Drowning pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


The Body's Reaction to Submersion

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.

Fresh Water vs. Salt Water Drowning

Although fresh-water drowning is often associated with aspiration of water into the lungs, the cause of death is not due to either hypoxia or pulmonary edema. When fresh water enters the lungs it is pulled into the pulmonary circulation via the alveoli because of the low capillary hydrostatic pressure and high colloid osmotic pressure. Consequently, the plasma is diluted and the hypotonic environment causes red blood cells to burst (hemolysis). The resulting elevation of plasma K+ level and depression of Na+ level, due to the hemolysis, alter the electrical activity of the heart. Ventricular fibrillation often occurs as a result of these electrolyte changes. Additionally, if drowning occurs in very cold water ( <10o C), the uptake of cold water into the vascular system can stop the heart. In open heart surgery, the technique of pouring cold saline solution over the heart is used to prevent heart action. If the victim is resucitated death can occur hours later due to renal failure. During hemolysis, hemoglobin is also released into the plasma which can accumulate in the kidneys leading to acute renal failure. In contrast, salt-water drowning does not lead to uptake of inspired water into the vascular system because it is isotonic to blood. Therefore, no red cell hemolysis occurs and the cause of death is asphyxia.

The Reaction to Oxygen Deprivation

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 Inhalation

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 Death

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.

Secondary Drowning

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.

Dry Drowning

The pathophysiology of this form of pulmonary oedema is multifactorial.

In normal breathing, the diaphragm contracts, causing it to drop and increase the volume of the chest. This increase in volume causes a partial vacuum, which draws air into the lungs from the outside. During laryngospasm, the person's larynx spasms shut. As a result, the partial vacuum created by contracting the diaphragm cannot be filled by the inrush of air into the lungs, and the vacuum persists. In an attempt to force air in through the spasmed larynx, the person may contract the diaphragm further, but this only increases the partial vacuum inside the chest.

The heart continues to beat during this time, and blood continues to flow, though it can neither pick up oxygen nor drop off carbon dioxide in the lungs. The volume of blood in the chest can increase, however, by pulling in more blood from the abdomen, head, arms and legs - abnormally large volumes of this blood enter the chest via the superior and inferior vena cavae (great veins) in response to the persistent partial vacuum. From the vena cavae, the increased volume of blood flows through the right atrium and into the right ventricle. The volume of blood is great enough to stretch out the ventricle, similar to water entering a balloon.

The ventricle typically responds to this increased volume of blood by contracting and pumping with increased strength - a phenomenon known as the Frank-Starling mechanism. On being ejected from the right ventricle, the blood is forced into the pulmonary artery and thence to the lungs.

In the lungs, the nature of the vasculature changes. The vessels become extremely narrow - narrow enough that red blood cells have to pass though in single file. The walls of the vasculature also become extremely thin to allow oxygen to enter the blood and carbon dioxide to leave it. In the case of dry drowning, however, there is no oxygen available in the lungs; there is only a partial vacuum. This partial vacuum draws some of the fluid from the vasculature and into the airspaces of the lungs, creating pulmonary oedma.

At the same time, the sympathetic nervous system responds to the emergency of the closed larynx. Among other things, it constricts much of the body's vasculature. This vasoconstriction increases the pressure against which the left ventricle must pump, and may cause enough backpressure to ripple back through the left ventricle, into the left atrium, and into the pulmonary vasculature. This additional pressure on the blood in the lungs' blood vessels exacerbates the oedema described above.

Additionally, the actions of the sympathetic nervous system can damage the lungs' vasculature, allowing even more fluid to escape into the lungs' airspaces.


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