Question of
the Week
Question:
Should additional time be allotted to the tables for the off-gassing of excess nitrogen...ie. in the older,
heavier diver or second dive for any diver? Are there any related articles or papers on this specific
subject within the medical-dive community?
Answer:
Numerous factors have been identified that would increase one's risk for developing decompression illness.
Here are some that have actually been found to be the causes of some accidents:
Repetitive dives
Exceeded No-decompression
limits
Running out of air, rapid
ascent
Diving on the edge of
No-decompression limits
Deep or repetitive dives
using computer outside the limits of the tables or no-decompression limits
Flying after diving
Diving at altitude
Patent foramen ovale
Vigorous exercise before
and after a dive
There are other factors that are thought to increase the chances of getting DCS but have little data in
support; some of these are:
Age; risk increases in proportion to increase in age
Obesity
Sex ? (Possibly more frequent in females )
Fatigue, Hard physical work
Dehydration, due to any cause (coffee, oral diuretics, alcohol, vomiting and diarrhea
states, failure to drink non-alcoholic liquids)
Alcohol and hangover state (related to dehydration)
Medical problems increasing the viscosity of the blood (Sickle cell anemia and trait)
Injury to muscle, bone or joint (due to increased blood flow to inflamed area)
Rate of ascent
Repetitive, multiday dives after a long lay-off; deep prolonged air diving
Failure to do safety stops
Smoking habits
Adaptation or recent diving history
Conditioning
Underestimated depth
Table "fudging"
Diving on Nitrox while using air tables gives a protective edge (estimated at 20% by some authorities).
Personally, and without any data to back me up, as I have grown older, fatter and in poorer physical
condition, I have used my own safety margin of "Campbell's 10% Rule" - diving 10% shallower, 10% less often,
adding 10% to all safety stops, and coming up 10% slower. I have not noticed any decrease in my diving
enjoyment!
Deep Thoughts
DAN Takes a Quick Look at the Makeup of Nitrogen Narcosis
By Renee Duncan Westerfield, Director, DAN Communications
From ‘Alert Diver’, June 2001, pp 16-19.
Re-printed with permission.
“I am personally quite receptive to nitrogen rapture. I like it and fear it like doom --- l’ivresse des
grandes profondeurs has one salient advantage over alcohol: no hangover. If one is able to escape from it’s
zone, the brain clears instantly and there are no horrors in the morning. I cannot read accounts of a record
dive without wanting to ask the champion how drunk he was.”
---Jacques Cousteau, in The Silent World
NITROGEN NARCOSIS
What is it?
Named by Jacques Cousteau “l’ivresse des grandes profondeurs,” or “the rapture of the deep,” nitrogen
narcosis is an ever-present factor for scuba divers.
Why so? Divers breathe compressed gas. Usually it’s air, but technical and commercial divers breathe
special mixtures of other gases. And for 165 years, beginning with the work of a French scientist named T.
Junod in 1835, scientists have recorded altered behavior in individuals breathing compressed gases.
Junod, for example, noted that when his divers were breathing compressed air, “the functions of the brain
are activated, imagination is lively, thoughts have a peculiar charm and, in some persons, symptoms of
intoxication are present.”
Similar signs and symptoms have been noted by other scientists throughout the years, including Paul Bert, a
scientist better known for his keystone work in decompression illness and oxygen toxicity. When tunnel workers
and divers breathed compressed air, strange – and sometimes dangerous—warning signs occurred, with euphoria,
intoxication, stupor, arrested activity and unconsciousness.
Later, in 1933, the British Royal Navy conducted an investigation and discovered that 17 of 58 dives
between 200 and 350 feet/61.7 and 107.9 meters resulted in a ‘semi-loss of consciousness.” The Royal Navy
scientists recognized this as a serious condition because, for example, the diver continued to give hand
signals at depth but later could not recall any of the events that had taken place underwater.
