This article represents the views of the author. The article has not been fact checked by myself, the Board of Directors or any member of the USA Dive Club.

Copyright Disclaimer under section 107 of the Copyright Act of 1976, allowance is made for “fair use” for purposes such as criticism, comment, news reporting, teaching, scholarship, education and research. Fair use is a use permitted by copyright statute that might otherwise be infringing.

Beyond the Soda Bottle: An In-Depth Look at Decompression Illness

By Alex Brylske

Like most divers, I have vivid memories of my basic scuba training. Perhaps the most memorable is the evening my instructor showed up for class with a large bottle of Coke.® He proceeded to explain that, like the bottle of soda he held in his hands, our bodies are under pressure when diving. He made his point while vigorously shaking the familiar hourglass-shaped bottle. Then he placed it before me and asked if I would open it. I resisted, but he insisted. So cautiously and reluctantly, I removed the top, expecting a vigorous eruption to spew forth. Much to my surprise, however, nothing happened. As it turned out, the bottle didn’t contain soda after all, but food-colored water.

“What did you expect?” my instructor asked, laughing.

“A big mess,” I replied, somewhat embarrassed.

The point of the lesson, as my instructor explained, was that while at that point we may not have known about the bends, we nonetheless understood full well the phenomenon of gas absorption and elimination in liquids — the essential concept of decompression illness. An hour later, after an informative discussion, we left the room confident of our in-depth and thorough understanding of the bends.

For most divers, the ubiquitous example of bubbling soda is about as far as it goes when it comes to insight into decompression illness. But the phenomenon is far more complex and infinitely more interesting than can be conveyed by any bottle of soda, diet or regular.

Your Body Ain’t No Bottle of Soda

The first thing we should understand about decompression illness is that our body, and the way gases behave when dissolved within its tissues, is far more involved than your instructor may have implied. That’s not a criticism of your training; it’s just that given all the other vital information that must be covered, a cursory overview of decompression — the bare essentials — is all that’s possible. Besides, it’s all most divers need to know, and about as much science as most students will tolerate anyway. But for the true aficionados, there’s a whole lot more.

Even the phenomenon of gas bubble formation in water is a good deal more involved than you might imagine. Because of special bonding characteristics, water molecules are very hard to separate. This gives water a high tensile strength, which is a measure of how resistant a substance is to being torn apart or separated. This characteristic makes spontaneous bubble formation in water very difficult. For example, you could theoretically compress a glass of pure water to over 200 atmospheres and immediately decompress it without forming a single bubble!

The trick to avoiding bubbles is not to shake the glass as it’s decompressing. This incredible resistance to bubble formation tells us that there must be something besides supersaturation of gas that produces bubbles. The other vital point is that the water in question must be pure free of all impurities. This point goes to the heart of one theory of bubble formation in divers.

To understand what’s happening, let’s look at something that has absolutely nothing to do with diving — how raindrops form. We’ve all known since elementary school that rain comes from clouds, which are made up of water vapor. But exactly how we go from water vapor to rain is similar to how bubbles form in us. At the core of every raindrop is a particle of dust. This dust particle acts as a “seed” — a point around which the water vapor can coalesce and grow into a drop.

Now, if we tried the previous experiment with a glass of water containing lots of impurities — even if we didn’t shake it — the results would be significantly different, too. Like raindrops, foreign particles in the water would seed the production of gas bubbles. Exactly how many bubbles would form depends on the number of particles in the liquid, the pressure differential and other factors. The point is, the seeds make all the difference.

But what does this have to do with the bends? More to the point, what are the “seeds” in our bodies that form bubbles? It may surprise you to learn that animals, including humans, have a proclivity for creating gas “seeds,” or what are more accurately termed gas micronuclei. These are microscopic pockets of gas caused by various factors, including movement. Just as in the shaken glass, the turbulence of blood flow itself and the natural movement of the body cause the formation of micronuclei. These seeds, like the impurities discussed previously, are the precursors to bubble formation. During an ascent from depth, nitrogen diffuses into these seeds (which are actually areas of low pressure), forming tiny microbubbles.

his phenomenon tends to occur in the capillaries — the smallest structures of the circulatory system. From there, many of the bubbles enter the venous circulation and flow back to the heart. Since they’re very tiny bubbles, they normally don’t cause any blockage in the vessels during their transit. From the heart, blood travels to the lungs. When the bubbles reach the extremely fine capillary bed of the alveoli, they’re trapped. The bubbles diffuse back into the alveoli, and nitrogen gas is expired in the normal respiratory process. Since these bubbles have no effect on us, they’re called subclinical, or asymptomatic. We also know them as “silent bubbles.”

So if the lungs filter out all the bubbles, why do we still get decompression illness? There are actually two answers. First, not all the bubbles are filtered out. Exactly how this happens is still debated by researchers, although several mechanisms have been proposed. One may involve the anatomy of the lungs. This theory holds that when bubbles in the capillary beds build to excessive levels, vessels can open up, allowing some blood to bypass the lungs altogether. This bypass mechanism is called shunting and allows bubbles present in the blood to migrate around the alveoli and into arterial circulation. This is a very big problem, because the path is now clear all the way to the brain.

Another bubble bypass theory has great implications for repetitive diving. The theory goes like this: On an initial dive, significant silent bubbles develop, but then, as described before, migrate to the tiny vasculature of the lungs. But if you make a repetitive dive, the bubbles may not be filtered and diffuse back into the alveoli. During a subsequent dive, the remaining bubbles are recompressed — possibly to the size where they can get through the capillaries and into the arterial circulation. This is one reason some researchers have cautioned against making deep, short-duration repetitive dives, sometimes called “bounce dives.”

