Hyperbaric medicine or hyperbaric oxygen therapy (HBOT) involves using high concentrations of oxygen (100%) at pressures greater than the surrounding ambient atmospheric pressure. This necessitates using a pressurized chamber where a single patient (monoplace) or several patients (multi-place) can be placed to facilitate treatment. Undersea medicine refers to the field of medicine concerned with humans in an undersea environment, such as divers, submariners, or caisson workers.
The first documented usage of hyperbaric medical therapy was in 1662. A British physician created the "domicillium" which consisted of a pressurized airtight chamber in which pressure could be increased using a bellows. Numerous afflictions were treated with unknown results. It is interesting to note that this was done before Boyle confirmed the relationship between volume and pressure of gases in the 1670s, the actual discovery of oxygen in 1774 by Joseph Priestly, or the development of Dalton’s and Henry’s laws of gases in the early 1800s. In 1872 Paul Bert researched and wrote about the physiological effects of pressurized air on the human body; the effects of Central Nervous System Oxygen Toxicity is also referred to as the “Paul Bert Effect”. This was followed by research by J Lorrain Smith into Pulmonary Oxygen Toxicity, also known as the “Lorrain Smith Effect.” In 1877 Fontaine built the first mobile hyperbaric operating theatre. In 1891 Dr J.L. Corning built the first North American hyperbaric chamber in New York, completing extensive hyperbaric research looking at its treatment feasibility with many conditions such as syphilis, arthritis, diabetes, and other afflictions. In 1928 he built a "hyperbaric hotel" in Cleveland Ohio that could accommodate more than 70 guests.
In 1908 Dr John Scott Haldane created the first decompression model based on inert gas uptake and saturation of tissues. World War II prompted the need for acceptable treatment modalities for treating Navy divers who suffered decompression sickness or the “Bends”. Detailed Navy dive charts and hyperbaric treatment tables were formulated for various diving and decompression scenarios. Interestingly the use of pressurized oxygen in the treatment of Decompression Sickness was not introduced until the 1930s by Behnke and Shaw. Research into the use of HBOT increased in the 1950s. One of the most famous studies “Life Without Blood” was published in 1959 by Dr. Ite Boerema who showed that he could keep swine alive using HBOT despite hemoglobin levels that would not normally be compatible with life. After draining all of their red blood cells, a plasma or plasma-like solution was used as volume replacement, which was hyperoxygenated with hyperbaric oxygen therapy. At the end of the treatment, they were reinfused with blood and recovery was uneventful. The use of HBOT has continued to be researched to the present day. [1][2][3][4][5]
The physics of light applies primarily to the undersea environment. Attenuation may occur due to absorption as light energy is converted to thermal energy; the red spectrum is absorbed first with blues absorbed last. This is why underwater pictures often appear blue! Diffusion may also occur as light is scattered secondary to interaction with substances in the water. Refraction of light occurs when the path of the light wave is altered due to a change in media. This occurs underwater when a diver is wearing a mask due to the interface between the surrounding water and the airspace within the mask. This results in objects being perceived as larger and closer than they truly are.
In the air, the localization of sound relies on the time delay between the sound wave being received between an individual’s ears. The velocity of sound is approximately 4 times faster in water as compared to air; as the time delay between ears is significantly reduced or lost, it is very difficult to localize sound underwater. The transmission of sound is also reduced due to the spreading and attenuation of the sound wave underwater.
Archimedes’ principle refers to the fact that any object partially or fully immersed in a liquid is buoyed up by a force that is equal to the weight of the fluid displaced by said object. An object that weighs less than the weight of the fluid it displaces while immersed would be positively buoyant or “float”. An object is neutrally buoyant (neither sinking nor floating) when its weight is equal to the weight of the fluid it displaces. An object will be negatively buoyant or “sink” if it weighs more than the weight of the fluid it displaces.
For example, a trained diver will balance the buoyancy of their body and wetsuit with a set amount of weights in order to achieve neutral buoyancy underwater. However, if they take a deep inspiration underwater (expanding their chest cavity), they will now displace more water and become positively buoyant. When they exhale and displace less water, they will return to neutral buoyancy or become negatively buoyant.
As the buoyant force refers to the mass of the fluid displaced, density (mass/volume) impacts buoyancy. As such, saltwater, which is denser than freshwater, results in increased buoyancy compared to freshwater
Wet suits, typically neoprene, provide thermal protection to a diver by insulating a layer of water that has been warmed by the body. Drysuits are aptly named as they allow a diver’s body to remain dry; they are composed of waterproof material with seals at the hands, feet, and neck.
