Venous Air Embolism

Definition

Air can enter the venous circulation when there is a negative pressure gradient between the right atrium and the upper area of incision or the air’s point of entrance. The pressure may be due to gravitational forces, and Albin and coworkers have reported that a 5.0 cm H ₂ O gravitational gradient was sufficient to entrain air in a neurosurgical case. Negative pressure gradients can also be due to increased ambient pressure as noted with various endoscopic procedures (gastrointestinal, ophthalmologic, etc.) where gases are employed as the pressurizing medium or where a narrow beam of fluid or gas may have a destructive (jet) effect on tissue aside from the response to an elevated pressure environment. The entry of a bolus of 100 mL of air into the venous circulation can be fatal, and it has been calculated that this volume of air can pass through a 14-gauge needle with a gradient of 5.0 cm H ₂ O in a matter of seconds. Factors modifying air entrainment include body position, depth of ventilation, volume of air entering the vessel, rate of gaseous entry, and composition and concentration of gases in the inhaled anesthetic mixture. Animal studies and human cases have shown that the transpulmonary passage of air can occur without a patent foramen ovale. Reduced central venous pressure due to a contracted blood volume (hemorrhagic hypovolemia), or decreased intrathoracic pressure due to the use of a table or frame to reduce abdominal compression, can help increase the gravitational pressure gradient and enhance the entrainment of air.

The fate of entrained air is illustrated in Fig. 186.1 . In the first case synopsis, the gravitational gradient was probably less than 10.0 cm H ₂ O, but was enhanced by blood loss and use of an orthopedic frame that reduced abdominal pressure, thus allowing the development of negative intrathoracic pressure with expiration. Because 50% nitrous oxide (N ₂ O) was used, this increased the air bubble size by a factor of about 2. Autopsy revealed air in the right side of the heart.

In the second case synopsis, a 6-year old child sustained four separate episodes of VAE while undergoing posterior fossa exploration with a considerable gravitational gradient. Although the anesthetic management in this case appears to be optimal, it appears that impeccable hemostasis was not carried out along with borders of the scalp incision. Hagen and coworkers studied the incidence of probe patent foramen ovale (PFO) in 965 normal hearts and noted an incidence of 27.3%, with the mean PFO diameter being 5.0 mm, making the pediatric population at high risk for paradoxic air embolism. It must be emphasized that because of solubility factors, air bubble size can be increased with the use of nitrous oxide, and at a 50% N ₂ O–O ₂ concentration, the entering air bubble volume is doubled, which may have occurred in the first case. In the second case synopsis, because of the large gravitational gradient, we are concerned that if VAE occurs in the presence of a probe PFO, air might pass into the coronary arteries in the left side of the heart and/or the cerebral vessels.

These cases demonstrate that VAE can occur in any position, as long as a pressure gradient allows the ingress of air between the procedural area and the heart. Evidence has accumulated that VAE is far from rare in patients undergoing procedures in the prone position, especially spinal procedures; there have been at least 22 cases reported, with a total of 13 deaths, 10 of which were in the pediatric age group ( ). In addition to neurosurgery, VAE has been reported with virtually all surgeries and endoscopy as well. It also occurs with catheterization for cardiac or central vascular access, arteriovenous shunts, intravenous infusions, and transfusion therapy.

Recognition

Physical signs and symptoms include gasping respiration in spontaneously breathing patients, increased central venous and pulmonary artery pressures, cardiac arrhythmias, electrocardiographic (ECG) changes, hypotension, abnormal heart sounds, changes in heart rate, decreased peripheral resistance, reduced cardiac output, cyanosis, a mill-wheel murmur, and cardiac arrest. Increased pulmonary artery pressure is the most prominent physical sign of VAE during controlled ventilation, irrespective of the volume or rate of air entrainment. The more rapidly air enters the pulmonary circulation, the more rapidly and severely the pulmonary artery pressure will rise. If it rises dramatically over the systemic pressure, a right-to-left shunt can occur through a septal defect (i.e., PFO) and cause paradoxic embolism of air into the left side of the heart. The ECG changes with air embolism are quite variable and include tachyarrhythmias, varying degrees of atrioventricular block, right ventricular strain, and ST-segment changes. Very large volumes of entrained air may cause such severely increased right ventricular afterload that the right ventricle becomes ischemic and fails acutely. Right-sided heart failure is the primary cause of acute hypotension, reduced cardiac output, and cardiac arrest after massive air embolism. A mill-wheel murmur indicates that a significant volume of air has entered the right-sided heart chambers. If so, cardiac arrest may be imminent. Air causes this churning sound and is one of the last signs observed before cardiac arrest.

Besides physical signs and symptoms, the other methods for detecting intraoperative air embolism, in order of sensitivity, are transesophageal echocardiography (TEE), precordial Doppler ultrasonography, ETCO ₂ , pulmonary artery catheter, pulse oximetry, and direct observation of the surgical site. TEE can detect both venous and paradoxic air embolism consisting of as little as 0.02 mL/kg of air. However, it is costly and may be inaccessible in some surgical locations; it has no audible alarms and may be difficult for solo practitioners to use when they are occupied with urgent patient care duties. A well-positioned precordial Doppler probe detects 0.05 mL/kg of intravascular air, is noninvasive, and alerts both the anesthesiologist and the surgeon simultaneously. As mentioned, although pulmonary artery catheters can show early and prominent signs of air embolism, they are highly invasive and less sensitive than precordial Doppler.

A sudden reduction in ETCO ₂ concentration is the most convenient and widely used noninvasive method for detecting air embolism. The magnitude and duration of the decrease in ETCO ₂ correlate positively with the volume of air entrained, and detection is possible during any general anesthetic. In contrast, pulse oximetry is relatively insensitive, because decreases in arterial oxygen saturation often occur late with a decrease in arterial oxygen tension. Further, the surgical field is often overlooked, especially in high-risk surgery where it may be easy to note whether there is a lack of venous oozing, indicating subatmospheric venous pressure. In high-risk procedures, combined precordial Doppler ultrasonography and ETCO ₂ monitoring should be used as Doppler tone activation and reduced ETCO ₂ signal air entrainment. VAE is confirmed if gas bubbles can be aspirated from a central line.