Another explanation, which has elicited renewed interest of late, is the “hole in the heart” theory. This mechanism involves what’s called a patent foramen ovale, or PFO. To understand what a PFO is, and how it affects divers, we must review some basic anatomy and human development. While in the womb, a fetus has no use for its lungs. It receives oxygen directly from the mother’s blood supply. Thus, in fetal circulation, blood bypasses the lungs. One way this bypass occurs is by shunting the blood entering the right atrium directly into the left atrium through an opening called the foramen ovale. The foramen ovale is similar to a one-way “flapper valve.”

At birth, when the newborn takes its first breath, the pressure in the left atrium increases and causes the flapper valve to close. Over time the valve normally seals shut. However, in perhaps as many as 25 to 30 percent of the population, the valve remains partially open. (The medical term is “patent.”) This allows small amounts of blood from the right atrium to seep into the left atrium. Under normal circumstances, this condition is of no consequence, because the pressure in the left atrium is higher than the right and tends to keep the valve closed.

The implications are pretty obvious. Silent bubbles that develop in the venous circulation eventually make their way back to the heart. Under normal conditions, these bubbles are trapped by minute blood vessels as the blood makes its way from the heart to be reoxygenated by the lungs. As described earlier, the trapped bubbles then diffuse into the lungs, and the gas is expired in the normal respiratory process.

But all is not necessarily well if you have a PFO. Under some circumstances — like when you equalize your ears — the pressure in the right atrium can increase slightly over the left atrium. It’s then possible and likely that blood will shunt from the right to left heart. This provides a pathway not only for small amounts of venous blood to bypass the lungs, but the silent bubbles contained in that blood as well.

Once in the left atrium, these micro-bubbles go directly into arterial circulation. Several studies have documented this phenomenon. Yet, as research is still limited on this subject, it’s impossible to draw any solid conclusions about the implications of PFO. Nonetheless, while the PFO does not cause decompression illness, additional bubbles entering the arterial blood flow in this manner may hasten the onset of symptoms or cause more severe forms of DCI. It could perhaps even cause arterial gas embolism.

One intriguing study comes from England, where a researcher examined over 100 cases of DCI. Of the test subjects who experienced symptoms of DCI within 30 minutes of surfacing, 66 percent had a PFO. In subjects experiencing symptoms after 30 minutes, only 26 percent had a PFO. This data suggests that a PFO may contribute to the early onset and severity of DCI.

Understand, however, that researchers caution against drawing any definitive conclusions about the ramifications of PFOs in divers, as the phenomenon requires far more study. While certainly inconclusive, the PFO issue provides yet another reason why we should dive conservatively. The PFO issue also offers one more example of how much science has yet to learn about the mechanism of DCI.

Bubbles That Stay Put

How bubbles bypass the lungs may be interesting, but that’s probably not what causes the vast majority of bends. The real culprits are the bubbles that don’t circulate, and with present technology, can’t even be detected. But the question remains, exactly how do they form?

One mechanism used to explain the phenomenon has to do with the nature of the blood vessels themselves. We know that bubbles form much more easily on surfaces that are termed nonwettable, or hydrophobic (like candle wax). This happens because less energy is required to form on them than on a wettable surface.

But you have to be wondering what in the world bubbles on candles have to do with bubbles in our bloodstream. Well, besides wax, another nonwettable substance is the interior surface of our blood vessels. These walls aren’t smooth, as you might have imagined, but highly irregular. They’re also made up of tissues that are primarily lipid (fat). Like a candle, this makes the interior walls of our blood vessels nonwettable surfaces. So it’s not a huge leap of the imagination to conclude that bubbles — or micronuclei — may form here as easily as on a candle.

As the diver ascends and continues offgasing, the bubbles or gas seeds grow. But unlike what you might imagine from day-to-day experience, these bubbles tend not to form the familiar spherical shape. Experiments in animals have shown that they instead become elongated — a shape that increases their surface area and resistance to movement. Bubbles in blood vessels can stop or interfere with normal blood flow. This further compounds the decompression process, because it’s now more difficult for dissolved nitrogen to escape from the tissues.

Some have termed this phenomenon the “bottleneck effect.” The dissolved nitrogen tries to escape or wash out, but the localized bubble formation impedes the flow of blood that would otherwise carry away the dissolved nitrogen. The nitrogen has to go somewhere, so it diffuses into the newly formed bubbles, causing them to grow even larger. It’s believed that this mechanism is a primary cause of neurologic DCI, the more serious and common form of the disorder in recreational divers.

But the story doesn’t end with blood vessels. Nitrogen can diffuse into seeds between tissues. In this case, the bubbles can distort and permanently damage the tissue. As they grow, the bubbles also put pressure on nerves. This type of bubble formation is called extravascular, meaning “outside the vessel.” Aqueous (watery) tissues — the type that make up ligaments and joints — are especially prone to developing these types of bubbles. That’s one reason for the widely held theory that extravascular bubbling is the primary mechanism for joint pain, one of the classic symptoms of DCI.

It Ain’t Just the Bubbles

Another misconception that many divers have about decompression illness is that it’s all about bubbles. Indeed, bubbles are the cause, but how our body reacts to this insult is a major factor in the eventual outcome. The mechanism of DCI involves a highly complex interplay of both bubble mechanics and biochemistry. During the treatment process, in fact, dealing with the biochemical complications of DCI is as important as recompression.

Research has shown that a substance in the blood called smooth muscle activating factor causes inflammation and could induce bends in decompressed animals. Conversely, a substance called anti-smooth muscle activating factor has just the opposite effect. This insight led to experiments where researchers were unable to induce DCI in animals given the smooth muscle activating factor, and the symptoms resolved once the animals were given anti-smooth muscle activating factor. These findings led to other exciting studies into the immunological involvement in DCI.

Other researchers have shown that gas bubble formation brings about important changes in blood chemistry. First, the presence of bubbles in the blood activates the clotting process. Platelets — blood components responsible for clotting — become sticky, attaching themselves to each other and to the newly formed bubbles. This was the genesis of the once popular practice of taking aspirin as a preventative to DCI — a practice that is now discouraged by most diving medical experts.

