Diving Physiology

The human body under water

Humans are known to be 80% water – so why is it so difficult for our bodies to be exposed to the pressure underwater and this heavy material around us?
We will explain in this chapter how the few air-filled cavities in our bodies can cause problems and how nitrogen moves through the body. And ask a few questions: Is a PFO really a big risk? Do divers:inside get DCS because they are dehydrated?
This is not a complete, comprehensive explanation of diving physiology, but illustrations and supplements to the SSI Science of Diving course or other training materials.

The lungs

Structure of the lungs

If you imagine such a lung, then just imagine such a sponge….

The somewhat flippant description is not that far off from what a lung is: a wobbly network of air sacs, alveoli, that carry oxygen into the blood. And in the process also take with it everything else that is inhaled. Fortunately, larger impurities such as fine dust are filtered out on the way in and transported back out with the lung mucus, but gases can reach the alveoli unhindered and from there enter the blood.
The inhaled air passes through the trachea into the bronchi, the larger airways, and from there into the increasingly branched bronchioles. These end in the alveoli, the air sacs surrounded by a fine membrane, where gas exchange with the blood takes place. This gas exchange is of particular interest to us in diving, so we devote an entire section to it.

The lungs are protected by the ribs in the chest cavity. It is not a muscle itself, but a soft tissue encased in the lung pleura that holds it together. The pleura adheres to the pleura, held in place by a film of fluid in the interstitial space, the pleural space.

When we inhale, we move the rib cage or diaphragm. The lung sticks to the pleura and thus has to grow larger – a negative pressure is created, which is filled with air from the outside. When we inhale, our respiratory muscles are tense; when we exhale, we let them slacken – the air escapes virtually by itself.



The lung. Image: Wikipedia

Lung Barotrauma

As we have seen, the lung is not a muscle in its own right, but a tissue permeated by alveoli and capillaries, which is kept in shape by the slight negative pressure in the pleural space.

Injuries to this tissue result in various forms of pulmonary barotrauma. Baro means nothing more than pressure, trauma is an injury, so translates to nothing more than pressure related lung injuries, or lung over-extension injuries.

Pulmonary barotrauma occurs when alveoli (or, rarely, other vessels) burst and gas escapes from the lungs. Depending on where this is located, it causes different injuries.

If air gets into the pleural space, pneumothorax may result. If air leaks from the alveoli, they may develop into subcutaneous or mediastinal emphysema. And in the worst case, if air gets into the capillaries and thus into the blood, arterial gas embolism can result.


When gas from the lungs enters the pleural space, the negative pressure that holds the lungs to the pleura can no longer be maintained. The affected lung collapses, and gas exchange is severely impaired.

The injury is not specific to diving but is well known to all paramedics: it often occurs after accidents when an injury causes air to enter the pleural space from the outside. Pneumothorax is dangerous but curable if detected in time.

Pneumothorax - Image: SSI

Subcutaneous emphysema

Subcutaneous emphysema is an accumulation of gas (emphysema) under the skin – sub means under, cutis is the skin.

From the outside, swellings of the skin are visible, which crackle slightly when palpated. Such gas accumulations can occur as a result of lung injuries; they occur mainly in the shoulder and neck area.
The emphysema itself is usually well treatable, but the underlying lung injury should of course be taken particularly seriously in divers:in.

Subcutaneous emphysema - Image: SSI

Mediastinal emphysema

In mediastinal emphysema, gas enters the mediastinum, which is the area in the chest.
This is dangerous mainly because a larger gas bubble can press on the heart. However, mediastinal emphysema is treatable if detected in time.

Mediastinal emphysema - Image: SSI

Arterial gas embolism

In the very worst case, gas (air) can escape from the arterial circulation. When that happens, the bubbles can block blood flow to the brain, causing symptoms similar to a stroke.

This is the most severe case of pulmonary hyperextension injury. AGE is easily confused with a severe form of DCS: In both, vesicles in the arterial circulation trigger the symptoms. An AGE is air coming out of the lungs, while a DCS is nitrogen that is not removed by the lung filter during the decompression phase. Usually, DCS occurs a little later than an AGE.
As divers, we do not need to be able to distinguish the symptoms – first aid is always the same: Call emergency services, oxygen, CPR if necessary.

Arterial gas embolism - image; SSI

How does the lung break down?

When diving courses are about the lungs, a balloon is always shown. The then changes its volume depending on the depth, and when it rises inflated, it bursts. This is how one likes to imagine the lungs then.

However, as we have already seen, the lung is not a balloon, but rather a sponge with air bubbles. What can burst are these air bubbles, the alveoli. And when many of them burst, the lungs are also ruptured.

How can this happen? Whenever the air cannot escape from the alveoli.

For example, because the alveoli (air sacs in the lungs) stick together. This can happen if the coating, the surfactant, is damaged, or because the bronchioles are slimy.


Air Trapping

When air cannot escape from the alveoli, this is called air trapping. Such a condition is known from people with severe lung diseases, for example, smoker-typical chronic obstructive pulmonary disease (COPD). On land, this results in less oxygen being absorbed. Underwater, however, it can cause very serious damage as it rises.