Hypothermia may be a concern for divers as water has high thermal conductivity. This is of particular concern on deep dives, or dives in cold water. Divers may use thicker wet suits, drysuits, or hot water suits depending on the dive depth/duration, and temperature of the water.
In addition, heat loss occurs due to breathing dry and cold compressed air. As the body must warm and humidify this air in the respiratory tract, there is both evaporative heat loss (humidifying) and convective heat loss (warming). In addition to protective clothing, divers may require warmed breathing gas if hypothermia is a concern. [6][7]
Pressure (P=F/A) is the force exerted on a surface per unit area.
On land, every creature is exposed to atmospheric pressure as a result of the weight of the atmosphere producing a force on the earth’s surface. As gas is compressible, pressure changes with altitude are curvilinear; with increased pressure closer to the earth’s surface, and decreased pressure experienced as you increase altitude. At approximately 18,000 feet, one would experience half the atmospheric pressure compared to standing at sea level.
Helpful conversions: surface atmospheric pressure 1 atmosphere (atm) = 760 mm Hg = 1.013 bar = 760 torr = 14.7 psi.
Immersion in water results in additional pressure due to the weight of the water exerting a force on the diver. As water is practically incompressible, there is an increase of 1 atm of pressure for every 33 feet of seawater (fsw)/10 meters seawater (msw), or 34 feet of freshwater (ffw)/10.3 meters freshwater (mfw) [remember salt water is denser than fresh water]. It is important to note that while the increase in pressure is a linear relationship (additional 1 atm of pressure for every 10msw), the relative pressure change is curved. For example: moving from surface to 10msw, the total pressure is increased from 1 ata to 2 ata, a relative 200% increase. Moving from 10msw to 20msw, the total pressure increases from 2 ata to 3 ata a relative increase of 150%. Moving from 20msw to 30msw the total pressure increases from 3 ata to 4 ata, a relative increase of 133%. Because of this, there are greater relative pressure changes underwater near the surface, which has implications for barotrauma and buoyancy.
Gauge pressure refers to the pressure relative to atmospheric; thus most pressure gauges used by divers will read 0 at surface level.
Due to the hydrostatic pressure, immersion results in a central redistribution of blood, which may be increased in the case of cold water due to peripheral vasoconstriction. Subsequently, anti-diuretic hormone (ADH) release results in diuresis. As such, divers may be relatively hypovolemic on surfacing after a dive. This fluid deficit may be exacerbated due to breathing the dry compressed gas as the body humidifies the breathing gas in the respiratory tract.
When a diver is underwater, they are exposed to the weight of the water column above them as well as the weight of the atmosphere. Absolute pressure refers to the total pressure experienced due to both the atmospheric pressure as well as the hydrostatic pressure. Depending on the country of origin, it is often written as atmospheres (absolute) or ata, or bar (absolute) or bar(a). For example, a diver at 20msw would experience 2 atm of hydrostatic pressure and 1atm of atmospheric pressure, for an absolute pressure of 3 ata. [6][8][7][9]
As gases are compressible, they are subject to 3 inter-related factors: volume, pressure, and temperature. It is important to note that absolute pressure and temperature must be used in calculations employing the following gas laws.
Charles’ law (V/T = V/T) refers to the fact that the volume of a gas will vary directly with the absolute temperature if pressure is kept constant. If the absolute temperature is increased, the volume of the gas will increase.
Gay-Lussac’s law (P/T = P/T) refers to the fact that the absolute pressure of a gas varies directly with the absolute temperature if the volume is kept constant. An increase in absolute temperature will result in an increase in absolute pressure.
Boyle’s law (PV=PV) is an extremely important law to understand in hyperbaric and undersea medicine as it is foundational in the pathophysiology of barotrauma, increased work of breathing at depth, and the use of HBOT. If the temperature remains constant, the volume of a gas is inversely proportional to the absolute pressure. If the ambient pressure is increased (i.e. descent in water, recompression in a hyperbaric chamber), then the volume of gas in a gas-filled body space will decrease. If ambient pressure is decreased, then the volume of gas will expand. This may result in barotrauma as described below.
Work of breathing in a hyperbaric chamber or underwater is also of concern. As the volume of gas decreases with increased ambient pressure, its density (mass/volume) increases. Combined with the central redistribution of blood due to immersion, as well as the breathing equipment itself (demand valve, flow resistance, dead space), the work of breathing will be increased as compared to breathing the same gas at surface level.
Dalton’s Law (P = P + P + … P) tells us that the total pressure exerted by a mixture of gases is equal to the sum of the pressures that would be exerted by each gas if it alone occupied the total volume. Thus, the partial pressure of a gas (P = P x %) is the portion of the total pressure of a gas mixture contributed by a single gas. For example, if a diver is breathing a mix of 40% oxygen at 2 ata, the partial pressure of oxygen would be 0.8 ata.
