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|Classification and external resources|
|Classification and external resources|
An air embolism, or more generally gas embolism, is a pathological condition caused by a gas bubble, or bubbles, in a vascular system although an embolism in a medical context refers to any large moving mass or defect in the blood stream. Air embolisms may also occur in the xylem of vascular plants, especially when suffering from water stress.
Small amounts of air often get into the blood circulation accidentally during surgery and other medical procedures (for example a bubble entering an intravenous fluid line), but most of these air emboli enter the veins and are stopped at the lungs, and thus a venous air embolism that shows any symptoms is very rare.
For venous air embolisms, death may occur if a large bubble of gas becomes lodged in the heart, stopping blood from flowing from the right ventricle to the lungs (this is similar to vapor lock in engine fuel systems). However, experiments in animals  show that the amount of gas necessary for this to happen is quite variable. Human case reports suggest that injecting more than 100 mL of air into the venous system at rates greater than 100 mL/s can be fatal. Very large and symptomatic amounts of venous air emboli may also occur in rapid decompression in severe diving or decompression accidents, where they may interfere with circulation in the lungs and result in respiratory distress and hypoxia.
Gas embolism into an artery, termed arterial gas embolism (AGE), is a more serious matter than in a vein, because a gas bubble in an artery may directly stop blood flow to an area fed by the artery. The symptoms of 'AGE' depend on the area of blood flow, and may be those of stroke or heart attack if the brain or heart, respectively, is affected. The amount of arterial gas embolism that causes symptoms depends on location - 2 mL of air in the cerebral circulation can be fatal, while 0.5 mL of air into a coronary artery can cause cardiac arrest.
Air embolism can occur whenever a blood vessel is open and a pressure gradient exists favoring entry of gas. Because the circulatory pressure in most arteries and veins is greater than atmospheric pressure, an air embolus does not always happen when a blood vessel is injured. In the veins above the heart, such as in the head and neck, the pressure is less than atmospheric and an injury may let air in. This is one reason why surgeons must be particularly careful when operating on the brain, and why the head of the bed is tilted down when inserting or removing a central venous catheter from the jugular or subclavian veins.
When air enters the veins, it travels to the right side of the heart, and then to the lungs. This can cause the vessels of the lung to constrict, raising the pressure in the right side of the heart. If the pressure rises high enough in a patient who is one of the 20% to 30% of the population with a patent foramen ovale, the gas bubble can then travel to the left side of the heart, and on to the brain or coronary arteries. Such bubbles are responsible for the most serious of gas embolic symptoms.
Trauma to the lung can also cause an air embolism. This may happen after a patient is placed on a ventilator and air is forced into an injured vein or artery, causing sudden death. Breath-holding while ascending from scuba diving may also force lung air into pulmonary arteries or veins in a similar manner, due to the pressure difference.
Air can be injected directly into the veins either accidentally or as a deliberate act. Examples include misuse of a syringe, failure to meticulously remove air from the vascular tubing of a haemodialysis circuit, and industrial injury resulting from use of compressed air. However, the amount of air that would be administered by a single small syringe is, in most cases, not enough to suddenly stop the heart, nor cause instant death. However, such bubbles may occasionally reach the arterial system through a patent foramen ovale, as noted above, and cause random ischemic damage, depending on their route of arterial travel.
There have been rare cases of air embolism being caused by air entering the bloodstream from the uterus or tears in female genitalia. The risk appears to be greater during pregnancy. Cases have been reported that resulted from attempts to perform an abortion by syringing. These appear to have been due to damage to the placenta allowing air to enter the bloodstream. Outside of pregnancy there is at least one case where an air embolism resulted from the insertion of an object into the vagina during masturbation.
As a general rule, any diver who has breathed gas under pressure at any depth who surfaces unconscious, loses consciousness soon after surfacing, or displays neurological symptoms within about 10 minutes of surfacing should be assumed to be suffering from arterial gas embolism.
Symptoms of arterial gas embolism may be present but masked by environmental effects such as hypothermia, or pain from other obvious causes. Neurological examination is recommended when there is suspicion of lung overexpansion injury. Symptoms of decompression sickness may be very similar to, and confused with, symptoms of arterial gas embolism, however, treatment is basically the same.
Discrimination between gas embolism and decompression sickness may be difficult for injured divers, and both may occur simultaneously. Dive history may eliminate decompression sickness in many cases, and the presence of symptoms of other lung overexpansion injury would raise the probability of gas embolism.
