Effects of lung volume on pulmonary vascular resistance

The pulmonary vascular resistance is calculated by dividing the driving pressure (pulmonary artery minus left atrial pressure) by the flow, so it includes the resistance of all the vessels between the right and left heart. The importance of the differentiation between intra- and extra-alveolar vessels is that changes in lung volume exert opposing effects on the two sets of vessels. Expansion of the lung will occur when transpulmonary pressure is increased, whether this is produced by a reduction in absolute pleural pressure or an increase in alveolar pressure, and this will compress the intra-alveolar vessels and so increase their resistance to blood flow. These changes will also tend to increase the size of zone 1 and so increase alveolar dead space. On the other hand, expansion of the lung, by whatever means, will increase the diameter of extra-alveolar vessels and so decrease their resistance. The diameter of the extrapulmonary vessels will also tend to increase when absolute pleural pressure is decreased, but as these vessels are large the effects on resistance will be relatively small, and these effects may be offset by local distortions of the hilum associated with the expansion of the lung.

As the extra-alveolar vessels are narrow at low lung volumes but expanded at high lung volumes, whereas the pulmonary capillaries are compressed at high lung volumes and open at low lung volumes, the pressure-volume curve for the whole lung is U shaped, the resistance being minimal at the normal end expiratory position or functional residual capacity (Fig. 5.2).

Regional inhomogeneity of blood flow

The gravitational model of the distribution of pulmonary blood flow was derived from radioisotope studies, which measured distribution in relatively large areas of lung. In recent years, methods yielding much higher resolution of the spatial distribution of blood flow have shown that, in humans, there is marked heterogeneity of distribution within an isogravitational plane, and that there is a radial distribution of flow with the greatest flow in the centre of lung lobes.11 12 There have also been a large number of studies in quadripeds which show: that there is a marked heterogeneity of flow between 1 and 2 cm samples of lung taken from isogravitational planes;13 that there is a distribution of flow which favours the dorsal regions of lung regardless of posture;14 15 and that flow distribution changes little when gravitational forces are increased by a factor of three.16 These studies

Lung Vascular Resistance

RV FRC TLC

Lung volume

Fig 5.2 The contribution of the resistance of the intra-alveolar (IAV) and extra-alveolar (EAV) vessels to the total pulmonary vascular resistance (PVR) at different lung volumes. Total resistance is minimal at the functional residual capacity (FRC).

suggest that distribution is mainly governed by variations in the resistive properties of the pulmonary vasculature resulting from asymmetrical branching, or other anatomical differences, and that gravity plays a much smaller role than had previously been thought. When considering the animal evidence, it must be remembered that the erect human tends to have a relatively higher lung volume, with distended extra-alveolar vessels, lower smooth muscle tone, and a greater proportion of the serial resistance in the middle (microvascular) segment than the animals studied. Although recent studies have shown that the gravitational gradient of distribution in baboons is decreased when they are held upside down, this finding could be explained by the effects of an alteration in pleural pressure gradient on extra-alveolar vessels. In the absence of firm evidence to the contrary, it seems reasonable to conclude that there is an important gravitational component to distribution in the human, but that there is much more inhomogeneity of distribution than had previously been assumed. How these local variations in pulmonary blood flow can be matched by ventilation distribution to minimise ventilation-perfusion inequalities has yet to be determined.17 18

Clinical implications

Fortunately, the gravitationally induced increase in blood flow down the lung is normally matched by an increase in ventilation. This increase is generated by the interaction between the non-linear pressure-volume curve of the lung and the gravitationally induced gradient of pleural pressure (Fig. 5.3). When the lung is vertical (height 30 cm) the pressure in the pleural space is about -1 kPa (-10 cm H^O) in the non-dependent areas and about -0-25 kPa (-2-5

cm H2O) in dependent zones at the normal end expiratory lung volume. The resulting transpulmonary pressure of 1 kPa (10 cm H2O) at the top of the lung and 0-25 kPa (2-5 cm

H2O) at the base causes the upper alveoli to have a larger resting volume than those at the base. When the transpulmonary pressure is increased by a reduction in absolute pleural pressure during inspiration, however, the lower alveoli will expand more than the upper because they lie on a steeper part of the pressure-volume curve. Thus, under normal conditions, the increase in ventilation down the lung (which is about half that of the increase in blood flow) minimises ventilation-perfusion inequalities (Fig. 5.4). If, however, there is dependent airway closure as a result of a loss of lung elastic recoil or of a reduction in functional residual capacity, there may be no ventilation to dependent zones during the early part of inspiration, so that these zones develop low ventilation-perfusion ratios and arterial PO2 (PaO2) is reduced.