Henry’s Law refers to the fact that the amount of gas that will dissolve in a liquid is directly proportional to the partial pressure of that gas above the liquid. An increase in ambient pressure (and thus partial pressure) results in more gas dissolving into the liquid portion of blood and tissues.
Boyle’s, Dalton’s and Henry’s law have significant implications in the development of decompression sickness, gas toxicities, as well as the use of HBOT. [6][8][7]
Barotrauma refers to trauma that results due to pressure changes. Any non-vented gas-containing space in the body is susceptible to barotrauma, such as the thorax, middle ear, sinus, intestines. It may also be an issue due to gas-filled spaces in dive equipment such as a dry suit or a mask. As relative pressure/volume changes underwater occur closer to the surface, barotrauma is more likely to occur as divers transit through these shallow waters.
Barotrauma of descent/compression (or colloquially a “squeeze”) results from the decrease in gas volume essentially creating a vacuum. Middle ear barotrauma is most commonly encountered in undersea and hyperbaric medicine due to a vacuum created in the middle ear space; if additional air from the nasopharynx is not introduced through the eustachian tube, the vacuum may result in a sensation of pressure or pain, fluid extravasation/hemorrhage, tympanic membrane perforation, or transmitted damage to the inner ear.
Barotrauma on ascent results from gas expansion due to decreasing ambient pressure. This is particularly concerning if compressed air within a gas-filled space cannot escape. For example, if compressed air in the lungs is prevented from escaping (gas trapping, bronchospasm, breath-holding etc.), as the gas continues to expand, focal shearing between vessels and airways and/or rupture of small airways/alveoli may occur. This may result in pneumothorax, mediastinal emphysema, subcutaneous emphysema, pneumopericardium, or arterial gas embolism. [10][6][8]
Due to the increase in ambient pressure at depth, there is an increase in the amount of gas that dissolves into the liquid portion of the blood and tissues (on-gassing) when divers breathe compressed gas underwater. Inert gases, particularly nitrogen, are often a component of these gas mixtures and the body does not metabolize these gases. As such, they must be removed as they come out of solution (off-gassing).
When a diver ascents (decrease ambient pressure) this inert gas will come out of solution. If the ascent is slow enough, the inert gas diffuses from the tissue into the blood and is filtered out by the lungs. However, if the ambient pressure is decreased too rapidly, bubbles may form within tissues or the vasculature, resulting in what is termed Decompression Sickness (DCS). Once bubbles form, they cause mechanical damage to tissues and endothelium, obstruction of blood flow. These bubbles interact with formed elements within the blood resulting in inflammatory and pro-coagulant reactions.
The full pathophysiology of DCS remains unclear and is beyond the scope of this article. What is known is that the on-gassing/off-gassing of tissues is impacted by the pressure gradient between the lungs/blood or blood/tissues, the duration of the dive, the gas mixtures, and the perfusion of the tissues. Some tissues that are very well perfused (lung, blood, brain, heart) may on-gas more readily, but may also off-gas more quickly if perfusion remains constant. Compared to tissues of lower perfusion such as ligaments, tendons, joint capsules who may on-gas more slowly, but may also off-gas more slowly.
Dive tables or computers employ mathematical models to predict inert gas on-gassing and off-gassing in order to guide divers on depth and time limits and whether they may need decompression stops (stop underwater to allow additional time to off-gas prior to further decreasing the ambient pressure). It is important to note that these algorithms are based on population data and theoretical inert gas uptake/excretion curves. There are many underlying factors that may impact an individual diver’s susceptibility to DCS, and a diver may develop DCS even if they have followed a dive table or computer [11][8][6][7][12]
Once again, a thorough understanding of physics, and in particular Dalton’s and Henry’s laws, are vital to the underlying pathophysiology of gas toxicities, as well as the choice of a gas mixture for diving or HBOT treatment. A partial pressure of a gas that may be safe on surface may become hazardous at increased ambient pressures. A full description of gas issues is outside the scope of this article, but three specific issues are outlined below to demonstrate the impact of understanding physics as it relates to the hyperbaric environment. The physics and function of HBOT are reviewed in a later section.
Oxygen toxicity results from breathing oxygen at higher partial pressure. Central Nervous System (CNS) oxygen toxicity is the main concern for divers and HBOT; pulmonary oxygen toxicity may become an issue with extended dive operations or HBOT. Oxygen toxicity is dose-dependent based on the partial pressure of oxygen and duration of exposure.
