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Shallow-water blackout and hypoxic blackout (SWB and HB; also referred to as ‘sudden underwater blackout syndrome’ and variations thereof; ILS, 2011) are characterized by the loss of consciousness in water. They can be fatal. They typically occur near the surface, but can occur at any depth and in many different circumstances and situations. SWB and HB often affect fit and healthy young people, but no one is safe. Understanding the risks and knowing how to avoid them when swimming underwater is thus essential in order to enjoy the water safely. The aim of this short paper is to help provide that understanding together with unified recommendations for prevention. SWB and HB have life-or-death consequences. Below are two personal experiences written to provide necessary context to the situations in which SWB and HB can arise, and the consequences and impact of it happening. It was 27 May 2020, and the first day on which the lockdown lifted to allow day trips. Oscar, my son, was 17 years old. Extraordinarily fit, he was a keen and talented rugby player. But his passion was the sea. Like me, he had been swimming from the age of 3, first used a mask and snorkel aged 4, and was a competent spear fisher at 12. By 16, every available recreational moment (even over Christmas) was spent in the sea, no matter how cold, rough or stormy. The day was hot and sunny, the sea glass-clear and calm. Oscar entered the water at ∼10.00 h. His camera suggests that he died not long afterwards. His body surfaced some weeks later. I am to blame. I gave him his love of the sea and of breath-holding to depth. I encouraged him to push himself, as I had always done. Nothing had ever gone wrong. For either of us. But, looking back, he had last snorkelled nearly 9 months earlier; surgery (a rugby injury), then lockdown, had prevented him. He was even hungrier to go and fitter than ever (again, lockdown allowed). He would have wanted to push himself. And such clear water would have made the depths all the more enticing. He had had a new wetsuit delivered (lockdown prevented him getting to his standard gear) and would probably have misjudged weighting himself or the degree of buoyancy loss at depth. Whatever. He died. And I miss him every day. Pushing oneself physically and mentally should not be avoided. Doing so was part of Oscar's passion. This document seeks to present information that can help others enjoy the water as much as he did, whilst perhaps also helping to keep them that bit safer. We were on a family holiday in the South of France on 28 July 2022. George and I were in the communal pool, having a bit of fun seeing who could swim the furthest underwater without coming up for a breath. We managed two attempts, going ∼25 m each time. Then I got out of the pool. George wanted to attempt the full length of the pool. He had another go, achieved 25 m or so again. He wanted one final attempt. After doing a little bit of hyperventilation, he went again. I was watching him closely, thankfully. As George passed me, it looked like he then came up for air. But then he suddenly seemed to slow under the water. At this point, I immediately stood up and started to realize something was wrong as he became static underwater. I became increasingly anxious, so I ran down the side of the pool and very quickly entered the water. When I reached George, he was lifeless at the bottom of the pool, eyes open facing me. I got him out of the pool and onto the side in one move. I immediately started chest compressions. As I was doing chest compressions, my daughter Serena had thankfully sensed something was wrong and ran over to where George and I were. On the way, she shouted for someone to call emergency services. Serena, now a qualified doctor, was a fifth-year medical student at the time and was truly brilliant. She checked George's airway whilst I continued chest compressions, and then Serena also performed chest compressions. I cannot remember the exact timings. George did not show an immediate response, perhaps another minute passed. I think he had had ∼3 min without oxygen in total, and I felt as if the world was quickly collapsing. Suddenly, some water started to dribble from his mouth, and he started to breathe slowly. He then started to make some horrific noises that will stay with me forever, I then thought he had serious brain damage at this time. However, things started to improve quickly, and within about the next 2 min, for the first time, I thought George might be okay. George was taken to the Nimes hospital, where he spent 4 days