Decompression Sickness: Amelioration of Risk Factors

Appropriate manipulation of the depth-time profile as discussed in the preceding section on decompression planning is obviously important in managing the risk of DCS. In addition, certain known or suspected risk factors for DCS, some of which have already been mentioned, can be manipulated or managed to reduce risk further.

Patent foramen ovale

The role of the patent foramen ovale (PFO) in the pathophysiology of DCS is discussed in Chapter 10, in which it was pointed out that PFO appears associated with an increased risk of cerebral, spinal, vestibulocochlear and cutaneous DCS. The most plausible explanation for this increase in risk is that a right-to-left shunt allows VGE to enter the arterial circulation, and these small bubbles can then distribute widely in the body and cause harm, as previously described. The degree of shunt facilitated by the PFO has consistently been found to be significant; with large and spontaneous shunts being important and very small shunts seemingly unimportant. The crucial question is this: ‘How should this knowledge be applied to reducing risk of DCS?’

One obvious strategy would be to screen divers for PFO after an episode of neurological, inner ear or cutaneous DCS and, possibly, to repair large PFOs in divers who wish to continue diving. Another more radical strategy would be to screen all prospective divers before entry to the sport. Many divers have enthusiastically embraced such ideas. When participants on Internet diving discussion forums report an episode of DCS, a chorus of advice to check for a PFO inevitably follows, even if the event involved a form of DCS that has never been associated with a PFO (e.g. musculoskeletal DCS). However, decisions to screen divers for PFO or to repair any lesion that is discovered are not straightforward.

As pointed out in Chapter 10, PFO is very common (around 30 per cent of divers or diving candidates can be expected to have one) and so is the formation of VGE after diving; yet cerebral, spinal and inner ear DCS cases remain rare. There are clearly factors beyond merely having a PFO and producing venous bubbles that are involved in the chain of events leading to the relevant forms of DCS, and at this time we are not certain what they are. Screening all prospective divers by using an expensive invasive test (see Chapter 10), which would detect the target lesion in about 30 per cent of subjects (and potentially exclude them from diving), with the aim of preventing an event that occurs perhaps once in 10 000 dives (even in an unscreened population), is neither sensible nor justified.

In contrast, it may be appropriate to test divers who have had one of the relevant forms of DCS, particularly if there have been multiple events or if the event(s) followed dives that seem unprovocative in terms of decompression stress. It is also inevitable that the diving physician will be approached by enthusiasts who have never had DCS but who are aware of the association of serious DCS with PFO and who wish to be tested for this heart condition. Referring for testing may be appropriate under these circumstances, but the following points should always be explained to the diver before testing is undertaken.

  1. The bubble contrast echocardiographic test is relatively safe, but there are some risks. Transient symptoms of cerebral arterial gas embolism have been reported following tests with strongly positive results for right-to-left shunt.
  2. The test result is likely to be positive in at least 30 per cent of cases (or more depending on the context), and the diver may then have some difficult options to choose from (see later). If the diver does not intend to take one of those options, then there is little practical point in having the test.
  3. A positive test result after an episode of DCS does not guarantee that the PFO was the cause of the DCS.
  4. As a corollary to point 3, repairing a PFO discovered after an episode of DCS does not guarantee that another event will not occur.
  5. A negative test result does not mean that the diver is ‘resistant’ to DCS, as many seem to believe.

If screening for a PFO is undertaken and the result is positive, the response should take account of the size or shunting behaviour of the lesion. There are data suggesting that a grade 1 PFO (see Chapter 10) is of little or no consequence and can be ignored. In contrast, a spontaneously shunting (grade 3) PFO is likely to confer increased risk and merits a response.

To mitigate the risk implied by a large PFO, the diver effectively has three options: cease diving, modify diving practice in an attempt to reduce VGE production or have the PFO repaired. The option to cease diving is self-explanatory and unpalatable to many. Modification of diving practice to reduce VGE production is an imprecise business, but the general aim is to reduce the provocation for bubble formation on arrival at the surface. Options for achieving this include diving well within no decompression limits, ensuring that safety stops are completed, using nitrox (see Chapter 62) but planning the dive as though using air and, if decompression diving using gradient factors, lowering the GF-High to force longer shallow decompression stops at the end of the dive. Breathing oxygen during those stops would also help. In a related vein, advice could also include avoidance of any heavy exercise that could open a pulmonary shunt, or manoeuvres that could encourage right-to-left shunting across a PFO (e.g. lifting or straining), over the typical 2-hour period of maximum VGE formation after a dive.

Having a PFO repaired involves the use of a transvenous catheter technique that leaves an occluder device across the atrial septum. It is an effective treatment, although repair may be incomplete in up to 10 per cent of cases. It is also an invasive procedure, and like many medical procedures considered ‘safe’, it nevertheless has significant risks, some of which are life-threatening. These risks include formation of blood clots on the device, loosening of the occluder from its position, the appearance of new heart rhythm disturbances and new mild aortic regurgitation. Patients are routinely required to take a potent antiplatelet agent for 6 months after placement. Occasionally, open heart surgery is required for explantation of devices that are causing complications. Despite these concerns, most procedures have satisfactory results, and the PFO is closed without complications. It is not known how many divers have taken this option to mitigate the risk of PFO in diving, but anecdotally the numbers are growing. Other than the potential for harm during and after the procedure, one of the concerns about the repair option is that data demonstrating that repair reduces subsequent risk of DCS are incomplete. There is one comparative study that followed divers with large PFOs discovered after DCS who self-selected into groups undergoing repair or not4. The study and its results are summarized in Figure 12.8.