Symptoms of CNS oxygen toxicity can include vision changes, tinnitus/auditory hallucinations, nausea, twitching/tremors, irritability or mood changes, dizziness, and convulsions. The risk of CNS oxygen toxicity is increased at a partial pressure of oxygen greater than 1.6 ata underwater, although a higher partial pressure is tolerated in resting and dry conditions like HBOT. There is significant inter- and intrapersonal variability in the presentation of CNS oxygen toxicity.
Pulmonary oxygen toxicity typically results from longer, lower pressure exposures and includes a recognizable pattern of an insidious onset of mild substernal irritation or chest tightness progressing to cough, then constant burning exacerbated by inspiration, to shortness of breath (on exertion and then at rest).
Inert gas narcosis is a reversible depression of neuronal excitability due to breathing inert gas at higher partial pressure. Clinical presentation can include decreasing cognitive and manual performance, euphoria, overconfidence, memory loss, perceptual narrowing, and impaired sensory functioning. Nitrogen narcosis is most commonly seen in recreational diving; onset varies but can be seen around 30msw or deeper.
Defective compressors used to fill diving tanks or compressors in poorly ventilated areas may cause exhaust fumes or oil vapors to contaminate the breathing gas. For example, a trace amount of Carbon Monoxide for which an individual would be asymptomatic at surface level, may become a lethal dose at deeper depths due to its increased partial pressure. CO disrupts oxygen delivery through its competitive binding of hemoglobin, inhibits mitochondrial respiration, and incites inflammatory effects. Clinical presentation may range from nausea and headache, to potentially fatal arrhythmias, loss of consciousness, or death. [8][6][7]
Hyperbaric Oxygen Therapy subjects a patient to 100% oxygen at increased pressures; typically between 2-3 ata, although some conditions may require higher pressures. The mechanism of action of hyperbaric therapy has been extensively studied, and includes the gas laws described above.
It is essential to understand the 14 conditions that are approved for hyperbaric medical therapy because many conditions rely on different aspects of hyperbaric medicine to be effective. The currently approved conditions include:
The complete explanation of the functions of hyperbaric medicine is complex. The Primary effect of HBOT is due to the increased ambient pressure itself.
While numerous types of diving and HBOT occur daily around the world, it is not without pitfalls.
Middle ear barotrauma (MEBT) remains the most common complication of diving and clinical hyperbaric oxygen treatment (HBO) and is directly related to the change in volume of a gas due to changing ambient pressure (Boyle’s law). In order to reverse the vacuum created by the increased ambient pressure, the addition of air from the nasopharynx into the middle ear space is required, known as equalization. If unsuccessful, decreasing the ambient pressure may also be used and equalization re-attempted. Divers may decrease their depth in the water by swimming toward the surface or hyperbaric chamber operators may decrease the depth of treatment by increasing the chamber exhaust until such time as the patient can clear their middle ear space.
The only absolute contraindication for hyperbaric treatment is an untreated pneumothorax. As patients are breathing compressed air while at depth, the gas within the pneumothorax will expand as the pressure is decreased at the end of the treatment (once again, Boyle’s law!) An untreated pneumothorax may convert to a tension pneumothorax due to this expansion of gas within the thorax.
As described above, oxygen toxicity occurs due to the increased partial pressure of oxygen. As such, treatment relies on decreasing the partial pressure of oxygen. In a recompression chamber, this can be achieved by removing the oxygen source and breathing air, or decreasing the depth of the treatment. Underwater, a diver may decrease their depth, or add a diluent gas into their breathing mix. With respect to pulmonary oxygen toxicity in HBOT, patients take several air breaks during a treatment to decrease the risk.
Caution must be maintained with the general usage of the chambers as pressurized oxygen can be explosive. Care must be taken to avoid excessively combustible materials and ignition sources. Patients must remove any makeup, oils, deodorants, and similar products. Recompression chambers are grounded, and all efforts are taken to eliminate static sparks. [17][18][10][8][6][1]
A thorough understanding of the physics principles outlined above cannot be understated as it is vital to the study of hyperbaric and undersea medicine. Physics provides a foundation for understanding the environmental stressors in a hyperbaric environment and the underlying mechanisms for many injuries encountered. Undersea and hyperbaric clinicians must be able to use their knowledge of physics and gas laws to appropriately diagnose and manage undersea and hyperbaric injuries and illnesses. For example, both inner ear barotrauma and inner ear DCS may offer similar clinical presentations however only the inner ear DCS requires treatment in a recompression chamber. In fact, not only is HBOT not indicated for inner ear barotrauma, it may worsen the condition. It is essential for a treating clinician to be able to recognize emergent hyperbaric indications, and to choose the most appropriate treatment modality.