A large bubble of air in the heart (as can follow certain traumas in which air freely gains access to large veins) will present with a constant "machinery" murmur. It is important to promptly place the patient in Trendelenburg position (head down)[dubious ] and on their left side (left lateral decubitus position). The Trendelendberg position keeps a left-ventricular air bubble away from the coronary artery ostia (which are near the aortic valve) so that air bubbles do not enter and occlude the cornonary arteries (which would cause a heart attack). Left lateral decubitus positioning helps to trap air in the non-dependent segment of the right ventricle (where it is more likely to remain instead of progressing into the pulmonary artery and occluding it). The left lateral decubitus position also prevents the air from passing through a potentially patent foramen ovale (present in as many as 30% of adults) and entering the left ventricle, from which it could then embolise to distal arteries (potentially causing occlusive symptoms such as stroke).
Administration of high percentage oxygen is recommended for both venous and arterial air embolism. This is intended to counteract ischaemia and accelerate bubble size reduction.
For venous air embolism the Trendelenberg or left lateral positioning of a patient with an air-lock obstruction of the right ventricle may move the air bubble in the ventricle and allow blood flow under the bubble.
Hyperbaric therapy with 100% oxygen is recommended for patients presenting clinical features of arterial air embolism, as it accelerates removal of nitrogen from the bubbles by solution and improves tissue oxygenation. This is recommended particularly for cases of cardiopulmonary or neurological involvement. Early treatment has greatest benefits, but it can be effective as late as 30 hours after the injury.
Bubbles in the bloodstream from any source are dangerous as they can form blockages and precipitate stroke or thrombosis. Pulmonary barotrauma is likely to affect oxygen supply to the brain because bubbles tend to be introduced into the venous system of the lungs where they will not be trapped in the alveolar capillaries, and will consequently be circulated to the rest of the body by the systemic circulation. Gas bubbles arising from decompression sickness are generally formed in the venous side of the systemic circulation, where inert gas concentrations are highest, the bubbles are smaller at first and they are generally trapped in the capillaries of the lungs where they will usually be eliminated without causing symptoms. If they are shunted to the systemic circulation through a patent foramen ovale they can travel to and lodge in the brain where they can cause stroke, or the coronary capillaries where they can cause coronary ischaemia. Decompression bubbles may grow in situ from supersaturated gas in local tissues. The first aid treatment for both is to administer oxygen, treat for shock and transport to hospital; at the hospital both may use a hyperbaric chamber, but otherwise different treatment strategies are used for each condition.
If an arterial gas embolism resulting from patent foramen ovale is suspected, an exam by echocardiography may be performed to diagnose the defect. In this test, very fine bubbles are introduced into a patient's vein by agitating saline in a syringe to produce the bubbles, then injecting them into an arm vein. A few seconds later, these bubbles may be clearly seen in the ultrasound image, as they travel through the patient's right atrium and ventricle. At this time, bubbles may be observed directly crossing a septal defect, or else a patent foramen ovale may be opened temporarily by asking the patient to perform the Valsalva maneuver while the bubbles are crossing through the right heart – an action which will open the foramen flap and show bubbles passing into the left heart. Such bubbles are too small to cause harm in the test, but such a diagnosis may alert the patient to possible problems which may occur from larger bubbles, formed during activities like underwater diving, where bubbles may grow during decompression.
Oxygen first aid treatment is useful for suspected gas embolism casualties or divers who have made fast ascents or missed decompression stops. Most fully closed-circuit rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as an alternative to pure open-circuit oxygen resuscitators. However pure oxygen from an oxygen cylinder through a Non-rebreather mask is the optimal way to deliver oxygen to a decompression illness patient.
Recompression is the most effective, though slow, treatment of gas embolism in divers. Normally this is carried out in a recompression chamber. As pressure increases, the solubility of a gas increases, which reduces bubble size by accelerating absorption of the gas into the surrounding blood and tissues. Additionally, the volumes of the gas bubbles decrease in inverse proportion to the ambient pressure as described by Boyle's law. In the hyperbaric chamber the patient may breathe 100% oxygen, at ambient pressures up to a depth equivalent of 18 msw. Under hyperbaric conditions, oxygen diffuses into the bubbles, displacing the nitrogen from the bubble and into solution in the blood. Oxygen bubbles are more easily tolerated. Diffusion of oxygen into the blood and tissues under hyperbaric conditions supports areas of the body which are deprived of blood flow when arteries are blocked by gas bubbles. This helps to reduce ischemic injury. The effects of hyperbaric oxygen also counteract the damage that can occur with reperfusion of previously ischemic areas; this damage is mediated by leukocytes (a type of white blood cell).
Air embolisms generally occur in the xylem of vascular plants because a fall in hydraulic conductivity results in cavitation. Possible causes of falling hydraulic conductivity include water stress and the freeze-thaw cycle.
A number of physiological adaptations serve to prevent embolisms. These include variations in the length and diameter of vessel elements in different parts of the plant; and the ability to reduce transpiration by closing off leaf stomata.