Bubbles also cause inflammation of the capillary walls, inducing leakage of fluid into the tissues, which contributes to dehydration. Eventually, the blood vessels themselves begin losing their integrity and start to break down. This causes the vessels to narrow and dislodges fat particles into the blood. These particles are yet another possible origin of gas seeds.

Other studies have shown that bubble formation activates antibodies called complement proteins. These substances cause the release of histamines and other chemicals that cause still further fluid leakage from the capillaries into the surrounding tissues (edema). This process, incidentally, is similar to the way our bodies react when we go into shock.

Amazingly, animal experiments have shown that if the release of these antibodies is stopped, the severity of decompression illness lessens. From this evidence, researchers hypothesize that a person’s susceptibility to DCI may depend on how easily his or her body releases these complement proteins. The implication of this is very exciting. Perhaps one day we may be able to develop a blood test that can identify divers who are prone to DCI. More recent studies have demonstrated that when DCI bubbles come into contact with white blood cells, the cells release toxic oxygen radicals. Their release also causes inflammation, which further slows the blood.

The overall effect of all this biochemical activity is like a snowball rolling downhill. The blood thickens, becomes sticky and cannot move as efficiently through the vessels. Red blood cells now clump or “sludge” together. This, in turn, decreases circulatory efficiency and nitrogen wash-out. More bubbles form, and bubbles that already exist grow. The blood flow slows even further, and the condition gets worse.

So while the decompression problem starts with the formation of bubbles, exactly how and why they form is more complex than you probably thought. Additionally, what happens after they form is almost incomprehensibly complex from a biochemical perspective. To add even more uncertainty to the recipe, very little of what you’ve just read has been definitively proven. It’s mostly informed speculation based on some preliminary experimentation and a lot of inferences based on how the body works under similar circumstances. But I, for one, am not about to buck the tide of medical opinion or speculation. If you’re smart, you won’t either. Dive conservatively, maintain good physical fitness and follow the advice of experts, and you’ll reduce your chances of experiencing a ride in a recompression chamber.

Isn’t science great?

Link to Dive Training magazine article.

Beyond The Soda Bottle: An In-Depth Look At Decompression Illness - Dive Training Magazine | Scuba Diving Skills, Gear, Education

This article represents the views of the author. The article has not been fact checked by myself, the Board of Directors or any member of the USADive Club.

Copyright Disclaimer under section 107 of the Copyright Act of 1976, allowance is made for “fair use” for purposes such as criticism, comment, news reporting, teaching, scholarship, education and research. Fair use is a use permitted by copyright statute that might otherwise be infringing.

By Robert N. Rossier

We all know there are medical factors that can prevent people from diving. Epilepsy, various heart conditions, loss of consciousness, pneumothorax, some chronic diseases and even some forms of anxiety can spell trouble that may be incompatible with diving. But over the years, the list of contraindications has narrowed, allowing more to enjoy exploration of the underwater world.

One condition that has prevented some people from becoming divers is diabetes. Diabetes affects the body’s ability to produce or respond to insulin — a hormone controlling the metabolism of carbohydrates. The result is abnormal carbohydrate metabolism leading to elevated glucose levels in the blood and urine.

While this might sound innocuous, the long-term effects of diabetes are dead serious. Diabetes takes more lives than AIDS (acquired immunodeficiency syndrome) and breast cancer combined, claiming one American life every three minutes. Diabetes is a leading cause of blindness, kidney failure, amputations, heart failure and stroke. What’s more, the incidence of diabetes is growing. According to diabetesresearch.org, the number of reported cases of people living with diabetes has jumped nearly 50 percent in the past decade and it now affects more than 29 million Americans. On a global scale, diabetes afflicts more than 380 million people, and the World Health Organization estimates that by 2030, the number of people living with diabetes will more than double. Clearly, diabetes is a growing health risk and one that could affect our ability to dive safely. But, at least for some, the door has been opened for scuba diving with diabetes — that is, if the proper conditions are met and the proper protocols are followed.

Defining Diabetes

Diabetes is categorized into two primary types, referred to as Type 1 and Type 2. In those with Type 1 diabetes, the pancreas does not produce insulin or it produces insufficient insulin to meet the body’s needs. Individuals with Type 1 diabetes must receive insulin injections regularly in order to metabolize blood glucose (blood sugar). In the more common Type 2 diabetes, the body may not produce enough insulin or the insulin does not trigger the cells to allow proper metabolism of glucose.

Type 1 and Type 2 diabetes are the most common forms of the disease but other forms exist. Many individuals are also diagnosed with pre-diabetes, a condition in which blood sugar is high but not significantly enough to warrant treatment. Unless changes are made to diet and 

exercise, those with pre-diabetes are likely to join the ranks of individuals diagnosed with diabetes.

Physiology of Diabetes

To understand the effects of diabetes, we need to have an understanding of some basic human biology. In a normally functioning body, a number of metabolic reactions occur in response to eating. First, the digestion process in the stomach breaks the food down into glucose (a form of sugar), which enters the blood stream and is transported to cells throughout the body. The hormone insulin is secreted by the pancreas, which triggers the cells to allow glucose to enter. Through a process called glycolysis, the glucose is broken down in the production of a molecule called ATP (adenosine triphosphate), which is the source of energy in the cell. Also in response to eating, the cells also synthesize and story fatty acids and proteins. These are all critical functions for a normal, healthy body.

For the person with diabetes, this process simply does not work properly. Type I diabetes is actually an autoimmune condition. The immune system destroys the beta cells in the pancreas, which are responsible for the production of insulin. And without that insulin, glucose does not enter the cells and they run out of energy.

For Type I diabetes, those affected must receive injections of insulin at the appropriate times to control blood glucose levels and allow cells to receive the needed glucose. Eating the right foods at the right time can also help control blood sugar by controlling how much glucose is produced through digestion. Other factors including exercise, stress and general health also affect the body’s need for insulin, so getting the correct timing and dosage for insulin injections can be a challenge.

