where: AP = driving pressure difference (PB - Ppi) k = constant

V = flow rate p = breathing gas density r = airway radius

Figure 1.3-9. Total diameter of airways from the trachea to alveolar level, at normobaric pressure gas flow is turbulent only in bigger airways where total diameter is small and gas flow is high. In peripheral airways, where total diameters of airways is bigger and gas flows slower, gas flow is laminar (Welslau2)

Figure 1.3-9. Total diameter of airways from the trachea to alveolar level, at normobaric pressure gas flow is turbulent only in bigger airways where total diameter is small and gas flow is high. In peripheral airways, where total diameters of airways is bigger and gas flows slower, gas flow is laminar (Welslau2)

During expiration gas flows from peripheral to central airways. Due to successive reduction of total diameter of airways towards the trachea gas flow is more and more accelerated. Hereby in the larger airways laminar gas flow changes to turbulent flow. During inspiration this happens vice versa. Breathing gas flow in human airways is a mixture of both laminar and turbulent flow3.

Figure 1.3-10. Total diameter of airways, due to higher gas density at hyperbaric perssure gas flow is turbulent also in more peripheral airways (Welslau2)

2.3.5 Ventilation response at increased pressure

For a gas with constant composition its density raises proportionally to increasing pressure. Gas flow during expiration always contains a turbulent component, so increasing gas density will always lead to a higher breathing resistance8. Because maximum expiratory gas flow at a given lung volume depends on airway resistance, maximum expiratory flow decreases when gas density is increasing. A higher gas density results in diminished maximum inspiratory and expiratory flow volume loops (figure 1.3-11, left side) as well as in more strenuous breathing work, when ventilation has to keep up with physical workload. The higher the gas density, the smaller is the flow volume loop. When drawing expiratory breathing gas flow at a given lung volume (e.g. 60% VC) as a function of increasing gas density, you will notice a reduction of gas flow as shown in figure 1.3-11 (right side)9.

When inspiratory and expiratory gas flows are reduced by increasing pressure, it is no surprise that maximum voluntary ventilation (MVV) is also reduced by increasing pressure. Ventilation response to increased pCO2 in inspiration gas at rest will decrease when ventilatory work is increased due to higher gas density10. The presumed reason why ventilation response is decreased is that the additional ventilation work requires a stronger CO2 stimulus. During physical work at increased gas density the breathing frequency is lower and the tidal volume is higher than normal. By this means required additional ventilation work and dead space ventilation are minimized while ventilation volume per minute is maintained3.


Figure 1.3-11. Reduction of expiratory breathing gas flow as a function of increasing pressure (Welslau2; modified from Miller9)


3.1 Nitrogen toxicity

3.1.1 Occurrence

Nitrogen intoxication is also called "nitrogen narcosis"1. It may occur at pN2 in excess of ~ 320kPa (3.2bar). When breathing air, this happens at a total pressure of 400kPa (4.0bar). When breathing gas mixtures with reduced nitrogen fraction (Fn2), symptoms will occur at higher total pressure depending on pN2. Inter-individual susceptibility to nitrogen varies widely. There is also great intra-individual variance for the occurrence of symptoms from day to day. Diverse factors may affect susceptibility to nitrogen narcosis. The list of influential factors is long and the risk of nitrogen narcosis can never be completely ruled out. Nitrogen narcosis will rarely occur in hyperbaric medicine because of limited pressure for standard treatments. But in treatments at higher pressure with mixed gases breathing for special indications (e.g. severe decompression incidents), it may become a problem for air breathing chamber attendants.

3.1.2 Symptoms

Nitrogen affects humans similarly to medical narcotic gases, but to a far less extent. Initial stages of nitrogen narcosis are described to be similar to alcohol or LSD intoxication. Symptoms may not be recognized by the affected individual.

Table l.3-2. Nitrogen narcosis: enhancing factors and symptoms1

Factors enhancing susceptibility to nitrogen narcosis

Nitrogen narcosis symptoms


euphoria / dysphoria


mental concentration impairment


logical thinking impairment


reaction time slowed down


short time memory impairment


mental arithmetic impairment


competence to judge impairment


Hallucinations (late)

Carbon dioxide intoxication

loss of consciousness (late)

3.1.3 Pathogenesis

A popular hypothesis explains narcotic effects of nitrogen with its high solubility in lipids, leading to N2 concentration in the lipophil layers of cell membranes and especially synaptic connections. This is believed to lead to swelling of cell and synaptic membranes with the effect of delayed impulse conduction between nerve cells11. One of the alternative explanations is that membrane proteins are the site of action, and that narcosis is the result of neurotransmitter mechanisms12.

When comparing different inert gases, i.e. gases not taking part in human metabolism, we can state a parallelism between relative narcotic potency and solubility in lipids. Provided the relative narcotic effect of nitrogen is 1, other gases may ranked according to their relative narcotic potency (see table 1.3-3). Solubility of gases in lipids shows that gases with a higher narcotic potency also have a higher solubility in lipids compared with less

narcotic gases .

Table 1.3-3. Comparison of molecular weight, solubility in lipid and narcotic potency of different gases (modified from Bennett and Elliott )_


Molecular weight

Solubility in lipid

Relative narcotic potency


[Bunsen coefficient]

[Nitrogen = 1]

Helium (He)




Neon (Ne)




Hydrogen (H2)




Nitrogen (N2)




Argon (Ar)




Krypton (Kr)




Xenon (Xe)




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