Hypoxia is an abnormal deficiency of oxygen in the arterial blood in which the partial pressure of oxygen is too low to meet the metabolic needs of the body (Wiebe et al., 1999). An environment is considered hypoxic when the partial pressure of oxygen in the breathing gas is below 0.16 ATA, regardless of depth. The onset of hypoxic effects can be sudden and can arise without warning. Additionally, hypoxia is a common cause of injury and fatality in semi or closed-circuit breathing rigs (Popa et al., 2022). On the surface, as the closed-circuit diver consumes oxygen, the oxygen fraction in the breathing loop will begin to decrease, as will the gas volume in the breathing bag. Oxygen is typically added on demand into the breathing loop. If the valves malfunction, no oxygen will be added and the oxygen fraction may drop to ten percent or less, instantiating hypoxic breathing conditions. Since the partial pressure of oxygen is constantly increasing on descent, hypoxia is less likely to occur while divers are descending. However, the reverse is also true. Hypoxia can be accelerated by the sudden decrease in oxygen partial pressure due to ascent.

The relevant biometric to measure hypoxia is SpO₂. SpO₂ is a proxy measurement of the percent of oxygenated hemoglobin in the arterial blood (Nitzan et al., 2014). SpO₂ measurements above 95% are considered healthy and values below 90% are generally considered hypoxic (American Thoracic SocietyAmerican College of Chest Physicians, 2003). Acute hypoxia, even acute profound hypoxia (SpO₂ <70%), for up to 10 min, is generally well tolerated in humans with no long-lasting effects (Bickler et al., 2017). However, increasingly prolonged exposure to hypoxic conditions can lead to progressively severe instances of shallow-water blackout (Bart and Lau, 2022). While ascending, the decreasing partial pressure of oxygen in the breathing loop, combined with the metabolic consumption of oxygen, creates an environment where there is a high demand for oxygen in the body, but oxygen is actively transferred back to the breathing loop. This combination leads to an increased risk of unconsciousness as cerebral oxygenation drops. Other relevant biometrics include SmO₂ and StO₂ (Hoiland et al., 2016), RR, and HR. Non-traditional oxygen saturation measurements are still an active area of research and are not as well established as SpO₂. Alternatively, well-established metrics, like HR and RR, may be particularly relevant as hypoxic conditions signal the cardiac output centers in the brain to increase HR and RR (Zhang et al., 2014; Brinkman et al., 2023). As the sympathetic nervous system affects these changes, it follows that HRV could be a relevant metric. However, the data does not support this relationship during physical activity (Buchheit et al., 2004), and the relationship between HRV and hypoxia (i.e., whether or not changes in HRV could be used to predict these events) warrants further study.

There are several clinical-grade medical devices, as well as commercial off-the-shelf (COTS) products, that can measure SpO₂ with a high degree of fidelity on land. Some researchers have made strides to adapt this technology to the underwater operating environment (Mulder et al., 2021; McKnight et al., 2021). A key challenge with these devices is their accuracy. The accuracy of pulse oximeters begins to decrease as the oxygenation percentage decreases because they are generally calibrated to a range of saturation between 70% and 100% (Torp et al., 2023). Other sources of inaccuracy include but are not limited to, skin tone, movement, body placement, core temperature, and blood flow (Fine et al., 2021). Similarly, the use of traditional methods such as an ECG to measure HR, presents challenges underwater versus on land. Specifically, ECG signal quality is dramatically impaired, particularly in seawater (Reyes et al., 2014). While there have been examples of ECG successfully measured in a dry suit configuration (Noh et al., 2018), additional developments are necessary to ruggedize ECG devices for all possible deployments. Furthermore, there are practical limitations to the adhesion of ECG pads. A surrogate measure such as pulse rate might be reasonable, but limitations also persist due to reductions in blood flow that occur in cold environments often present during dives (Yeung et al., 2016). Moreover, the pulse rate may misreport HR if an arrhythmia is present, as each heartbeat may not result in changes in blood flow, blood pressure, and pulse rate. Finally, accurate measurement of the gasses (O₂, CO₂) could factor into a novel safety system; however, further exploration is needed.