In Type 2 diabetes, the pancreas has a deficiency of beta cells that create insulin, making it unable to supply enough insulin to the body. In addition, insulin receptors at the cellular level may not respond properly to insulin, limiting the amount of glucose entering the cells and allowing blood glucose to remain elevated. Controlling diet is also important for those with Type 2 diabetes to prevent spikes in blood glucose. Medications are available to help maintain an appropriate low level of blood glucose. For some, additional medications may be available to increase insulin production by the pancreas.

A Balancing Act

The factors that determine blood glucose levels fluctuate greatly throughout every day, so for a Type 1 diabetic, determining the proper dose of insulin to take can be a complex and sometimes delicate balancing act. Too much insulin means the body consumes too much glucose, which can drive blood glucose to a dangerously low level. This low blood glucose condition, referred to as hypoglycemia, can sometimes be fatal if prompt corrective action is not taken.

With too little insulin, blood glucose can soar to dangerous levels while at the cellular level the body is starved of energy. This condition is referred to as hyperglycemia, and it poses a risk of long-term complications.

The goal, then, is to take the necessary steps to maintain a relatively constant blood glucose level as we eat and perform various activities throughout the day. One way that those challenged with diabetes can help avoid the spikes that can come, is to pay attention to what they eat and when they eat it. If such an individual doesn’t eat at the right time or eats too much of the wrong thing (or right thing) at the wrong time, the system can easily be thrown out of balance. In addition to proper eating and dietary habits, other natural remedies have also been widely used to help keep blood sugar levels in check. For example, Gymnemate Sylvestre is an herb used for centuries in India to help control blood glucose by stimulating pancreatic function.

Contributing Factors

Numerous factors affect blood glucose levels, as well as overall health for all of us. These are of particular importance to those with pre-diabetes or diabetes. One factor that contributes to elevated blood glucose is stress. The stress hormone adrenaline increases blood glucose, releasing it into the blood to provide a needed boost of energy to meet the fight or flight needs. In a situation such as being chased by a shark, we would react physically by fighting or fleeing and that glucose would soon be used up. But what if instead we remain stationary? Many of us deal with stress on a daily basis, but we don’t deal with that stress by engaging in physical activity. Instead, we are forced to sit and deal with it. One result of that inaction can be elevated blood glucose levels.

Cortisol is a hormone generated by the adrenal glands that can elevate blood glucose. Under conditions of high stress, cortisol provides the body with glucose by tapping into protein stored in the liver. This energy can help an individual in a fight or flight situation. However, if we’re constantly subjected to stress, the resulting chronic elevated cortisol can lead to increased blood glucose levels. To help reduce the effects of stress, we need to find ways to prevent or cope with it. Strategies include everything from exercise to nutrition, hydration, music and meditation.

Sleep is not a luxury — it is a necessity that also has an impact on blood glucose. In fact, a chronic lack of sleep is another form of stress that can result in elevated blood glucose, according to an article in the December 2015 issue of Diabetes Therapy. The National Sleep Foundation recommends seven to nine hours of sleep every night to enjoy its restorative health effects.

Another factor that can predispose individuals to Type 2 diabetes is a chronically low level of Vitamin D. A study reported in Scientific American in 2009, found that 45 percent of Americans are deficient in Vitamin D and more recent studies corroborate a rising trend in Vitamin D deficiencies. But here is the kicker: a Tufts-New England Medical Center study found that those who are chronically low on Vitamin D had a 46 percent increased risk of Type 2 diabetes. While the mechanism of Vitamin D with regards to diabetes is not crystal clear, researchers suspect that Vitamin D enhances the cells’ response to insulin.

As it turns out, precautions against skin cancer may actually be depressing our levels of Vitamin D. In a 2009 Article in Scientific American, co-author Adit Ginde, an assistant professor at the University Of Colorado Denver School Of Medicine, reveals that using a sunscreen with as little as an SPF 15 reduces the skin’s Vitamin D production by 99 percent.

For the remainder of this article use the link below,

 Click on the link.

A Primer On Diving With Diabetes | Dive Training Magazine

This article represents the views of the author. The article has not been fact checked by myself, the Board of Directors or any member of the USADIVE Club

Copyright Disclaimer under section 107 of the Copyright Act of 1976, allowance is made for “fair use” for purposes such as criticism, comment, news reporting, teaching, scholarship, education and research. Fair use is a use permitted by copyright statute that might otherwise be infringing.

The Misguided Assist

By Jon Hardy

Ed.'s note: The incidents described here are real. Names of locations and people have been changed or deleted.

As part of a major "Dive-In" event, Mary, a nurse and master diver with six years of diving experience, was making a shore dive with her local dive club. She planned a 30-minute, 100-foot dive to a near-shore underwater wall with one of the club's divemasters, Tom, and a friend of his named Susan. All three were using dive computers and knew that most of the dive would be spent on the swim out and back, following the slope of the bottom. The surf was up, but the three were ready to dive and standing at the water's edge when a middle-aged man and his young adult son bungled their entry, and the father was pulled out of the water with a medical emergency. Medical help was immediately available on the beach and the father was given first aid. The ailing father pleaded with Mary to let his son, Chuck, dive with them. Mary agreed and became Chuck's buddy.

The first problem occurred when Chuck refused to put on his fins to make the surf entry. Without fins, he struggled through the surf, wasting a good deal of air. The group met, as planned, at a buoy to check buoyancy. Chuck arrived at the buoy short of breath, but neither he nor any of the other divers checked his air,

Going Down

The four divers then descended to 40 feet. Tom was not only buddying with Susan, but he had moved off separately with her and she was receiving all of his attention.

At the same time, Chuck was flapping his hands and arms while going nowhere. Mary checked her pressure gauge and found that she had 2,600 psi. She thought that Chuck probably had less air, but figured he was still OK, so she didn't check his pressure gauge.

