Ventilation Perfusion Mismatching
At rest, alveolar ventilation and pulmonary blood flow are similar, each being around 5 L/min. Ventilation (V- A) and perfusion (Q- ) may vary in different lung regions, but for optimal gas exchange they must be matched. Areas with high perfusion need high ventilation, and, ideally, local ventilation-perfusion ratios (VA/Q) should be close to 1. Ventilation-perfusion mismatching or inequality is said to occur when regional VA/Q ratios vary, with many being much greater or less than 1 (Fig. 14a). A right-to-left shunt from complete collapse or consolidation of a region (Chapter 13) has VA/Q = 0, and can be viewed as an extreme example of ventilation-perfusion mismatching.
At the other extreme, alveolar dead space from a pulmonary embolus is a ventilated region without perfusion and VA/Q = ∞. Regions where VA/Q is much greater than 1 have excessive ventilation or dead space effect and blood from them has a high Po2 and a low Pco2. Regions with VA/Q much less than 1 behave qualitatively like shunts and are sources of shunt effect or venous admixture. Blood draining them has undergone some gas exchange, but Po2 is lower and Pco2 higher than normal. The effect on Po2 and O2 content draining different VA/Q regions both during air breathing and during oxygen breathing is shown in Fig. 14a (lower panel).
Effect of the upright posture on perfusion, ventilation and VA/Q (Fig. 14b)
Hydrostatic pressure in all vessels varies with vertical height above or below the heart because of the weight of blood. On standing, the increased pressure at the lung bases distends vessels, increasing f ow. Pressures generated by the right side of the heart are low, and higher up the lung vascular pressures in diastole may fall below alveolar pressure at the venous end of the pulmonary capillary. In such regions, fl w is reduced and determined by the difference between arterial and alveolar pressure. There may be regions at the apices - especially in haemorrhage or positive-pressure ventilation where alveolar pressure also exceeds pressure at the arterial end of the pulmonary capillaries. The vessels collapse completely for part of each cardiac cycle, giving low intermittent flow. The net result is a blood flow per unit volume of lung tissue that falls progressively from base to apex.
Gravity also affects intrapleural pressure, which is less negative at the base than at the apex. As a result, at functional residual capacity, apical alveoli are more expanded with less capacity for further expansion during inspiration than at the bases. Consequently, ventilation is also higher at the base than at the apex. The effect of gravity on ventilation is less marked than on perfusion and so VA/Q is higher at the apex than at the base. In young people, the degree of mismatching is modest and has little effect on blood gases because the regions with low VA/Q are still ventilated enough to nearly saturate the blood passing through them with oxygen. The scatter of ventilation-perfusion ratios increases with age and contributes to the reduction in Pao2 seen in the elderly.
Ventilation–perfusion matching in disease
Increased ventilation-perfusion mismatching is an important cause of gas exchange problems in many respiratory diseases, including asthma, chronic obstructive pulmonary disease (COPD), pneumonia and pulmonary oedema. Regions of low VA/Q may arise when airways are partly blocked by bronchoconstriction, inflammatio or secretions and high VA/Q areas arise in emphysematous areas where capillaries are lost or pulmonary emboli are partially blocking blood fl w. Hypoxic vasoconstriction (Chapter 13) helps reduce the severity of ventilation-perfusion mismatching by diverting blood from regions with low VA/Q to regions that are better ventilated.
Effect of ventilation–perfusion mismatching on arterial blood gases
Blood emerging from areas with high VA/Q might be expected to compensate for blood from areas with low VA/Q. This is not the case, for two reasons (Fig. 14c). First, although Po2 will be increased in high VA/Q regions, oxygen content is raised little, as blood is normally nearly saturated. Blood draining regions with low VA/Q and low Po2 (especially if <8 kPa, 60 mmHg) will have significantl reduced oxygen content. In addition, these areas contribute more blood than areas with high VA/Q, which are typically caused by reduced perfusion. The net effect of mixing blood from areas with a wide range of ventilation-perfusion ratios is a low arterial O2 content and Pao2. CO2 content is less severely affected because the over ventilated areas do lose extra CO2 and partly compensate for low VA/Q regions. Moreover, any abnormalities of Pao2 and Paco2 will lead to a reflex increase in ventilation, which usually corrects or overcorrects the raised Paco2 while being less effective at raising Pao2. The fina arterial blood gas picture, a low Pao2 and a normal or low Paco2, is similar to that resulting from anatomical right-to-left shunts (Chapter 13).
One difference is that arterial hypoxia caused by ventilation-perfusion mismatching improves much more with oxygen therapy than that caused by a shunt. In a hypoxic patient with a pure shunt, the oxygen-enriched air fails to reach the shunted blood. In VA/Q mismatching, increased oxygen fraction can increase local Po2 in areas of low VA/Q (Fig. 14a), giving rise to significan improvement in arterial oxygen content and pressure.
Assessment of ventilation–perfusion mismatching
Regional ventilation and perfusion can be visualized by inhalation and infusion of appropriate radioisotopes (Chapter 21). A simple but useful index of the degree of mismatching is the difference between Po2 in gas-exchanging or 'ideal' alveoli and in arterial blood. Ideal alveolar Po2 can be calculated from the alveolar air equation (Fig. 14d). An increased A–a Po2 gradient (A = alveolar Po2, a = arterial Po2) is usually caused by ventilation-perfusion mismatching or anatomical right-to-left shunts. In healthy young people, there is a small A-a gradient (<2 kPa) arising from the normal anatomical right-to-left shunts, discussed in Chapter 13. The normal value for A-a gradient increases with age and in a healthy 80-year-old may be as high as 5 kPa (38 mmHg).