Human physiology of underwater diving
Human physiology of underwater diving is the physiological influences of the underwater environment on the human ambient pressure diver, and adaptations to operating underwater, both during breath-hold dives and while breathing at ambient pressure from a suitable breathing gas supply. It, therefore, includes the range of physiological effects generally limited to human ambient pressure divers either freediving or using underwater breathing apparatus. Several factors influence the diver, including immersion, exposure to the water, the limitations of breath-hold endurance, variations in ambient pressure, the effects of breathing gases at raised ambient pressure, effects caused by the use of breathing apparatus, and sensory impairment. All of these may affect diver performance and safety.
Immersion affects fluid balance, circulation and work of breathing. Exposure to cold water can result in the harmful cold shock response, the helpful diving reflex and excessive loss of body heat. Breath-hold duration is limited by oxygen reserves, the response to raised carbon dioxide levels, and the risk of hypoxic blackout, which has a high associated risk of drowning.
Large or sudden changes in ambient pressure have the potential for injury known as barotrauma. Breathing under pressure involves several effects. Metabolically inactive gases are absorbed by the tissues and may have narcotic or other undesirable effects, and must be released slowly to avoid the formation of bubbles during decompression. Metabolically active gases have a greater effect in proportion to their concentration, which is proportional to their partial pressure, which for contaminants is increased in proportion to absolute ambient pressure.
Work of breathing is increased by increased density of the breathing gas, artifacts of the breathing apparatus, and hydrostatic pressure variations due to posture in the water. The underwater environment also affects sensory input, which can impact on safety and the ability to function effectively at depth.
Immersion
Immersion of the human body in water has effects on the circulation, renal system and fluid balance, and breathing, which are caused by the external hydrostatic pressure of the water providing support against the internal hydrostatic pressure of the blood. This causes a blood shift from the extravascular tissues of the limbs into the chest cavity, and fluid losses known as immersion diuresis compensate for the blood shift in hydrated subjects soon after immersion. Hydrostatic pressure on the body due to head out immersion causes negative pressure breathing which contributes to the blood shift.The blood shift causes an increased respiratory and cardiac workload. Stroke volume is not greatly affected by immersion or variation in ambient pressure but slowed heartbeat reduces the overall cardiac output, particularly due to the diving reflex in breath-hold diving. Lung volume decreases in the upright position due to cranial displacement of the abdomen due to hydrostatic pressure, and resistance to air flow in the airways increases significantly because of the decrease in lung volume. There appears to be a connection between pulmonary edema and increased pulmonary blood flow and pressure which results in capillary engorgement. This may occur during higher intensity exercise while immersed or submersed. Negative static lung load due to hydrostatic pressure difference between ambient pressure on the chest and breathing gas supply pressure can cause a reduction in compliance of the soft lung tissues leading to increased work of breathing.
Exposure
Cold shock response is the physiological response of organisms to sudden cold, especially cold water, and is a common cause of death from immersion in very cold water, such as by falling through thin ice. The immediate shock of the cold causes involuntary inhalation, which if underwater can result in drowning. The cold water can also cause heart attack due to vasoconstriction; the heart has to work harder to pump the same volume of blood throughout the body, and for people with heart disease, this additional workload can cause the heart to go into arrest. A person who survives the initial minute of trauma after falling into icy water can survive for at least thirty minutes provided they don't drown. However, the ability to perform useful work like staying afloat declines substantially after ten minutes as the body protectively cuts off blood flow to "non-essential" muscles.The diving reflex is a response to immersion that overrides the basic homeostatic reflexes, and which is found in all air-breathing vertebrates. It optimizes respiration by preferentially distributing oxygen stores to the heart and brain which allows staying underwater for extended periods of time. It is exhibited strongly in aquatic mammals, but exists in other mammals, including humans. Diving birds, such as penguins, have a similar diving reflex. The diving reflex is triggered specifically by chilling the face and breath-hold. The most noticeable effects are on the cardiovascular system, which displays peripheral vasoconstriction, slowed pulse rate, redirection of blood to the vital organs to conserve oxygen, release of red blood cells stored in the spleen, and, in humans, heart rhythm irregularities. Aquatic mammals have evolved physiological adaptations to conserve oxygen during submersion, but the apnea, bradycardia, and vasoconstriction are shared with terrestrial mammals as a neural response.
Hypothermia is reduced body temperature that happens when a body dissipates more heat than it absorbs and produces. Clinical hypothermia occurs when the core temperature drops below. Heat loss is a major limitation to swimming or diving in cold water. The reduction in finger dexterity due to pain or numbness decreases general safety and work capacity, which consequently increases the risk of other injuries. Reduced capacity for rational decision making increases risk due to other hazards, and loss of strength in chilled muscles also affects the capacity to manage both routine and emergency situations. Low tissue temperatures and reduced peripheral perfusion affect inert gas solubility and the rate of ingassing and outgassing, thereby affecting decompression stress and risk. Body heat is lost much more quickly in water than in air, so water temperatures that would be quite reasonable as outdoor air temperatures can lead to hypothermia in inadequately protected divers, although it is not often the direct clinical cause of death.
Persistent exposure of the external auditory canal to cold water can induce the growth of exostoses.
Non-freezing cold injury is a form of localised cold injury in which there is no freeze–thaw damage. The tissue damage is caused by sustained exposure to low temperature without actual freezing.
