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Venous air embolism (VAE). Dr . S. Parthasarathy MD. DA. DNB., Dip.diab . MD( acu ) , DCA, Dip. PhD ( physio ) Mahatma Gandhi medical college and research institute , puducherry – India . What is it ??.

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venous air embolism vae

Venous air embolism (VAE)

Dr . S. Parthasarathy

MD. DA. DNB., Dip.diab. MD(acu) , DCA, Dip. PhD (physio)Mahatma Gandhi medical college and research institute , puducherry – India

what is it
What is it ??
  • Venous air embolism (VAE), a subset of gas embolism, is an entity with the potential for severe morbidity and mortality
  • iatrogenic complication
  • atmospheric gas is introduced into the systemic venous system
when will it occur
When will it occur ??
  • neurosurgical procedures conducted in the sitting position
  • central venous catheterization,
  • penetrating and blunt chest trauma
  • high-pressure mechanical ventilation thoracocentesis,
  • hemodialysis
other causes
Other causes
  • diagnostic studies, such as during radiocontrast injection for computerized tomography
  • carbon dioxide and nitrous oxide during medical procedures
  • invasive vascular procedures
  • Massive Air Embolism After Central Venous Catheter Removal
during lscs
During LSCS
  • The incidence of VAE during cesarean delivery ranges 10 %
  • The risk factors
  • operation in the Trendelenburg position, abruptioplacentae, placenta previa, exteriorization of the uterus,
  • extraction of the placenta, preeclampsia,
two prerequisites
Two prerequisites
  • (1) a direct communication

between a source of air

and the vasculature

(2) a pressure gradient

favoring the passage of air

into the circulation.

open vessels collapse usually
Open vessels collapse usually
  • When open vessels cannot collapse,
  • which is the case with major venous sinuses as well as bridging and epidural veins,
  • the risk of VAE increases substantially
what is important
What is important ??

The key factors determining the degree of morbidity and mortality

  • volume of gas entrainment,
  • the rate of accumulation,
  • the patient’s position at the time of the event
Volume ??
  • 5 ml/kg is routine – but
  • 20 ml (the length of an unprimed IV infusion tubing)
  • 2 or 3 mL of air into the cerebral circulation
  • 0.5 ml in coronaries
Rate ??
  • >0.30 mL/kg/min–
  • 60 kg man – 18 ml/min.
  • can overwhelm the air-filtering capacity of the pulmonary vessels, resulting in symptoms
  • Venous air emboli pose a risk anytime the surgical wound is elevated more than 5 cm above the right atrium
  • Sitting !!
  • A pressure gradient of 5 cm H2O between air and venous blood across a 14-gauge needle allows the entrance of air into the venous system at a rate of 100 mL per second
  • 0.13%during the insertion and removal of central venous catheters
  • The neurosurgical procedure-related complications of venous air embolism have been estimated to be between 10-80 %
  • Reports of venous air embolism in the setting of severe lung trauma have been estimated between 4-14%.
  • Catheter-associated VAE mortality rates have reached 30%.
  • In a case series of 61 patients with severe lung trauma, the mortality rate associated with concomitant VAE was 80% in the blunt trauma group and 48% in the penetrating trauma group
why is it not great
Why is it not great ??
  • Often it is asymptomatic
  • Symptoms even present – trivial
  • Are we diagnosing ??
why it is great
Why it is great??

It is iatrogenic

patho physiology
Patho physiology
  • large volumes of air
  • Strain RV
  • rise in pulmonary artery (PA) pressures.
  • RV outflow obstruction
  • decreased pulmonary venous return.
  • Decreased LV preload
  • decreased cardiac output
  • systemic cardiovascular collapse
air embolism and sirs
Air embolism and SIRS
  • Air embolism has also been described as a potential cause of the systemic inflammatory response syndrome triggered by the release of endothelium derived cytokines
  • Acute dyspnea, Continuous cough
  • •"Gasp" reflex (a classic gasp at times reported when a bolus of air enters the pulmonary circulation and causes acute hypoxemia)
  • •Dizziness/lightheadedness/vertigo
  • •Nausea, Substernal chest pain
  • •Agitation/disorientation/sense of "impeding doom"
respiratory symptoms
Respiratory symptoms
  • Adventitious sounds (rales, wheezing)
  • Tachypnea
  • Hemoptysis
  • Cyanosis
  • Acute altered mental status
  • Seizures
  • Transient/permanent focal deficits (weakness, paresthesias, paralysis of extremities)
  • Loss of consciousness, collapse
  • Coma (secondary to cerebral edema)