undergoing numerous tests to identify an underlying cause for his cardiac arrest. There was none. None of us had ever heard of SWB or knew of the risks George was taking. We were so, so lucky that the situation allowed a complete recovery for George. I cannot imagine life without George, but I think about that every single day. We went to the edge of the abyss, but luckily returned. The key to avoiding a problem is to understand its evolution. In terms of SWB and HB, this means identifying the physical and physiological mechanisms by which they come about (i.e., ‘the cause of the cause of death’). There are many routes by which a breath-hold diver can become unconscious when underwater [e.g., ‘cold shock’ (cardiac and respiratory consequences) (Tipton, 1989), traumatic injury, seizure, swim failure or a fall in blood oxygen (‘hypoxia’; ILS, 2011)]. A variety of factors thus influence risk (e.g., recent experience, speed and route of entering the water, equipment worn, water temperature, duration of exposure and depth). Other factors (e.g., degree of physical fitness, acclimatization to breath-holding, and psychological drive) also play a part. Here, we focus on otherwise fit and healthy individuals undertaking breath-hold diving (BHD). The pressure exerted by the weight of the 38.6 km of the Earth's atmosphere above us is 760 mmHg (101.3 kPa or 14.7 psi). Because water is a lot denser than air, 10 m of water provides one atmosphere of pressure. Therefore, at the surface of the water, the body is at one atmosphere. Swimming down increases pressure by a 10th of an atmosphere each metre, hence at 10 m the pressure exerted is two atmospheres (one of air and one of water). Doubling the atmospheric pressure on the chest also doubles the pressure of air in the lungs and halves the volume of the air contained within them (Boyle's law). On return to the surface, the pressure halves (from two to one atmosphere), and if nothing else has changed, the volume returns to its original level. In the lung, there is a mixture of gases [primarily nitrogen (N2), oxygen (O2) and carbon dioxide (CO2)]. The pressure exerted by each of these gases is proportional to the percentage of volume occupied (Dalton's law): if 21% of the gas is oxygen at the surface, then it exerts 21% of one atmosphere of pressure (21% of 760 mmHg or 160 mmHg; this is its ‘partial pressure’, P). As pressure changes with depth, so too does that exerted by each gas, in proportion. Thus, at 10 m, the pressure of gas in the lungs is two atmospheres or 1520 mmHg, meaning that the pressure exerted by the 21% which is oxygen will be 319 mmHg. It is the difference between the partial pressure of gas in our lungs and in our blood that drives gas exchange in our bodies, with gases moving along the pressure gradient from higher- to lower-pressure areas. Normally, for oxygen this is from the lungs ( P A O 2 ${P_{{\mathrm{A}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ) to the circulating blood ( P a O 2 ${P_{{\mathrm{a}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ) and for carbon dioxide from the circulating blood ( P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ) to the lungs ( P AC O 2 ${P_{{\mathrm{AC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ). These partial pressures of gases are particularly important in BHD. The urge to breathe is driven principally by three factors: a raised P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ or lowered P a O 2 ${P_{{\mathrm{a}}{{\mathrm{O}}_{\mathrm{2}}}}}$ in the blood, in addition to the duration of ‘inactivity’ in breathing muscles. The drive to breathe can also be influenced by other factors, including cold receptor afferent input when immersed in cold water (Tipton, 1989). The urge to breathe can also be overridden with increasing success by physiological and psychological adaptation (Barwood et al. 2024). Breathing is controlled by the central chemoreceptors (in the medulla oblongata of the brain) and peripheral chemoreceptors (in the carotid arteries [‘carotid bodies’] and arch of the aorta). Both provide input to the nucleus tractus solitarii and ventrolateral medulla (medullary respiratory centres). The peripheral chemoreceptors do not provide input to the central chemoreceptors directly (although the central chemoreceptors are found in the medullary centres). These receptors respond to changes in hydrogen ion concentration ([H+]), which is largely proportional to the P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ , with a rise in P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ causing a proportional rise in [H+], stimulating the chemoreceptors and thus the urge to breathe (or to return to the surface, if snorkelling or BHD). The central chemoreceptors are also sensitive to cerebrospinal fluid pH, whilst the peripheral chemoreceptors respond to both CO2/pH and O2, in addition to some metabolites and temperature. Unlike many physiological responses, breathing (rate and depth) are also under voluntary control. People can hyperventilate when they want to or can, for a period, overcome the drive to breathe (breath-hold). The terms SWB and HB are often used interchangeably, but they are not synonymous, although both do result in a rapid fall in blood oxygen (hypoxia) supply to the brain that causes unconsciousness. HB typically occurs whilst breath-hold swimming (for instance, ‘doing lengths underwater’). Exercising muscle consumes oxygen. As the oxygen content of arterial blood falls, muscle extracts all the oxygen it can, leading to a steepening fall in venous oxygen content. As the heart pumps harder and faster, the speed of blood transit through the lungs increases, meaning that there is less time for it to pick up oxygen. As the oxygen content in the inflated lung reduces, there is less ‘driving pressure’ for oxygen to enter the circulation. Arterial blood oxygen content thus falls even more dramatically. This rapid fall means that the time between the initial drive to breathe and unconsciousness can be very short. If that drive is overridden voluntarily or by diminished brain function, unconsciousness and drowning can occur at any depth. SWB refers to loss of consciousness on ascent from a breath-hold swim to depth (e.g., free-diving and spear fishing). A similar process to that in HB may contribute to SWB, although exercise is not necessary for this to occur, and changes in pressure on the body with submersion play an important role. An increase in intrathoracic pressure when diving raises the partial pressure of CO2 in the alveoli of the lung ( P AC O 2 ${P_{{\mathrm{AC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ), driving diffusion of it into the blood. With time, CO2 produced by body metabolism diffuses into the alveoli. Given that no air is being exchanged with the atmosphere, the P AC O 2 ${P_{{\mathrm{AC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ slowly rises until it reaches equilibrium with the P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ (Figure 1). This can mean that it takes a long time for P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ to reach a level that stimulates a drive to breathe. This situation is made worse if there is hyperventilation prior to diving; this lowers both total body CO2 content and P AC O 2 ${P_{{\mathrm{AC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ . Swimming when underwater consumes oxygen, the ‘supply’ of which is supplemented by that from the raised (by being at depth) alveolar partial pressure of O2 ( P A O 2 ${P_{{\mathrm{A}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ). Thus, the drive to breathe, which comes from a low P a O 2 ${P_{{\mathrm{a}}{{\mathrm{O}}_{\mathrm{2}}}}}$ is also delayed. Furthermore, deoxygenated blood also has an increased capacity for CO2 carriage (Haldane effect), limiting the increase in P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ and the drive to breathe. Some examples follow, each of which ends with loss of consciousness and commencement of the drowning process. Firstly, let us imagine someone in a swimming pool who is determined to beat their record for distance swum underwater (1 m depth). Swimming underwater consumes oxygen rapidly, resulting in a drop in the oxygen content of the body (hypoxia) that can cause loss of consciousness if the drive to breathe is overridden or, eventually, dulled by the impact of extreme hypoxia on neuronal activity. Secondly, let us imagine someone in a swimming pool who is determined to beat their record for distance swum underwater (1 m depth). They know that hyperventilation immediately before the underwater swim will extend their breath-hold time. By hyperventilating, they empty CO2 from their blood and lungs, lowering P AC O 2 ${P_{{\mathrm{AC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ and P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ and delaying the urge to breathe and return to the surface. Swimming underwater consumes oxygen, resulting in a drop in the oxygen content of the body (hypoxia) that can cause loss of consciousness before a sufficient level of CO2 is re-established to evoke the urge to breathe. Thirdly, let us imagine someone who free-dives to 10 m (two