The first quantitative evidence of narcotic effect of compressed air at depths came in 1937 when two United
States Navy scientists, C.W. Shilling and W.W. Willgrube, tested the effects of compressed air between 90 and
300 feet/27.8 and 92.5 meters on 46 men who performed addition, subtraction, multiplication and division
exercises. Shilling and Willgrube recorded the time it took each man to perform these tasks and the number of
errors each made at increasing depths.
They found that experienced workers were less affected, and that the most severe signs and symptoms
appeared immediately when the subjects arrived at the target pressure. They discovered that the narcosis
intensified with rapid compression.
In the 1950s, a growing number of quantitative experiments began using different tests to determine
subjects’ intoxication levels. With studies still ongoing in nitrogen narcosis, scientists have measured
slower arithmetic and motor skills in affected divers, a decrease in attentiveness and slower responses; and
they have documented physical effects such as body sway, manual dexterity and disturbances in vision in
“narked” divers.
Throughout the years, navigating the complexities of each successive set of experiments, the big picture
comes into focus: Breathing compressed air or gas at depths can be intoxicating.
Background
Nitrogen narcosis is part of a larger syndrome called inert gas narcosis. Tracing the symptoms of narcosis
specifically to nitrogen, the most common inert gas in air (79 percent), came around 1935 – a century after
narcosis was first identified by Junod.
He observed that as the pressure of inhaled nitrogen in compressed air increased, warning signs of
intoxication progressed, moving from an initial feeling of euphoria to drunkenness and finally to
unconsciousness.
It was U.S. Navy physicians A.R. Behnke, E.P. Motley and R.M. Thomson who first attributed the narcosis to
the raised partial pressure of nitrogen in compressed air. They demonstrated that when their subjects breathed
compressed air deeper than 66 feet/20 meters, it caused “euphoria, retardation of the higher mental processes
and impaired neuromuscular coordination.”
At 100 feet/30 meters, the signs and symptoms became more apparent. Divers experienced “a feeling of
stimulation, excitement and euphoria, occasionally accompanied by laughter and loquacity,” signs and symptoms
similar to those effected from alcohol, oxygen deprivation (hypoxia) and the early stages of anesthesia.
The subjects also experienced a slowing in their thought processes, and their responses to visual,
auditory, olfactory and tactile stimulation were delayed. Concentration was difficult, memory became faulty,
and the subjects experienced a tendency to fixate on ideas. Their powers of association became limited. They
made errors in recording data, and mathematical exercises became more difficult. Fine movements were more
difficult, but in general intellectual functions were more impaired than their physical dexterity.
In other words, moving around wasn’t a big issue for them, but keeping their thoughts focused became a lot
harder.
Sound familiar?
If any of this rings a bell, you’ve experienced nitrogen narcosis, too.
When Does It Strike?
Researchers believe the potential for narcosis exists as soon as a diver begins to descend, but generally
most divers have felt the effects beginning somewhere around 100 feet/30 meters. Narcosis has hit other divers
sooner, however, as shown with Behnke and associates’ experiments, demonstrating that individuals have varying
levels of susceptibility. A recent test in a Navy recompression chamber, for example, showed a definite
alteration in thinking skills when divers reached 33 feet/10 meters.
Nitrogen narcosis has been called “the martini effect,” or “Martini’s Law, “ because of it’s alcohol-like
effect, a feeling often compared to drinking a martini on an empty stomach: being slightly giddy, woozy, a
little off-balance. One rule of thumb states that divers should consider the narcotic effect of one martini
foe every 50 feet/15.4 meters of seawater.
Deaths attributed to nitrogen narcosis occur mostly among sport divers who exceed recreational limits.
Scientists believe narcosis results from a slowing of nerve impulses precipitated by the effect of inert gas
under high pressure. How does this happen? The narcotic potency of inert gases is related to their affinity to
lipids, or fat. When nitrogen seeps into the fatty substances around the brain, it slows the communication
between cells, and therefore, slows down your thinking and reaction times.
Narcosis is not unique to nitrogen; however, it can occur with many of the so-called “noble” or inert
gases, with the exception of helium. Add to this the fact that other inert gases each have their own brand of
narcotic effects at depth, and you have a complicated picture for technical and commercial divers. One of
these rare gases, argon, for example, has about twice the narcotic potency of nitrogen, but helium has very
weak narcotic properties and is less soluble than nitrogen in body tissues.
