Basics of Dead Space Ventilation

• Alveolar dead space:
  Normally, ventilation and perfusion of respiratory zones (lung units) are nicely matched (normal V/Q ~0.9). Consider a scenario where a small embolus blocks all perfusion to a lung unit. Since the perfusion of the lung unit reduces to zero, the V/Q ratio for this unit is infinity (V÷0 = ∞). A V/Q of infinity is the definition of alveolar dead space.
  

• Increased heterogeneity of V/Q ratio:
  This is the most difficult to grasp but also perhaps the most important factor in many disease states. Normally, there is only mild heterogeneity of V/Q ratios but this is increased in various pathological states. If a substantial proportion of lung units have a very high V/Q (e.g. >= 10), this can cause a ‘dead space effect’. Again, this is not truly alveolar dead space since the V/Q ratio is not infinity.

Let’s take the example of a patient with ARDS who is set on a high PEEP and high tidal volume. The dependent lung units are inflated normally but the non-dependent units are now overinflated. Lung overinflation compresses the capillaries and reduces blood flow to those units. Hence, the V/Q in non-dependent regions rises to 10. 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. You can think of low V/Q as ‘relative hypoventilation’ of that lung unit 🡪 alveolar pCO2 increases. 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.

• Shunt dead space

This is a misnomer. A significant shunt fraction can cause a dead space effect but this has obviously nothing to do with true dead space. The basic idea behind this is that the CO2 in the shunted blood never makes it to the respiratory zone and is hence retained by the body. However, this is a mild effect and a very large shunt fraction is needed to cause a significant dead space effect.[2]

Physiological dead space: a cumulative measure of wasted ventilation

Physiological dead space (VDphys) is another term that is troublesome but is commonly used in the literature. The term “wasted ventilation” has been proposed as an alternative, which sounds less technical but is certainly more accurate.[3] It is a cumulative index that incorporates all aforementioned causes of true dead space and dead space effects. Its formula is as follows – 

(PaCO2 – PECO2)/PaCO2

, where PECO2 is the mixed expired PCO2. The widely available index of end-tidal CO2 can be used as a surrogate for PECO2 to calculate physiological dead space but they are not interchangeable. Calculation of PECO2 requires a technique called volumetric capnography that can be performed by some ventilators or dedicated devices.

It is easier to understand the concept of VDphys concept if we consider a lung model with only two units – one with normal perfusion and other with no perfusion (V/Q = ∞). Physiological dead space is then equal to the proportion of tidal volume that would have to be delivered to the unperfused unit to account for the measured difference between PaCO2 and PECO2. Although it is an excellent global measure of wasted ventilation, it doesn’t differentiate between the relative contribution of the four factors listed above.

Practical implications

The practical implications of dead space in disease states are immense and impossible to cover in a limited space. I will highlight just two important examples that relate to anatomical dead space, as it is the most intuitive.

Impact of breathing pattern on dead space fraction

Clinical example: A patient is mechanically ventilated and paralyzed on VC mode. Initial settings: TV = 700cc, RR = 10/min, V̇E = 7L/min. To enforce lung protective ventilation, the tidal volume is halved (350cc) and respiratory rate doubled (20/min), thereby achieving the same V̇E of 7L/min. Will PaCO2 be unaffected after this change?

To learn the answer, we need to calculate the alveolar minute ventilation in each case. Let’s assume the anatomical dead space (VD) is 150 cc/min, and there is no alveolar dead space or V/Q heterogeneity.

• V̇A with initial settings = (VT – VD)xRR = (700–150)x10 = 5,500cc/min
• V̇A after changing settings = (VT – VD)xRR = (300–150)x20 = 3,000cc/min

Hence, even though the minute ventilation remained the same, the alveolar ventilation reduced by 45%! Another way to look at this is to calculate the dead space fraction (VD/VT) for each breath. In the first case, it is 150/700 = 0.21. After changing the settings, it would be 150/300 = 0.5. Hence, for the same minute ventilation, a rapid shallow breathing pattern increases anatomical dead space fraction. It is important to be mindful of this factor while managing mechanical ventilation.

Impact of apparatus (instrumental) dead space

Another important factor often overlooked in clinical practice is that of apparatus dead space (VDapp). In a non-intubated patient, the source of gas is the ambient air and the anatomical dead space starts at the mouth opening. In an intubated patient, the source of gas is the ventilator and its tubing (inspiratory limb). The basic anatomy of this circuit is presented in Figure 2. The key point to appreciate is that the inspiratory limb is constantly filled with fresh gas and can be thought of as an extension of the ventilator itself. So practically speaking, the source of gas in an intubated patient is the wye (Y-piece) of the ventilator circuit. Any equipment distal to the wye constitutes apparatus dead space. At minimum, this includes the endotracheal tube (see appendix). Other potential sources include heat and moisture exchanger (HME), sensors (flow, end-tidal etc.), catheter mount (ETT extension) etc.