![]() ![]() , where P E CO 2 is the mixed expired PCO 2. It is a cumulative index that incorporates all aforementioned causes of true dead space and dead space effects. The term “wasted ventilation” has been proposed as an alternative, which sounds less technical but is certainly more accurate. Physiological dead space (VDphys) is another term that is troublesome but is commonly used in the literature. Physiological dead space: a cumulative measure of wasted ventilation However, this is a mild effect and a very large shunt fraction is needed to cause a significant dead space effect. The basic idea behind this is that the CO 2 in the shunted blood never makes it to the respiratory zone and is hence retained by the body. A significant shunt fraction can cause a dead space effect but this has obviously nothing to do with true dead space. Furthermore, since the majority of the perfusion is happening in the dependent region, the global gas exchange mirrors the gas exchange in this area – overall resulting in a dead space effect. You can think of low V/Q as ‘relative hypoventilation’ of that lung unit □ alveolar pCO2 increases. At the same time, most of the blood flow is now diverted to the dependent lung units, where the V/Q drops down to 0.5. Hence, the V/Q in non-dependent regions rises to 10. Lung overinflation compresses the capillaries and reduces blood flow to those units. The dependent lung units are inflated normally but the non-dependent units are now overinflated. Let’s take the example of a patient with ARDS who is set on a high PEEP and high tidal volume. ![]() Again, this is not truly alveolar dead space since the V/Q ratio is not infinity. >= 10), this can cause a ‘dead space effect’. If a substantial proportion of lung units have a very high V/Q (e.g. Normally, there is only mild heterogeneity of V/Q ratios but this is increased in various pathological states.
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