Air embolism pathophysiology

Jump to: navigation, search

Air Embolism Microchapters


Patient Information


Historical Perspective




Differentiating Air embolism from Other Diseases

Epidemiology and Demographics

Risk Factors


Natural History, Complications, and Prognosis


History and Symptoms

Physical Examination

Laboratory Findings


Chest X Ray



Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies


Medical Therapy


Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Air embolism pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides


American Roentgen Ray Society Images of Air embolism pathophysiology

All Images
Echo & Ultrasound
CT Images

Ongoing Trials at Clinical

US National Guidelines Clearinghouse

NICE Guidance

FDA on Air embolism pathophysiology

CDC on Air embolism pathophysiology

Air embolism pathophysiology in the news

Blogs on Air embolism pathophysiology

Directions to Hospitals Treating Air embolism

Risk calculators and risk factors for Air embolism pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


The pathogenesis varies depending on the cause of air embolism.

  • Iatrogenic causes involve access to an open blood vessel.
  • Scuba diving or decompression sickness occurs due to an accumulation of nitrogen bubbles.


Air embolism can occur whenever there is access to an open blood vessel and a pressure gradient exists favoring entry of gas. Because the pressure in most arteries and veins is greater than atmospheric pressure, an air embolus does not always happen when a blood vessel is injured. In the veins above the heart, such as in the head and neck, the pressure is less than atmospheric and an injury may let air in. This is one reason why surgeons must be particularly careful when operating on the brain, and why the head of the bed is tilted down when inserting or removing a central venous catheter from the jugular or subclavian veins.

When air enters the veins, it travels to the right side of the heart, and then to the lungs. This can cause the vessels of the lung to constrict, raising the pressure in the right side of the heart. If the pressure rises high enough in a patient who is one of the 20% to 30% of the population with a patent foramen ovale, the gas bubble can then travel to the left side of the heart, and on to the brain or coronary arteries. Such bubbles are responsible for the most serious of gas embolic symptoms.

Trauma to the lung can also cause an air embolism. This may happen after a patient is placed on a ventilator and air is forced into an injured vein or artery, causing sudden death. Breath-holding and rapid ascent from scuba diving may also force nitrogen air into pulmonary arteries or veins causing Decompression Sickness During a deep sea dive nitrogen accumulates in the tissues of the body, as the diver ascends, the nitrogen leaves the body through the lungs, if the ascent occurs too rapidly nitrogen bubble can form and diffuse into the circulation causing an air embolism.[1]

Air can be injected directly into the veins either accidentally or as a deliberate act. Examples include misuse of a syringe, and industrial injury resulting from use of compressed air. However, despite being employed by writers of fiction as a clandestine method of murder, amounts of air such as would be administered by a single small syringe are not likely to suddenly stop the heart, nor cause instant death. Single air bubbles in a vein do not stop the heart, due to being too small. However, such bubbles may occasionally reach the arterial system through a patent foramen ovale, as noted above, and cause random ischemic damage, depending on their route of arterial travel.


  1. Asadullah Naqvi & Derrick Clarence (2018). "A case of decompression illness not responding to hyperbaric oxygen". Journal of intensive care. 6: 29. doi:10.1186/s40560-018-0299-3. PMID 29796283.