When a diver breathes oxygen at high partial pressures, this can prompt the diver to become over-oxygenated (hyperoxia), which can subsequently lead to a diving disorder known as oxygen toxicity (O₂ toxicity) (Cooper et al., 2023). In hyperbaric conditions, the increase in partial pressure of the oxygen in the lungs has several physiological effects, with known and unknown mechanisms (Thomson and Paton, 2014). O₂ toxicity is understood to be dose-dependent. Both dive depth (pressure) and dive duration can be altered to mitigate the effects of oxygen on the body. There are two main types of O₂ toxicity: pulmonary (Jackson, 1985) and CNS (Rodgers et al., 2018); the former is better understood than the latter (Naval Sea Systems Command, 2016). Pulmonary O₂ toxicity likely occurs as the result of free radical oxidation in the pulmonary tissue. Oxidative stress causes lung irritation, with symptoms including chest pain, cough, and pain on inspiration. These symptoms can develop slowly and become increasingly worse as long as elevated oxygen levels are inspired, with prolonged exposure to high concentrations of oxygen leading to pulmonary edema. Pulmonary O₂ toxicity can occur whenever the partial pressure of oxygen exceeds 0.5 ATA. In place of personal physiological monitoring, established safety factors have successfully mitigated oxygen toxicity. However, monitoring RR may provide utility for detecting oxygen toxicity, as changes in RR often occur downstream of pulmonary O₂ toxicity (Cooper et al., 2023; Lellouche and L’Her, 2020).

The more insidious form of oxygen toxicity is CNS O₂ toxicity. High partial pressures of oxygen are associated with many biochemical changes in the brain, but it is unknown which specific changes are responsible for the signs and symptoms of CNS O₂ toxicity. CNS O₂ toxicity can occur whenever the oxygen partial pressure exceeds 1.3 ATA in a wet diver or 2.4 ATA in a dry diver. The symptoms of CNS O₂ toxicity may be remembered with the following acronym, VENTIDC (Naval Sea Systems Command, 2016):

V: Visual symptoms. Tunnel vision, a decrease in the diver’s peripheral vision, and other symptoms, such as blurred vision, may occur.

The exact mechanism of CNS O₂ toxicity is unknown; however, it is hypothesized that reactive oxygen species interrupt neural networks and function (Manning, 2016). Initial studies have demonstrated that electrodermal activity can predict CNS O₂ toxicity in divers (Posada-Quintero et al., 2021). However, this measure has not yet been ruggedized and implemented in a technology suitable for the underwater operating environment. Although HRV could be relevant due to its utility as a measure of sympathetic outflow, research is lacking in this area and the inclusion of HRV would be an exploratory biometric. Reductions in HR stroke volume and cardiac output have been shown in patients suffering from hyperoxia (Rodgers et al., 2018); however, it is not understood how this translates to an underwater environment.

Hypercapnia is a condition that is either due to hypo-ventilation or the inhalation of a gas mixture with a substantial fraction of carbon dioxide (CO₂). More specifically, a build-up of CO₂ in the breathing supply will accumulate in the diver’s blood and tissues (Dunworth et al., 2017), which can lead to symptoms such as headaches, mild dizziness, and confusion (Sterba, 2024). In high quantities, this excess CO₂ can cause cognitive/physiological impairment and ultimately lead to diving accidents. The principal causes presented in the US Navy Dive Manual are the following:

1) Excess carbon dioxide levels in compressed air supplies due to improper placement of the compressor inlet.

