Special Feature: Air Embolism in Patients with Central Venous Catheters
December 1, 2001
Special Feature: Air Embolism in Patients with Central Venous Catheters
By Uday Nanavaty, MD
Central venous catheters (CVC) are commonly inserted in patients admitted to the ICU. One of the complications that develop in patients with CVCs is air embolism. This form of embolic phenomenon can be noted during insertion of catheter, when the catheter is in place, and also after the removal of the catheter. It is obviously difficult to have an estimate of the incidence of this complication—venous air embolism (VAE). However, it is important to recognize it, as it can be fatal if massive amounts of air enter the circulation rapidly. On the other hand, its prompt recognition can lead to successful therapy that can be life saving. Of note, a variety of surgical procedures are complicated by development of VAE, but the clinical manifestations are the same and range from no manifestations at all to cardiac arrest. Systemic air embolism beyond the pulmonary circulation and into the systemic arterial circulation can develop even if the patient does not have a patent foramen ovale and should be suspected in appropriate clinical settings.
Pathogenesis of Venous Air Embolism
Three conditions are required for air embolism to develop around CVCs.
1. A direct communication must exist between the atmospheric air and the venous circulation. This does not necessarily mean that there has to be an open communication as when one of the lumens is uncapped or when a syringe with some air in it is used for administration of medications inadvertently. A potential for such communication often exists when a catheter is removed after several days of use. Similarly, it has been noted that VAE can develop when air gains entry around a catheter if a large bore catheter (for example, the sheath of a PA catheter) is replaced over a wire with a smaller gauge catheter.
2. A gradient of pressure should exist between the entry site for air and the heart. Air travels from higher to lower pressure, especially if gravity favors the flow. This is one of the reasons why patients are placed in the Trendelenburg (head down) position during insertion and removal of CVC, so that the air would have to travel against gravity or a pressure gradient in order to enter the central circulation. Such pressure gradients (negative pressures in the thorax compared to entry site) are often formed when a patient has a violent cough (as it is preceded by a deep breath) or a sudden change in posture with sudden but dramatic changes in intra-thoracic pressure unfortunately favoring air entry into the circulation.
3. A large amount of air must enter at a relatively rapid rate to form big enough emboli to manifest clinically. Although it is hard to measure the exact amounts of air that enter patients, based on animal studies it is estimated that between 50 and 500 mL of air entering the circulation rapidly can be fatal in human beings. A 14-gauge catheter can introduce about 100 mL/sec of air with a 5 cm H2O pressure gradient.
If a large amount of air enters the circulation rapidly, it can form a large bubble embolus and can occlude the pulmonary outflow tract, resulting in cardiac arrest. When air enters the pulmonary circulation, with constant motion of the heart and blood flow, it often breaks into smaller bubbles. The miniscule amount of CO2 in air is rapidly dissolved in the blood. Oxygen is dissolved rather slowly, and nitrogen in air is almost insoluble, accounting for most of the bubbles in the circulation.
Platelets and other cells are activated at the sites of obstruction of the circulation and on the surfaces of smaller bubbles, and result in the release of inflammatory products. This inflammatory state often results in pulmonary edema. It is thought that increased pulmonary arterial pressure from obstruction by air bubbles and pulmonary vasoconstriction by inflammatory cytokines and prostaglandins also contributes to edema formation. The platelet products are also thought to result in increases in airway pressures and clinical wheezing, similar to the wheezing seen in venous thromboembolism. Air bubbles can cross pulmonary capillaries, or larger bubbles can cross at a patent foramen ovale or an arteriovenous malformation, and result in systemic manifestations ranging from cardiac dysrrhythmias and acute myocardial infarction to various neurological phenomena.
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