atmospheres). This causes P A O 2 ${P_{{\mathrm{A}}{{\mathrm{O}}_{\mathrm{2}}}}}$ to double, driving oxygen into the blood. Our diver swims at depth, their muscles consuming oxygen all the time, meaning that P a O 2 ${P_{{\mathrm{a}}{{\mathrm{O}}_{\mathrm{2}}}}}$ and P A O 2 ${P_{{\mathrm{A}}{{\mathrm{O}}_{\mathrm{2}}}}}$ fall. The CO2 generated by the muscle work diffuses into the lungs until P AC O 2 ${P_{{\mathrm{AC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ matches P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ , at which point P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ begins to rise to a point that stimulates the drive to breathe. They thus begin to swim to the surface. Between 10 m and the surface, P A O 2 ${P_{{\mathrm{A}}{{\mathrm{O}}_{\mathrm{2}}}}}$ drops by half (from two to one atmosphere), which now might be lower than P a O 2 ${P_{{\mathrm{a}}{{\mathrm{O}}_{\mathrm{2}}}}}$ . Oxygen will now start dumping from the blood to the lungs. Near the surface, as the relative pressure change maximizes, P a O 2 ${P_{{\mathrm{a}}{{\mathrm{O}}_{\mathrm{2}}}}}$ falls rapidly to a level at which the brain cannot function. Loss of consciousness (ascent blackout) or a seizure occurs. The free-diver drowns. If this occurs at sufficient depth, lung volume may be so low that the diver may be negatively buoyant (or they may breathe out as they lose consciousness), and they sink to the bottom. Hyperventilation before diving introduces the additional problems described above in the second scenario (Figure 1). Craig (1961) describes eight incidents where the above occurred and, in 1976, described 58 more (Craig, 1968). Edmonds and Walker (1999) suggested that 15 of 60 snorkelling deaths in Australia also occurred in this way. Those who died were all males and were usually <40 years of age (Bart & Lau, 2023). In many cases, a focus on achieving a goal (competing on breath-hold time or performing a task underwater, such as spear fishing) played a part by altering the interpretation of, or overriding, the physiological urge to breathe (Craig, 1961; Craig & Babcock, 1962; Craig & Medd, 1968; Craig & Harley, 1968). The effect of hydrostatic pressure on alveolar gases is usually seen with dives beyond a depth of 5 m. However, SWB and HB incidents are commonly reported in shallower dives, such as in swimming pools. Therefore, BHD depth cannot account for all the incidents of SWB and HB. Hyperventilation reduces CO2 levels in the body, and the resulting increase in serum pH (alkalosis) promotes the binding of calcium ions to proteins such as albumin, reducing the amount of free (unbound) calcium in the blood. Given that calcium is involved in both muscle contraction and neurotransmitter function (possibly including the oxygen receptors), this can result in reduced transmission of neurotransmitters, loss of motor control, and bilateral fine motor tremor with head bobbing. Competitive free-divers call the euphoric sensations, disinhibition and altered perception they experience at the breath-hold breakpoint ‘Samba’ (Gibson et al., 1981). It is associated with arterial hypoxia and possibly also a reduction in cerebral metabolic rate. Hypoxia and hypocapnia can result in arrhythmias (Windsor et al., 2010). A low P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ can also reduce cerebral blood flow. It can drive a left shift in the oxyhaemoglobin dissociation curve, impairing tissue oxygen delivery. In addition, high vagal tone from the ‘diving response’ to face immersion in cold water can result in vagal arrest of the heart (Bayne & Wurzbacher, 1982; ILS, 2011). ‘Autonomic conflict’ (vagal stimulation as above, but with simultaneous sympathetic activation [e.g., ‘cold shock’]) can also cause lethal arrhythmias (Shattock & Tipton, 2012; Figure 2). Finally, breath-holding at total lung capacity can, owing to intrathoracic compression, result in a fall in stroke volume and cardiac output when at the surface. This response is exacerbated with any form of glossopharyngeal insufflation (Ferrigno et al., 1986; Schipke et al., 2015). Andrew H. Baker, Hugh Montgomery and Mike Tipton were involved in the conceptualization of the article. All authors contributed to the acquisition, analysis and interpretation of the work and drafting of the article and revising it for intellectual content. All authors approved the final version of the manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. Thanks to Dr Paddy Morgan and Professor Mike Shattock for their comments on the manuscript. None declared. None. No data were generated or analysed for this study.