Recompression treatment in a hyperbaric chamber was initially used as a life-saving tool to treat decompression sickness in caisson workers and divers who stayed too long at depth and developed decompression sickness. Now, it is a highly specialized treatment modality that has been found to be effective in the treatment of many conditions where the administration of oxygen under pressure has been found to be beneficial. Studies have shown it to be quite effective in some 13 indications approved by the Undersea and Hyperbaric Medical Society.

Hyperbaric oxygen treatment is generally preferred when effective, as it is usually a more efficient and lower risk method of reducing symptoms of decompression illness, However, in some cases recompression to pressures where oxygen toxicity is unacceptable may be required to eliminate the bubbles in the tissues that cause the symptoms.

All divers should be free of conditions and illnesses that would negatively impact their safety and well-being underwater. The diving medical physician should be able to identify, treat and advise divers about illnesses and conditions that would cause them to be at increased risk for a diving accident.

Some reasons why a person should not be allowed to dive are as follows:

- Disorders that lead to altered consciousness: conditions that produce reduced awareness or sedation from medication, drugs, marijuana or alcohol; fainting, heart problems and seizure activity.

- Disorders that substantially increase the risk of barotrauma injury conditions or diseases that are associated with air trapping in closed spaces, such as sinuses, middle ear, lungs and gastrointestinal tract. Severe asthma is an example.

- Disorders that may lead to erratic and irresponsible behavior: included here would be immaturity, psychiatric disorders, diving while under the influence of medications, drugs and alcohol or any medical disorder that results in cognitive defects.

Conditions that may increase risk of diving disorders:

- Patent foramen ovale

- Diabetes mellitus — No serious problems should be expected during dives due to hypoglycaemia in divers with well-controlled diabetes. Long-term complications of diabetes should be considered and may be a contrindication.

- Asthma

Conditions considered temporary reasons to suspend diving activities:

- Pregnancy—It is unlikely that literature research can establish the effect of scuba diving on the unborn human fetus as there is insufficient data, and women tend to comply with the diving industry recommendation not to dive while pregnant.

The most straightforward way to avoid nitrogen narcosis is for a diver to limit the depth of dives. Since narcosis becomes more severe as depth increases, a diver keeping to shallower depths can avoid serious narcosis. Most recreational dive schools will only certify basic divers to depths of , and at these depths narcosis does not present a significant risk. Further training is normally required for certification up to on air, and this training should include a discussion of narcosis, its effects, and cure. Some diver training agencies offer specialized training to prepare recreational divers to go to depths of , often consisting of further theory and some practice in deep dives under close supervision. Scuba organizations that train for diving beyond recreational depths, may forbid diving with gases that cause too much narcosis at depth in the average diver, and strongly encourage the use of other breathing gas mixes containing helium in place of some or all of the nitrogen in air – such as trimix and heliox – because helium has no narcotic effect. The use of these gases forms part of technical diving and requires further training and certification.

While the individual diver cannot predict exactly at what depth the onset of narcosis will occur on a given day, the first symptoms of narcosis for any given diver are often more predictable and personal. For example, one diver may have trouble with eye focus (close accommodation for middle-aged divers), another may experience feelings of euphoria, and another feelings of claustrophobia. Some divers report that they have hearing changes, and that the sound their exhaled bubbles make becomes different. Specialist training may help divers to identify these personal onset signs, which may then be used as a signal to ascend to avoid the narcosis, although severe narcosis may interfere with the judgement necessary to take preventive action.

Deep dives should be made only after a gradual training to test the individual diver's sensitivity to increasing depths, with careful supervision and logging of reactions. Diving organizations such as Global Underwater Explorers (GUE) emphasize that such sessions are for the purpose of gaining experience in recognizing the onset symptoms of narcosis for an individual , which are somewhat more repeatable than for the average group of divers. Scientific evidence does not show that a diver can train to overcome any measure of narcosis at a given depth or become tolerant of it.

