Venous Air Embolism

Venous Air Embolism

Venous air embolism (VAE), a subset of gas embolism, is an entity with the potential for severe morbidity and mortality. Venous air embolism is a predominantly iatrogenic complication that occurs when atmospheric gas is introduced into the systemic venous system. More recently, venous air embolism has been associated with central venous catheterization, penetrating and blunt chest trauma, high-pressure mechanical ventilation, thoracocentesis, hemodialysis, and several other invasive vascular procedures. The use of gases such as carbon dioxide and nitrous oxide during medical procedures and exposure to nitrogen during diving accidents can also result in VAE.


Two preconditions must exist for venous air embolism to occur: (1) a direct communication between a source of air and the vasculature and (2) a pressure gradient favoring the passage of air into the circulation. The key factors determining the degree of morbidity and mortality in venous air emboli are related to the volume of gas entrainment, the rate of accumulation, and the the systemic venous circulation puts a substantial strain on the right ventricle, especially if this results in a significant rise in pulmonary artery (PA) pressures. This increase in PA pressure can lead to right ventricular outflow obstruction and further compromise pulmonary venous return to the left heart. The diminished pulmonary venous return will lead to decreased left ventricular preload with resultant decreased cardiac output and eventual systemic cardiovascular collapse. With venous air embolism (VAE), resultant tachyarrhythmias are frequent, but bradyarrhythmias can also occur.


The potentially life-threatening and catastrophic consequences of venous air embolism (VAE) are directly related to its effects on the affected organ system where the embolus lodges. VAE may be fatal and frequently carries high neurologic, respiratory, and cardiovascular morbidity. The morbidity and mortality associated with traumatic VAE, as with non traumatic VAE, depends not only on associated injuries but also on the volume and rate of air entry, underlying cardiac condition, and the patient's position.


No specific age preference exists for venous air embolism.


No racial preference exists for venous air embolism.


No gender preference exists for venous air embolism.


Key Symptoms/ History

If venous air embolism is suspected, inquiry about the following key historical elements should be obtained:

  • Patients with HD access catheters or other indwelling central venous catheters
  • Patients on positive pressure ventilation
  • Recent surgical procedures especially neurosurgical, otolaryngological, cardiovascular, or orthopedic
  • Scuba diving trips and a history of decompression injuries or decompression sickness
  • Blunt or penetrating trauma to the head, face, neck, thorax, and/or abdomen
  • Invasive therapeutic and/or diagnostic procedures such as central venous catheterization; lumbar puncture; high-pressure infusion of medications, blood products, and/or IV contrast agents
  • Peripartum/postpartum orogenital sex (air may enter veins of the myometrium)
  • Ingestion of hydrogen peroxide (rare)


Clinical Presentation

Many cases of venous air embolism (VAE) are subclinical and do not result in untoward outcomes. However, severe cases are characterized by cardiovascular collapse and/or acute vascular insufficiency of several specific organs, including, but not limited to, the brain, spinal cord, heart, and skin. The spectrum of effects is largely dependent on the rate and volume of entrained VAE. An arterial air embolism can also form if passage of air occurred through a right-to-left shunt, as in the case of apatent foramen ovale. The arterial air emboli can then lodge in the coronary or cerebral circulation, causing myocardial infarction or stroke. Symptoms (awake patients)

  1. Nausea
  2. Acute dyspnea
  3. Agitation/disorientation/sense of "impending doom"
  4. Continuous cough
  5. Substernal chest pain
  6. "Gasp" reflex (a classic gasp at times reported when a bolus of air enters the pulmonary circulation and causes acute hypoxemia)
  7. Dizziness/lightheadedness/vertigo



  1. Transient/permanent focal deficits (weakness, paresthesias, paralysis of extremities)
  2. Loss of consciousness, collapse
  3. Acute altered mental status
  4. Seizures
  5. Coma (secondary to cerebral edema)


  1. Myocardial ischemia
  2. Dysrhythmias (tachyarrhythmias/bradycardias)
  3. Increased CVP
  4. "Mill wheel" murmur - A temporary loud, machinerylike, churning sound due to blood mixing with air in the right ventricle, best heard over the precordium.
  5. JVD
  6. Pulmonary artery hypertension
  7. Hypotension
  8. Circulatory shock/cardiovascular collapse
  9. Nonspecific ST-segment and T-wave changes and/or evidence of right heart strain


  1. Livedo reticularis
  2. Crepitus over superficial vessels (rarely seen in setting of massive air embolus)


  1. Hemoptysis
  2. Adventitious sounds (rales, wheezing)
  3. Tachypnea
  4. Pulmonary edema
  5. Cyanosis
  6. Decreased end-tidal carbon dioxide, arterial oxygen saturation, and tension
  7. Hypercapnia
  8. Increased pulmonary vascular resistance and airway pressures
  9. Apnea


  1. Funduscopic examination may reveal air bubbles in the retinal vessels.

The above hemodynamic, pulmonary, and neurologic complications primarily result from gas gaining entry into the systemic circulation, occluding the microcirculation and causing ischemic damage to these end organs.


