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Air embolism Dx

An air embolism can be detected many different ways.

  • Doppler ultrasound: most sensitive noninvasive monitor capable of detecting 0.05ml/kg of air.
  • Transesophageal echo (TEE): most sensitive invasive monitor can detect as little as 0.02ml/kg of air.
  • PA Catheter – increase PAP.
  • Increase ET N2
  • Decrease ETCO2 due to increase in functional dead space.
  • Hypercapnea
  • Precordial/esophageal stethoscope-mill wheel murmur.

1. General

  • predominantly iatrogenic complication
  • atmospheric gas is introduced into the systemic venous system
  • mostly associated with neurosurgical procedures conducted in the sitting position.

Now, associated with

  • central venous catheterization
  • penetrating and blunt chest trauma,
  • high-pressure mechanical ventilation,
  • thoracocentesis
  • hemodialysis and several other invasive vascular procedures

2. Pathophysiology

a. What FAVORS air embolus? TWO preexisting Conditions 1) DIRECT communication btn source of air and vasculature 2) Pressure gradient favoring passage of air

b. What determines MORBIDITY AND MORTALITY? VERY HIGH Mortality (80%)

  1. Volume of air entrained: as little as 20 mL of air can be fatal!, but typical 5mL/kg is bad
  2. Rate of accumulation–>puts BIG strain on RV and increases PA pressures–>decreases pulmonary venous return–>decreases CO–> circulatory collapse–> tachyarrhythmia(sometimes brady’s occur)–> cardiac arrest
  3. Pt’s position: Fowlers/sitting

c. Tissue Level changes occur:

  • inflammatory change in pulmonary vessels
  • direct endothelial damage: accumulation of plt, fibrin, and lipid droplets
  • activation of complement and release of free radicals –>capillary damage and non-cardiogenic pulmonary edema
  • all these changes lead to V/Q mismatching –> increase in alveolar dead space
  • arterial HYPOXEMIA and hypercapnea

3. Dx

  • most go unrecognized, b’c s/s can mimic other cardiopulmonary dz
  • Hx: recent neurosurgery, indwelling catheter presence, blunt/penetrating trauma, positive pressure ventilation
  • Sx: dyspnea, N/V, dizziness, substernal CP


Mill WHEEL murmur: constant machine like sound, late sign, heard over precordium

  1. Dysrhythmias: either tachy or brady
  2. Myocardial Ischemia
  3. Circulatory/Cardiovascular collapse
  4. Hypotension
  5. rales, wheezing
  6. hemoptysis
  7. tachypnea
  8. pulmonary edema


  • ABG can show metabolic ACIDOSIS as a result of hypoxemia
  • TEE: highest SENSITIVITY for detecting AIR in RV and pulmonary vessels
  • Precordial Doppler: most SENSITIVE NON-invasive test
  • CT: HCT can reveal air, chest CT can show blunt trauma/penetrating of chest wall
  • MRI: NOT reliable for detecting gas emboli
  • EKG: low sensitivity, can show RV strain pattern, ST depression
  • ETCO2: look for it to DECREASE, nonspecific finding
  • SPO2: late finding

4. Rx a. 100% O2, intubate if there are any signs of respiratory distress b. Durant Maneuver: place pt in L Lat decubitus and T-berg c. one MAY attempt to remove air via aspiration with CVC d. Supportive: CPR (can break big small bubbles), Hyperbaric Oxygen therapy, fluid resuscitation, pressors


  1. Marek A Mirski, Abhijit Vijay Lele, Lunei Fitzsimmons, Thomas J K Toung Diagnosis and treatment of vascular air embolism. Anesthesiology: 2007, 106(1);164-77 PubMed Link