  • Recumbent position,
  • gas proceeds into the right ventricle and pulmonary circulation, subsequently causing pulmonary hypertension and systemic hypotension
  • sitting position,

gas will travel retrograde via the internal jugular vein to the cerebral circulation, leading to neurologic symptoms secondary to increased intracranial pressure

  • spontaneously breathing (yielding negative thoracic pressure)
  • or under
  • controlled positive pressure ventilation
  • Dysrhythmias
  • "Mill wheel" murmur - A temporary loud, machinery like, churning sound due to blood mixing with air in the right ventricle, best heard over the precordium (a late sign
  • Hypotension
  • Circulatory shock/cardiovascular collapse
paradoxical embolism
Paradoxical embolism
  • Arterial embolism as a complication of venous air embolism (VAE) can occur through direct passage of air into the arterial system via anomalous structures such as an atrial or ventricular septal defect,
  • a patent foramen ovale,
  • pulmonary arterial-venous malformations.
preop test for pfo
Preop test for PFO??
  • a preoperative ‘‘bubble test’’ in conscious patients using TEE is advocated by some investigators if the sitting position is considered
various investigations
Various investigations
  • Doppler,
  • TEE,
  • ETCO2
  • ETN2
  • Pulse oximetry,
  • CT scan
  • CxR
  • device can detect 1 mL of air or less
  • The Doppler probe should be placed after the patient is in the operative position. The probe is usually positioned at the middle third of the sternum on the right side
  • Can be confirmed with agitated saline
  • Pulmonary artery catheter – Can detect increases in pulmonary artery pressures, which may be secondary to mechanical obstruction/vasoconstriction from the hypoxemia induced by the VAE
  • Pulse oximetry– Changes in oxygen saturation are late findings with VAE.
end tidal carbon dioxide etco2
End-tidal carbon dioxide (ETCO2)
  • – VAE leads to V/Q mismatching and increases in physiologic dead space.
  • This produces a fall in end-tidal CO2 (normal value is < 5).
  • A change in 2 mm Hg ETCO2 can be an indicator of VAE.
  • this finding is nonspecific, slow
end tidal nitrogen etn2
End-tidal nitrogen (ETN2)
  • Most sensitive gas-sensing VAE detection modality;
  • usually less then 2%,
  • measures increases in ETN2 as low as 0.04%.
  • Response time is much faster than ETCO2
  • False positives ??
  • The optimal management of venous air embolism prevention.
  • 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 use
principles of therapy
Principles of therapy
  • Management of venous air embolism (VAE), once is suspected,
  • identification of the source of air,
  • prevention of further air entry (by clamping or disconnecting the circuit),
  • a reduction in the volume of air
  • and hemodynamic support.
useful measures
Useful measures
  • N2O is used, it should be discontinued
  • The surgeon should flood the surgical field with fluids while open veins are cauterized or exposed bone is waxed
  • compress both jugular veins lightly to minimize air entrainment.
catheter removal
Catheter removal
  • During catheter insertion/removal, place the patient in the supine position with head lowered).
  • 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
  • Central venous catheter – If in place, aspiration of air may help make the diagnosis. It is also helpful in monitoring central venous pressures, which may be increased in VAE.
  • Any procedure posing a risk for venous air embolism (VAE), if in progress, should be aborted
  • Administer 100% O 2 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%) O 2 will help reduce the bubble's nitrogen content and therefore size
  • hyperbaric oxygen therapy (HBOT)
durant maneuver
(Durant maneuver)
  • left lateral decubitus and Trendelenburg position.
  • CPR required – supine and Trendelenburg position.
  • Direct removal of air from the venous circulation by aspiration from a central venous catheter
special situations
Special situations
  • cross-clamping the aorta,
  • cardiac massage, and aspirating air from the left ventricle, aortic roots, and pulmonary veins
  • emergency thoracotomy with clamping of the hilum of the injured lung
  • Supportive therapy should include fluid resuscitation
  • increase venous pressure and venous return.
  • gas emboli may cause a relative

haemo concentration

vasopressors and ventilation
Vasopressors and ventilation
  • The administration of vasopressors and mechanical ventilation are two other supportive measures that may necessary
  • Usually ephedrine may be enough
  • Suspicion in possible situations
  • Diagnosis
  • Prevention
  • Stop nitrous , flood fields
  • 100 % O2 , fluids, vasopressors,
  • Ventilation SOS
  • Aspirate if possible