Key features and results of the study by Billinger and associates on the efficacy of repair of patent foramen ovale (PFO) in preventing serious neurological decompression sickness (DCS).
Figure 12.8 Key features and results of the study by Billinger and associates on the efficacy of repair of patent foramen ovale (PFO) in preventing serious neurological decompression sickness (DCS). The final results are based on very small numbers of cases (1 case of DCS in the closure group and 4 cases of DCS in the no closure group). DCI, decompression illness. (Data from Billinger M, Zbinden R, Mordasini R, et al. Patent foramen ovale closure in recreational divers: effect on decompression illness and ischaemic brain lesions during long-term follow-up. Heart 2011;97:1932–1937.)

In this study, divers who continued diving without repair had a markedly higher rate of DCS than those who had a repair, but caution is required in interpreting these data because the numbers of DCS cases arising after the repair decision were so small, and the divers were not randomized. Notwithstanding this concern, the study does provide some reassurance that there is a positive return on the risk exposure associated with having a repair. Many diving enthusiasts may well be prepared to take this risk for the apparent benefit of eliminating their anatomical right-to-left shunt. This may be particularly true of those conducting deep technical dives who may see little practical potential for improving the conservatism of their dives.


The relationship between DCS risk and exercise is a complex and evolving issue, and exercise needs to be considered in multiple contexts, specifically exercise before diving, exercise during diving and exercise after diving.

Until the early 2000s, little attention had been given to the issue of exercise before diving and its relationship with risk of DCS, other than general speculation that being physically fit was probably a good thing. Things changed with the publication of a remarkable series of experiments demonstrating that a single bout of heavy exercise approximately 20 hours before diving markedly reduced mortality in a rodent model of severe DCS. By 48 hours after exercise, the protective effect seemed to wear off. Translation of this finding into human research is incomplete, but there have been several studies demonstrating that heavy exercise between 2 and 20 hours before diving reduces VGE counts after diving. The mechanism for this protective effect is unclear. Early speculation that it was mediated by nitric oxide seemed disproved when protection persisted in the presence of a nitric oxide synthase inhibitor, although as a sidebar to this line of research it was discovered that exogenously administered nitric oxide also appeared to reduce post-dive VGE. It has been suggested that exercise produces some sort of endothelial conditioning effect that results in fewer suitable sites for micronuclei to grow when the surrounding tissue becomes supersaturated. Similarly, exercise may disturb stable micronuclei so that they subsequently involute, thus reducing the population transiently. Restoration of micronuclei numbers by whatever process is responsible for producing them would explain the decay in benefit over time following the exercise episode. There are no widely recommended practical strategies designed to take advantage of this phenomenon. Perhaps the best that can be said is that going for a run (or something similar) between 2 and 24 hours before diving may help reduce the risk of DCS.

The effect of exercise during diving may depend on its timing. The typical pattern is that activity during the bottom time sees the diver exercising moderately, and then ascent and decompression (if any) are largely done at rest. This is probably a disadvantageous pattern of exercise because it will result in increased perfusion and inert gas uptake (in some tissues at least) during the bottom phase of the dive and then decreased perfusion and inert gas elimination during the decompression. It is widely accepted that this explains the perception that dives involving hard work at the bottom are associated with greater risk of DCS. A reduction in risk may therefore be achieved by reducing work at depth and maintaining gentle levels of exercise during decompression. There is some evidence in support of these notions. Although a reduction in work at depth can be impractical in occupational diving, in recreational diving it is afforded by, for example, use of diver propulsion vehicles. Similarly, in a decompression diving situation, to maintain gentle exercise during decompression it is usually possible to fin gently against the resistance of the down line or decompression stage. In diving where hard work at the bottom cannot be avoided, the use of a longer safety stop (for a no decompression dive) or lengthening of the prescribed shallow stops in a decompression dive would be an appropriate precaution. There are no universally accepted guidelines for ‘padding’ decompression in this way.

Exercise after diving has generally been considered unwise, although the timing is unclear. Several concerns are noted, not the least of which is that there are many reports of symptoms of DCS arising during periods of work soon after diving. This, of course, may be coincidental, but there are plausible reasons to believe that exercise may have a causative role in such cases. First, exercise may promote the passage of VGE across pulmonary shunts into the arterial system, where they may be more harmful, as described in Chapter 10. Second (and similarly), exercise (particularly that involving lifting or straining) may promote right-to-left shunting of VGE across a PFO with the same result. Finally, it is speculated that where there are micronuclei in tissues supersaturated with inert gas, exercise may contribute to their excitation into growth, thus producing bubbles. This would be analogous to shaking an open bottle of carbonated drink, but the validity of this concern is unknown. At a practical level, mitigation of this risk involves refraining from exercise or lifting for a period after diving. This ‘period’ should definitely extend for at least several hours because this corresponds to the peak and duration of VGE formation after typical dives. Longer would be better, but how long is unknown.


Hydration (or more correctly, dehydration) is one of the most widely recognized of the alleged risk factors for DCS among divers. For all the attention given to the matter, there is remarkably little proof that dehydration actually imputes increased risk.