Notably, inadequate lung ventilation is often caused by skip breathing, increased apparatus dead space, excessive breathing resistance, or increased oxygen partial pressure (Dunworth et al., 2017). To mitigate instances of hypercapnia, specific procedures for filling, packing, and weighing the CO₂ absorbent material are followed. Additionally, diving profiles and water temperatures are meticulously calculated and factored into operational planning. These steps are taken to ensure diver safety, not just to prevent hypercapnia, but also CNS O₂ toxicity. It is hypothesized that hypercapnia greatly increases the risk of CNS O₂ toxicity by increasing brain blood flow and consequently brain oxygen levels, leading to toxic concentrations of oxygen in the brain (Eynan et al., 2020). CO₂ sensors in the breathing apparatus in conjunction with SpO₂ monitors could potentially help mitigate hypercapnia events. Additionally, insight into the diver’s RR (i.e., rapid increases or decreases) could help identify hypercapnic breathing patterns (Brinkman et al., 2023). In contrast to hypoxia, hypercapnia decreases RR, triggering a pattern of slow, deep breaths, as the lungs aim to limit dead space and optimize CO₂ clearance. Finally, HR may also be relevant, as a rise in CO₂ in the bloodstream initially depresses HR due to an increasing intercellular pH (van Beek et al., 1998).

Nitrogen narcosis is a condition that temporarily impairs the neurological function of a diver, resulting from the inhalation of high concentrations/partial pressures of nitrogen in the breathing apparatus (Rocco et al., 2019). Similar to oxygen toxicity, as the diver descends, the partial pressure of nitrogen increases, leading to an increased concentration of nitrogen in the bloodstream. While the exact mechanism is unknown, a leading hypothesis suggests that there is a correlation between the lipid solubility of an inert gas and its narcotic effect (Kirkland et al., 2022). Therefore, at higher concentrations, more gas is dissolved in the lipid bilayer of cells, leading to greater interaction with cellular processes and disrupted cell signaling (Hapfelmeier et al., 2000). As a diver descends to greater depths, the probability of experiencing narcotic effects from the gases that interfere with the diver’s nervous system increases, potentially leading to a significant impairment in their judgment or adherence to protocol. Nitrogen narcosis effects are progressive, as an increase in the diver’s depth can lead to complete incapacitation if not recognized promptly. Measurements of electrical activity in the central nervous system (electroencephalography; EEG) or measurements of other autonomic processes could be leading indicators of a narcotic event (Dolmierski et al., 1988; Pastena et al., 2005). Although nitrogen narcosis can be evaluated at depth during a dive using the critical flicker fusion frequency (CFFF; see Section 4), other methods have been employed to prevent nitrogen narcosis, such as the utilization of other gas mixes (helium-oxygen; heliox), which eliminates the narcotic effects of nitrogen, especially at deeper depths. Helium, unlike other inert gases, does not have narcotic properties when inhaled at high partial pressures.

Chemical injury is often referred to as a “caustic cocktail” and can have immediate adverse effects on a diver (Minns et al., 2010). This injury is caused by excessive humidity mixing with a carbon dioxide absorbent (Sodasorb; soda lime) to create a caustic alkaline solution in the breathing loop of a closed-circuit diving apparatus. If inhaled, the solution can cause corrosive esophageal and lung injuries. Choking, gagging, foul taste, and burning of the mouth and throat may begin immediately (Buzzacott et al., 2022). Although the onset of a “caustic cocktail” in itself does not cause a diving physiological disorder, the exposure to this solution underwater may cause a diver to immediately ascend to the surface, which could be the impetus for an AGE, barotraumas, a hypoxia event, or DCS, depending on the diving modality. If this caustic solution reaches the upper airway of the diver, it can cause several adverse effects including hyperventilation, headache, and with prolonged exposure, significant injury to the pulmonary system (Minns et al., 2010).

The extent of the chemical injury depends on the amount and distribution of the solution. Additionally, the accumulation of the caustic solution in the canister can impair the carbon dioxide absorption properties of the system, leading to other issues like hypoxia and hypercapnia. Advancements in breathing loop sensing technologies could lead to diver warnings that could alert the diver ahead of a chemical injury; however, no known interventions have been operationalized. Poisonings and other chemical ingestions have been shown to alter some biometrics (abnormal heart rates, body temperatures, blood pressures, etc.) (Lee et al., 2008; Gorguner and Akgun, 2010), and therefore the sudden inhalation of a strong alkaline solution would likely cause some detectable change in a diver’s vital signs. However, there is no research showing a causal relationship between any biometric data to these events.