It should be noted that the topical application of 100% oxygen to a body surface or breathing 100% oxygen at 1 ata is not HBOT.
All hyperbaric and undersea medicine team members should have an understanding of the physics principles outlined above. There are several emergent/ urgent HBOT indications that must be recognized early in order to improve patient outcomes. Complications of hyperbaric therapy must also be recognized and managed efficiently and expeditiously.
[1] | Lam G,Fontaine R,Ross FL,Chiu ES, Hyperbaric Oxygen Therapy: Exploring the Clinical Evidence. Advances in skin [PubMed PMID: 28301358] |
[2] | Carney AY, Hyperbaric oxygen therapy: an introduction. Critical care nursing quarterly. 2013 Jul-Sep; [PubMed PMID: 23736666] |
[3] | JACOBSON JH 2nd,MORSCH JH,RENDELL-BAKER L, CLINICAL EXPERIENCE AND IMPLICATIONS OF HYPERBARIC OXYGENATION. THE HISTORICAL PERSPECTIVE OF HYPERBARIC THERAPY. Annals of the New York Academy of Sciences. 1965 Jan 21; [PubMed PMID: 14255570] |
[4] | Camporesi EM,Bosco G, Mechanisms of action of hyperbaric oxygen therapy. Undersea [PubMed PMID: 24984320] |
[5] | BOEREMA I,MEYNE NG,BRUMMELKAMP WH,BOUMA S,MENSCH MH,KAMERMANS F,STERN HANF M,van AALDEREN, [Life without blood]. Nederlands tijdschrift voor geneeskunde. 1960 May 7; [PubMed PMID: 13802034] |
[6] | Spira A, Diving and marine medicine review part I: diving physics and physiology. Journal of travel medicine. 1999 Mar; [PubMed PMID: 10071371] |
[7] | Flook V, Physics and physiology in the hyperbaric environment. Clinical physics and physiological measurement : an official journal of the Hospital Physicists' Association, Deutsche Gesellschaft fur Medizinische Physik and the European Federation of Organisations for Medical Physics. 1987 Aug; [PubMed PMID: 3304804] |
[8] | Levett DZ,Millar IL, Bubble trouble: a review of diving physiology and disease. Postgraduate medical journal. 2008 Nov; [PubMed PMID: 19103814] |
[9] | Harding RM,Mills FJ, Aviation medicine. Problems of altitude I: hypoxia and hyperventilation. British medical journal (Clinical research ed.). 1983 Apr 30; [PubMed PMID: 6404482] |
[10] | ONeill OJ,Brett K,Frank AJ, Middle Ear Barotrauma 2020 Jan; [PubMed PMID: 29763026] |
[11] | Strauss MB,Lu LQ,Miller SS, The Gradient Perfusion Model Part 1: Why and at what sites decompression sickness can occur. Undersea [PubMed PMID: 30028915] |
[12] | Papadopoulou V,Eckersley RJ,Balestra C,Karapantsios TD,Tang MX, A critical review of physiological bubble formation in hyperbaric decompression. Advances in colloid and interface science. 2013 May; [PubMed PMID: 23523006] |
[13] | Leach RM,Rees PJ,Wilmshurst P, Hyperbaric oxygen therapy. BMJ (Clinical research ed.). 1998 Oct 24; [PubMed PMID: 9784458] |
[14] | Thom SR, Hyperbaric oxygen: its mechanisms and efficacy. Plastic and reconstructive surgery. 2011 Jan; [PubMed PMID: 21200283] |
[15] | Weaver LK, Hyperbaric medicine for the hospital-based physician. Hospital practice (1995). 2012 Aug; [PubMed PMID: 23086098] |
[16] | Chen W,Liang X,Nong Z,Li Y,Pan X,Chen C,Huang L, The Multiple Applications and Possible Mechanisms of the Hyperbaric Oxygenation Therapy. Medicinal chemistry (Shariqah (United Arab Emirates)). 2018 Dec 18; [PubMed PMID: 30569869] |
[17] | An Update on the Appropriate Role for Hyperbaric Oxygen: Indications and Evidence., Fife CE,Eckert KA,Carter MJ,, Plastic and reconstructive surgery, 2016 Sep [PubMed PMID: 27556750] |
[18] | Cho K,Minami T,Okuno Y,Kakuda Y,Tsutsumi T,Kogame T,Ohtsuru S,Sato N,Koike K, Convulsive seizure and pulmonary edema during hyperbaric oxygen therapy:A case report. The journal of medical investigation : JMI. 2018; [PubMed PMID: 30282875] |