There is one study in which pigs deprived of water and administered a diuretic during a saturation pressure exposure had more severe DCS than normally hydrated pigs after decompression. In addition, limited human data have shown that supplemental hydration just before diving reduces VGE numbers after diving, especially in subjects who appear prone to VGE formation. This finding is encouraging but falls short of proving that good hydration is protective in humans. Nevertheless, the proposition makes sense. There is evidence that divers are prone to dehydration through factors such as exposure to hot conditions, poor availability of water on boats, sea sickness and immersion diuresis. There is also evidence that realistic levels of ‘dehydration’ reduce regional tissue perfusion during exercise, and because perfusion is important for inert gas washout, it seems plausible that dehydration could impair this process. It is certainly true to say that no one has ever demonstrated dehydration to be beneficial.

It follows that maintenance of hydration can probably only be good. As a somewhat arbitrary guide, the supplementation of normal fluid intake with a litre of water over the hour before diving would make sense.


It has long been observed that the risk of DCS seems higher when diving is conducted in cold conditions. The potentially dramatic effect of temperature on risk of DCS was demonstrated in a landmark study performed by the US NEDU5. It is a complicated study with multiple arms and profiles, but the most important observation was the comparison of outcomes when divers undertook a 120-foot for 30-minute dive with decompression as prescribed by a US Navy dive table under two different thermal conditions. In one set of dives (referred to as cold/warm), the divers were immersed in water at a temperature of 26°C for the bottom phase of the dive and 36°C for the decompression. In the second set of dives (referred to as warm/cold), the temperature conditions were reversed between the bottom and decompression phases. The divers wore no thermal protection. In the cold/warm series, there were no cases of DCS in 80 dives (0 per cent), whereas in the warm/cold series, there were 7 cases of DCS in 32 dives (22 per cent).

The water temperatures and the lack of exposure protection make the conditions difficult to interpret in real-world terms, but the dramatic change in DCS risk between the cold/warm and warm/cold conditions is highly relevant. It can be argued that the condition most analogous to real diving would be the markedly more hazardous warm/cold situation. Thus, divers tend to start a dive warm and become progressively colder during the dive. If there is a lesson to be learned from the NEDU temperature study it is that becoming cold during a dive should be avoided as much as possible.

Practical strategies to mitigate the risk of diving in cold water include optimizing exposure protection, which would include the use of drysuits with state of the art undergarments and possibly even active heating systems, which are now widely available. The ideal time to turn these heating systems on would be during decompression. Extreme divers in cold water caves have even established underwater habitats where the diver can remain under pressure, but not immersed, thus giving an opportunity to reduce conductive heat loss into the water and to take hot fluids orally. As previously, there is always the option of ‘padding’ or extending decompression for decompression dives conducted in cold water.

Some data suggest that remaining warm after diving (despite a cold environment) may reduce production of VGE and the incidence of DCS. It is therefore probably sensible to avoid becoming cold early after a dive, especially one that was provocative from a decompression point of view. Almost paradoxically, however, there is a report of two cases of DCS arising in temporal relation to exposure to hot water in a shower early after diving. This single report has achieved considerable penetration into the diving community and is the cause of much anxiety about showers after diving. It is plausible that sudden warming of supersaturated superficial tissue could decrease gas solubility and precipitate symptomatic bubble formation. However, many divers take showers early in the post-diving period with no problems, and the risk of such events seems very low.


It has long been believed that obesity is a risk factor for DCS, based largely on the ‘first principle’ belief that because nitrogen is highly soluble in fat, an obese person can absorb more nitrogen. Whether this is a practically relevant consideration is controversial. There is conflict in the literature with some studies (probably the majority of those that have addressed this issue) purporting to show an association between risk of DCS and obesity, whereas others have not. Whatever the truth of this matter, obesity is a condition that is often associated with reduced functional capacity and other health problems. Obese divers would benefit from losing weight for multiple reasons.


There are some data suggesting that older divers are at higher risk of DCS and perhaps at higher risk of an incomplete recovery if they suffer serious event. However, once again, there is conflict in the literature on this subject. The fact that older divers are likely to have a lower functional capacity and a higher risk of cardiac events is probably of greater importance than concern about the risk of DCS.

Dive sequences

As alluded to earlier, multiple dives in a single day are common in recreational diving. Sequential dives conducted while dissolved inert gas in tissue remains after a previous dive are referred to as ‘repetitive dives’. The definition of repetitive diving differs according to which table or decompression algorithm is used because there is variability in assumptions about total outgassing time. For example, the Professional Association of Diving Instructors, Inc. considers that complete outgassing occurs after 6 hours, whereas the Canadian Defence and Civil Institute of Environmental Medicine (DCIEM) table works on a much longer total outgassing time of 18 hours.

