹	0.24 kPa.L ⁻¹ .min
Conventional units	9 mmHg	5 L.min ⁻¹	1.8 mm Hg.L ⁻¹ .min
Absolute CGS units	12’000 dyn.cm ⁻²	83 cm ³ .s ⁻¹	144 dyn. s.cm ⁻⁵

See Appendix A for explanation of units

Localization of the pulmonary vascular resistance

In the systemic circulation the greatest part of resistance is in the arterioles, along which the pressure falls from a mean value of approximately 12 kPa (90 mmHg) down to approximately 4 kPa (30 mmHg; Fig. 6.2 ). This pressure drop largely obliterates the pulse pressure wave, and the systemic capillary flow is not pulsatile to any great extent. In the pulmonary circulation, the pressure drop along the arterioles is very much smaller than in the systemic circulation and, as an approximation, the pulmonary vascular resistance is equally divided between arteries, capillaries and veins. Pulmonary arteries and arterioles, with muscular vessel walls, are mostly extraalveolar and involved in active control of pulmonary vascular resistance by mechanisms such as nervous, humoral or gaseous control. In contrast, pulmonary capillaries are intimately associated with the alveolus (see Fig. 1.8 ), so resistance of these vessels is therefore greatly influenced by alveolar pressure and volume. Thus in the pulmonary circulation, vessels without the power of active vasoconstriction play a major role in governing total vascular resistance and the distribution of the pulmonary blood flow.

Passive changes in pulmonary vascular resistance

Effect of pulmonary blood flow (cardiac output)

The pulmonary circulation can adapt to large changes in cardiac output with only small increases in pulmonary arterial pressure. Thus pulmonary vascular resistance must decrease as flow increases. Reduced resistance implies an increase in the total cross-sectional area of the pulmonary vascular bed, and particularly the capillaries. These adaptations to increased flow occur partly by passive distension of vessels and partly by recruitment of collapsed vessels, and the former is the more important factor.

Recruitment of previously unperfused pulmonary vessels occurs in response to increased pulmonary flow. This is particularly true of the capillary bed, which is devoid of any vasomotor control, so allowing the opening of new passages in the network of capillaries lying in the alveolar septa, and is most likely to occur in the upper part of the lung where capillary pressure is lowest (zone 1, see later). Capillary recruitment was first described in histological studies involving sections cut in lungs rapidly frozen while perfused with blood, which showed that the number of open capillaries increased with rising pulmonary arterial pressure. Recruitment of capillaries in the intact lung remains poorly understood. Animal studies using colloidal particles in the blood demonstrate that there is perfusion in all pulmonary capillaries, including in zone 1, during normal ventilation, but when airway pressure is increased there is no flow in almost two-thirds of capillaries in zone 1. It therefore seems that, with increased alveolar pressure unperfused capillaries are available for recruitment, but that under normal circumstances, with low airway pressures, there is flow in all capillaries. However, these studies using colloidal particles cannot discriminate between plasma or blood flow, and have led to speculation that some, almost collapsed, capillaries may contain only plasma (‘plasma skimming’) or even blood flow from the bronchial circulation.

Distension in the entire pulmonary vasculature occurs in response to increased transmural pressure gradient and is again most likely to occur in capillaries devoid of muscular control. In one animal study, capillary diameter increased from 5 to 10 µm as the transmural pressure increased from 0.5 to 2.5 kPa (5–25 cmH ₂ O). As described in the previous section, it now seems likely that capillaries never collapse completely, and therefore passive distension is clearly the more important adaptation to increased flow.

A striking example of the ability of the pulmonary vasculature to adapt to changing flow occurs after pneumonectomy (page 401), when the remaining lung will normally take the entire resting pulmonary blood flow without a rise in pulmonary arterial pressure. There is, inevitably, a limit to the flow that can be accommodated without an increase in pressure, and this will be less if the pulmonary vascular bed is affected by disease. The most important pathological cause of increased pulmonary blood flow is left-to-right shunting through a patent ductus arteriosus or through atrial or ventricular septal defects. Under these circumstances the pulmonary blood flow may be several-fold greater than the systemic flow before pulmonary hypertension develops. Despite this, remodelling of the pulmonary vessels commonly results in an increase in vascular resistance, causing an earlier and more severe rise in pulmonary arterial pressure.

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