<unk>  can be considered as going through four stages: # Breath-hold under voluntary control until the urge to breathe due to hypercapnia becomes overwhelming # Fluid is swallowed and/or aspirated into the airways # Cerebral anoxia stops breathing and aspiration # Cerebral injury due to anoxia becomes irreversible Generally, in the early stages of<unk> , a person holds their breath to prevent water from entering their lungs. When this is no longer possible, a small amount of water entering the trachea causes a muscular spasm that seals the airway and prevents further passage of water. If the process is not interrupted, loss of consciousness due to hypoxia is followed rapidly by cardiac arrest. Oxygen deprivation A conscious person will hold their breath (see Apnea) and will try to access air, often resulting in panic, including rapid body movement. This uses up more oxygen in the bloodstream and reduces the time until unconsciousness. The person can voluntarily hold his or her breath for some time, but the breathing reflex will increase until the person tries to breathe, even when submerged. The breathing reflex in the human body is weakly related to the amount of oxygen in the blood but strongly related to the amount of carbon dioxide (see Hypercapnia). During an apnea, the oxygen in the body is used by the cells and excreted as carbon dioxide. Thus, the level of oxygen in the blood decreases, and the level of carbon dioxide increases. Increasing carbon dioxide levels lead to a stronger and stronger breathing reflex, up to the breath-hold breakpoint, at which the person can no longer voluntarily hold his or her breath. This typically occurs at an arterial partial pressure of carbon dioxide of 55 mm Hg but may differ significantly between people. The breath-hold breakpoint can be suppressed or delayed, either intentionally or unintentionally. Hyperventilation before any dive, deep or shallow, flushes out carbon dioxide in the blood resulting in a dive commencing with an abnormally low carbon dioxide level; a potentially dangerous condition known as hypocapnia. The level of carbon dioxide in the blood after hyperventilation may then be insufficient to trigger the breathing reflex later in the dive. Following this, a blackout may occur before the diver feels an urgent need to breathe. This can occur at any depth and is common in distance breath-hold divers in swimming pools. Both deep and distance free divers often use hyperventilation to flush out carbon dioxide from the lungs to suppress the breathing reflex for longer. It is important not to mistake this for an attempt to increase the body's oxygen store. The body at rest is fully oxygenated by normal breathing and cannot take on any more. Breath-holding in water should always be supervised by a second person, as by hyperventilating, one increases the risk of shallow water blackout because insufficient carbon dioxide levels in the blood fail to trigger the breathing reflex. A continued lack of oxygen in the brain, hypoxia, will quickly render a person unconscious, usually around a blood partial pressure of oxygen of 25–30 mmHg. An unconscious person rescued with an airway still sealed from laryngospasm stands a good chance of a full recovery. Artificial respiration is also much more effective without water in the lungs. At this point, the person stands a good chance of recovery if attended to within minutes. More than 10% of<unk> s may involve laryngospasm, but the evidence suggests that it is not usually effective at preventing water from entering the trachea. The lack of water found in the lungs during autopsy does not necessarily mean there was no water at the time of<unk> , as small amounts of freshwater are readily absorbed into the bloodstream. Hypercapnia and hypoxia both contribute to laryngeal relaxation, after which the airway is effectively open through the trachea. There is also bronchospasm and mucous production in the bronchi associated with laryngospasm, and these may prevent water entry at terminal relaxation. The hypoxemia and acidosis caused by asphyxia in<unk>  affect various organs. There can be central nervous system damage, cardiac arrhythmia, pulmonary injury, reperfusion injury, and multiple-organ secondary injury with prolonged tissue hypoxia. A lack of oxygen or chemical changes in the lungs may cause the heart to stop beating. This cardiac arrest stops the flow of blood and thus stops the transport of oxygen to the brain. Cardiac arrest used to be the traditional point of death, but at this point, there is still a chance of recovery. The brain cannot survive long without oxygen, and the continued lack of oxygen in the blood, combined with the cardiac arrest, will lead to the deterioration of brain cells, causing