Physiological consequences of increased dead space

This chapter is most relevant to Section F6(v) from the 2017 CICM Primary Syllabus, which expects the exam candidates to be able to "describe the physiological impact of increased dead space". This is a highly examinable topic which has come up twice in the past papers:

• Question 3 from the first paper of 2018
• Question 7(p.2) from the first paper of 2010

 This is a fairly narrow topic, and can be summarised easily:

 The section from the 8th edition of Nunn's (p.123) which deals with this topic is relatively short, but that appears to be all that is required to answer CICM primary exam questions. 

Consequences of increased dead space

At a fundamental level, increasing the dead space functionally indistinguishable from hypoventilation:

• Dead space is a fraction of the total tidal volume
• Of the tidal volume, only the non-dead fraction participates in gas exchange
• Ergo, increasing dead space has the same effect as reducing the tidal volume.

Theoretically, it should not matter which dead space component has increased: this effect would be the same. However, functionally there may be some differences. 

Consequences of increased apparatus dead space

Consider: let's say you have a patient who is breathing comfortably with tidal volumes of 500ml, of which there is 150ml of total dead space which is all anatomical. Let's say you have now increased your dead space by introducing an extra 1000ml of apparatus dead space into the respiratory circuit.

Now, your alveolar ventilation remains the same, around 350ml, but now the tidal volume, moving 500ml of gas in and out of the respiratory circuit, is composed just of rebreathed gas. No added oxygen is inhaled, unless it has mixed by diffusion with the contents of the apparatus. No CO₂ removal occurs, unless it is also by diffusion. The consequence of this is that the patient will now need to increase their tidal volume by at least the same volume as the apparatus dead space in order to get back to something resembling normal gas exchange.

This effect was demonstrated by Kelman et al (1973). The investigators we are to secure the cooperation of several young fit physiology students. Each student was then attached to an apparatus dead space, "a partitioned Perspex box of total internal volume 1,200 ml". Their minute volume was found to increase signficantly, mainly due to an increase in the tidal volume.  For some reason, it seemed important for the investigators to choose students who had not yet studied any respiratory physiologyand were therefore completely ignorant of the purpose of the experiment. The concern was that though junior, "they were however not unintelligent; and it is, of course, possible that they were consciously evolving a strategy to deal with the respiratory hindrance of the increased dead-space". 

One might complain that the example offered above has minimal relevance to the ICU environment, as our patients rarely have massive perspex boxes hanging off their endotracheal tubes. A more relevant example of the same situation is ARDS, where the dead space may be small but the tidal volume is decreased. In these scenarios, a small volume of apparatus dead space can make all the difference. Hinkson et al (2006) found that removing a HME and 15cm of flexible tubing from the circuit of an ARDS patient can decrease the PaCO₂ by about 11 mmHg, all though the magic of decreasing dead space.

Consequences of increased alveolar dead space

Increasing the alveolar dead space with a normal anatomical/apparatus component will increase your minute volume requirements proportionally to the change in the rato of dead space to alveolar ventilation. Consider: if the increasing alveolar dead space has halved your alveolar ventilation, you need to double your minute volume to restore your alveolar ventilation back to the original levels. If your dead space has increased to 80% of the tidal volume, you need to increase your minute volume by five times. This is seen in extremely large pulmonary emboli.