When the alveoli or bronchioles become stuck and the air can’t get out, but you still rise, the air expands. And this is exactly what leads to the bursting of pulmonary alveoli – a pulmonary barotrauma.

Fast ascents

Even with healthy lungs, overpressure injuries can occur, namely if the air cannot escape from the alvels quickly enough.
Alveoli cannot remove unlimited amounts of expanding air. Thus, overpressure can develop in them during ascent even when you exhale. And the only thing that helps against this is a slow ascent, even and especially from shallow depths.

Surfactant | Image: physiologie.cc
Air trapping in COPD - Image: Huether and McCance, 2008

Does the lung burst when you hold your breath?

Among the first rules of diving you learn never to hold your breath. Mancmal it is somewhat specified: At least not in the ascent.

In principle, this is certainly a good idea; if you exhale consciously, you ensure a good gas exchange.

However, it is unclear whether it is even possible to create a dangerous overpressure in the lungs at will by closing the airways. If you just “hold your breath,” your airways are not hermetically sealed, and air always seeks the easiest way out. Even though it is fundamentally important to keep the airways open during ascent: Probably the ascent speed is more important.

It is also possible that glottis spasm plays a role in lung hyperextension injuries. It can be triggered by panic, or by water droplets hitting the vocal cords – for example, by a regulator that is not quite tight. In such a spasm, the airways close completely. The person can’t breathe, panics, and rises – and really serious lung injuries can occur.
Because the spasm resolves as soon as the person becomes unconscious, it is unclear whether this is actually the cause of relatively unexplained lung hyperextension injuries. Precisely because such a climb from greater depths can end tragically, such accidents are difficult to comprehend. However, since it is definitely a realistic possibility, gt maintained controllers and anything that helps prevent panic are certainly always a good idea.


Vocal cords

How much does a person breathe?

How much air do we actually move? To give you an idea: although an average man has a lung capacity of about 6l, he moves only about 0.5l with a normal breath. With effort, of course, it becomes more.

The lung volume is divided into a residual volume of about 25% of the total volume and the vital capacity from the remaining 75%. The residual volume is the volume that remains when one has completely exhaled as deeply as only possible.
Normally, our breathing takes place in the lower to middle range of the lung volume: We breathe in a relaxed manner when we do not have to exert ourselves either when breathing in or when breathing out. Of course, we can also control the area of the lungs in which we breathe to a certain extent and influence our buoyancy in the short term – the most important contribution to relaxation is that the lungs are as empty as possible.


Lung volume - graphic: Wikipedia

Gas exchange

With every breath, new air flows into our lungs and enters the millions of alveoli. Here, in the alveoli, oxygen and inert gases enter the bloodstream.

The oxygen binds to the hemoglobin until it is saturated. It then diffuses into the blood.

Nitrogen, on the other hand, is an inert gas – gases that do not form chemical bonds. When the pressure is elevated, it enters the bloodstream; when the pressure in the lungs is lower, it is exhaled through the lungs.

What happens to the nitrogen in the process follows two basic physical rules:

“Henry’s law”: concentration of a gas dissolved in a liquid is proportional to the partial pressure of the gas above the liquid

“Principle of Le Chatelier“: It is in nature to avoid constraints. With partial pressure – increase à increased dissolution of gas

Gas exchange - Image: SSI

DCS: Deco diseases

Ask an OWD student about DCS, and you’ll get in response “DCS…don’t know exactly, something about bubbles maybe.”.

Ask an experienced diver about DCS, and the answer consists of a long explanation that surfacing too quickly or disregarding stops causes bubbles in body tissues, and that triggers DCS.

Ask an instructor about DCS, and you’ll get a half-hour lecture on different profiles, decompression models, surface breaks, and strategies to reduce bubble load and avoid DCS.

Ask an experienced diving physician about DCS, and you’ll get an hour-long lecture on arterialization of bubbles, the different forms of DCS, echocardiograms, and how to get the bubbles gone with HBO.

Ask a scientist who has studied DCS all his life, and the answer will be “DCS…don’t know exactly, something about bubbles maybe.”


All deco theory strives for one thing: to minimize the risk of healthy problems after diving. How Deko’s disease occurs, what symptoms it causes, and how to treat it is fairly well known – commensurate with its rare occurrence. What is much less clear, however, is what exactly causes them.

It is reasonably certain that nitrogen bubbles in the body have a lot to do with it. However, exactly when the blisters lead to symptoms and when they don’t is not conclusively understood: two people can have an identical blister load, one gets sick, and the other feels nothing at all. So the bubbles don’t seem to be doing it alone.

Which tissues are affected also seems to play a role. Certain symptoms seem to correlate with supersaturations in certain tissues.

However, it is not known exactly. Every dive carries a certain risk of suffering from decompression sickness afterwards. We can minimize this risk to the best of our knowledge, but can never completely exclude it. Therefore, it is important to recognize the symptoms and react appropriately in case of doubt.


What divers have: “A little DCS”.