Irrespective of the definition, it is clear that if a second dive takes place in the presence of residual dissolved inert gas remaining after a previous one, then tissue gas loading during the second will compound on that remaining from the first. Perhaps for this reason it has frequently been taught that repetitive diving is a risk factor for DCS, although it is not clear why it should be, provided residual inert gas is adequately accounted for in calculation of no decompression limits or decompression protocols for subsequent dives. One argument that is sometimes advanced in this regard is that bubble formation after the first dive alters inert gas kinetics on the second dive, or those bubbles may undergo further growth after the second dive. There are no convincing data that clearly identify repetitive dives per se as being associated with increased risk. Indeed, the situation is made even less clear by the existence of an acclimatization phenomenon reported from occupational environments in which the incidence of DCS among a cohort of workers undertaking diving or compressed air work is reliably noted to fall over a multiday sequence of exposures. These exposures frequently differ (e.g. in being once daily) from the typical repetitive dives undertaken by recreational divers that may involve up to four or more short exposures per day. Nevertheless, the truth relating to risk in these situations is unclear. Part of the problem relates to the fact that so much of the diving undertaken by recreational divers is repetitive, so it is not surprising that many of the DCS cases arise in repetitive diving.

One particular form of repetitive diving that is associated with considerable controversy is so-called ‘reverse profile’ diving. This is the performance of a repetitive dive deeper than the previous dive (or than another dive in the repetitive sequence). In this sense, the term ‘reverse profile’ is a misnomer because what is really being discussed is reverse depth diving. The origins of the edict that reverse profile diving is hazardous are unclear. Cursory manipulation of the repetitive function of common dive tables reveals that avoidance of reverse profiles results in more allowable bottom time over the sequence. That alone could be reason enough to avoid reverse profiles, but as in repetitive diving itself, it is not clear why reverse profile diving should be considered more hazardous provided residual inert gas from the previous shallower dive(s) is adequately accounted for in calculation of no decompression limits or decompression protocols for the subsequent deeper excursion.

Decompression Planning: Dive Tables, Planning Software and Dive Computers

Dive tables are pre-calculated and pre-printed implementations of a decompression algorithm that divers can use to plan their dives. These were most popular before the 1990s among recreational scuba air divers wanting to plan simple dives, and their use was taught as part of all recreational scuba diving courses. The most frequently used items of information were the no decompression limits (see earlier) provided by these tables. Thus, divers could look up the allowable bottom time they could spend at any particular depth and still make a direct ascent to the surface without decompression stops. Even though no decompression was prescribed for dives ‘inside’ the no decompression limits, most training agencies advocated the use of a 3- to 5-minute ‘safety stop’ at 3 to 5 metres during the final part of the ascent, as an added precaution. Such stops are probably useful in reducing the incidence of DCS on routine no decompression dives.

The dive tables also provided a series of steps (with minimal calculation) for divers to account for the effect of inert gas accumulated but not yet eliminated after previous dives when planning further ‘repetitive’ dives. In air diving, this is referred to as ‘residual nitrogen’, and its presence, not surprisingly, has the effect of reducing the no decompression limit for subsequent dives.

The use of dive tables has declined dramatically with the rise in use of dive computers (see later), and some entry level diving courses no longer teach their use. Whether this is a good or bad thing is impossible to say. Tables were inexpensive and readily available, whereas in the early days this was not true of computers. More recently, however, entry level dive computers have become much more reasonably priced and have the advantages of avoiding calculation errors, thus ensuring that the diver who carries one is receiving accurate time and depth information, and most of these computers provide ascent rate alarms.

Planning software that runs a decompression algorithm (and often multiple decompression algorithms) can be purchased for use on desktop, laptop and tablet computers, as well as telephones. Such software is effectively an electronic dive table and is often used to generate tables that are transcribed onto underwater slates for specific missions. The advantage of such software is that the decompression plan can be tailored specifically to the diver’s equipment, gas mixes and decompression preferences (e.g. gas content model, bubble model, gradient factors). The multitude of combinations and permutations of circumstances that can be ‘run’ by such software would be very difficult, if not impossible, to replicate on pre-printed tables.

Dive computers that the diver carries underwater have become increasingly popular since the early 1990s and are now almost ubiquitous. These computers run software with one or more decompression algorithms programmed into them and with various levels of adaptability for decompression planning. They track time and depth exposures in real time and provide a constant display of parameters such as depth, dive duration, decompression ceiling and expected time to surfacing. These parameters are continuously updated as the depth varies and the dive duration lengthens, all with little or no effort on the part of the diver. Advanced computers allow the diver to choose the equipment being used (e.g. open-circuit or rebreather systems) and the gas mixes being breathed and to adjust decompression preferences such as gradient factors. Some computers can connect to the oxygen cells in a rebreather (see Chapter 62) so that they ‘know’ the inspired partial pressure of oxygen used by the diver and can incorporate this information in calculating decompression. Advanced computers that perform these functions and provide all relevant information in a head-up display constantly visible to the diver are now available.

Decompression Sickness: Decompression Planning ( Gas Content Versus Bubble Models )

As described earlier, gas content models regulate ascent and impose decompression stops to maintain tissue supersaturation below empirically derived thresholds across the range of tissues with different kinetic behaviour. Such models have been very successful, but are not invariably so; that is, DCS can certainly still occur even when divers decompress according to the model. The occurrence of such events always results in interest in alternative approaches that may (potentially) be more successful. Moreover, as discussed in Chapter 10, it has long been known that even decompressions performed in accordance with established guidelines frequently result in the formation of venous gas emboli (VGE), whose numbers can be correlated (albeit imprecisely) with the risk of DCS. Much of the early research that revealed this VGE phenomenon took place when the use of gas content models to control decompression was almost ubiquitous. Thus, the emerging recreational technical diving world of the late 1990s and early 2000s was fertile ground for well-meaning advocates of alternative approaches to decompression.

