Venous Air Embolism Treatment & Management

Updated: Dec 30, 2017
  • Author: Brenda L Natal, MD, MPH; Chief Editor: Erik D Schraga, MD  more...
  • Print

Emergency Department Care

If venous air embolism (VAE) is known about before presentation to the emergency department (ED), affected patients should be transported in the left lateral decubitus position. [7]

Management of VAE, once it is suspected, includes identification of the source of air, prevention of further air entry (by clamping or disconnecting the circuit), reduction of the volume of air entrained, and hemodynamic support. 

Administer 100% O2 and perform endotracheal intubation for severe respiratory distress or refractory hypoxemia or in a somnolent or comatose patient in order to maintain adequate oxygenation and ventilation. Institution of high-flow (100%) O2 will help reduce the bubble's nitrogen content and therefore size. [1, 4, 7, 10, 11, 15, 23, 30]

Immediately place the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg position. This helps to prevent air from traveling through the right side of the heart into the pulmonary arteries, leading to right ventricular outflow obstruction (air lock). If cardiopulmonary resuscitation (CPR) is required, place the patient in a supine and head-down position. [1, 7, 11, 15, 23]

Direct removal of air from the venous circulation by aspiration from a central venous catheter in the right atrium may be attempted. However, no current data support emergency catheter placement for air aspiration during an acute setting of VAE-induced hemodynamic instability. [1, 4, 11, 15]

If necessary, initiate CPR. Besides maintaining cardiac output, CPR may also serve to break large air bubbles into smaller ones and force air out of the right ventricle into the pulmonary vessels, thus improving cardiac output. Even without the need for CPR, this rationale holds for closed-chest massage. Animal studies have shown that the benefit of cardiac massage equals that of left lateral recumbency, as well as intracardiac aspiration of air. [1, 4, 11, 15]

Admit patients to the intensive care unit (ICU), as they may develop cardiopulmonary distress/failure following VAE.

Consider transfer to a hyperbaric oxygen therapy (HBOT) facility. Indications for HBOT include neurologic manifestations and cardiovascular instability. Potential benefits include compression of existing bubbles, establishing a high diffusion gradient to speed resolution of existing bubbles, improved oxygenation of ischemic tissues, and lowered intracranial pressure.

Immediate HBOT, once VAE is diagnosed, is recommended; however, prognosis may still be good if therapy is initiated beyond 6 hours of event. Prompt transfer to an HBOT center has been reported to decrease mortality in patients with cerebral air embolism. If transfer is necessary, ground transportation is preferred. If air transportation cannot be avoided, the lowest altitude should be sought. [1, 4, 7, 11, 14, 15, 18, 42]

Supportive therapy should include fluid resuscitation (to increase intravascular volume, increase venous pressure and venous return). There is also some evidence that gas emboli may cause a relative hemoconcentration, which increases viscosity and impairs the already compromised circulation. Hypovolemia is less tolerated than relative anemia. In animal studies, moderate hemodilution to a hematocrit of 30% reduces neurologic damage. Crystalloids may cause cerebral edema; therefore, colloids are preferred for hemodilution. [1, 4, 18]

The administration of vasopressors and mechanical ventilation are two other supportive measures that may be necessary. [1, 4, 41] In a case report of a patient undergoing a craniotomy who showed cardiopulmonary findings suggestive of acute VAE, inotropic treatment with ephedrine seemed to rapidly reverse the cardiopulmonary abnormalities. Early inotropic support of the right ventricle has been recommended if venous air embolism is suspected. [41]

In animal studies, the use of perfluorocarbons (FP-43) has been shown to enhance the reabsorption of bubbles and the solubility of gases, thereby decreasing both neurologic and cardiovascular complications of systemic and coronary VAE. These benefits, however, have not been validated in humans. [1]



The optimal management of VAE is prevention. Minimizing the pressure gradient between the site of potential entry and the right atrium is essential in prevention of VAE.

Potential measures to reduce the risk and/or severity of VAE during neurosurgical interventions include the following [38] :

  • Using a modified semisitting or lounging position for the patient, in which the head is lower than the legs to create a positive pressure in the transverse and sigmoid sinuses
  • Avoiding hyperventilation in the sitting position
  • Using a sitting position, under strict protocol, for procedures in patients with known patent foramen ovale 

Measures to reduce the risk of air embolism during mechanical ventilation and central line insertion/removal/manipulation should be taken. With regard to these two procedures, the following interventions should be implemented:

  • Prevent barotraumas by minimizing airway pressures during mechanical ventilation
  • Avoid positive end-expiratory pressure (PEEP); it impairs hemodynamic performance, does not protect against air embolism, and probably increases the risk of paradoxic emboli
  • Avoid and treat hypovolemia prior to catheter placement
  • Occlude the needle hub during catheter insertion/removal
  • Maintain all connections to the central line closed/locked when not in used (use Luer-Lok syringes for blood draws from catheters)
  • During catheter insertion/removal, place the patient in the supine position with head lowered (insertion site should be 5 cm below right atrium); if the patient is awake he or she may assist by holding his or her breath or by doing a Valsalva maneuver, both of which can increase the central venous pressure