Especially after several days of diving, it is not uncommon to notice mild symptoms of DCS. On liveaboards with unlimited dives, sometimes it’s the moments when you don’t feel so comfortable after all that slow you down.

Typical of milder forms of deco disease is a slight tingling sensation on the skin, formerly known as “diving fleas.” Sometimes there is slight redness, leicten pain in the joints, and you just feel tired – more than you would expect from the effort.

Often such rather mild symptoms are not noticed or denied and can then develop into more severe symptoms Therefore, one should also observe mild complaints well.

Such symptoms were previously referred to as “DCS I,” but are now taken more seriously as possible precursors to more severe symptoms.

Marble skin – Cutis marmorata

Blue spots after diving are known as a typical diver’s disease, especially in the older age groups. They can be observed especially when many dives have been made in a row and the middle tissues have reached their saturation limits.
To be seen are bruises on the skin, often on the abdomen or thighs, painful and sometimes slightly bulging. Often they change their shape and size over time.

For a very long time they were not taken too seriously. In the meantime, however, it must be assumed that they are often accompanied by other symptoms that should not be overlooked.

DCS: Severe symptoms

Nitrogen can sometimes cause very severe failure symptoms in our bodies – but in order to assess this appropriately, such cases are extremely rare. Among the few fatalities in diving, DCS plays a minor role, and cases with severe, persistent damage are so rare that (almost) everyone is personally known.

Nevertheless, it is a serious risk. If paralysis, speech problems, weakness, dizziness and other clear signs appear immediately after the dive, it may be a serious decompression accident. Something like this is extremely rare and can be mistaken for a lung injury. Since the distinction is irrelevant at the outset of treatment, it is sufficient for first responders:in to recognize that the problem is life-threatening.

Other severe symptoms may include moderate to severe pain, incoordination, impaired vision and speech, dizziness and loss of consciousness. In addition, there is a wide range of possible symptoms: Since nitrogen bubbles can cause problems in a wide variety of places in the body, there is no single set of symptoms. So if you have complaints after diving, you should consider whether there might be a connection.

First aid - Image: Mares

PFO: Persistent Foramen Ovale

A patent foramen ovale, a small hole between the two atria of the heart, occurs in quite a few people – it is estimated in about 10-33%.

It is something quite normal: every human being has this connection when growing up in the womb. This small hole allows blood exchange between oxygenated and deoxygenated blood while the fetus is not yet breathing on its own. After birth it closes by itself, but in some people not completely.

A small opening may be left, usually 1-19mm in size. In normal life, it’s usually not even noticeable – but when diving, it could be a problem.



Why might a PFO be relevant to us?


A PFO allows blood to leak from one side of the heart to the other. What is rarely a problem in normal life – maybe it has something to do with migraines, maybe it plays a part in strokes, but doesn’t actually affect us directly – can definitely gain importance in diving.

Nitrogen bubbles can form even during quiet dives within no-stop limits. These normally first pass through the atrium into the lungs and are filtered out there. However, through a PFO, they can pass directly into the arterial circulation. Especially when additional pressure is applied to the chest, e.g., during forced pressure equalization, the pathway through the PFO may be more inviting than the pathway to the lungs.

Vesicles in the arterial circulation are irritating because they can cause neurological symptoms. Studies of those affected by DCS suggest that a PFO leads to a significantly increased risk of severe DCS.



But: The details are important

Although it must be assumed that the risk of DCS increases with a PFO, the data on this should be taken with caution. Why? Particularly in the case of risks that are small in absolute terms, a reference to a relatively increased risk does not always make sense.

The one thing (DCS) is very rare (about 1 per 10 000 TGs). The other thing (PFO) is very common (about 1 per 4 divers). And the postulated connection between the two extremely sexy. So you just want to believe that there is a connection well, because it is so clear and logical on the hand. Such a situation may cause other possible causes to be overlooked.

Bubbles can only enter the arteries through a PFO if they exist at all. This means that after dives with few bubbles, or when the person tends to train less, the problem does not arise in the first place.

In addition, the PFO is not the only place where bubbles can cross over. Other coronary shunts exist, and besides them not quite rare pulmonary shunts. Even with arterialized bubbles, the inference to a PFO does not work.

In no way is a PFO to blame for everything

When someone suffers a DCS, the PFO is always high on the list of suspected causes. That is human, one would like to have nevertheless so gladly a reason, a “guilty one” to make out. Unfortunately, in this case it is not so simple.

DCS – Cases with a well-motivated suspicion of being related to a PFO appear to have neurological symptoms, inner ear problems, and skin bends in particular.

However, a large number of all diving accidents happen without us being able to identify a direct cause – the so-called “undeserved hits”. The statistical probability that someone will be hit every now and then can only extremely rarely be assigned to a clear cause (except, of course, diving itself).

So, under no circumstances should any diver who wants to dive more challenging or has had an accident be persuaded to get tested after all. Testing for a PFO and possibly considering surgery itself carries such extensive risks that it is important to carefully consider whether one really wants to accept the risk compared to a DCS risk, which is still quite low.

PFO - Image: MAYO Foundation
Info PFO from DAN