A school of thought that had been around for some time, but came to prominence during this period, was the so-called ‘bubble-model’ approach. Bubble model advocates had taken note of the frequently high VGE counts after decompression conducted according to gas content models and advanced the notion that, at least in part, the failure of these models to control bubble formation effectively could increase the risk of DCS even when the diver did everything right. Moreover, they proposed that initiation of bubble formation probably occurred during exposure to the relatively large supersaturations allowed by gas content models during the long ascent to the first decompression stop. Using advanced physics, bubble modellers purported to be able to quantify bubble formation from micronuclei (see Chapter 10) of a given size for a given level of supersaturation, and their calculations suggested that shorter initial ascents (and therefore smaller initial supersaturations) than allowed by gas content models would result in ‘excitation’ of smaller populations of micronuclei and therefore help prevent initiation of bubble formation. It was even suggested that by imposing deeper initial decompression stops a diver could reduce the requirement for the shallow decompression stops later in the ascent because initiation of bubble formation would have been controlled earlier. A stylized comparison between these two approaches to decompression using the same format as previous figures is shown in Figure 12.5.

Figure 12.5 Stylized depiction of differences between decompression of a hypothetical single tissue prescribed by a gas content model (black line) and a bubble model (grey line). See text for further explanation.
Figure 12.5 Stylized depiction of differences between decompression of a hypothetical single tissue prescribed by a gas content model (black line) and a bubble model (grey line). See text for further explanation.

As in Figures 12.3 and 12.4, line A in Figure 12.5 represents descent to the bottom depth indicted at point 1, and line B represents the increase in tissue gas pressure as inert gas is absorbed during the time spent at that depth (bottom time). By the end of the bottom time the illustrated tissue has reached the ambient pressure line (grey dot at point 2) and is thus saturated with inert gas. As in Figure 12.4, the supersaturation limit or M-value line as prescribed by a gas content model is depicted, and if the diver was following such a model, then direct ascent (line C) would proceed until the tissue gas pressure equalled the maximum allowed (point 3), at which time the first decompression stop would be imposed at a depth corresponding to point 4. After the tissue has off-gassed sufficiently, the ascent would be resumed with stops imposed each time the maximum supersaturation is approached.

In contrast, the ascent prescribed by a typical bubble model (depicted by the grey arrows) involves shorter initial ascents, deeper initial decompression stops and smaller initial supersaturations. A bubble model could also (as depicted) allow surfacing with a tissue gas supersaturation greater than the maximum allowed by the gas content model, based on the belief that the process of bubble initiation had been controlled earlier and that this allowed exposure to greater supersaturation later in the ascent.

There was a compelling theoretical attraction to the concept of using ‘deep stops’ to ‘control bubble formation early in the ascent’. There were also some widely discussed anecdotal observations from several prominent divers that insertion of deep stops into their ascents seemed to result in feeling less fatigued after dives. In the early 2000s these factors, combined with the burgeoning influence of Internet communication, became an article of faith among deep recreational technical divers that bubble model approaches to decompression were superior even though no formal testing of the algorithms had been undertaken. There was widespread adoption of the two most readily available bubble model algorithms (the varying permeability model [VPM] and the reduced gradient bubble model [RGBM]). It largely went unnoticed when VPM was revised into VPM-B to increase shallow stop time after reports of DCS began to emerge. Gas content models with their relatively rapid early ascents and longer shallow stops were derided as being a recipe for ‘bending and mending’ (an allusion to causing bubble formation with supersaturation of fast tissues early in the ascent and then fixing the problem with long shallow stops late in the ascent).

The use of gas content models did persist, perhaps because they were easier to understand or to program for use in computers, but even users of these algorithms began to manipulate them to make them behave more like bubble models. One technique for such a manipulation that became and remains popular is the use of so-called ‘gradient factors’. This involves limiting supersaturation to less than permitted by the conventional supersaturation limit by redefining maximal permissible supersaturation as a fraction of the difference between ambient pressure and the limit. These fractions have come to be known as gradient factors. Thus, if a diver elects to limit supersaturation to 80 per cent of the usual difference between ambient pressure and the supersaturation limit, this is referred to as ‘gradient factor 80’ or ‘GF 80’. Typical implementations of the gradient factor method require the diver to select two gradient factors: the first (often referred to as GF-Low) notionally controls supersaturation in the fast tissues early in the ascent, and the second (often referred to as GF-High) controls supersaturation in the slower tissues at the point of surfacing. The algorithm then interpolates a series of modified M-values in between these two user-specified points. Not surprisingly, lowering the first gradient factor limits supersaturation in the fast tissues early in the ascent by imposing deeper decompression stops, and lowering the second will produce longer shallower stops to reduce supersaturation in the slower tissues at the point of surfacing. Choosing a low GF-Low and a higher GF-High produces a decompression profile that resembles a bubble model decompression. This is illustrated in Figure 12.6 for a GF-Low of 20 per cent and a GF-High of 90 per cent (in common use this terminology would be abbreviated to ‘GF 20/90’).

Figure 12.6 The stylized effect of imposing gradient factors GF 20/90 on the decompression prescribed by a gas content model for a single hypothetical tissue. See text for further explanation.
Figure 12.6 The stylized effect of imposing gradient factors GF 20/90 on the decompression prescribed by a gas content model for a single hypothetical tissue. See text for further explanation.