Now it was just the two of them, and as they moved down the slope, they encountered a thermocline at 80 feet. At this point, they checked their gauges and Chuck was down to 300 psi, less than 15 minutes into the dive.

Panic Attack

Mary and Chuck did not make physical contact and did not prepare to share air. Chuck appeared to have a panic attack and bolted for the surface. Mary raced after him, hoping to stop him and make a shared air ascent. But Chuck arrived at the surface first, so Mary slowed as she approached the surface and even included a pause in shallow water. On the surface, they both inflated their BCs and proceeded to swim in. As they were swimming in, Mary heard a popping sound in her chest, then she started wheezing, as it also became difficult and painful to breathe.

Medical personnel on the beach checked Mary and agreed with her that she needed to go to an emergency room, not a recompression chamber. Chuck disappeared, never to be seen again. Mary went by ambulance to the hospital and was diagnosed with a partial pneumothorax and other respiratory complications. After 12 months out of the water, and lots of medical tests, Mary finally received medical clearance to return to diving.

Lessons For Life

• Do not let yourself be talked into being someone's buddy, particularly as a last-minute change. If something has already gone wrong, more problems are likely.

• If your dive buddy makes bad dive decisions or uses incorrect dive procedures (like Chuck's surf entry in this case), terminate the dive before these errors become compounded.

• Checking air is a three-step process: Check your own, check your buddy's and show your buddy yours.

• Allow or request that the most qualified diver in the group, in this case the divemaster, handle or deal with the weakest diver.

• Part of dive planning is to agree on procedures to use in a low-air or out-of-air situation.

• Do not put yourself at risk of a rapid ascent because of someone else's errors.

This article represents the views of the author. The article has not been fact checked by myself, the Board of Directors or any member of the USADive Club.

Copyright Disclaimer under section 107 of the Copyright Act of 1976, allowance is made for “fair use” for purposes such as criticism, comment, news reporting, teaching, scholarship, education and research. Fair use is a use permitted by copyright statute that might otherwise be infringing.

Making a Clean Sweep: The Regulator Retrieval Skill

By Barry & Ruth Guimbellot

Keeping your regulator in place when underwater is a top priority for divers whether novice or advanced. Most of us never expect to have our regulators pulled from our mouth. However, accidents do happen. For example, you and your buddy are swimming side by side when your buddy taps you on the right shoulder. You turn your head in response and your buddy’s hand gets tangled in the regulator hose. In an effort to withdraw their hand, they pull the regulator from your mouth. Or perhaps a diver is swimming in front of you and gets pushed close to you due to a current. In an effort to move away, he accidently kicks you in the face with his fin. Out comes the second stage with a flip of the fin. If it falls in front of you, quickly grab the second stage, place it in your mouth, clear it of water and continue the dive. If the regulator falls out of sight or gets caught on some object behind you, there are two specific ways to perform the regulator retrieval skill — the sweep and the reach methods.

Keeping your regulator in place when underwater is a top priority for divers whether novice or advanced. Most of us never expect to have our regulators pulled from our mouth. However, accidents do happen. For example, you and your buddy are swimming side by side when your buddy taps you on the right shoulder. You turn your head in response and your buddy’s hand gets tangled in the regulator hose. In an effort to withdraw their hand, they pull the regulator from your mouth. Or perhaps a diver is swimming in front of you and gets pushed close to you due to a current. In an effort to move away, he accidently kicks you in the face with his fin. Out comes the second stage with a flip of the fin. If it falls in front of you, quickly grab the second stage, place it in your mouth, clear it of water and continue the dive. If the regulator falls out of sight or gets caught on some object behind you, there are two specific ways to perform the regulator retrieval skill — the sweep and the reach methods.

The sweep method of regulator retrieval consists of several steps. Follow the sequence as listed:

Step 1: When the regulator is dislodged from your mouth, immediately begin to slowly and continuously exhale a stream of small bubbles. This will help prevent overexpansion of the lungs if you unknowingly ascend during the recovery effort.

Step 2: Regardless of your position in the water column, you will be able to use the sweep method for retrieval of the regulator. Whether vertical or horizontal, begin the sweep by leaning with the right shoulder downward, allowing the regulator hose to swing and hang away from your body.  In the horizontal position, it is helpful to have your head and torso slightly lower than your feet. This position allows the hose to swing to the side and slightly forward, making recovery easier.

Step 3: While continuing to slowly exhale and lean to the right, begin a downward sweep with the right arm, fully extending the arm behind you. During the sweep, the arm should maintain contact with the right side of your body. Close contact with the body helps prevent missing the regulator hose if it is located close to the body. With the right arm fully extended behind you, swing the arm up and out until perpendicular to your body. The hose should now be lying across your arm.

As you swing your arm in front of you, the second stage should be close to your right hand .

With either hand, place the regulator in your mouth, immediately clear the regulator of water using the blast or purge methods and begin breathing normally. Remember, when taking the first breath after clearing the regulator, do so cautiously to avoid inhaling a drop or two of water that might remain inside.

Link to article with photos:

Making A Clean Sweep: The Regulator Retrieval Skill - Dive Training Magazine.

Trouble at the Surface

By Jon Hardy

Ed.'s note: The incidents described here are real. Names of locations and people have been changed or deleted.

A middle-aged couple, Joe and Margaret Kirby, had recently been certified along with their teenage daughter, Becky. The family had made a few resort dives before signing up for their first really independent boat trip closer to home. The dive operator offered a dive guide for the day as the three were still novices, but they declined.

The day was beautiful with rolling waves, clear skies and a moderate breeze. Complete briefings were conducted at the dock and on arrival at the dive site. The dive area was popular, and several dive boats had already arrived and taken the available mooring buoys. The boat carrying Joe, Margaret and Becky anchored beside the reef in a sandy area. All of the dive boats there that day had student divers on board and planned their dives within the skill level of these divers.

