An air embolism occurs when a bubble of air or other gas enters the bloodstream and travels through the circulatory system. It prevents blood from flowing normally through a vessel. When blood flow is blocked, the tissue supplied by that vessel is deprived of oxygen, which is a serious, potentially life-threatening medical event. The severity depends on the size of the bubble, the speed of its entry, and where it ultimately lodges within the body.
The Physiological Mechanism
The consequences of an air bubble depend primarily on whether it enters the venous or arterial side of the circulation. A Venous Air Embolism (VAE) occurs when air enters a vein, traveling back toward the heart’s right side. From the right ventricle, the air bubble is then pumped into the pulmonary arteries, which carry deoxygenated blood to the lungs.
If the bubble is large, it can become lodged at the outflow tract of the right ventricle, creating a mechanical barrier known as an “air lock.” This obstruction immediately halts the heart’s ability to pump blood forward into the lungs, leading to a sudden and severe drop in cardiac output. Smaller bubbles can pass into the pulmonary arterioles, where they trigger local inflammation and vasoconstriction, raising the pressure within the pulmonary circulation.
An Arterial Air Embolism (AAE) occurs when air travels directly into the systemic circulation, which feeds the major organs. These bubbles can easily travel to the brain, where they block blood flow in the cerebral arteries, leading to a stroke-like event and rapid neurological damage. Air bubbles that enter the coronary arteries can block circulation to the heart muscle itself, resulting in myocardial ischemia or sudden cardiac arrest. In some cases, venous air can cross into the arterial circulation through a Patent Foramen Ovale, an opening between the upper chambers of the heart present in up to 25% of the population.
Sources and Entry Points
For air to enter the circulatory system, there must be a direct opening into a blood vessel and a pressure gradient that favors the air moving inward. Most air embolisms are iatrogenic, meaning they occur as a complication of medical procedures. Any procedure involving the insertion or removal of a central venous catheter carries a risk of air entry, especially if the patient takes a deep breath during the process.
Surgical procedures, particularly those involving the head, neck, or spine, carry an elevated risk because the surgical site may be elevated above the heart. In this position, the pressure within the veins can be lower than atmospheric pressure, causing air to be drawn into the open vessel. Other medical sources include high-pressure injection of contrast agents during imaging or air introduced through an intravenous line.
Non-medical causes often relate to rapid changes in pressure. Scuba diving accidents, where a diver ascends too quickly while holding their breath, can cause the air in the lungs to over-expand and rupture the delicate air sacs, forcing air into the pulmonary veins and resulting in an arterial air embolism. Blunt or penetrating chest trauma can tear lung tissue and blood vessels, allowing air to enter the circulation directly.
The Critical Volume Threshold
The outcome of an air embolism is determined by the rate of air introduction, the total volume, and the final location of the air bubble. In the venous system, a slow introduction of air allows the lungs to filter and absorb the gas, often preventing symptoms.
A rapid infusion of air into the venous system is dangerous. Clinical estimates suggest that an adult may tolerate up to 50 milliliters of air introduced slowly, but volumes ranging from 200 to 300 milliliters are often cited as the lethal dose if introduced rapidly. A rapid infusion of 300 to 500 milliliters of air at a rate of 100 milliliters per second can cause immediate cardiac collapse due to the “air lock” effect.
For arterial air embolisms, because the arterial system directly feeds the most sensitive organs, even a tiny bubble can cause tissue damage. As little as 0.5 milliliters of air entering a coronary artery has been reported to cause ventricular fibrillation and cardiac arrest. The introduction of only 1 to 2 milliliters of air into the cerebral circulation can be fatal due to the brain’s extreme sensitivity to any disruption in oxygen supply.
The location of entry also modifies the risk, as air introduced into veins close to the heart is less likely to be absorbed before reaching the right ventricle. While a few milliliters of air in a small peripheral vein may be harmless, the same volume introduced into a large central vein carries a much higher risk of severe symptoms or death.
Immediate Recognition and Response
Recognizing an air embolism is important, especially when a patient is undergoing a procedure with known risk factors. Symptoms often appear suddenly and are related to the affected organ system. A person may experience acute shortness of breath, chest pain, or a rapid drop in blood pressure.
When the air travels to the brain, neurological symptoms such as confusion, focal weakness, or stroke-like deficits can be the first sign. In a monitored setting, an unexplained drop in the end-tidal carbon dioxide level indicates a venous air embolism, signaling a blockage of blood flow to the lungs. A late-stage physical sign is the “mill-wheel” murmur, a churning sound heard over the heart caused by the mixture of air and blood.
The immediate response involves several steps. The source of air entry must be sealed or clamped immediately to stop the flow of gas into the circulation. High-flow oxygen at 100% is administered, which helps to shrink the nitrogen-containing air bubbles by increasing the pressure gradient for gas absorption into the blood.
For a suspected venous air embolism, the patient is immediately placed in the left lateral Trendelenburg position—lying on the left side with the head tilted downward. This maneuver is intended to trap the air bubble in the non-obstructive apex of the right ventricle, keeping it away from the pulmonary artery outflow tract. For arterial air embolisms, definitive treatment involves hyperbaric oxygen therapy, which uses high pressure to physically compress the air bubbles and accelerate their dissolution back into the bloodstream.