As in previous figures, line A in Figure 12.6 represents descent to the bottom depth indicted at point 1, and line B represents the increase in tissue gas pressure as inert gas is absorbed during the time spent at that depth (bottom time). By the end of the bottom time the illustrated tissue has reached the ambient pressure line (grey dot at point 2) and is thus saturated with inert gas. At the start of decompression, the initial ascent (line C) is allowed to proceed until the tissue reaches 20 per cent of the supersaturation limit, at which point a stop is imposed at the depth corresponding to point 3. The ascent then continues with further stops imposed when the tissue supersaturation approaches the modified supersaturation limit defined by a line joining the chosen GF-Low (black dot labelled 20 per cent) and the chosen GF-High (black dot labelled 90 per cent). If this approach is compared with the two profiles shown in Figure 12.5, it is clear that it is now very different from the unmodified gas content model decompression and substantially similar to the bubble model decompression. For obvious reasons, the use of gradient factors with a low GF-Low and bubble model decompressions are collectively referred to as ‘deep stop’ approaches to decompression.

The ZH-L Buhlmann gas content model that forms the basis for most tables and computers designed to guide decompression diving by recreational divers was subjected to some human testing; albeit minimal for the trimix diving and depth range for which it is now implemented. The bubble models and gradient factor manipulations of gas content models have had essentially no testing. It is acknowledged that the preceding discussion of bubble model theory represents a gross oversimplification of a complicated matter, but the fact remains, no matter how attractive the theory, it has never been tested in a practical sense. Advocates frequently cite the ubiquitous nature of deep stop approaches as some sort of proof that they are optimal, but this is an invalid argument in the absence of comparative outcome data. These approaches clearly work in the majority of dives, but whether they are optimal is an unresolved question.

Debate over this issue has been rekindled with the publication of several studies that have suggested that the emphasis on deep stop approaches to decompression may need to be reconsidered. Several of these studies have focussed on measuring VGE after diving and suggest that deep stops may not reduce the appearance of VGE as previously widely assumed. However, by far the most significant development has been the 2011 publication of a study performed by the US Navy Experimental Diving Unit (NEDU) at Panama City in Florida3. The investigators compared outcomes after air dives to 170 feet for 30 minutes with same-duration decompression on air prescribed by either a gas content model or a bubble model. Both decompression protocols are US Navy models that are not used by recreational divers, but they nevertheless have characteristics that reflect the respective approaches; the gas content model allows greater supersaturation in faster tissues early in the ascent and distributes decompression time shallower, and the bubble model imposes deeper stops early in the ascent and thereby distributes decompression time deeper. The remarkable feature of this study was that the primary outcome measure was DCS in human subjects. The divers performed a standardized workload during the bottom time, and temperature effects were standardized across the groups by having all divers wear no thermal protection in water at a temperature of 30°C. There were 11 cases of DCS in 198 dives in the deep stops group and 3 cases in 192 dives in the shallow stops group. The trial was ceased at this point because the difference became significant on sequential analysis.

This result was not the outcome expected or hypothesized by the investigators. Attempts to explain it have focussed on the likelihood that protection of fast tissues from supersaturation early in the ascent does not seem to be as effective as thought, and it comes at the expense of increased supersaturation in the slow tissues later in the ascent because they are continuing to absorb gas during deep stops. This principle is illustrated in Figure 12.7. As in previous figures, line A in Figure 12.7 represents descent to the bottom depth (indicted at point 1), and line B represents the increase in tissue gas pressure as inert gas is absorbed during the time spent at that depth (bottom time). By the end of the bottom time the tissue represented by the grey dot at point 2 has reached the ambient pressure line and is thus saturated with inert gas, whereas the slower tissue represented by the grey dot at point 3 is still absorbing inert gas. At the start of decompression, gas content model decompression allows an the initial ascent (line C) to proceed until the faster controlling tissue reaches the maximum supersaturation limit, where the first decompression stop is imposed at a depth indicated by point 4. In contrast, the bubble model allows a shorter ascent (line D) to the first stop at a depth indicated by point 5. In the slower tissue, whose tissue gas pressure at the beginning of ascent is indicated by point 3, the gas content model decompression gives the tissue little more time to absorb inert gas as illustrated by line E because absorption ceases and outgassing begins once the tissue reaches then crosses the ambient pressure line. In contrast, the deep stops prescribed by the bubble model will result in further inert gas absorption by this tissue (line F).

Figure 12.7 The stylized effect of a gas content model decompression (solid black arrows) and a bubble model decompression (grey arrows) on tissue gas pressure in a hypothetical fast tissue (arrows originating at point 2) and a hypothetical slower tissue (arrows originating at point 3). See text for further explanation.
Figure 12.7 The stylized effect of a gas content model decompression (solid black arrows) and a bubble model decompression (grey arrows) on tissue gas pressure in a hypothetical fast tissue (arrows originating at point 2) and a hypothetical slower tissue (arrows originating at point 3). See text for further explanation.

The NEDU study forces us to question whether the proposed benefit of using a bubble model (protection of fast tissues early in the ascent) is worth the disadvantage of the increased gas loading that occurs in slower tissues as a result. Bubble model advocates have tried to portray the study as irrelevant because the experiments involved air diving and used a deep stop profile that is not exactly the same as that prescribed by VPM-B. Nevertheless, analyses of ‘real-world’ VPM-B profiles prescribed for dives using accelerated decompression on oxygen (such as are typically undertaken by technical divers) suggest that the same disadvantageous pattern of protecting fast tissue from supersaturation early in the ascent at the expense of slower tissue supersaturation later still occurs.