Equivalent narcotic depth (END) is a commonly used way of expressing the narcotic effect of different breathing gases. The National Oceanic and Atmospheric Administration (NOAA) Diving Manual now states that oxygen and nitrogen should be considered equally narcotic. Standard tables, based on relative lipid solubilities, list conversion factors for narcotic effect of other gases. For example, hydrogen at a given pressure has a narcotic effect equivalent to nitrogen at 0.55 times that pressure, so in principle it should be usable at more than twice the depth. Argon, however, has 2.33 times the narcotic effect of nitrogen, and is a poor choice as a breathing gas for diving (it is used as a drysuit inflation gas, owing to its low thermal conductivity). Some gases have other dangerous effects when breathed at pressure; for example, high-pressure oxygen can lead to oxygen toxicity. Although helium is the least intoxicating of the breathing gases, at greater depths it can cause high pressure nervous syndrome, a still mysterious but apparently unrelated phenomenon. Inert gas narcosis is only one factor influencing the choice of gas mixture; the risks of decompression sickness and oxygen toxicity, cost, and other factors are also important.

Because of similar and additive effects, divers should avoid sedating medications and drugs, such as marijuana and alcohol before any dive. A hangover, combined with the reduced physical capacity that goes with it, makes nitrogen narcosis more likely. Experts recommend total abstinence from alcohol for at least 12 hours before diving, and longer for other drugs. Abstinence time needed for marijuana is unknown, but owing to the much longer half-life of the active agent of this drug in the body, it is likely to be longer than for alcohol.

Narcosis is potentially one of the most dangerous conditions to affect the scuba diver below about . Except for occasional amnesia of events at depth, the effects of narcosis are entirely removed on ascent and therefore pose no problem in themselves, even for repeated, chronic or acute exposure. Nevertheless, the severity of narcosis is unpredictable and it can be fatal while diving, as the result of illogical behavior in a dangerous environment.

Tests have shown that all divers are affected by nitrogen narcosis, though some experience lesser effects than others. Even though it is possible that some divers can manage better than others because of learning to cope with the subjective impairment, the underlying behavioral effects remain. These effects are particularly dangerous because a diver may feel they are not experiencing narcosis, yet still be affected by it.

First aid is common for both DCS and AGE:

- Monitor the patient for responsiveness, airway, breathing and circulation, resuscitate if necessary.

- Treat for shock.

- Lay the patient on their back, or for drowsy, unconscious, or nauseated victims, on their side.

- Administer 100% oxygen as soon as possible.

- Seek immediate medical assistance, locate a hospital with hyperbaric facilities and plan for possible transport.

- Allow the patient to drink water or isotonic fluids only if responsive, stable, and not suffering from nausea or stomach pain. Administration of intravenous saline solution is preferable.

- Record details of recent dives and responses to first aid treatment and provide to the treating medical specialist. The diving details should include depth and time profiles, breathing gases used and surface intervals.

Genetic testing is being performed in a limited fashion to determine susceptibility to MH. In people with a family history of MH, analysis for "RYR1" mutations may be useful.

The main candidates for testing are those with a close relative who has suffered an episode of MH or have been shown to be susceptible. The standard procedure is the "caffeine-halothane contracture test", CHCT. A muscle biopsy is carried out at an approved research center, under local anesthesia. The fresh biopsy is bathed in solutions containing caffeine or halothane and observed for contraction; under good conditions, the sensitivity is 97% and the specificity 78%. Negative biopsies are "not" definitive, so any patient who is suspected of MH by their medical history or that of blood relatives is generally treated with non-triggering anesthetics, even if the biopsy was negative. Some researchers advocate the use of the "calcium-induced calcium release" test in addition to the CHCT to make the test more specific.

Less invasive diagnostic techniques have been proposed. Intramuscular injection of halothane 6 vol% has been shown to result in higher than normal increases in local among patients with known malignant hyperthermia susceptibility. The sensitivity was 100% and specificity was 75%. For patients at similar risk to those in this study, this leads to a positive predictive value of 80% and negative predictive value of 100%. This method may provide a suitable alternative to more invasive techniques.

A 2002 study examined another possible metabolic test. In this test, intramuscular injection of caffeine was followed by local measurement of the ; those with known MH susceptibility had a significantly higher (63 versus 44 mmHg). The authors propose larger studies to assess the test's suitability for determining MH risk.

Below is a summary comparison of the signs and symptoms of DCI arising from its two components: "Decompression Sickness" and "Arterial Gas Embolism". Many signs and symptoms are common to both maladies, and it may be difficult to diagnose the actual problem. The dive history can be useful to distinguish which is more probable, but it is possible for both components to manifest at the same time following some dive profiles.