Carbon monoxide (CO) is a colorless, odorless, tasteless gas that, when inhaled, will ultimately bind to hemoglobin present in red blood cells and thus prevent oxygen from being circulated throughout the body (Long and Flaherty, 2017). The inability to adequately oxygenate the body (tissue hypoxia) due to the binding of CO is referred to as CO poisoning. Despite being an uncommon diving hazard (Hampson, 2020), CO poisoning can be very dangerous. One of the most common causes of CO poisoning in a diving context is procedural error when charging air cylinders or nitrogen and air gas mixes used in Nitrox diving. Accordingly, closed-circuit UBAs that only employ oxygen are not rigs involved with CO poisoning. Charging these cylinders in the presence of other contaminants can contaminate the pressurized gas. Although the presence of small amounts of CO can be unnoticeable at low pressures, the effects of CO poisoning worsen as the gas is present at higher partial pressures. CO poisoning can be particularly detrimental to divers, as it can be confused with decompression illnesses such as DCS (Allen, 1992) or AGE (Holt and Weaver, 2012). Treatment of CO poisoning is similar to the treatment of decompression illnesses, which is to have the diver breathe high concentrations/partial pressures of oxygen in hyperbaric environments (Köhler et al., 2022).

Similar to sensing chemical injuries, advancements in breathing loop sensing technologies could provide a diver with an advanced warning that CO is present in the breathing apparatus. However, given the seemingly infrequent occurrence of CO poisoning, no known interventions for CO poisoning have been operationalized. One physiological device that may be capable of detecting CO poisoning is a pulse CO-oximeter (Hampson, 2012). Analogous to pulse oximeters collecting peripheral oxygen saturation (SpO2), these devices are capable of detecting CO saturation, or more specifically, elevated blood carboxyhemoglobin (COHb) levels. This would be a novel addition to an underwater physiological monitoring system; however, it has been suggested that COHb levels do not correlate well with the clinical severity of CO poisoning (Garg et al., 2018). Critically, elevated COHb levels have also been shown to incorrectly elevate the oxygen saturation from pulse oximetry, which suggests that metrics such as SpO2 may not provide utility for CO poisoning (Hampson, 1998). Nevertheless, other physiological metrics that may help to detect CO poisoning can include HR and RR, as both of these metrics have been well characterized in the literature, albeit in a clinical setting. Analyzing these metrics for an underwater use case will require additional research.

Barotrauma associated with the ear canal, colloquially referred to as “ear squeeze,” (Mawle and Jackson, 2002) is one of the most commonly reported injuries that occur when diving that can vary in severity depending on where trauma occurs. Ear squeezes can occur at depths of as little as eight feet and stem from blockages in the nasal tissue when a diver has a head cold or cannot clear their ear passages (eustachian tube) correctly (Sheridan et al., 1999). While middle ear barotrauma usually resolves on its own, inner ear barotrauma typically requires medical intervention for symptoms related to tinnitus, hearing loss, vertigo, or permanent auditory disability (Sheridan et al., 1999). More specifically, if a person does not ascend to more shallow depths when pain is observed, this can lead to increasingly more severe injuries (i.e., tympanic membrane perforation), which occur suddenly and would require inspection of the ear canal to confirm. Thus, ear squeeze currently lends itself to be exceptionally difficult for physiological monitoring systems to detect and prevent, and currently relies on the diver to discern during descent.

Subcutaneous emphysema is a type of barotrauma that occurs when gases are trapped under the skin and inside body tissues (Aghajanzadeh et al., 2015). Although subcutaneous emphysema is considered to be a common, non-life-threatening diving complication, it can range in severity, appearing as swelling in regions such as the face, neck, upper chest, and shoulders. The presence of subcutaneous emphysema can also be a sign that air is occupying somewhere deeper in the body and can be a symptom of another type of barotrauma known as pneumothorax, which is described later in this review. Treatment of subcutaneous emphysema is dependent on various methods that can be used to release the trapped air such as incisions, needles, or drains (Aghajanzadeh et al., 2015). Non-invasive methods to detect subcutaneous emphysema in real-time currently do not exist.