After the student divers had entered the water, the Kirbys did likewise and made a free descent to the 40- to 60-foot depth range and, using a compass course, proceeded along the coral reef.

At about 70 feet, Becky indicated she had some difficulty, so they all surfaced together. At the surface, they discovered that they were quite far from their own boat and that they had traveled opposite from their intended direction but were near another boat that was on a mooring. They signaled back to their boat, giving the OK signal and what appeared to be a "come get me" signal. The skipper, seeing the conflicting signals, sent the divemaster out to investigate, while he continued to bring the students on board.

The divemaster swam out, made contact with the three divers and inflated all of their BCs, while evaluating the situation and making sure everyone was breathing OK. The divemaster provided reassurance while they waited for their boat to pick them up. Suddenly, Margaret, who was using her regulator to breathe on the surface, said she was out of air. A quick check of her pressure gauge showed 1,100 psi. She then dropped her regulator second stage from her mouth. The divemaster replaced it, and she dropped it again. At this point, he gave the emergency signal and started in-water mouth-to-mouth resuscitation.

The nearby dive boat dropped its mooring and was beside the divers in two to three minutes. Margaret was brought aboard and full CPR was administered during the rushed trip back to the dock, but to no avail.

In the legal action against the dive boat, skipper, divemaster and dive business, the family claimed that:

• The conditions were unsafe, in particular that an extremely strong current of over three knots was running.
• There was no dive briefing.
• The divemaster did not swim out fast enough.
• They should have used a chase boat, surfboard or float, pocket mask and an underwater recall.

NOAA had a continuously recording current meter on the reef at the site and depth of their dive, and, at the time of the accident, it recorded a variable current between zero and one-quarter of a knot.

Many student dives were made at the same time and place with no accidents or incidents. The procedures outlined in the briefings for divers who surface away from the boat indicated that divers should inflate their BCs, signal the boat and wait for pick-up. Of course, the boat would not put multiple students at risk by running the propellers while they were surfacing.

The divers did not follow the instructions to go down the anchor line and swim into the current; they incorrectly used their compass and went in the wrong direction.

When they first surfaced, Margaret was not having a problem. When she claimed she was out of air at 1,100 psi, it was a clear indication of stress, over breathing or circulatory distress.

The whole family was using private-label, mail-order BCs and regulators.

The autopsy gave drowning as cause of death, due to a heart attack brought on by morbid obesity, coronary atherosclerosis and other medical problems.

The court dismissed the case based on the waiver and release form signed by the victim.

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How to Control Seasickness

There are many ways to describe it: tossing your cookies, hugging the porcelain, calling for Ralph or letting out a technicolor yawn. but no matter what you call it, it’s no laughing matter. Motion sickness (seasickness, or “mal de mer”) is a common problem of boaters and divers. At best it is annoying, and at worst it becomes totally disabling. I will never forget crossing the ocean between Truk Lagoon and Pohnpei through very rough seas. As our boat scaled 10-foot/3-m swells and bounced off the backside of the rhythmic aquatic heights, my shipmates, a group of bronzed, sun-worshipping divers, went from golden-hued to green around the gills as soon as the seas picked up. Fortunately, I had placed a scopolamine patch (see below) behind my ear as soon as the surface began to get choppy. The drug worked well, and I was spared the wrath of an unsettled sea — and stomach.

What Causes Seasickness?

Seasickness is a complex phenomenon that involves the cerebellum (part of the brain that controls, among other things, balance), vestibular system (labyrinth of the inner ear that plays a major part in the control of equilibrium), the nerve connections between the eyes and the inner ear, and the gastrointestinal tract. It is made worse by alcohol ingestion, emotional upset, noxious odors (e.g., diesel exhaust fumes) and inner ear injury or infection. Motion sickness can be induced in a person who is not moving by having him watch an image of changing motion, such as a car chase or roller-coaster ride. Some of the special effects in current movies, particularly large-format ones like IMAX, can cause viewers to become dizzy or even mildly motion sick. Most persons adapt to real motion after a few days, but may require medication until they are adjusted to the environment.

Signs and symptoms of seasickness include a sensation of dizziness or spinning, a sensation of falling, pale skin color, sweating, nausea, weakness, yawning and increased salivation. Vomiting may provide temporary relief, but prolonged salvation does not occur until the inner ear labyrinth acclimatizes to motion or someone intervenes with medication.

How to Manage Motion Sickness

Here are a few tips to help you treat — or possibly prevent — a bout of seasickness:

Keep your eyes fixed on a steady point in the distance. If on board a ship, stay on deck. Splash your face with cold water. If the seas are rough, be careful not to slip or fall overboard.

1. Take meclizine (Antivert, Bonine) or cyclizine (Marezine) 25 mg orally, or dimenhydrinate (Dramamine) 50 mg orally, every six to 12 hours as necessary to prevent and control motion sickness. To be most effective, the first dose of medication should precede the environmental change by one hour. Medication given after the onset of seasickness will often be ineffective.
   Obviously, if you are vomiting and cannot keep any medication down, you may need to use a suppository, such as prochlorperazine (Compazine) 25 mg or promethazine (Phenergen) 25 mg, noting that these drugs won’t cure the motion sickness. They might control vomiting, but have the side effect of drowsiness. Astemizole (Hismanal) is a nonsedating antihistamine that appears to suppress motion sickness as a side effect in some individuals. The dose is 10 mg by mouth every 24 hours. Persons with impaired liver function or who are taking ketoconazole, itraconazole, erythromycin, clarithromycin, or troleandomycin should not take this drug.

2. Place a transdermal scopolamine patch (Transderm-Scop) on the skin behind the ear. This patch releases the drug slowly through the skin and is effective against motion sickness for up to three days. Side effects include drowsiness, blurred vision (sometimes with a dilated pupil in the eye on the side of the patch), decreased sweating, difficulty with urination (particularly in elder males with enlarged prostate glands), dry mouth and a propensity to be susceptible to heat illness during times of heat exposure. On rare occasions, a person who uses a patch can become delirious as a side effect. Normal behavior returns within a few hours after the patch is removed.