It is clear that the optimal approach to decompression from the deep bounce dives undertaken by recreational technical divers is not established; however, it seems plausible to suggest that we have evolved an approach that risks overemphasizing deep stops. One trend that is emerging as this book goes to press is the use of gradient factors to reduce the emphasis on deep stops (by increasing the GF-Low) and re-emphasizing shallow stops (by decreasing the GF-High). Thus, whereas gradient factor combinations such as 10/90 were popular during the height of belief in deep stops, it is increasingly common to see combinations such as 40/70 or 50/70 now.

Decompression Sickness: Decompression Planning ( Basic Principles )

As discussed in Chapter 10, DCS occurs when supersaturation of inert gas during decompression causes bubbles to form in sufficient numbers or size (and in the right location) such that some poorly defined clinical threshold is exceeded and symptoms occur. Decompression planning is the process of controlling depth, time and the ascent (‘decompression’) to reduce the probability of DCS.
Because tissue gas supersaturation is the fundamental condition required for bubbles to form, it is not surprising that all decompression planning approaches have, at their core, a means of calculating the pressure of dissolved inert gasses in a range of tissues throughout a dive. These dissolved gas pressures can then be compared with ambient pressure to establish the degree of supersaturation, and adjustments to the dive profile can be made to prevent supersaturation from exceeding safe thresholds. With the intended audience in mind, it is the express intent of this account to discuss the broad principles of adapting tissue supersaturation calculations into decompression planning tools, rather than the related mathematics. Those wishing to study the mathematical principles and methods can find relevant accounts elsewhere1,2.
Basic principles

As mentioned earlier, virtually any approach to decompression planning assumes that the inert gas tensions within tissues can be calculated and thereby tracked throughout a dive. As could be anticipated from the discussion of gas uptake and elimination in Chapter 10, the mathematical models that allow such calculations include tissue perfusion and the blood-tissue partition coefficient for the relevant gas(es) as inputs. It is also pertinent to reiterate that the ‘tissues’ considered in these models are not real or identifiable tissues per se. The models merely consider a range of hypothetical tissues with different inert gas kinetics and assume that the relevant real tissues behave in a manner analogous to one of the hypothetical compartments used in decompression calculations.

To illustrate the incorporation of tissue gas supersaturation data into decompression planning, the relevant events during a dive are depicted using the format introduced in Figure 12.1. It is important to appreciate that this and subsequent figures in this chapter are illustrating principles and do not purport to be scaled correctly or to –represent any particular tissue accurately.

Depiction of changes in inert gas tension in a hypothetical single tissue during the early part of a dive. See text for explanation.
Figure 12.1 Depiction of changes in inert gas tension in a hypothetical single tissue during the early part of a dive. See text for explanation.

In Figure 12.1, ambient pressure (depth) is shown on the horizontal axis, and tissue gas pressure is shown on the vertical axis. Time is not illustrated in the diagram but requires assumptions to be made about its passage, as will be described. Line A represents descent at the start of a dive. The descent occurs over a short space of time, and so there is little time for inert gas uptake and little increase in tissue gas pressure. The bottom depth is reached at the point indicated; therefore, there is no further change in ambient pressure until the ascent begins (see later). During time spent at the bottom depth, inert gas will dissolve into the tissue and the tissue inert gas tension will increase, as depicted by line B. The other notable feature in Figure 12.1 is the line labelled ‘Tissue pressure = ambient pressure’. This represents the point, for all depths, where the pressure of dissolved gas in tissue is equal to the ambient pressure and is often referred to as the ‘ambient pressure line’. It should be clear that while remaining at any particular depth, the tissue gas pressure cannot rise above this line because once tissue gas pressure equals ambient pressure, there can be no further pressure gradient to drive diffusion of gas into the tissue unless the diver descends deeper. Depending on the kinetics of individual tissues and the time spent at depth, at the end of a period at the bottom depth, tissue gas pressure may have equilibrated with ambient pressure in some ‘fast’ tissues, whereas in other ‘slower tissues’ it may not (Figure 12.2).

Gas pressures in a range of hypothetical tissues at the end of a period at depth. See text for further explanation.
Figure 12.2 Gas pressures in a range of hypothetical tissues at the end of a period at depth. See text for further explanation.

Figure 12.2 illustrates a hypothetical situation that could prevail at the end of a period at depth in respect of tissue gas pressures in a range of tissues (represented by the grey dots) with differing kinetic properties. Depending on the duration of the bottom time, the tissue gas pressure in one or more tissues may have reached equilibrium with ambient pressure (thus having reached the ambient pressure line), and these tissues can be described as ‘saturated’ with inert gas for that depth. Other tissues with slower kinetics will have absorbed less inert gas and will have lower tissue gas pressures.

For the purposes of illustrating the principles of decompression, this discussion temporarily ignores the fact that multiple tissues are involved and focusses on the behaviour of a single tissue. For the sake of simplicity, it is assumed that this tissue has reached the ambient pressure line (and is thus saturated with inert gas) at the end of a long bottom time. This is illustrated in Figure 12.3.

