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Chapter four: Pressure regulation
1. High pressure nervous syndrome (HPNS) is caused by the hydrostatic pressure inducing tremors and convulsions.
2. Nitrogen narcosis is caused by the anesthetic effect of certain gases at high pressure
ultimately leading to loss of consciousness at deeper depths.
3. Decompression sickness (DCS) is caused by the dissolved gas coming out of solution
and forming bubbles during a reduction in pressure. Bubbles may cause lesions or
embolize blood vessels leading to ischemic damage.
4. Shallow-water blackout is the loss of consciousness due to cerebral hypoxia caused by
depletion of blood O 2 associated with a rapid drop in partial pressure of lung O 2
toward the end of a breath-hold dive.
5. Oxygen toxicity is caused by the high partial pressure of O 2 with short exposure causing central nervous system toxicity, longer exposures causing pulmonary or ocular
toxicity.
We are familiar with these syndromes due to their effect on human divers, and primarily
scuba divers. While scuba divers breathe compressed air and are, therefore, exposed to the
deleterious effects of increased blood gas concentrations (i.e., at 30 m depth they breathe
four times the gas concentrations as would someone breathing at the surface), breath-hold
divers bring down only what is contained in the lungs, which mixes with gases previously absorbed and only causes problems if it is not completely removed during the surface interval. Consequently, scuba divers absorb significantly more N 2 as compared to
breath-hold divers, which may have deleterious effects. This was well demonstrated by
Scholander (1940) who pressurized a container with two frogs, one held underwater and
one breathing under pressure. The frog breathing under pressure died while that held
underwater (breath-holding) survived.
Thus until recently, it has been widely believed that free-divers, and particularly those
with shallow depths of alveolar collapse (such as incurred by exhalation prior to diving),
would be relatively immune from diving diseases. Alveolar collapse at shallow depths
(Figure 4.2) would reduce the amount of inert gas absorbed and minimize the likelihood
of supersaturation and bubble formation during ascent. However, recent work looking at
human free-divers has suggested otherwise (Lemaitre et al. 2009). In fact, rapid, repetitive
breath-hold diving in humans can result in decompression sickness (Schipke et al. 2006)
and modeling work suggests that it may even be possible to develop DCS after a single
deep breath-hold dive (Fitz-Clarke 2009). It seems that in free-diving animals, tissues can
become highly saturated under certain circumstances depending on the iterative process
of loading during diving and washout at the surface (Paulev 1967); and there is ample
evidence that marine mammals are living with blood and tissue N 2 tensions that exceed
ambient levels (de Quiros et al. 2013b; Falke et al. 1985; Moore et al. 2009; Ridgway and
Howard 1979).
4.2.6.1 High pressure nervous syndrome and nitrogen narcosis
In humans, the symptoms of HPNS appear at pressures exceeding 11 ATA (Halsey 1982;
Jain 1994), although individual differences make it difficult to give an absolute pressure (or
depth) at which the symptoms first appear (Bennett and Rostain 2003; Brauer et al. 1975).
Although species show differences in their susceptibility to elevated pressures, this variability appears to be related to the complexity of the CNS, and organisms with a less complex CNS seem to have a higher tolerance (Hunter and Bennett 1974; Rostain et al. 1983).
Many marine mammals would therefore appear to be at risk of HPNS since they have fast
descent rates (1–2 m/s), and spend time at pressures far exceeding 11 ATA.
Chapter four: Pressure regulation
1. High pressure nervous syndrome (HPNS) is caused by the hydrostatic pressure inducing tremors and convulsions.
2. Nitrogen narcosis is caused by the anesthetic effect of certain gases at high pressure
ultimately leading to loss of consciousness at deeper depths.
3. Decompression sickness (DCS) is caused by the dissolved gas coming out of solution
and forming bubbles during a reduction in pressure. Bubbles may cause lesions or
embolize blood vessels leading to ischemic damage.
4. Shallow-water blackout is the loss of consciousness due to cerebral hypoxia caused by
depletion of blood O 2 associated with a rapid drop in partial pressure of lung O 2
toward the end of a breath-hold dive.
5. Oxygen toxicity is caused by the high partial pressure of O 2 with short exposure causing central nervous system toxicity, longer exposures causing pulmonary or ocular
toxicity.
We are familiar with these syndromes due to their effect on human divers, and primarily
scuba divers. While scuba divers breathe compressed air and are, therefore, exposed to the
deleterious effects of increased blood gas concentrations (i.e., at 30 m depth they breathe
four times the gas concentrations as would someone breathing at the surface), breath-hold
divers bring down only what is contained in the lungs, which mixes with gases previously absorbed and only causes problems if it is not completely removed during the surface interval. Consequently, scuba divers absorb significantly more N 2 as compared to
breath-hold divers, which may have deleterious effects. This was well demonstrated by
Scholander (1940) who pressurized a container with two frogs, one held underwater and
one breathing under pressure. The frog breathing under pressure died while that held
underwater (breath-holding) survived.
Thus until recently, it has been widely believed that free-divers, and particularly those
with shallow depths of alveolar collapse (such as incurred by exhalation prior to diving),
would be relatively immune from diving diseases. Alveolar collapse at shallow depths
(Figure 4.2) would reduce the amount of inert gas absorbed and minimize the likelihood
of supersaturation and bubble formation during ascent. However, recent work looking at
human free-divers has suggested otherwise (Lemaitre et al. 2009). In fact, rapid, repetitive
breath-hold diving in humans can result in decompression sickness (Schipke et al. 2006)
and modeling work suggests that it may even be possible to develop DCS after a single
deep breath-hold dive (Fitz-Clarke 2009). It seems that in free-diving animals, tissues can
become highly saturated under certain circumstances depending on the iterative process
of loading during diving and washout at the surface (Paulev 1967); and there is ample
evidence that marine mammals are living with blood and tissue N 2 tensions that exceed
ambient levels (de Quiros et al. 2013b; Falke et al. 1985; Moore et al. 2009; Ridgway and
Howard 1979).
4.2.6.1 High pressure nervous syndrome and nitrogen narcosis
In humans, the symptoms of HPNS appear at pressures exceeding 11 ATA (Halsey 1982;
Jain 1994), although individual differences make it difficult to give an absolute pressure (or
depth) at which the symptoms first appear (Bennett and Rostain 2003; Brauer et al. 1975).
Although species show differences in their susceptibility to elevated pressures, this variability appears to be related to the complexity of the CNS, and organisms with a less complex CNS seem to have a higher tolerance (Hunter and Bennett 1974; Rostain et al. 1983).
Many marine mammals would therefore appear to be at risk of HPNS since they have fast
descent rates (1–2 m/s), and spend time at pressures far exceeding 11 ATA.