Positive pulmonary barotrauma, or pulmonary overinflation syndrome (POIS), is a lung overexpansion injury that occurs during ascent. It is primarily caused by inadequate exhalation, especially during rapid ascent, as lung volume expands with decreasing environmental pressure (Kennedy-Little and Sharman, 2024). Expansion exceeding the elastic limit of alveoli can lead to rupture, and subsequent release of air (Bove, 2014). In severe cases, alveolar air can enter pulmonary capillaries and central circulation, leading to an AGE. Depending on the rupture location, air may move centrally, entering the mediastinum, or peripherally to the pleural space. Central movement may result in pneumomediastinum or subcutaneous emphysema, if air dissects upwards toward the head and neck. Peripheral movement to the pleural space may result in a pneumothorax or tension pneumothorax (Kennedy-Little and Sharman, 2024). Patients with pneumomediastinum may be asymptomatic, or may experience chest pain, coughing, shortness of breath, or dysphagia. Hamman’s sign, a crunching sound heard during auscultation, is also a symptom of pneumomediastinum. Most mediastinal air reabsorbs on its own and does not require treatment, however breathing 100% oxygen can increase reabsorption rate (Bove, 2014). To our knowledge, there are currently no real-time monitoring devices capable of assessing pulmonary overinflation.

A pneumothorax is a condition where air becomes trapped in the pleural space between the lung and the chest wall. It occurs when differences in pressures result in a one-time leakage of air, causing partial lung collapse and varying degrees of respiratory distress (Zarogoulidis et al., 2014). Symptoms of a pneumothorax include sudden, sharp chest pain, shortness of breath, labored breathing, rapid heart rate, weak pulse, and anxiety. In severe cases, a damaged lung may allow gas to enter, but not leave. Successive breaths increase the volume of this gas pocket, in turn increasing pressure on the lung and heart, potentially leading to a tension pneumothorax (Zarogoulidis et al., 2014). If unmitigated, a tension pneumothorax eventually leads to complete lung collapse and consequently, impaired respiration and circulation. A tension pneumothorax will become progressively more severe, eventually leading to shock and death.

The treatment approach depends on the size and severity of the pneumothorax. Smaller pneumothoraxes (less than 15%) may resolve on their own as the trapped air is reabsorbed spontaneously (Naval Sea Systems Command, 2016) and can be managed by having the affected individual breathe 100% O₂. However, more significant pneumothoraxes (with cardio-respiratory compromise) may require active intervention such as insertion of a chest tube, large-bore intravenous catheter, or other devices designed to remove intrathoracic gas. Patients with pneumothorax may develop tachycardia, tachypnea, and hypoxia, especially as the injury progresses (McKnight and Burns, 2023). As with a number of the other diving disorders, monitoring HR, RR, and pulse oximetry levels could potentially help detect the presence of a pneumothorax (Gustman et al., 1983), however, further research is required to deploy these methods underwater. Other monitoring technologies include ultrasound imaging, which is used clinically to diagnose the presence of pneumothorax, but again has not been outfitted to underwater applications (Alrajhi et al., 2012).

On one end of the spectrum, hypothermia is a condition characterized by a drop in the body’s core temperature, which poses a significant risk during diving operations in cool and cold waters. Hypothermia occurs when the body loses more heat than it generates due to the temperature difference between the body and water (Aguilella-Arzo et al., 2003). Critically, the thermal conductivity of water is 26 times greater than the thermal conductivity of air (Sterba, 1989), which suggests that divers may become hypothermic faster underwater. Therefore, a diver’s response to immersion depends on the level of thermal protection worn and the ambient water temperature. Even in relatively warm water, if given enough time, a diver can become hypothermic without an adequate level of protection. Initially, cold-induced vasoconstriction reduces blood flow to the skin, lowering heat conductance and preserving the body’s core temperature (Sterba, 1989). However, this vasoconstrictive regulation has limitations, and prolonged exposure to frigid water can lead to fluctuating blood flow and increased heat loss. Exercise in cold water accelerates heat loss, as movement stirs water in contact with the skin, promoting convection (Kuehn, 1978). For context, an average core temperature is approximately 98.6°F. As a diver’s core temperature drops, symptoms of hypothermia progress from uncontrolled shivering and slurred speech in mild cases (core temperatures between 95°F and 97°F) to loss of shivering, impaired mental status, irregular heartbeat, and shallow respirations in the most severe cases (core temperatures between 88°F and 93°F) (Mccullough and Arora, 2004). A core temperature of 84°F or below generally results in a loss of consciousness (Mccullough and Arora, 2004). Given enough time in cold water, even the most protected divers can experience severe core temperature drops and resultant hypothermic symptoms.

