Air embolism is a rare, but potentially fatal, event that occurs when a bolus of air enters the vascular space. There are two types of air embolism – venous and arterial.

To really understand this concept, you need to have a good understanding of cardiopulmonary circulation. So let’s review that pathway. 

Deoxygenated blood comes from venous circulation throughout the body and enters the right atrium. From there it flows into the right ventricle and out through the pulmonary artery into pulmonary circulation. This is where gas exchange takes place. The red blood cells offload CO2 and pick up oxygen. This oxygenated blood then returns to the heart via the pulmonary veins. It enters at the left atrium, flows into the left ventricle and is pumped out through the aorta into systemic circulation. 

Venous air embolism

A venous air embolism occurs when air enters venous circulation and moves to the right ventricle of the heart and then into pulmonary circulation where it becomes lodged. Because it enters pulmonary circulation, you may see this referred to as a pulmonary air embolism. If the air embolism is small, it may diffuse into the alveolar space. However, larger air embolisms can obstruct pulmonary circulation leading to obstructive shock and cardiovascular collapse. The bubbles associated with the embolism can be small or large. 

If the bubbles of air are small, they usually obstruct pulmonary microcirculation, which impairs blood flow and also causes vasoconstriction (which further impairs blood flow). When this occurs, patients can experience increased pulmonary pressures, increased pulmonary vascular resistance, and increased pressure in the right ventricle. Ultimately the patient experiences decreased cardiac output, right ventricular overload and myocardial ischemia due to hypoxia. 

Large bubbles of air usually block the pulmonary outflow tract which decreases the circulation of blood from the right side of the heart. This leads to increased central venous pressure, decreased pulmonary pressure and hypotension.

Some patients also suffer from arterial embolization as a consequence of a venous air embolism. If venous air passes through the pulmonary capillary bed and enters the arterial side, organ ischemia can occur, including cardiac ischemia if the coronary arteries are affected.

How dangerous the venous air embolism is depends on how much air enters the vascular space, how quickly it enters, and where it ultimately lodges. Some studies show that as little as 50 ml of air entering the venous circulation may be fatal.

Venous air embolism can also cause tissue damage in the lungs which leads to the accumulation of neutrophils, platelets and other inflammatory substances collecting where gas exchange should take place. Patients may experience pulmonary edema, hypoxemia, increased airway resistance and bronchoconstriction. Some patients may progress to acute respiratory distress syndrome.

Arterial air embolism

An arterial air embolism enters arterial circulation and travels to organs and tissues throughout the body. If the affected organ or tissue does not have adequate collateral circulation, tissue ischemia and tissue necrosis can result. The brain and the heart are the two organs most likely to be detrimentally affected by microbubbles in circulation, though any organ or tissue can suffer ischemia. Air emboli can occur through direct introduction of air into the arterial side of circulation such as in surgery or trauma. It can also occur in patients with a patent foramen ovale, a pulmonary AVM or in patients with a septal defect. Studies suggest that even just 2 ml of air in the cerebral arteries and as little as 0.5 ml of air in coronary circulation can be fatal. Aside from direct tissue damage, the body’s inflammatory response can also cause endothelial damage that ultimately leads to organ dysfunction.

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How do air embolisms occur?

Air can enter the vascular space any time the vasculature is exposed to air or when a pressure gradient exists that allows air to enter circulation (as opposed to blood exiting the vessel). For example, surgery, vascular cannulation, trauma and barotrauma can all cause air embolism to occur. Though rare, some specific procedures that may cause venous air embolism are needle biopsies of lung tissue, coronary artery bypass graft surgery, cardiac ablation procedures, total joint arthroplasty, cesarean section, ERCP, and pacemaker placement.

Two types of surgery are specifically higher risk for air embolism due to the presence of a distinct pressure gradient. In neurosurgical procedures and surgeries involving the ear, nose and throat, the surgical incision is generally at a location where pressures are higher than central venous pressure. This pressure gradient makes it easier for air to enter circulation, especially if the patient is in a more upright position.

In cases of trauma, penetrating and blunt trauma to the chest or abdomen can cause either venous or arterial air embolism as air enters through the wound. Additionally, head and neck injuries specifically, have been identified as a risk for arterial air embolism as well.

Barotrauma, which occurs with positive pressure ventilation, can also cause air emboli. Trauma to the alveoli allows gas to enter pulmonary circulation. Studies show it is most likely to occur in those with ARDS and in scuba divers who ascend too quickly.

Another significant risk factor for air embolism is the use of IV catheters. Venous air embolism can occur with the use of hemodialysis catheters, central venous catheters, and pulmonary artery catheters, and it can even occur with power injection of contrast dye. Arterial air embolism is a known risk with arterial catheters (such as those used to monitor blood pressure), and with intra-aortic balloon pumps. Embolisms can occur at the time of catheter insertion, removal, or even while the catheter is in place if connections are not secure. Conditions which place patients at higher risk for air embolism during insertion are generally those in which central venous pressure is lower than atmospheric pressure. This can occur when the patient is hypovolemic, if they take a deep breath during insertion, or if they are in an upright position.

What are the signs and symptoms of venous air embolism?

Signs and symptoms of venous air embolism can include:

Respiratory symptoms – Shortness of breath, cough, tachypnea, wheezing and/or crackles, hypoxia, respiratory failure. 

Cardiac symptoms – Chest pain, right-sided heart failure, jugular vein distention, hemodynamic compromise (due to obstructive shock), cardiac arrest.