3. Place a transdermal scopolamine patch (Transderm-Scop) on the skin behind the ear. This patch releases the drug slowly through the skin and is effective against motion sickness for up to three days. Side effects include drowsiness, blurred vision (sometimes with a dilated pupil in the eye on the side of the patch), decreased sweating, difficulty with urination (particularly in elder males with enlarged prostate glands), dry mouth and a propensity to be susceptible to heat illness during times of heat exposure. On rare occasions, a person who uses a patch can become delirious as a side effect. Normal behavior returns within a few hours after the patch is removed.
   The patch should be positioned at least three hours before rough seas are encountered. If you touch the medicated (sticky) side of the patch with a finger and then let that finger come in contact with your eye, your pupil will almost certainly dilate and stay that way for up to eight hours.

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   By Paul Auerbach, M.D.

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What is visibility? Illuminating facts about an unclear situation

By Robert N. Rossier

What’s the difference between a great dive and a mediocre dive? In most cases, it’s a matter of feet — not in terms of depth, but underwater visibility.

One of the most important considerations for diving is the “viz”. Clear water can make a mundane dive site shimmer in glory. Conversely, even the best coral reef can be a disappointment when it’s clouded by a veil of murky water.

Visibility is generally considered to be the distance at which an object underwater can be readily identified. Underwater visibility is measured two ways. There is horizontal visibility —how far you can see looking straight ahead — and vertical visibility — how far you can see looking up or down.

Horizontal visibility is usually more important, since it affects our ability to view the underwater environment and keep track of our dive buddies.

Despite its importance, visibility receives precious little attention in a basic scuba course.

That’s too bad because if you know something about the factors that affect visibility, you’ll

have a better chance of locating clearer waters.

Three factors primarily affect underwater visibility: light penetration, biological species and particulates. Not surprisingly, these factors are often related to one another, as well as to other environmental factors.

LIGHT PENETRATION

It only takes a couple of dives before we realize that sunlight plays a very important role in the visibility equation. Just as we can usually see better on the surface during a sunny day, the same generally holds true underwater.

The amount of light that will penetrate the water depends on three things: overall light levels (i.e., a cloudy versus a sunny day), the angle at which the light rays meet the water (called the “angle of incidence”) and the roughness of the surface.

While you may not be able to do anything about the clouds, you can plan your dives to take advantage of optimum light levels. In a geographic sense, when you’re near the equator,

where the sun’s rays are most intense, more light penetrates the water surface. In higher latitudes, the lower angle of incidence causes more light to be reflected, and less enters the water column. That’s one of the reasons why the water is almost always clearer in Bonaire (which is very close to the equator) than it is off the coast of New Jersey.

The location of the sun in the sky also affects light penetration, with the best light levels occurring around noon. The further the sun sinks on the horizon, the smaller its angle of incidence and the worse the visibility.

Sea state is another factor affecting light penetration. Rough seas reflect more light, thus reducing the underwater illumination. So if you’re choosing between two dive sites, opt for the one with calmer waters. The visibility will probably be better.

THE BIOLOGY OF VIZ

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Delays and Misdiagnosis

By Jon Hardy 

A physician named George took a tropical dive vacation with his wife Eve and teenage son Todd. The family took advantage of the two boat dives per day and unlimited shore diving offered by their resort. By Friday, George and his family were 13 dives into their weeklong vacation and planned only two morning boat dives so that they would have a 24-hour surface interval before their Saturday afternoon flight home.

When they surfaced at the stern of the dive boat after their second dive Friday morning, George and Todd let Eve board first. George started to tell Todd that he felt something was wrong when he suddenly lost consciousness.

Todd swam to his father immediately and yelled for help. The crew jumped into action and promptly got George and Todd out of the water and out of their dive gear. George regained consciousness quickly and, other than feeling out of sorts, he seemed to be all right.

While the crew secured the boat, George's symptoms worsened. Because English was not the boat crew's primary language, the family had difficulty communicating with them. No neurological exam was performed, no first aid was provided and George, the only person on hand with any medical training, was in no shape to provide a diagnosis. On the ride back to shore, the crew told the family that George must have been stung by something in the water and he would be better soon. They volunteered to arrange a ride to a local medical clinic.

When they arrived on shore, the dive guide called a cab, and George and his family went on their way. But the cab driver, seeing they were scuba divers, took them to the local hyperbaric chamber rather than the clinic. While paperwork was being completed and a medical exam was started for George, the dive guide from the boat caught up with them. The dive guide convinced George that he should go to the clinic, rather than be treated at the chamber.

After some delay, the clinic began administering oxygen, but stopped the oxygen treatment during the night when the oxygen supply was needed for another patient. The next day, with worsening symptoms, George was returned to the hyperbaric chamber and treated.

After multiple treatments at the local chamber and then back home, George was left with residual damage that precluded his continuing to perform surgery as part of his medical practice. He brought a legal action that was decided in his favor at trial.

George likely suffered from a poorly understood form of decompression illness that appears to be caused when a minor arterial gas embolism occurs in a diver who has significant nitrogen loading. This causes a hard-to-treat form of decompression sickness, Type III DCS.

Administering oxygen promptly to an injured diver is the best first aid, and getting hyperbaric oxygen therapy without needless delays is the definitive treatment.

If a diver suffers a lapse of consciousness upon surfacing, immediately suspect arterial gas embolism, administer first aid and get proper medical care.

Carry dive accident insurance so there is no question about payment for treatment.

Be assertive. Insist on medical care, and make it clear to the medical professionals that the injured person has been scuba diving.

Contact Divers Alert Network (919-684-4326) and enlist their help to find proper medical support or to consult with local physicians for you.