This is why we find helium used in deep and saturation diving, as demonstrated by diving physiologist R.W.
Hamilton in groundbreaking experiments he conducted in 1966. Mixed with oxygen and called heliox, this mixture
is less likely to impair deep divers, although they still have to undergo decompression in order to prevent
decompression sickness (DCS). Helium has it’s drawbacks, however: it has a high thermal conductivity, which
requires the use of heated diving suits and breathing gas; it is quite expensive and difficult to store, and
it distorts the voice.
What Can You Do?
As to the cause of narcosis, there is one prevalent theory that states nitrogen partial pressure is
responsible. One fact that emerges from all this research is that there is a wide range of susceptibility
among individuals. And individual sensitivity can vary from day to day.
The fact is that if you dive, you take the chance of getting narked. The good news is that if you do
experience narcosis, the shallower you get the less you will feel the effects. And it doesn’t take long at all
for the effects to wear off once you get topside.
Before you dive, however, stop and take stock of these suggestions:
· Know your limits
Exercise your discipline. Diving is a multitasked activity: You have to pay close attention to your thoughts,
feelings, attentiveness – in addition to your buddy, depth and air consumption. If you notice a sudden
lightheadedness or experience confusion, try to step back mentally and take stock of what’s happening to you
and around you. Then slowly ascend to a shallower depth.
· Watch your carbon dioxide levels
Increased levels of CO2 can increase your potential for nitrogen narcosis. The working or swimming diver
wearing a breathing device is more susceptible to narcosis than a diver in a chamber. And the effect is
synergistic: that means the effect CO2 wields can have a greater wallop.
· Avoid alcohol
When you’re planning your dive excursion, keep in mind that alcohol augments the signs and symptoms of
nitrogen narcosis. Why? “Because of the similar (and additive) effects to excess nitrogen, alcohol should be
avoided before any dive. A reasonable recommendation is total abstinence at least 24 hours before diving; by
that time effects of alcohol should be gone, “ advises dive physician, Dr. Lawrence Martin.
· Be rested when you dive
Refrain from hard work and it’s resultant fatigue before and immediately after your dives. Work and fatigue
can cause higher levels of CO2 in the body, which results in metabolic effects on the neurotransmitters in
your brain.
· Be calm before you dive
Go well prepared so you can look forward to your trip. Anxiety increases you r susceptibility to narcosis.
“The exact mechanism isn’t known,” adds Dr. Peter Bennett, DAN Chie Executive Officer, “but it has an effect
on the brain’s neurotransmitters, in the same place anxiety operates.”
· Descend slowly on deep dives
Experiments have shown that rapid compression affects divers more severely than slow compression.
· Stay Warm
Cold makes narcosis worse. As with anxiety, the precise mechanism is unknown, but cold can have analgesic and
anesthetic effects. These reactions in turn can be synergistic, packing a greater than expected punch.
If you feel the effects of narcosis and recognize it, head for the surface and fresh air. Remember to
breathe, ascend slowly, make your safety stop, then get out into the open. You’ll be back to normal in no
time. And if you have questions about nitrogen narcosis, call DAN Medical Information Line.
References
The Physiology and Medicine Of Diving. 4th Edition, by Peter Bennett, PhD, D.Sc. and David Elliott, D.Sc.;
Chapter 7: Inert Gas Narcosis, 1995.
Bove and Davis’ Diving Medicine, 3rd Edition; by Alfred Bove: Chapter 9: Inert gas Narcosis and High
Pressure Nervous Syndrome; 1997.
Scuba Diving Explained, Questions and Answers on Medical Aspects of Scuba Diving: Lawrence Martin, MD;
1997.
Diving Medicine Online: by Ernest S Campbell, MD, FACS: www.gulftel.com/~scubadoc
‘Nitrogen Narcosis’, by John Francis, Field Editor, Rodale’s Scuba Diving Magazine, www.scubadiving.com/training/instruction/narced.shtml
It doesn't matter which dive tables or computer you don't use!