Pleural Pressure Mechanical Ventilation

Fig 5.3 Distribution of ventilation. Above: during spontaneous ventilation the gravitationally induced gradient of pleural pressure causes the non-dependent alveoli to lie on the upper, curved part of the lung pressure-volume curve, whereas the dependent alveoli lie on the lower, steep portion. As a result the increase in transpulmonary pressure (AP) during inspiration causes more ventilation to enter the dependent zones of the lung. Below: the absence of diaphragmatic activity during controlled ventilation permits the hydrostatic pressure generated by the abdominal contents to influence distribution. The position of the alveoli on the pressure-volume curve of the total respiratory system (that is, lung plus chest wall) now causes ventilation to be preferentially distributed to the non-dependent zones. Note that changes in end expiratory lung volume may modify the distribution by moving the alveoli to different portions of the P/V curves.

Fig 5.3 Distribution of ventilation. Above: during spontaneous ventilation the gravitationally induced gradient of pleural pressure causes the non-dependent alveoli to lie on the upper, curved part of the lung pressure-volume curve, whereas the dependent alveoli lie on the lower, steep portion. As a result the increase in transpulmonary pressure (AP) during inspiration causes more ventilation to enter the dependent zones of the lung. Below: the absence of diaphragmatic activity during controlled ventilation permits the hydrostatic pressure generated by the abdominal contents to influence distribution. The position of the alveoli on the pressure-volume curve of the total respiratory system (that is, lung plus chest wall) now causes ventilation to be preferentially distributed to the non-dependent zones. Note that changes in end expiratory lung volume may modify the distribution by moving the alveoli to different portions of the P/V curves.

During controlled ventilation the distribution of ventilation is determined by the shape of the total respiratory (lung plus chest wall) pressure-volume curve because the inspiratory muscles are no longer active. Furthermore, in the supine position, the hydrostatic pressure produced by the semiliquid abdominal contents exerts an upward pressure on the dependent areas of the diaphragm so that ventilation is preferentially directed into non-dependent zones. As the distribution of blood flow is still gravitationally determined there is gross mismatching of ventilation and perfusion (Figs. 5.3 and 5.4). The situation is exacerbated if there is a decrease in pulmonary artery pressure resulting from a reduction in blood volume, peripheral pooling of blood, or the administration of oxygen or a pulmonary vasodilator drug, because this will result in an increase in zone 1 with a further increase in alveolar dead space. Similar changes may occur if mean alveolar pressure is increased by mechanical ventilation with positive end expiratory pressure (PEEP), or if the emptying of the lung is delayed in patients with increased airway resistance (auto or intrinsic PEEP). When there is an increase in dead space/tidal volume ratio in the spontaneously breathing patient with normal respiratory control mechanisms, minute ventilation will tend to increase to compensate for the increased dead space

Airway Resistance

Fig 5.4 Distribution of ventilation ^ v J and blood flow plotted against lung height during spontaneous respiration (left) and during anaesthesia with controlled ventilation (right). Note that the small alveolar dead space (VDalv) associated with zone 1 conditions during spontaneous respiration is increased by the greater ventilation to non-dependent zones during controlled ventilation. In elderly people there is often an area with

Fig 5.4 Distribution of ventilation ^ v J and blood flow plotted against lung height during spontaneous respiration (left) and during anaesthesia with controlled ventilation (right). Note that the small alveolar dead space (VDalv) associated with zone 1 conditions during spontaneous respiration is increased by the greater ventilation to non-dependent zones during controlled ventilation. In elderly people there is often an area with

low ventilation-perfusion ^ ratios at the base of the lung associated with airway closure. General anaesthesia usually results in the development of a shunt in dependent lung zones as a result of compression collapse.

so that PCO2 is maintained at normal levels, but if the minute volume is controlled by a ventilator, PCO2 may increase. If the rest of the lung is normal there will be no effects on PaOj other than those arising from any increase in PCO2.