In order for venous air embolism (VAE) to occur, 2 physical preconditions for the entry of gas into the venous system must be met.

  1. A pressure gradient (sub-atmospheric pressure in the vessels) favoring the passage of air into the circulation must be present.
  2. A direct communication between a source of air/gas and the vasculature (incising of non collapsed veins) must exist.

Classically, venous air embolism has been recognized as occurring in the context of decompression illness in divers, aviators, and astronauts. However, the most common cause of VAE is iatrogenic.

  1. Surgical procedures are the primary cause of venous air emboli. Neurosurgical procedures, especially those performed in the Fowler’s (sitting) position, and otolaryngological interventions are the two most common surgeries complicated by venous air emboli.
  2. Venous air emboli pose a risk anytime the surgical wound is elevated more than 5 cm above the right atrium. The presence of numerous, large, non-compressed, venous channels in the surgical field (especially during cervical procedures and craniotomies that breach the dural sinuses) also increase the risk of VAE.
  3. The incidence of mild or clinically silent venous air embolism (VAE) during neurosurgical procedures has been estimated to range between 10% in cervical laminectomy surgeries where the patients are in the prone position, and 80% during posterior fossa surgeries (e.g., repair of cranial synostosis) where patients are placed in the Fowler’s position.
  4. Entrainment of air/gas facilitated by the patient's intra operative position causing VAE may result from other surgical procedures. These include, craniofacial surgery, dental implant surgery, vascular procedures (e.g., endarterectomies), liver transplantation, orthopedic procedures (e.g., hip replacement, spine surgery, arthroscopy), lateral decubitus thoracotomy, genitourinary surgeries in the Trendelenburg position, and surgeries involving tumors/malformations with high degree of vascularity or compromised vessels, as in the context of trauma.
  5. Venous air embolism may also result from the iatrogenic creation of a pressure gradient for air entry. Procedures causing such a pressure gradient include lumbar puncture, peripheral intravenous lines, and central venous catheters.
  6. Obstetric/gynecological procedures (cesarean delivery) and laparoscopic surgeries each carry their own risk for venous air embolism.
  7. Venous air embolism is a potentially life-threatening and under-recognized complication of central venous catheterization (CVC), including central lines, pulmonary catheters, hemodialysis catheters and Hickman (long-term) catheters. A number of factors increase the risk of catheter-related VAE, including the following:
  1. Hypovolemia, which reduces central venous pressure
  2. Deep inspiration during insertion or removal, which increases the magnitude of negative pressure
  3. Fracture or detachment of catheter connections (accounts for 60-90%)
  4. Dysfunction of self-sealing valves in plastic introducer sheaths
  5. Failure to occlude the needle hub and/or catheter during insertion or removal
  6. Presence of a persistent catheter tract following the removal of a central venous catheter
  7. Upright positioning of the patient, which reduces central venous pressure
  8. Mechanical insufflation or infusion is another cause of venous air emboli.
  1. Several different procedures involve the use of insufflation, including arthroscopic procedures, CO 2hysteroscopy, laparoscopy, urethral procedures, and orogenital sexual activity during pregnancy (by entering veins of the myometrium during pregnancy and/or after delivery).
  2. Inadvertent infusion of air can also occur during the injection of IV contrast agents for CT scans, angiography, and cardiac catheterization, as well as during cardiac ablation procedures.
  3. Positive pressure ventilation during mechanical ventilation places patients at risk for barotrauma and, subsequently, arterial and/or venous air emboli. Entry of gas into the circulation may result in violation of pulmonary vascular integrity occurs at the same time alveoli rupture from over distension of the airspaces.
  4. The occurrence of venous air embolism (VAE) has also been described in the setting of blunt and penetrating chest and abdominal trauma as well as in neck and craniofacial injuries.

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