AN OVERVIEW OF DECOMPRESSION SICKNESS (DCS):
DCS is that illness which follows a reduction in environmental pressure sufficient to cause the formation of
bubbles from gases dissolved in body tissues (see Dalton's and Henry's laws). The consequence of such bubble
formation is twofold:
(1) Bubbles may obstruct blood vessels and lead to ischemia and infarction (death) of tissues beyond the
obstruction.
(2) Bubbles may also initiate an inflammatory response which can lead to bleeding into the tissues, further
compromising the circulation and resulting in tissue swelling
A Chronological History:
1670- Robert Boyle described a furiously tortured viper with a bubble in its eye after observing it in a
vacuum chamber. He suggested that the rapid reduction of pressure caused the production of bubbles in the
tissues of the body.
1840- The Royal Navy used a diving dress developed by Siebe to salvage the Royal George-a naval vessel sunk in
the Thames river. He noted that 'Not a man escaped the repeated attacks of the cold and rheumatism'.
1845- Triger provided the first description of DCS in humans by noting that French caisson workers suffered
sharp pains in the arms and knees after emerging from long exposure. Treated by 'rubbing the spirits with
wine.' We do the same today but the wine
is applied by a different route.
1854-Pol and Wattle noted that 'one pays only upon leaving' the compressed air environment and that the
symptoms are relieved upon returning.
1863- Foley suggests a return to pressure as a treatment for the pains.
1871-Workers on the Brooklyn Bridge coined the term 'bends' because sufferers assumed a posture resembling the
'Grecian bend', an affectation of that era in which women bent over to accentuate their derrieres.
1878-Paul Bert publishes his monumental work 'Barometric Pressure' and demonstrates that bubbles associated
with DCS formed during rapid decompression and consisted mainly of nitrogen.
1888-Moir installed onsite recompression chambers. The incidence of death dropped from 1/4 to 1/60 on the
Hudson River tunnel project.
1906-JBS Haldane develops decompression tables based on tissue half-lives. He demonstrated that the body could
tolerate a 2:1 reduction in ambient pressure without symptoms. This results in the publication of the first
dive tables.
1915-USN accepts Haldane's tables.
1937-Behnke proposes O2 plus recompression as a treatment for DCS. Unfortunately, this pioneering work is
ignored till 1967.
1947- USN develops tables for divers using compressed air.
1967-USN recompression tables 5, 6, 5A, and 6A are published.
Conventional DCS Classifications:
TYPE I:
Also known as minor or pain only bends. It usually involves the limbs, with the shoulder being most frequently
involved, and, in descending order of frequency, the elbows, hands, and lower limbs. It has been described as
a 'toothache in a joint'. This type of DCS responds rapidly to recompression on 100% O2 at 2.8 ATA (60 FSW)-usually
within 5-10 min.
Skin bends ('niggles' or itching) is also in this category. However, skin 'marbling' can be a precursor to
shock (10%) and indicative of a far more severe form of DCS
Generalized severe fatigue/malaise may also be a manifestation of type I DCS but may also be associated with
more ominous forms of DCS.
Type I DCS is the most common presentation in commercial divers, but only represents about 20% of the cases in
sport SCUBA divers.
Permanent residua after treatment ranges from 7-20%. (DAN 1994 data).
TYPE II:
'Major' or neurological bends-present usually as spinal cord hits from T12-L1 with incontinence, paralysis,
and IMPOTENCE. Also can see parasthesias, numbness, weakness, and girdling abdominal pain in a bathing suit
distribution with progressive loss of
strength. THIS IS THE COMMONEST PRESENTATION OF DCS IN THE SPORT SCUBA DIVER, with the incidence representing
~60% of all cases of DCS. Experimental evidence suggests that the threshold for bubble formation in the spinal
cord is 86 fsw-does this give you
a hint as to how deep you should dive??