In most patients undergoing anaesthesia or intensive care there is some alveolar collapse in dependent lung zones and this creates an intrapulmonary right to left shunt.19 This is usually quantified by expressing the shunt as a percentage of the cardiac output. The PaO2

resulting from a given shunt depends on the alveolar PO2 (PAO2) (which in turn depends on the inspired PO2 (PIO2), the alveolar PCO2 (PACO2) and the respiratory exchange ratio) and on the mixed venous (Fig. 5.5). Normally, it is assumed that an increase or decrease in the percentage shunt means that the volume of collapsed lung has increased or decreased. The percentage shunt may, however, change with no alteration of the volume of collapsed lung if the proportion of blood flowing through the oxygenated and collapsed zones is changed by an alteration in the pulmonary vascular pressures. For

Oxygen Tension Venous Blood
Fig 5.5 Factors governing arterial oxygen tension, PIO2, PAO2, PACO2, inspired and alveolar gas tensions; R,

respiratory exchange ratio (normally 0.8); /Ja02. arterial and mixed venous oxygen tensions;

, shunt flow and cardiac output; 2 , oxygen consumption per minute. Note that the Pa02 depends on both the proportion of blood flowing through the shunt and the depends on the relationship between Or and 2.

example, blood flow through a collapsed area of lung is maximal when it is in the dependent position but can be reduced by rotating the patient so that the collapsed area is uppermost, with a resultant decrease in shunt and increase in PaO2?^ (The improvement in oxygenation is not, however, usually sustained because collapse soon develops in the areas of lung now made dependent, whereas the collapse in the non-dependent zones disappears.)

The opposite effect can be seen in patients with dependent zone collapse when pulmonary artery pressure and cardiac output are decreased by vasodilator drugs. Under such circumstances the continued flow through the dependent zone with reduced flow to the ventilated area of lung will cause an apparent increase in the proportion of shunt, even though the actual flow through the shunt is unchanged (Fig. 5.6). The application of a high peak airway pressure or PEEP will also reduce flow through the ventilated non-dependent zones and so will have a similar effect. Another example is the redistribution of flow which may be seen during anaesthesia for thoracic surgery with a double lumen tube. When the upper lung is collapsed the effects of gravity and hypoxic vasoconstriction in the upper lung decrease the upper lung blood flow so that the shunt is only 20-30% instead of the 45-55% predicted from the relative volume of each lung. If the mean airway

Lung Po2 Distribution

Fig 5.6 The effect of a decrease in pulmonary artery pressure (P) resulting from a decrease in cardiac output on percentage shunt in the presence of dependent zone collapse or consolidation. If flow to the ventilated area of lung is decreased from 3 1/min to 2 1/min whilst flow through the shunt remains at 11/min the percentage shunt & will increase from 25% to 33%. Note that the resulting fall in arterial PO2 (PaO2) will be accentuated by the decrease in mixed venous

Po2 (Pfo2)

Fig 5.6 The effect of a decrease in pulmonary artery pressure (P) resulting from a decrease in cardiac output on percentage shunt in the presence of dependent zone collapse or consolidation. If flow to the ventilated area of lung is decreased from 3 1/min to 2 1/min whilst flow through the shunt remains at 11/min the percentage shunt & will increase from 25% to 33%. Note that the resulting fall in arterial PO2 (PaO2) will be accentuated by the decrease in mixed venous

Po2 (Pfo2)

resulting from the decrease in output.

Vascular Resistance Percentage
Fig 5.7 Factors that may increase flow through the non-dependent collapsed lung during one lung anaesthesia in the lateral position. The distribution of blood flow and ventilation with lung height is shown on the left of the diagram.

pressure in the dependent lung is increased, however, by the use of high peak or end expiratory pressures, shunt will increase because the compression of capillaries in the dependent lung increases pulmonary artery pressure and so diverts blood flow into the non-dependent collapsed lung (Fig. 5.7). The injection of pulmonary vasoconstrictor drugs will have a similar effect.

Another factor that affects the PaO2, even when the areas of shunt are scattered throughout the lung and are not changed by alterations in lung volume, is the direct relationship between shunt and cardiac output. The increase in shunt with cardiac output occurs when the output is changed by altering blood volume or the administration of inotropic drugs but the cause is not properly understood. It is possible that the increase in flow increases pulmonary artery pressure and so opposes hypoxic vasoconstriction. An p-

increase in output will usually increase and this may also reduce the magnitude of the vasoconstrictor response (see below). Although the increase in may increase the proportion of shunt it will also increase the oxygen saturation of the blood flowing through the shunt and so tend to offset the effects of the increased percentage shunt on PaO2.

Obviously, these interactions may lead to very variable effects on PaO2.

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  • anselma
    How will increased lung volume affect PVR?
    11 months ago

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