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. This is the most difficult to grasp but also perhaps the most important factor in many disease states. A V/Q of infinity is the definition of alveolar dead space. Since the perfusion of the lung unit reduces to zero, the V/Q ratio for this unit is infinity (V÷0 = ∞). Consider a scenario where a small embolus blocks all perfusion to a lung unit. Normally, ventilation and perfusion of respiratory zones (lung units) are nicely matched (normal V/Q ~0.9). The dead space in an average adult has been reported to be ~150 cc or 2cc/kg ideal body weight. Anatomical dead space is thus defined as the volume of the conducting zone (Figure 1). The remaining circuit: respiratory bronchioles to alveolar sacs (generation 23) participate in gas exchange and is called the respiratory zone. The entire airway circuitry all the way from mouth to the terminal bronchioles (~generation 14-16) is the conducting zone of the respiratory system. Mechanisms that create ‘dead space effect’.A conceptual, simplistic categorization is as follows: The nomenclature describing dead space can be quite confusing (see for in-depth reading). , where V̇CO 2 = CO 2 production by the body (units: cc/min) and V̇ A = alveolar ventilation. The alveolar ventilation controls CO 2 homeostasis according to the alveolar ventilation equation : Mathematically, V̇ A is total ventilation minus anatomical dead space ventilation. Its calculation requires exclusion of ventilation occurring in the anatomical dead space. in a passive mechanically ventilated patient on volume control (VC) mode, V̇ E = V T x RR.Īlveolar ventilation ( V̇ A the subscript ‘A’ denotes ‘alveolar’) is the amount of ventilation occurring in the alveoli in one minute. Minute ventilation ( V̇ E the subscript ‘E’ denotes ‘exhaled’) is the total ventilation in one minute (units: L/min). At this point, it is helpful to define minute ventilation and alveolar ventilation : V D /V T is a common way to quantify dead space. The fraction of the tidal volume that does not contribute to gas exchange is known as dead space fraction (V D /V T where V T = tidal volume and V D = dead space volume). A certain amount of dead space is normally present in every person (this is known as anatomical dead space: see below). This concept can be extended to include factors that cause a dead space effect. Simply put, dead space represents the volume of ventilated air that does not participate in gas exchange.
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