To the Editor:—
We read with great interest the comprehensive work on vascular embolism by Dr. Mirski et al .1but would like to elaborate on some clinically important points. In some situations, this must include an active therapeutic role for the physician.
The ability of a patient to tolerate gas embolism is critically dependent not only on the volume and rate of accumulation, but also on the type of gas injected. Carbon dioxide, for example, is 25 times more soluble in blood than nitrogen, the primary constituent of air. Carbon dioxide can be carried in the blood not just in the dissolved form, but also takes advantage of bicarbonate buffering and combination with hemoglobin and plasma proteins. Increased solubility and rapid elimination explain why the lethal dose of carbon dioxide is approximately 5 times greater than that of air.2For these reasons, carbon dioxide is often chosen over air for laparoscopy, and because of carbon dioxide’s relative safety, it is used as an intravascular contrast agent for angiography. Radiologists commonly inject carbon dioxide intraarterially and do so safely, although inadvertent contamination of the carbon dioxide with air may lead to embolic complications.3
In addition, the clinician should be aware of the distinction between arterial and venous gas embolism. Even relatively small amounts of intraarterial air can cause bubble obstruction and resultant distal ischemia in at-risk brain or myocardial tissue, leading to stroke or myocardial infarction. Intracardiac air leading to potential arterial air embolism is a common event in open-heart procedures, prompting many surgeons to instill the more soluble carbon dioxide into the chest cavity to displace air before separation from cardiopulmonary bypass.4Venous gas, as well described by Dr. Mirski, often passes into the left heart through a patent foramen ovale and then becomes arterial gas as well. In the supine patient, aortic root gas preferentially flows into the nondependent right coronary artery, eventually leading to the Bezold-Jarisch reflex, bradyarrhythmias, hypotension, and inferior myocardial infarction. Inferior ischemia from this cause can be difficult to manage, although when caused by arterial gas embolism, precordial thumps (or vigorous coughing) have been shown to be effective. The precordial thump physically disrupts large gas bubbles and empties the left heart of these bubbles. Otherwise, the ventricle serves as a gas reservoir, prolonging right coronary artery obstruction as gas exits the left ventricle in small amounts. Precordial thumps lead to nearly complete resolution within two cardiac cycles in the case of carbon dioxide embolism in a pig model.5
Finally, transesophageal echocardiography (TEE) can play a vital role not only in detecting air embolism, but also in managing patients at high risk for embolism. TEE is considered minimally invasive in contrast to the pulmonary artery catheter and has a long track record of safety.6It is the study of choice to determine right-to-left shunt through the atrial septum, which increases the chance of a venous embolism reaching the arterial tree. It can also be used in real time to properly position a central venous catheter. Further, evaluating and treating patients with hemodynamic instability is a class I indication for its use. We agree that TEE requires training to be used effectively; however, more and more anesthesiologists are developing this skill and are routinely using it for cardiac and other complex cases.
Gas embolism should be recognized quickly in the appropriate setting, especially if TEE is ongoing in an operative patient, and prompt therapy should be applied. If aortic root gas is probable or known through the use of TEE or another definitive method, several prompt precordial thumps are justified if symptoms are severe.
*The Texas A&M University System Health Science Center College of Medicine, Scott & White Hospital, Temple, Texas. email@example.com