Venous Air Embolism

Keith J Ruskin, MD
Assistant Professor of Anesthesia
Yale University School of Medicine


Air embolism can occur during any surgical procedure in which the operative site is 5 cm or higher above the right atrium. It incidence has been reported to be 35% in sitting craniotomies (occurrence rates of nearly 100% have recently been reported). Air embolism can also occur during surgical procedures involving the head and neck (i.e., neck dissection), vaginal delivery and caesarean section, and spinal instrumentation procedures. It has also been reported to occur during liver transplantation.


Because of the near 100% likelihood of air embolism during sitting craniotomies, some type of monitoring for air embolism during this procedure is essential.

Doppler ultrasound is the most sensitive noninvasive monitor, and is commonly used. The monitor uses ultrahigh frequency sound waves (usually between 2 and 3 megahertz) to measure blood flow velocity and changes in blood density. This information is converted to a characteristic sound.

The Doppler ultrasound monitor is useful because it detects air before it enters the pulmonary circulation. The characteristic sound of venous air embolism is readily identifiable, even when the anesthesiologist is attending to other tasks in the operating room. [Sound]

The Doppler ultrasound is not quantitative, however, and may be difficult to place on some patients, especially those with a chest wall deformity or who are obese. The Doppler is overly sensitive, and does not differentiate between a massive air embolism and a physiologically insignificant embolism. Crystallized mannitol may mimic intravascular air. The Doppler does not function during electrocautery because of radio frequency interference, and is unable to detect air embolism during that time.

Transesophageal echocardiography is more sensitive than Doppler ultrasound, and is also more invasive and technically more difficult to place and to interpret. It does, however, allow determination of the volume of air aspirated. Transesophageal echocardiography will also show air passing through a patent foramen ovale into the left atrium and into the systemic circulation.


A "four-chamber" view. The right atrium is in the upper left corner of the picture. The central venous catheter can be seen as a small dot in the center of the atrium.


Another four-chamber view recorded during dissection of a vascular tumor. Air bubbles are visible as a "snow-storm" appearance in the right atrium. Note that no air is crossing into the left atrium. (The left atrium is above and to the right of the right atrium.)

The pulmonary artery catheter is the next most sensitive monitor. Air entering the pulmonary circulation causes mechanical obstruction and reflex vasoconstriction due to pulmonary hypoxemia. The pulmonary artery catheter is easy to place in experienced hands, but is invasive. Its disadvantages are that its small lumen makes air aspiration difficult, placement for air aspiration may not allow PCWP measurement, and increases in PA pressure are not specific for air.

Mass spectrometry for end-tidal nitrogen is as sensitive as the pulmonary artery catheter. It is highly specific for air, but is not widely available. The concentration of exhaled nitrogen is usually less then 2%, and is below the threshhold of some commercial mass spectrometers.

End-tidal carbon dioxide is commonly used, widely available, and sensitive. It is not specific for air embolism, however. Hyperventilation, low cardiac output, other types of emboli, and COPD can also decrease ETCO2.

The least sensitive monitor is the precordial or esophageal stethoscope. A "millwheel murmur" indicates a massive air embolism. When a millwheel murmur is heard, cardiovascular collapse is imminent.

A multiorifice central venous catheter should be placed in patients at risk of air embolism. The optimal site for the tip of the catheter is at the SVC-RA junction. If an embolus occurs, air can be aspirated through the catheter before it enters the pulmonary circulation.


Venous air embolism produces several effects. Pulmonary microvascular occlusion results in increased dead space. Bronchoconstriction may result from release of endothelial mediators, complement production, and cytokine release. A large, rapidly-entrained bolus of air can fill the right atrium with air and cause an air lock, which leads to obstruction of the right ventricular outflow tract, decreased venous return, and decreased cardiac output. Myocardial and cerebral ischemia soon follow.

Morbidity and mortality from air embolism are directly related to the size of the embolus and the rate of entry. Doses of air greater than 50 ml (1 ml/kg) cause hypotension and dysrhythmias. 300 ml of air entrained rapidly can be lethal. Bronchoconstriction results in increased airway pressure, and wheezing. Other manifestations of air embolism include hypoxemia, hypercapnia and decreased ETCO2 (due to increased functional dead space). Hypotension, cardiac dysrhythmias, and cardiovascular collapse occur as air entrainment continues.


Treatment of air embolism is largely supportive. The surgeon should be informed as soon as the diagnosis is made. N2O diffuses into air bubbles faster than nitrogen can diffuse out, and increases the size of the bubble. If N2O is used, it should be discontinued when an air embolism occurs. FiO2 should be increased to 1.0. The surgeon should flood the surgical field with fluids while open veins are cauterized or exposed bone is waxed. If significant amounts of air have entered the circulation, the jugular veins should be manually occluded. This will prevent additional air from being entrained while the surgeons obtain hemostasis. The blood pressure should be supported with fluid and vasopressors.

If possible, the operative site should be positioned below the level of the heart. This can be done by tilting the table into the Trendelenberg position. This will increase venous pressure at the operative site and reduce air entrainment. If a large volume of air has been entrained, and surgical conditions permit (i.e., the head is not in pins), positioning the patient in the left lateral decubitus position will help to keep air in the right atrium from entering the ventricle. The right atrial catheter should be aspirated until no more air can be obtained.

If the air embolism is treated promptly and the ETCO2 and pulmonary artery pressures (if monitored) return to normal, then N2O can be carefully reintroduced while monitoring the doppler, ETCO2 and PAP.


Preventive strategies include elevating the head only as much as necessary to obtain adequate exposure. The patient should be hydrated to increase CVP, which decreases the risk of embolism, and to increase LAP, which minimizes the risk of paradoxical embolism to the left side of the circulation. The surgeons should be meticulous about cauterizing and tying blood vessels and applying bone wax.

The use of PEEP during surgery is controversial. Although small amounts of PEEP (5 - 10 cm H20) may reduce the risk of air entrainment, sudden loss of PEEP with air in the right side of the heart (as may happen if the endotracheal tube is disconnected from the anesthesia circuit) may result in a paradoxical air embolus.

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