A more detailed account of the signs and symptoms of Decompression Sickness can be found here.

There is no one single test for confirming that breathlessness is caused by pulmonary edema; indeed, in many cases, the cause of shortness of breath is probably multifactorial.

Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. Chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edema

Lung ultrasound, employed by a healthcare provider at the point of care, is also a useful tool to diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water, track changes over time, and differentiate between cardiogenic and non-cardiogenic edema.

Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous pressures and high pulmonary artery pressures.

Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT) are also typically requested. B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) suggest a cardiac cause is unlikely.

Given the constant threat of bioterrorist related events, there is an urgent need to develop pulmonary protective and reparative agents that can be used by first responders in a mass casualty setting. Use in such a setting would require administration via a convenient route for e.g. intramuscular via epipens. Other feasible routes of administration could be inhalation and perhaps to a lesser extent oral – swallowing can be difficult in many forms of injury especially if accompanied by secretions or if victim is nauseous. A number of in vitro and in vivo models lend themselves to preclinical evaluation of novel pulmonary therapies.

In those with underlying heart disease, effective control of congestive symptoms prevents pulmonary edema.

Dexamethasone is in widespread use for the prevention of high altitude pulmonary edema. Sildenafil is used as a preventive treatment for altitude-induced pulmonary edema and pulmonary hypertension, the mechanism of action is via phosphodiesterase inhibition which raises cGMP, resulting in pulmonary arterial vasodilation and inhibition of smooth muscle cell proliferation. While this effect has only recently been discovered, sildenafil is already becoming an accepted treatment for this condition, in particular in situations where the standard treatment of rapid descent has been delayed for some reason.

Specific pretreatments, drugs to prevent chemically induced lung injuries due to respiratory airway toxins, are not available. Analgesic medications, oxygen, humidification, and ventilator support currently constitute standard therapy. In fact, mechanical ventilation remains the therapeutic mainstay for acute inhalation injury. The cornerstone of treatment is to keep the PaO2 > 60 mmHg (8.0 kPa), without causing injury to the lungs with excessive O2 or volutrauma. Pressure control ventilation is more versatile than volume control, although breaths should be volume limited, to prevent stretch injury to the alveoli. Positive end-expiratory pressure (PEEP) is used in mechanically ventilated patients with ARDS to improve oxygenation. Hemorrhaging, signifying substantial damage to the lining of the airways and lungs, can occur with exposure to highly corrosive chemicals and may require additional medical interventions. Corticosteroids are sometimes administered, and bronchodilators to treat bronchospasms. Drugs that reduce the inflammatory response, promote healing of tissues, and prevent the onset of pulmonary edema or secondary inflammation may be used following severe injury to prevent chronic scarring and airway narrowing.

Although current treatments can be administered in a controlled hospital setting, many hospitals are ill-suited for a situation involving mass casualties among civilians. Inexpensive positive-pressure devices that can be used easily in a mass casualty situation, and drugs to prevent inflammation and pulmonary edema are needed. Several drugs that have been approved by the FDA for other indications hold promise for treating chemically induced pulmonary edema. These include β2-agonists, dopamine, insulin, allopurinol, and non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. Ibuprofen is particularly appealing because it has an established safety record and can be easily administered as an initial intervention. Inhaled and systemic forms of β2-agonists used in the treatment of asthma and other commonly used medications, such as insulin, dopamine, and allopurinol have also been effective in reducing pulmonary edema in animal models but require further study. A recent study documented in the "AANA Journal" discussed the use of volatile anesthetic agents, such as sevoflurane, to be used as a bronchodilator that lowered peak airway pressures and improved oxygenation. Other promising drugs in earlier stages of development act at various steps in the complex molecular pathways underlying pulmonary edema. Some of these potential drugs target the inflammatory response or the specific site(s) of injury. Others modulate the activity of ion channels that control fluid transport across lung membranes or target surfactant, a substance that lines the air sacs in the lungs and prevents them from collapsing. Mechanistic information based on toxicology, biochemistry, and physiology may be instrumental in determining new targets for therapy. Mechanistic studies may also aid in the development of new diagnostic approaches. Some chemicals generate metabolic byproducts that could be used for diagnosis, but detection of these byproducts may not be possible until many hours after initial exposure. Additional research must be directed at developing sensitive and specific tests to identify individuals quickly after they have been exposed to varying levels of chemicals toxic to the respiratory tract.