Neurological symptoms – Lightheadedness, loss of consciousness, sense of impending doom.

What are the signs and symptoms of arterial air embolism?

Signs and symptoms of arterial air embolism vary depending on which organ is suffering ischemia. Since the brain is the most commonly affected organ, patients generally show mental status changes and neurological compromise. In severe cases, patients may become comatose or suffer cardiac arrest. If other organs are affected, the patient will exhibit signs and symptoms associated with that particular organ, including the skin. 

What tests are conducted if an air embolism is a risk or suspected?

ABG – An arterial blood gas will show hypercapnia and hypoxemia.

EKG – Patients typically have tachycardia and may show changes depending on whether the embolism is arterial or venous. An arterial embolism may cause T-wave changes and ST depression or elevation secondary to myocardial ischemia or myocardial infarction. Venous air embolism may cause a right bundle branch block and peaked p-waves. 

End-tidal CO2 – A decrease in end-tidal CO2 can be associated with the VQ mismatch that occurs with pulmonary air embolism. End-tidal CO2 is often used during high-risk surgeries to catch an embolism at the time of occurrence.

Transcranial doppler – Observation of transcranial blood flow may be conducted during high risk surgical procedures.

Echocardiogram – Ultrasound studies of the heart can be utilized to detect air in the heart and great vessels as well as increased pulmonary pressures and right ventricular enlargement.

Imaging studies – Various imaging studies may be utilized including chest X-ray, chest CT, brain CT (if cerebral embolism is suspected), abdominal CT (if organ ischemia is suspected) and MRI. 

Other studies – Though not the most common diagnostic tests, VQ scan or pulmonary angiography may be utilized to evaluate a patient with suspected air embolism.

How is the patient with an air embolism managed?

Upon suspicion of an air embolism, the initial key treatments are oxygenation, positioning and supportive therapies. Which treatments the patient receives will depend on the severity, location, and type of embolism. 

Oxygenation – Oxygen supplied at a high FiO2 helps the body resorb the air bolus more quickly. Some patients may require emergent intubation and mechanical ventilation.

Positioning – For a venous air embolism, the studies show that patients should be positioned in the left lateral decubitus position, Trendelenberg position with the head 15 to 30 degrees lower than the feet, or in left lateral decubitus with the head down. This traps the air bolus in the right ventricle and prevents it from entering pulmonary circulation. 

If an air bolus is suspected on the arterial side, studies indicate the preferred positioning is the supine position, though you may also see right lateral decubitus or Trendelenberg utilized. The reason the supine position is utilized for arterial embolisms is that arterial blood flow is stronger than venous blood flow and the air bubbles can enter circulation even in Trendelenberg position. And since cerebral edema is often a consequence of arterial embolism, this head down position can exacerbate cerebral edema.

Removal of air from the heart – Though not a common procedure, some of the air may be removed from the heart chambers directly through a needle inserted into the heart or through a central venous catheter or pulmonary artery catheter. 

Chest compressions – Chest compressions may be utilized if no other options are effective or available, and the patient is severely hemodynamically compromised. The forceful compression of the heart may improve cardiac output by moving the bolus out of the pulmonary outflow tract into smaller vessels of the pulmonary vasculature.

Hyperbaric oxygen – Hyperbaric oxygen may be utilized in severe cases, though it is not always readily available and the risks associated with transporting the patient may outweigh the potential benefits.

IV fluids – A fluid bolus can increase central venous pressure, which helps prevent further air from entering venous circulation.

Vasopressors – Patients with hemodynamic compromise that persists after fluid administration may benefit from a vasopressor such as norepinephrine.

Additional specific treatments – Further treatment for each patient will vary depending on which organ or organs have been affected. For example, a patient suffering from ARDS will require specific treatment for that condition, and a patient with acute kidney failure due to organ ischemia may need temporary (or permanent) dialysis.

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How is an air embolism prevented?

As a nurse, one of the most important ways you can prevent an air embolism is to manage central lines and arterial lines with unsurpassed diligence. 

  • Ensure patients are positioned in Trendelenburg when central venous catheters are inserted in the subclavian and jugular veins. If the femoral vein is being used, the supine position may be utilized.
  • Place patients in Trendelenburg when removing central venous catheters from the subclavian or jugular veins. Again, the supine position may be utilized when removing a femoral central venous catheter. 
  • Take measures to avoid inspiration during removal by instructing the patient not to inhale, cough or speak during the procedure.
  • Having the patient perform a Valsalva maneuver can elevate central venous pressure significantly and is a great option for a cooperative patient. Another option is having the patient inhale and then hold their breath. This method has benefits over having them hold their breath and end exhalation since they could potentially abruptly inhale during removal if the lungs are empty.
  • Hold manual pressure after removal for at least ten minutes or longer as needed to achieve homeostasis. 
  • Immediately apply an occlusive dressing to the site and instruct the patient to keep it in place for 24 hours.
  • Keep all connections secure.
  • Keep catheters clamped closed when not in use.
  • Remove all air from syringes prior to saline flushes or medication administration.
  • Place the patient in a supine position when drawing blood or administering IVP medications through a central venous catheter.

Want to learn more about managing a central venous catheter? This article discusses the prevention of central line infections so you can help keep your patients safe!

Review the basics of air embolisms for your exams, clinicals, and NCLEX while you’re on the go by tuning in to episode 338 of the Straight A Nursing podcast. Tune in wherever you get your podcast fix, or straight from the website here.


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