Other forms of type II DCS include inner ear/vestibular DCS ('staggers') presenting with vertigo, tinnitus,
nystagmus, hearing loss, and nausea and vomiting, and brain hits (may be cerebral gas embolism), presenting as
visual blurring, blind spots, headache, spotty motor or sensory loss, personality changes, seizures, or
unilateral paresthesias (usually seen in altitude-induced DCS).
Permanent Residua after treatment in Type II DCS ranges from 15-36%. (DAN 1994 data)
AGE (ARTERIAL GAS EMBOLISM):
The most dramatic and disastrous type of DCS in which pulmonary overpressure causes bubbles in the arterial
side of the circulation. These may cause the sudden onset of chest pain, hemoptysis, stroke, heart attack,
dyspnea, nonproductive cough, shock, an
d gas emboli in the lungs ('chokes'). (? role of a PFO-patent foramen ovale- in allowing bubbles to cross from
the venous side to the arterial side via a hole in the atrium.)
This catastrophe accounts for about 8% of reported cases of DCS. (DAN 1994 data)
These divers are very ill-~5% die and another 35% have major permanent residua.
TYPE III:
This is a combination of AGE and Type II DCS in divers with a large N2 load who then develop an AGE due to a
rapid ascent. These cases have a very high mortality, and those who survive usually have permanent residua.
May be more common than we suspect.
DYSBARIC OSTEONECROSIS:
Despite what you may have read, this problem is seen almost exclusively in commercial, mixed-gas technical,
and saturation divers and essentially never in sport SCUBA divers. However, with the increasing popularity of
mixed gas, NITROX, and decompression
diving in what was formerly the sport SCUBA population, we are now starting to see this problem in the
non-commercial population.
DAN 1994 DATA: 1164 DCS cases: 227 TYPE I, 664 TYPE II, 91 AGE, 202 couldn't categorize from the data
DAN 1997 DATA: 972 DCS cases with 82 fatalities (2 in technical divers)
DCS RISK DATA: approximately 1/5000 dives
TREATMENT:
a) Early recognition!
90% of all DCS symptoms will appear in the first 12 hours after a dive and an additional 9% in the next 12
hours.
'If there's anything wrong with you within 12-24 hours after diving, it's DCS until proven otherwise.' Don't
take 'no' from an ER doc. They don't know anything about DCS unless they dive. Call DAN (919) 684-8111 for
advice and help.
Be responsible for each other. Be aware of DENIAL. Timely referral to a hyperbaric chamber results in a better
salvage rate. Statistics from DAN suggest that the overall permanent improvement from DCS is only 60-80% and
that the long delays often associated with the treatment of sport SCUBA divers is responsible for the
relatively poor outcomes when compared to military or commercial divers.
b) O2 by tight fitting mask.
Leave it on, even if the diver temporarily improves, until he/she is in the recompression chamber. ABC's if
the diver is unconscious.
c) Aspirin (2 tabs) and fluids (orally or IV ) 1 liter/hour
d) Transport to the nearest chamber ASAP.
Remember:
Oxygenation and recompression are the sine qua non of DCS treatment. The most common error in the medical
management of DCS is the failure to recognize and treat minor or confusing manifestations. Delay in treatment
markedly lowers the treatment success
rate. If done in a timely fashion, 80-85% of DCS cases resolve completely.
US Navy table 6 is the current gold standard for the treatment of most types of DCS (100% O2 at 2.8 ATA /60
fsw with air breaks over a 4 hour and 45 min. time period).
Some closing observations:
'No bubbles, no bends.'
'The deeper you go, the longer you stay there, and the faster you come up, the more likely you are to get
bent.'
Ascent rates should be no faster than 30 feet/min and a safety stop for 3-5 mins. at 10-20 feet should be
mandatory.
Dive well within the computer or table 'no D' limits and preferably above 90 fsw. Your computer algorithms are
not designed to accurately calculate the safe limits for more than 4 dives a day over multiple consecutive
days of diving.
Unlike the 'good old days' when SCUBA meant 'Some Come Up Barely Alive, sex was safe, and diving was
dangerous, now sport SCUBA is inherently a safe sport and and sex can be_______'(fill in the blank).
How about a review on Gases?
