Drowning is death as caused by suffocation when a liquid causes interruption of the body's absorption of oxygen from the air leading to asphyxia. The primary cause of death is hypoxia and acidosis leading to cardiac arrest.
Near drowning is the survival of a drowning event involving unconsciousness or water inhalation and can lead to serious secondary complications, including death, after the event. Cases of near drowning are often given attention by medical professionals.
Secondary drowning is death due to chemical or biological changes in the lungs after a near drowning incident.
The pathophysiology of drowningEdit
The body's reaction to submersionEdit
Submerging the face in water triggers the mammalian diving reflex. This is found in all mammals, and especially in marine mammals such as whales and seals. This reflex is designed to protect the body by putting it into energy saving mode to maximize the time it can stay under water. The effect of this reflex is greater in cold water than in warm water and has three principal effects:
- Bradycardia, a slowing of the heart rate of 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 under water than in a comparable situation on dry land.
The reaction to oxygen deprivationEdit
A conscious victim will hold his or her breath (see Apnea) and will try to access air, often resulting in panic, including rapid body movement. This uses up more oxygen in the blood stream and reduces the time to unconsciousness. The victim can voluntarily hold his or her breath for some time, but the breathing reflex will increase until the victim will try 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. During 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 victim 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 from individual to individual and can be increased through training.
The breath-hold break point 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 and a blackout may occur without warning and before the diver feels any urgent need to breathe. This can occur at any depth and is common in distance breath-hold divers in swimming pools, refer to shallow water blackout for more detail. Hyperventilation is often used by both deep and distance free-divers 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.
The reaction to water inhalationEdit
If water enters the airways of a conscious victim the victim will try to cough up the water or swallow it thus inhaling more water involuntarily. Upon water entering the airways, both conscious and unconscious victims experience laryngospasm, that is the larynx or the vocal cords in the throat constrict and seal the air tube. This prevents water from entering the lungs. Because of this laryngospasm, water enters the stomach in the initial phase of drowning and very little water enters the lungs. Unfortunately, this can interfere with air entering the lungs, too. In most victims, the laryngospasm relaxes some time after unconsciousness and water can enter the lungs causing a "wet drowning". However, about 10-15% of victims maintain this seal until cardiac arrest, this is called "dry drowning" as no water enters the lungs. In forensic pathology water in the lungs indicates that the victim was still alive at the point of submersion; the absence of water in the lungs may be either a dry drowning or indicates a death before submersion.
A continued lack of oxygen in the brain, hypoxia, will quickly render a victim unconscious usually around a blood partial pressure of oxygen of 25-30mmHg. An unconscious victim 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 victim stands a good chance of recovery if attended to within minutes. In most victims the laryngospasm relaxes some time after unconsciousness and water fills the lungs resulting in a wet drowning. Latent hypoxia is a special condition leading to unconsciousness where the partial pressure of oxygen in the lungs under pressure at the bottom of a deep free-dive is adequate to support consciousness but drops below the blackout threshold as the water pressure decreases on the ascent, usually close to the surface as the pressure approaches normal atmospheric pressure. A blackout on ascent like this is called a deep water blackout.
Cardiac arrest and deathEdit
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. 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 will die after approximately six minutes without oxygen but special conditions may prolong this (see 'cold water drowning' below). Freshwater contains less salt than blood and will therefore be absorbed into the blood stream by osmosis. In animal experiments this was shown to change the blood chemistry and led to cardiac arrest in 2 to 3 minutes. Sea water is much saltier than blood. Through osmosis water will leave the blood stream and enter the lungs thickening the blood. In animal experiments the thicker blood requires more work from the heart leading to cardiac arrest in 8 to 10 minutes. However, autopsies on human drowning victims show no indications of these effects and there appears to be little difference between drownings in salt water and fresh water. After death rigor mortis will set in and remains for about two days, depending on many factors including water temperature.
Water, regardless of its salt content, will damage the inside surface of the lung, collapse the alveoli and cause edema in the lungs with a reduced ability to exchange air. This may cause death up to 72 hours after a near drowning incident. This is called secondary drowning. Inhaling certain poisonous vapors or gases will have a similar effect.