NFCI is caused by microvascular endothelial damage, stasis and vascular occlusion and is characterised by peripheral neuropathy. NFCI generally affects the hands or feet during exposure to temperatures just above freezing, often wet.
The thermal status of the diver has a significant influence on decompression stress and risk, and from a safety point of view this is more important than thermal comfort. Ingassing while warm is faster than when cold, as is outgassing, due to differences in perfusion in response to temperature perception, which is mostly sensed in superficial tissues. Maintaining warmth for comfort during the ingassing phase of a dive can cause relatively high tissue gas loading, and getting cold during decompression can slow the elimination of gas due to reduced perfusion of the chilled tissues, and possibly also due to the higher solubility of the gas in chilled tissues.
Breath-hold limitations
Breath-hold diving by an air-breathing animal is limited by the physiological capacity to perform the dive on the oxygen available until it returns to a source of fresh breathing gas, usually the air at the surface. When this internal oxygen supply is depleted, the animal suffers an increasing urge to breathe caused by a buildup of carbon dioxide in the circulation, followed by loss of consciousness due to central nervous system hypoxia. If this occurs underwater, it will drown. Breath-hold diving depth is limited in animals when the volume of rigid walled internal air spaces is occupied by all of the compressed gas of the breath and the soft spaces have collapsed under external pressure. Animals that can dive deeply have internal air spaces that can extensively collapse without harm, and may actively exhale before diving to avoid absorption of inert gas during the dive.Breath-hold blackout is a loss of consciousness caused by cerebral hypoxia towards the end of a breath-hold dive, when the swimmer does not necessarily experience an urgent need to breathe and has no other obvious medical condition that might have caused it. It can be provoked by hyperventilating just before a dive, or as a consequence of the pressure reduction on ascent, or a combination of these. Victims are often established practitioners of breath-hold diving, are fit, strong swimmers and have not experienced problems before.
Divers and swimmers who blackout or grey out underwater during a dive will usually drown unless rescued and resuscitated within a short time. Freediving blackout has a high fatality rate, and mostly involves males younger than 40 years, but is generally avoidable. Risk cannot be quantified, but is clearly increased by any level of hyperventilation.
Freediving blackout can occur on any dive profile: at constant depth, on an ascent from depth, or at the surface following ascent from depth and may be described by a number of terms depending on the dive profile and depth at which consciousness is lost. Blackout during a shallow dive differs from blackout during ascent from a deep dive in that deep water blackout is precipitated by depressurisation on ascent from depth while shallow water blackout is a consequence of hypocapnia following hyperventilation.
The minimum tissue and venous partial pressure of oxygen which will maintain consciousness is about. This is equivalent to approximately in the lungs. Approximately 46 ml/min oxygen is required for brain function. This equates to a minimum arterial partial pressure of oxygen of at 868 ml/min cerebral flow.
Hyperventilation depletes the blood of carbon dioxide, which causes respiratory alkalosis, and causes a leftward shift in the oxygen–hemoglobin dissociation curve. This results in a lower venous partial pressure of oxygen, which worsens hypoxia. A normally ventilated breath-hold usually breaks with over 90% saturation which is far from hypoxia. Hypoxia produces a respiratory drive but not as strong as the hypercapnic respiratory drive. This has been studied in altitude medicine, where hypoxia occurs without hypercapnia due to the low ambient pressure. The balance between the hypercapnic and hypoxic respiratory drives has genetic variability and can be modified by hypoxic training. These variations imply that predictive risk cannot be reliably estimated, but pre-dive hyperventilation carries definite risks.
There are three different mechanisms behind blackouts in freediving:
Duration-induced hypoxia occurs when the breath is held long enough for metabolic activity to reduce the oxygen partial pressure sufficiently to cause loss of consciousness. This is accelerated by exertion, which uses oxygen faster or hyperventilation, which reduces the carbon dioxide level in the blood which in turn may increase the oxygen-haemoglobin affinity thus reducing availability of oxygen to brain tissue towards the end of the dive, and suppress the urge to breathe, making it easier to hold the breath to the point of blackout. This can happen at any depth.
Ischaemic hypoxia is caused by reduced blood flow to the brain arising from cerebral vasoconstriction brought on by low carbon dioxide following hyperventilation, or increased pressure on the heart as a consequence of which can reduce blood circulation in general, or both. If the brain used more oxygen than is available in the blood supply, the cerebral oxygen partial pressure may drop below the level required to sustain consciousness. This type of blackout is likely to occur early in the dive.
Ascent-induced hypoxia is caused by a drop in oxygen partial pressure as ambient pressure is reduced on ascent. The oxygen partial pressure at depth, under pressure, may be sufficient to maintain consciousness but only at that depth and not at the reduced pressures in the shallower waters above or at the surface.
The mechanism for blackout on ascent differs from hyperventilation induced hypocapnia expedited blackouts and does not necessarily follow hyperventilation. However, hyperventilation will exacerbate the risk and there is no clear line between them. Shallow water blackouts can happen in extremely shallow water, even on dry land following hyperventilation and apnoea but the effect becomes much more dangerous in the ascent stage of a deep freedive. There is considerable confusion surrounding the terms shallow and deep water blackout and they have been used to refer to different things, or been used interchangeably, in different water sports circles. For example, the term shallow water blackout has been used to describe blackout on ascent because the blackout usually occurs when the diver ascends to a shallow depth.