Currently there are no clinically approved agents that can reduce pulmonary and airway cell dropout and avert the transition to pulmonary and /or airway fibrosis.

1.escape when filling refillable vapourizers,

2.Leaks in the high pressure system between the nitrous oxide (N2O) cylinder,

3.Can escape from around the patient's anesthesia mask,

4.Can escape from around the patient's endotracheal tube

5.Can in an anesthetic medical procedure.

Inert gas asphyxiation is a form of asphyxiation which results from breathing a physiologically inert gas in the absence of oxygen, or a low amount of oxygen, rather than atmospheric air (which is largely composed of nitrogen and oxygen). Examples of physiologically inert gases, which have caused accidental or deliberate death by this mechanism, are: argon, helium, nitrogen and methane. The term "physiologically inert" is used to indicate a gas which has no toxic or anesthetic properties and does not act upon the heart or hemoglobin. Instead, the gas acts as a simple diluent to reduce oxygen concentration in inspired gas and blood to dangerously low levels, thereby eventually depriving all cells in the body of oxygen.

According to the U.S. Chemical Safety and Hazard Investigation Board, in humans, "breathing an oxygen deficient atmosphere can have serious and immediate effects, including unconsciousness after only one or two breaths. The exposed person has no warning and cannot sense that the oxygen level is too low." In the US, at least 80 people died due to accidental nitrogen asphyxiation between 1992 and 2002. Hazards with inert gases and the risks of asphyxiation are well established.

An occasional cause of accidental death in humans, inert gas asphyxia with gases including helium, nitrogen, methane, and argon, has been used as a suicide method. Inert gas asphyxia has been advocated by proponents of euthanasia, using a gas-retaining plastic hood device colloquially referred to as a suicide bag.

Nitrogen asphyxiation has been suggested by a number of lawmakers and other advocates as a more humane way to carry out capital punishment. In April 2015, the Oklahoma Governor Mary Fallin signed a bill authorizing nitrogen asphyxiation as an alternative execution method in cases where the state's preferred method of lethal injection was not available as an option.

On average the incidence of nausea or vomiting after general anesthesia ranges between 25 and 30% [Cohen 1994]. Nausea and vomiting can be extremely distressing for patients and is therefore one of their major concerns [Macario 1999]. Vomiting has been associated with major complications such as pulmonary aspiration of gastric content and might endanger surgical outcomes after certain procedures, for example after maxillofacial surgery with wired jaws. Nausea and vomiting can delay discharge and about 1% of patients scheduled for day surgery require unanticipated overnight admission because of uncontrolled postoperative nausea and vomiting.

Treatment of the underlying cause is required. Endotracheal intubation and mechanical ventilation are required in cases of severe respiratory failure (PaO2 less than 50 mmHg). Respiratory stimulants such as doxapram are rarely used, and if the respiratory failure resulted from an overdose of sedative drugs such as opioids or benzodiazepines, then the appropriate antidote (naloxone or flumazenil, respectively) will be given.

There is tentative evidence that in those with respiratory failure identified before arrival in hospital, continuous positive airway pressure can be useful when started before conveying to hospital.

It is likely that HPNS cannot be entirely prevented but there are effective methods to delay or change the development of the symptoms.

Utilizing slow rates of compression or adding stops to the compression have been found to prevent large initial decrements in performance.

Including other gases in the helium–oxygen mixture, such as nitrogen (creating trimix) or hydrogen (producing hydreliox) suppresses the neurological effects.

Alcohol, anesthetics and anticonvulsant drugs have had varying results in suppressing HPNS with animals. None are currently in use for humans.

Nitrous oxide, desflurane, and isoflurane are most the most commonly used anesthetic gases. They may cause some complications due to their leakage and storage failure.

Efforts to prevent poisoning include child-resistant packaging and a lower number of pills per package.

