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Welcome back to the tasty morsels of critical care podcast.
Today we’re talking about dead space. While it may sound like something from The Expanse, we’re actually talking about the physiological concept of dead space here. This is pretty core physiology that crops up in clinical practice all the time so I think it’s worth thinking about.
As usual this represents a sort of idiot’s guide to the topic with just enough information to scrape by in an exam and in clinical practice but likely with large gaps, simplifications and occasional frank errors in description.
Definition is “the fraction of tidal volume which does not participate in gas exchange.” But let’s be clear the word participation here refers more to an inability rather than a surly choice by the dead space fraction not to participate as it didn’t get picked for football till last. The dead space fraction never has the option of participating in gas exchange as it never reaches any functional gas exchange surface.
At its most basic (and that’s the only form I’m interested in) it can be split into:
- Apparatus dead space – the amount of gas in the circuit and associated dongles like ETT, an NIV face mask or an HME.
- Physiological dead space – this is split further into:
- anatomic- gas in the conducting airways and
- alveolar – gas in non perfused alveoli
Phsyiological dead space usually takes up ~20-30% of the Vt. As mentioned above it splits into two components, anatomic and alveolar. As you can imagine the anatomic is pretty fixed but the alveolar dead space can vary markedly depending on V/Q matching.
Anatomic dead space is ~2ml/kg (about 150mls) but this includes the oropharynx that will be bypassed with the placement of an ETT or even better a tracheostomy with both of these interventions reducing anatomic dead space. I think the most important clinical take away about anatomical dead space is that it is fairly fixed. Assuming a 2ml/kg anatomic dead space, if you’re ventilating someone at 8ml/kg PBW and want to reduce to 6ml/kg PBW the fraction of anatomic dead space in each breath goes from 20% to 33%. In other words, while you’ve only reduced the Vt by 20% you’ve reduced the portion of gas participating in gas exchange by a third. There is of course good empiric evidence that a lower Vt is better but in terms of clearing CO2 dropping the Vt disproportionately reduces the fraction of gas available at the alveolus and may cause big issues with your CO2. Indeed at some point a rate reduction rather than Vt reduction may be the more favorable factor to reduce overall mechanical power delivered to the lung. That all seees very persuasive and logical but is countered by the simple fact that it doesn’t seem to be true when tested.
It seems that at very low Vt gas exchange continues to be more effective than one might expect likely due to 2 mechanisms beyond simple mass gas movement.
- laminar flow occurs allowing a central column of gas to move in and out
- there is expiratory gas mixing – basically diffusive gas mixing that ensures the right molecules are in the right place at the right time
Moving onto alveolar dead space, there are a number of things that might increase it:
- reduced cardiac output: eventually lung units stop receiving perfusion
- parenchymal disease: air space cavities no longer with effective perfusion due to thickening of interstitium
- high airway pressures: ensures aerated alveoli but may limit blood inflow to the lung unit
- pulmonary vascular occlusion: eg PE (one of probably several mechanisms of hypoxia)
- Posture – this will affect the west zone of particular lung units
The main consequence of increased dead space will be primarily seen in your CO2 with either hypercapnia or a requirement for a huge minute volume. As noted in the alveolar gas equation it will affect oxygenation much less but eventually it will impair oxygenation.
The unfortunately short lived and much missed basic science clinic podcasts from Steve Morgan and Sophie Connolly.