To the best of your ability, ensure that the dive boats you use have radios and oxygen, and that the crew is trained and prepared to use them. At least one crew member should be able to recognize and deal with the signs and symptoms of diving accidents. In countries where English is not the primary language, try to determine if the boat crews can function in English, even if things become difficult.

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Scuba diving PTSD: how common is it, why does it matter and what may be done? – Fit To Dive

How common is scuba diving PTSD?2

Experiencing some lingering distress, mental or emotional issues after a traumatic experience is relatively common. Mostly, the person heals and the problem resolves naturally. However, for a proportion of people this reaction may develop into psychological stress injury or post-traumatic stress (disorder, i.e. PTSD). Divers do occasionally face challenging incidents or circumstances, such as decompression illness, barotrauma, entrapment/entanglement, lost gas events and rapid ascents. So it is reasonable to anticipate that some divers would be affected by psychological trauma issues.

This is likely partly due to the fact that these reports relate to the incident, any rescue and acute medical treatment. Data from longer-term follow up is harder to access. With psychological conditions, the impact of a traumatic event is not always apparent immediately. Also, during an incident and subsequent medical treatment, distress may be a normal response to what has happened. Diagnosis of PTSD would be much later, and so this data is not available for those reports.3

There is one study that specifically examined the psychological impact of accidents on recreational scuba divers. The research was carried out at the hyperbaric chamber in Orkney, which covers diving-related injuries in one of the world’s best known wreck diving locations: Scapa Flow. The study followed up all divers attending the chamber for diving-related conditions across two years. (Issues included: DCI, barotrauma, non-fatal drowning, marine stings, missed deco stops due to buoyancy or lack of gas supply). It measured reported symptoms of psychological trauma in: (a)victims of scuba diving accidents, (b) their buddies, and (c) another member of group who was not (or at least less) involved in the incident. All were measured at 3 months, 6 months and 12 months after the diving medical contact.

A few optional notes on quality of evidence

Before looking at the results of a study, it’s important to check the quality of the design and methods. This one has some good points. First of all, it’s prospective, that means it took a sample of people and followed them to see if there was an issue. (This is different from studying a group of people who are already reporting symptoms, for example). It could be said that to be truly prospective, it would start prior to the incident occurring at all. However, the authors considered this and included assessments of general mental health and a control group. In addition, they considered the statistical power of the study in advance and made sure to get enough participants to be confident that any difference in symptoms was not due to chance. The study also used a reliable and validated measure, one which is also clinically useful.

The study found that quite a substantial portion of the divers reported symptoms of psychological trauma, 3 months, 6 months and (in some cases) 12 months after the event. The victims reported significantly more symptoms than their buddy or the control. Divers were reporting symptoms of trauma on all three domains: avoidance, re-experiencing and arousal. So, we have an estimate that 25 to 50 % of divers are experiencing scuba diving PTSD symptoms after accidents. It is important to be clear that this does not mean that many divers get diagnosable PTSD. Instead, it is the number of the divers who reported some symptoms psychological trauma.

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Waiting to Exhale: Diving’s Golden Rule Explained

by Alex Brylske

As a child of the ’50s, I was a big fan of the hallmark TV series Sea Hunt and its indomitable hero, Mike Nelson, played by the late actor Lloyd Bridges. One episode I particularly remember involved the kidnapping of a scientist. As this was the era of Sputnik, it was implied — though never overtly stated — that the culprits were a group of “stinking commies.” The scientist was being held in a cave on an island. Central to the story line was the fact — seemingly unknown to the bad guys — that the cave could be entered from underwater.

Of course, Mike Nelson knew all about the underwater entryway and planned a highly sophisticated escape: he swam into the cave, distracted the guards, gave the scientist a 30-second scuba lesson, dodged a few bullets on the way out and — fade to black — the world was once again a safe place for mom, apple pie and clean-cut capitalists.

For years, I thought the episode was pretty bogus. Even as a kid I knew that becoming a scuba diver required hours of arduous training. I never gave the show much thought until years later when, following in my hero’s footsteps, I, too, became a scuba instructor. Even back then, everyone wanted to be like Mike. I soon came to realize that my hero hadn’t let me down after all. In fact, his 30-second lesson was brilliant in its cut-to-the-chase elegance, and certainly could have been enough training given the dire circumstance and high motivation of the unlucky victim. I don’t remember the dialogue verbatim, but it went something like this: “You see this thing? [pointing to the regulator mouthpiece] You put it in your mouth and breathe. Whatever you do, keep breathing; don’t ever hold your breath, or your lungs will burst and you’ll die!”

End of lesson. Any questions?

It was one of the few instances where Hollywood actually got the facts straight. If you had but 30 seconds to teach someone to scuba dive, what would you tell them? The same thing Mike did — the Golden Rule of scuba diving. Breathe normally; never hold your breath. The rest, in most cases, is pretty much secondary.

Of course, if you’re learning to dive without the distraction of gunfire, and your instructor has a bit more time to explain the nuances and importance of breathing, you probably will be subjected to either an illustration or an actual example of the most commonly used prop in diver training — the ubiquitous balloon. And the explanation, though lacking the dramatic effect that Lloyd Bridges could bring to the lesson, will be something like: If a flexible, gas-filled container — like a lung — can’t vent excess pressure as it rises in the water column, its volume will expand until it bursts. Of course, today you might have sophisticated video or computer-based graphics, but the essence of what Mike told the scientist remains the same.

Unfortunately, the balloon-aided explanation is about all that most divers ever learn. Now, there’s nothing really wrong with the balloon analogy. It’s just a bit oversimplified, especially if you really want to fully understand the consequences of forgetting what Mike Nelson so succinctly told the scientist. For one thing, our lungs bear little resemblance to balloons. (A sponge is a much more accurate analogy.) And due to the intricate and delicate nature of their anatomy, severe problems occur from lung expansion long before, as Mike so aptly put it, “your lungs burst and you die.”

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