This inherited condition can be diagnosed with a blood test. If the total cholinesterase activity in the patient's blood is low, this may suggest an atypical form of the enzyme is present, putting the patient at risk of sensitivity to suxamethonium and related drugs. Inhibition studies may also be performed to give more information about potential risk. In some cases, genetic studies may be carried out to help identify the form of the enzyme that is present.

When humans breathe in an asphyxiant gas, such as pure nitrogen, helium, neon, argon, sulfur hexafluoride, methane, or any other physiologically inert gas(es), they exhale carbon dioxide without re-supplying oxygen. Physiologically inert gases (those that have no toxic effect, but merely dilute oxygen) are generally free of odor and taste. As such, the human subject detects little abnormal sensation as the oxygen level falls. This leads to asphyxiation (death from lack of oxygen) without the painful and traumatic feeling of suffocation (the hypercapnic alarm response, which in humans arises mostly from carbon dioxide levels rising), or the side effects of poisoning. In scuba diving rebreather accidents, there is often little sensation but euphoria—however, a slow decrease in oxygen breathing gas content has effects which are quite variable. By contrast, suddenly breathing pure inert gas causes oxygen levels in the blood to fall precipitously, and may lead to unconsciousness in only a few breaths, with no symptoms at all.

Some animal species are better equipped than humans to detect hypoxia, and these species are more uncomfortable in low-oxygen environments that result from inert gas exposure.

To counter the effects of high-altitude diseases, the body must return arterial p toward normal. Acclimatization, the means by which the body adapts to higher altitudes, only partially restores p to standard levels. Hyperventilation, the body’s most common response to high-altitude conditions, increases alveolar p by raising the depth and rate of breathing. However, while p does improve with hyperventilation, it does not return to normal. Studies of miners and astronomers working at 3000 meters and above show improved alveolar p with full acclimatization, yet the p level remains equal to or even below the threshold for continuous oxygen therapy for patients with chronic obstructive pulmonary disease (COPD). In addition, there are complications involved with acclimatization. Polycythemia, in which the body increases the number of red blood cells in circulation, thickens the blood, raising the danger that the heart can’t pump it.

In high-altitude conditions, only oxygen enrichment can counteract the effects of hypoxia. By increasing the concentration of oxygen in the air, the effects of lower barometric pressure are countered and the level of arterial p is restored toward normal capacity. A small amount of supplemental oxygen reduces the equivalent altitude in climate-controlled rooms. At 4000 m, raising the oxygen concentration level by 5 percent via an oxygen concentrator and an existing ventilation system provides an altitude equivalent of 3000 m, which is much more tolerable for the increasing number of low-landers who work in high altitude. In a study of astronomers working in Chile at 5050 m, oxygen concentrators increased the level of oxygen concentration by almost 30 percent (that is, from 21 percent to 27 percent). This resulted in increased worker productivity, less fatigue, and improved sleep.

Oxygen concentrators are uniquely suited for this purpose. They require little maintenance and electricity, provide a constant source of oxygen, and eliminate the expensive, and often dangerous, task of transporting oxygen cylinders to remote areas. Offices and housing already have climate-controlled rooms, in which temperature and humidity are kept at a constant level. Oxygen can be added to this system easily and relatively cheaply.

A prescription renewal for home oxygen following hospitalization requires an assessment of the patient for ongoing hypoxemia.

Intravenous fluids containing dextrose such as D5W are recommended to keep a urinary output between 2 and 3 ml/kg/h.

Sodium bicarbonate is given in a significant aspirin overdose (salicylate level greater than 35 mg/dl 6 hours after ingestion) regardless of the serum pH, as it enhances elimination of aspirin in the urine. It is given until a urine pH between 7.5 and 8.0 is achieved.

Fasting guidelines often restrict the intake of any oral fluid after two to six hours preoperatively. However, it has been demonstrated in a large retrospective analysis in Torbay Hospital that unrestricted clear oral fluids right up until transfer to theatre could significantly reduce the incidence of postoperative nausea and vomiting without an increased risk in the adverse outcomes for which such conservative guidance exists.

Prognosis for recovery following administration of succinylcholine is excellent when medical support includes close monitoring and respiratory support measures.

In nonmedical settings in which subjects with pseudocholinesterase deficiency are exposed to cocaine, sudden cardiac death can occur.