first brain damage and eventually brain death from which recovery is generally considered impossible. The brain will die after approximately six minutes without oxygen at normal body temperature, but hypothermia of the central nervous system may prolong this. The extent of central nervous system injury to a large extent determines the survival and long term consequences of<unk> , In the case of children, most survivors are found within 2 minutes of immersion, and most fatalities are found after 10 minutes or more. Water aspiration If water enters the airways of a conscious person, the person will try to cough up the water or swallow it, often inhaling more water involuntarily. When water enters the larynx or trachea, both conscious and unconscious persons experience laryngospasm, in which the vocal cords constrict, sealing the airway. This prevents water from entering the lungs. Because of this laryngospasm, in the initial phase of<unk> , water generally enters the stomach, and very little water enters the lungs. Though laryngospasm prevents water from entering the lungs, it also interferes with breathing. In most persons, the laryngospasm relaxes sometime after unconsciousness, and water can then enter the lungs, causing a "wet<unk> ." However, about 7–10% of people maintain this seal until cardiac arrest. This has been called "dry<unk> ", as no water enters the lungs. In forensic pathology, water in the lungs indicates that the person was still alive at the point of submersion. An absence of water in the lungs may be either a dry<unk>  or indicates a death before submersion. Aspirated water that reaches the alveoli destroys the pulmonary surfactant, which causes pulmonary edema and decreased lung compliance, compromising oxygenation in affected parts of the lungs. This is associated with metabolic acidosis, secondary fluid, and electrolyte shifts. During alveolar fluid exchange, diatoms present in the water may pass through the alveolar wall into the capillaries to be carried to internal organs. The presence of these diatoms may be diagnostic of<unk> . Of people who have survived<unk> , almost one-third will experience complications such as acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). ALI/ARDS can be triggered by pneumonia, sepsis, and water aspiration and are life-threatening disorders that can result in death if not treated promptly. During<unk> , aspirated water enters the lung tissues, causes a reduction in alveolar surfactant, obstructs ventilation, and triggers a release of inflammatory mediators which ultimately results in hypoxia. Specifically, upon reaching the alveoli, hypotonic liquid found in freshwater dilutes pulmonary surfactant, destroying the substance. Comparatively, aspiration of hypertonic seawater draws liquid from the plasma into the alveoli and similarly causes damage to surfactant by disrupting the alveolar-capillary membrane. Still, there is no clinical difference between salt and freshwater<unk> . Once someone has reached definitive care, supportive care strategies such as mechanical ventilation can help to reduce the complications of ALI/ARDS. Whether a person drowns in freshwater versus salt water makes no difference in respiratory management or the outcome of the person. People who drown in freshwater may experience worse hypoxemia early in their treatment, however, this initial difference is short-lived and the management of both fresh water and salt water<unk>  is essentially the same. Cold-water immersion Submerging the face in water cooler than about triggers the diving reflex, common to air-breathing vertebrates, especially marine mammals such as whales and seals. This reflex protects the body by putting it into energy-saving mode to maximise the time it can stay underwater. The strength of this reflex is greater in colder water and has three principal effects: * Bradycardia, a slowing of the heart rate by up to 50% in humans. * Peripheral vasoconstriction, the restriction of the blood flow to the extremities to increase the blood and oxygen supply to the vital organs, especially the brain. * Blood Shift, the shifting of blood to the thoracic cavity, the region of the chest between the diaphragm and the neck, to avoid the collapse of the lungs under higher pressure during deeper dives. The reflex action is automatic and allows both a conscious and an unconscious person to survive longer without oxygen underwater than in a comparable situation on dry land. The exact mechanism for this effect has been debated and may be a result of brain cooling similar to the protective effects seen in people who are treated with deep hypothermia. The actual cause
Drowning
Arrhythmia
Heat stroke
Hypoglycemia
Sudden wealth syndrome
Murder
Heat exhaustion
Seizure