Venous Air Embolism Workup

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

Laboratory tests are neither sensitive nor specific for the diagnosis of venous air embolism (VAE). The only indication for obtaining routine laboratory tests is to evaluate the associated end-organ injury resulting from air embolism.

Extravasation of fluid into inflamed tissue may result in laboratory findings consistent with intravascular depletion.

Arterial blood gas samples often show hypoxemia, hypercapnia, and metabolic acidosis secondary to right-to-left pulmonary shunting.

Patients may develop a clinical picture similar to that of classic pulmonary embolism, with hypoxia, decreased PCO2 levels, and respiratory alkalosis.


Imaging Studies

Transesophageal echocardiography 

Transesophageal echocardiography (TEE) has the highest sensitivity for detecting the presence of air in the right ventricular outflow tract or major pulmonary veins. It can detect as little as 0.02 mL/kg of air administered by bolus injection. [1, 2, 5, 11, 15, 18, 22, 23, 38] It also has the added advantage of identifying paradoxical air embolism (PAE), and Doppler allows audible detection of venous air embolism (VAE).

Echocardiography, both TEE and transthoracic echocardiography (TTE), not only allows diagnosis of VAE but also aids in the diagnosis of cardiac anomalies, assessment of volume status, pulmonary hypertension, and cardiac contractility, thereby allowing exclusion of other causes of hypotension, dyspnea, and aiding in further patient management. The use of bedside TTE has become more common in emergency medicine. Its use in a case of VAE described by Maddukuri et al aided in the diagnosis and prompt initiation of appropriate therapy. [39]

Doppler ultrasonography

Precordial Doppler ultrasonography is the most sensitive noninvasive method for detecting venous air emboli. This modality is capable of detecting as little as 0.12 mL of embolized air (0.05 mL/kg). [1, 15, 22, 23, 38]

Transcranial Doppler ultrasonography is another imaging modality commonly used to detect cerebral microemboli. [1]


Chest radiography may be normal or may show gas in the pulmonary arterial system, pulmonary arterial dilatation, focal oligemia (Westermark sign), and/or pulmonary edema. [11, 15, 22]

CT and MRI

Computed tomography (CT) can detect air emboli in the central venous system (especially the axillary and subclavian veins), right ventricle, and/or pulmonary artery. Small (< 1 mL) air defects, usually asymptomatic, occur during 10-25% of contrast-enhanced CT scans; thus, the specificity of this modality is best with large filling defects. [1, 11] CT of the head may show intracerebral air, cerebral edema, or infarction. Chest CT in lung trauma may show underlying conditions such as pneumothorax, hemothorax, or emphysematous blebs that may have led to air embolism but is not helpful for initial diagnosis. [40]

MRI of the brain may show increased water concentration in affected tissues, but this finding alone may not be reliable for the detection of gas emboli.


Other Tests


Electrocardiography (ECG) has a low sensitivity for VAE detection. The findings closely resemble those seen with venous thromboembolism and include tachycardia, right ventricular strain pattern, and ST depression. Transient myocardial ischemia may also occur (severe bradycardia, ST elevation in inferior leads and ST depression in L1 and avL, observed 3 minutes post CVC removal (case report). [1, 37]

End-tidal carbon dioxide (ETCO2)

VAE leads to ventilation/perfusion (V/Q) mismatching and increases in physiologic dead space. This produces a fall in end-tidal CO2 (normal value, < 5). A 2 mm Hg change in end-tidal carbon dioxide (ETCO2) can be an indicator of VAE. However, this finding is nonspecific and may also occur with other disease states, such as pulmonary embolism (PE), massive blood loss, hypotension, circulatory arrest, upper-airway obstruction, mouth breathing, and/or disconnection from monitor. The detector also has a slow response time. [1, 4, 15, 22, 23]

End-tidal nitrogen (ETN2)

End-tidal nitrogen (ETN2) is the most sensitive gas-sensing VAE detection modality; it measures increases in ETN2 as low as 0.04%. Response time is much faster than ETCO2 (30-90 s earlier). However, it does not detect subclinical VAE or decreases with hypotension and may falsely indicate resolution of VAE too prematurely. [1, 41]

Pulse oximetry

Changes in oxygen saturation are late findings with VAE. Measurement is often skewed secondary to exposure to high fraction of inspired oxygen. Like carbon dioxide measuring, it is on the lower end of sensitive measurements. [1]

Pulmonary artery catheter

A pulmonary artery catheter can detect increases in pulmonary artery pressures, which may be secondary to mechanical obstruction or vasoconstriction from the hypoxemia induced by the VAE. However, it is a relatively insensitive/nonspecific monitor of air entrainment (0.25 mL/kg). [1] The lumen catheter is also too small for air to be removed, thereby limiting its function.

Central venous catheter

If a central venous catheter is in place, aspiration of air may help to make the diagnosis. It is also helpful in monitoring central venous pressures, which may be increased in VAE. [1]



Any procedure posing a risk for VAE, if in progress, should be aborted immediately once VAE is suspected.

During central venous catheter (CVC) insertion/removal, one attempt at aspirating air back from line may be useful. Prior to aspiration, the tip of the CVC should be optimally placed 2 cm below the junction of the superior vena cava and the right atrium; however, it may have to be advanced to optimize results.

The placement of a CVC (multiorifice) or PA catheter to attempt aspiration of air, if not already done, has been recommended by several authors. [1, 4, 18, 22, 41] When appropriately placed, it may be possible to aspirate approximately 50% of the entrained air with a right atrial catheter.

Catheter removal should be performed with the patient supine or in a Trendelenburg position while holding his/her breath at the end of inspiration or during a Valsalva maneuver. [2, 14, 22]

In the event of circulatory collapse, cardiopulmonary resuscitation (CPR) should be initiated in order to maintain 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. [18]

If an arrest is refractory to CPR, an immediate thoracotomy in the emergency department (ED) may be indicated. An emergency thoracotomy with clamping of the hilum of the injured lung is currently recommended for SAE-associated with unilateral lung injury. This prevents continued passage of air into the coronary, cerebral, and other systemic arteries. [11, 18]

Other measures include cross-clamping the aorta, cardiac massage, and aspirating air from the left ventricle, aortic roots, and pulmonary veins. [11]