At the other end of the spectrum, hyperthermia is a condition characterized by a high core body temperature due to either excessive thermal protection or prolonged exposure to warmer ambient water temperatures (Looney et al., 2019). One of the primary methods that the body uses to reduce core body temperature is to sweat. Moreover, the evaporation of sweat is what aids in the cooling process (Gagnon et al., 2018). However, being immersed underwater prevents this process and hinders a diver’s ability to shed excess heat. When the core body temperature gets too high, a person can experience symptoms such as nausea, slurred speech, headache, vertigo, body weakness, and dehydration. In severe cases, a diver would experience heat fatigue, a drop in blood pressure, and loss of consciousness. To mitigate the occurrence of these diving complications, divers are advised to wear appropriate thermal protection based on water temperature, expected bottom time, and individual factors. Monitoring of ambient water, skin, and core temperatures could help detect these events before they become dangerous. Monitoring skin temperature to predict diving disorders would require extensive algorithm development, as skin temperature can fluctuate across a wide range of temperatures in response to environmental conditions (Yousef et al., 2024). However, some efforts have been made to correlate core body temperature with skin temperature readings (Eggenberger et al., 2018; Xu et al., 2013). Recent developments related to skin surface heat flux sensors, could provide a more ergonomic, less invasive solution to traditional core temperature measurements (Daanen et al., 2023; Ajčević et al., 2022), however more research is needed to validate these sensors at depth and in water.

Immersion pulmonary edema, also referred to as swimming-induced pulmonary edema (SIPE), is a condition that causes infiltration of fluid from the bloodstream into the alveoli (Harper, 2011). Since first being reported in the late 1980s (Wilmshurst et al., 1989), no single pathophysiology adequately describes the occurrence of SIPE. However, multiple intrinsic and extrinsic factors have been proposed which contribute to an individual’s risk (Moon et al., 2016; Peacher et al., 2015; Sames et al., 2019). Chronic hypertension is the greatest predictor for those who experience SIPE, including individuals who develop hypertension later in life. While typically a result of cardiac problems, such as heart failure, SIPE has a high incidence in healthy swimmers during strenuous activity (Shupak et al., 2000; Miller et al., 2010). Additionally, water immersion leads to an increased central blood volume and thus raised cardiac filling pressures (Koehle et al., 2005). In colder water, this effect is further exacerbated due to the vascular response to cold temperatures in addition to immersion. Finally, negative lung breathing pressures, due to use of different breathing apparatus and immersed postures, contribute to hydrostatic pressures driving fluid movement into the alveoli from pulmonary capillaries (Wilmshurst, 2019; Shupak et al., 2003). Each unique risk factor may act to increase the pressure gradient across the pulmonary capillary membrane, which in turn increases the combined likelihood of SIPE. SIPE can be fatal in severe cases, and otherwise presents with symptoms of dyspnea, cough, hemoptysis, and sputum production (Adir et al., 2004). Monitoring of pulmonary capillary pressure would enable the calculation for the risk of developing SIPE, however, this is typically an invasive process involving right heart catheterization (Ranu et al., 2010). Noninvasive measurements have been shown to correlate with pulmonary capillary wedge pressure at normobaric conditions (Nagueh et al., 2019; Genovese et al., 2021), but a dive-ready monitoring method has not been developed. More research is needed to identify correlates to pulmonary capillary pressure or alternate approaches that can be applied in wet, hyperbaric conditions to enable better tracking and understanding of SIPE pathophysiology.