In Figure 12.3 (as in Figure 12.1), line A represents descent to the depth indicated at point 1 at the start of the dive, and line B represents the increase in tissue gas pressure as inert gas is absorbed during the time at depth. This tissue has reached the ambient pressure line (grey dot at point 2) and is thus saturated with inert gas. Line C represents the changes in tissue gas pressure and ambient pressure during the early part of the ascent. Ambient pressure decreases quickly as depth changes, whereas in this tissue the accumulated inert gas is not washed out at a rate that matches the fall in ambient pressure. In a tissue with very fast kinetics, the fall in tissue gas pressure could more closely match the falling ambient pressure, but in this tissue it can be seen that by point 3 on the ascent, the tissue gas pressure (point 4) markedly exceeds the ambient pressure (point 5) and the tissue is thus ‘supersaturated’. The supersaturation pressure is indicted by the double-ended arrow in Figure 12.3.

Development of supersaturation in a hypothetical single tissue during ascent. See text for further explanation.
Figure 12.3 Development of supersaturation in a hypothetical single tissue during ascent. See text for further explanation.

It should be clear at this point that the key question when modelling decompression in this way is ‘How much supersaturation is acceptable?’ The means of deriving an answer to this question introduces a controversial dichotomy in decompression science between the so-called ‘gas content models’ and ‘bubble models’. For the moment, the focus of this discussion is on the more traditional gas content models, and this approach is contrasted with bubble models later.

The original gas content model proposed by Haldane held that ascent could proceed until such time as the tissue gas pressure in any tissue reached twice the ambient pressure. This was Haldane’s often-cited 2:1 ratio. At this point a decompression stop was imposed to allow the tissue gas pressure to fall while the ambient pressure remained constant. This approach was moderately successful, but it evolved over time, and the fixed ratio concept was eventually dropped in favour of ascent rules that prescribed maximum allowable supersaturations (sometimes referred to as ‘M-values’) for different tissues across a range of depths. The most famous of these sets of rules were the Zurich Limits for 16 hypothetical tissues (the ZH-L16 limits) prescribed by A. A. Buhlmann and based on physiological predictions with subsequent empirical modifications. The principles by which these work are illustrated for a single tissue in Figure 12.4.

Figure 12.4 Representation of a decompression protocol determined by a gas content model ascent rule for a hypothetical single tissue. See text for further explanation.
Figure 12.4 Representation of a decompression protocol determined by a gas content model ascent rule for a hypothetical single tissue. See text for further explanation.

As in Figure 12.3, line A in Figure 12.4 represents descent to the bottom depth indicted at point 1 at the start of the dive, and line B represents the increase in tissue gas pressure as inert gas is absorbed during the time spent at that depth (bottom time). By the end of the bottom time the illustrated tissue has reached the ambient pressure line (grey dot at point 2) and is thus saturated with inert gas. As in Figure 12.3, line C in Figure 12.4 represents the changes in tissue gas pressure and ambient pressure during the early part of the ascent. In Figure 12.4, the ascent rule is shown as a series of values for maximum allowable tissue gas pressures plotted against depth and is labelled ‘supersaturation limit’ for simplicity. As is typical, especially for tissues with fast kinetics, the rule allows greater supersaturation at deeper depths. Direct ascent (line C), at a rate not exceeding a maximum prescribed by the model, proceeds until the tissue gas pressure equals the maximum allowed (point 3), at which time the first ‘decompression stop’ is imposed at a depth corresponding to point 4. After the tissue has ‘off-gassed’ sufficiently, the ascent is resumed with stops imposed each time the supersaturation limit is approached as depicted in Figure 12.4. Eventually, there is sufficient outgassing in the tissue to allow direct ascent to the surface while remaining just under the supersaturation limit.

Although diagrams such as Figure 12.4 are useful for illustrating some of the basic concepts underlying decompression planning, the process is much more complex in reality. In ‘real’ decompression modelling, we are usually not considering only one tissue but multiple tissues simultaneously. Whichever tissue is closest to its maximum supersaturation limit at any stage of the ascent becomes the ‘controlling tissue’. Typically, this will be one of the tissues with faster kinetics early in the ascent (because these tissues are likely to have accumulated higher levels of inert gas during the bottom time). This means that the early decompression stops are shorter because the faster tissues that are controlling at that point will outgas quickly. Similarly, the tissues with slower kinetics tend to be controlling later in the ascent for the shallower stops. These stops tend to be longer because the slower tissues take longer to outgas. The involvement of multiple tissues and the effect of tissue gas kinetics on decompression stop durations are not captured in diagrams such as Figure 12.4.

It is appropriate to acknowledge at this point that recreational divers undertaking entry level courses are taught ‘no decompression diving’. This means that dives are planned to be of modest depth and duration so that a direct ascent to the surface (at the correct rate) can be made at any point in the dive without the gas pressure in any tissues crossing the supersaturation limit. Because tissue inert gas pressures will reach higher levels more quickly at greater depths (where the inspired inert gas pressures are higher), the permitted duration for a no decompression dive (referred to as a ‘no decompression limit’) becomes progressively shorter as the depth increases. For example, for many years the US Navy air diving table prescribed no decompression limits for 18-, 30- and 40-metre dives as 60, 25 and 5 minutes, respectively. Dives requiring decompression stops are routinely undertaken by recreational divers who refer to themselves as ‘technical divers’ (see Chapter 62).