Intracardiac Aspiration for Life-Threatening Air Embolism During Cardiac Catheterization in Tetralogy of Fallot: An Aborted Sudden Death

ABSTRACT: Accidental introduction of air into veins can occur during a variety of surgical operations or diagnostic procedures. High mortality rate results without early diagnosis and appropriate treatment. This is due to “air lock” at the right ventricular outflow tract, compromising the left ventricular filling. We describe a 2-year-old male with Tetralogy of Fallot who developed air embolism due to unexpected rupture of Swan-Gang catheter during a cardiac catheterization study, which was managed successfully by intracardiac aspiration.

J INVASIVE CARDIOL 2012;24(11):E294-E296

Key words: catheters, cardiac arrest, cardiogenic shock, complications, pulmonary embolism

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Case Report. A 2-year-old male was referred to our tertiary care cardiac center with history of cyanosis noticed at 3 months of age and recurrent cyanotic spells. Clinical examination and basic investigations were consistent with Tetralogy of Fallot. The diagnosis was confirmed on transthoracic echocardiography, which showed nonrestrictive perimembranous ventricular septal defect (VSD) and overriding aorta with severe infundibular stenosis as well as hypoplastic pulmonary annulus and arteries. According to institutional policy, he received a cardiac catheterization study with angiography to assess pulmonary annulus, pulmonary artery size, and aortopulmonary collaterals.

Under general anesthesia, vascular access was obtained from the right femoral vein and artery. The Swan-Ganz balloon flotation catheter was introduced into the right atrium. As soon as the catheter was inflated with room air, it burst and an air pocket was seen within the right ventricle (Figure 1; Video 1) resulting in “air lock,” or venous air embolism. Within fractions of a second the patient’s blood pressure started falling and arterial saturation dropped to 50%. The cardiac monitor showed sinus tachycardia with gross ST segment elevation and hypotension (mean blood pressure 36mm Hg; Figure 2A). Immediately, we started high flow oxygen and we planned to aspirate the air. A 6 Fr angiographic catheter (Berman) was introduced into the right ventricle and directed toward the air pocket, and manual aspiration (Video 2) was initiated. During the process of aspiration, a few smaller bubbles embolized into the pulmonary and systemic circulation (via large nonrestrictive VSD and overriding aorta), however we aspirated the majority of the air. As soon as the air was aspirated blood pressure dramatically improved, tachycardia improved, and ST elevation settled (Figure 2B).

After the patient’s vital parameters improved, we observed the patient and then completed the cardiac catheterization study. Saturation and pressure data were consistent with Tetralogy of Fallot. There was severe infundibular stenosis with hypoplastic pulmonary annulus and pulmonary arteries and a few major aortopulmonary collaterals. The Nakata index was 134 mm2/m2 with Z value of -4. There was no evidence of neurologic or other organ damage. He was advised Blalok-Taussig shunt.

Discussion. Venous air embolism, a subset of gas embolism, can cause severe morbidity and mortality if unrecognized. Venous air embolism is a predominantly iatrogenic complication^1,2 that occurs when atmospheric gas is introduced into the systemic venous system.³ Many cases of venous air embolism are subclinical with no adverse outcome and thus go unreported. A high index of clinical suspicion of possible venous air embolism is required to prompt investigations and initiate appropriate therapy.

Even though air embolism is mostly associated with percutaneous cardiac interventions it can also occur in other situations like neurosurgical procedures conducted in the sitting position⁴ central venous catheterization,^3,5 penetrating and blunt chest trauma,^6,7 high-pressure mechanical ventilation,³ thoracocentesis,¹ hemodialysis,³ and several other invasive vascular procedures and also during diagnostic studies, such as during radiocontrast injection for computerized tomography.⁸

Venous air embolism is a potentially life-threatening and under-recognized complication of central venous catheterization, including central lines, pulmonary catheters, and hemodialysis catheters. As mentioned earlier, the frequency of venous air embolism associated with central venous catheterization use ranges from 1 in 47 to 1 in 3000. The emboli may occur at any point during line insertion, maintenance, and/or removal of catheters.³ A number of factors increase the risk of catheter-related venous air embolism, including fracture or detachment of catheter connections (accounts for 60%-90%);^1,2 failure to occlude the needle hub and/or catheter during insertion or removal; dysfunction of self-sealing valves in plastic introducer sheaths; presence of a persistent catheter tract following the removal of a central venous catheter; deep inspiration during insertion or removal, which increases the magnitude of negative pressure; hypovolemia, which reduces central venous pressure; and upright positioning of the patient, which reduces central venous pressure.

The key factors determining the degree of morbidity and mortality in venous air emboli are related to the volume of gas entrainment, the rate of accumulation, and the patient’s position at the time of the event.^1,5,9 Rapid entry or large volumes of air entering the systemic venous circulation puts a substantial strain on the right ventricle, especially if this results in a significant rise in pulmonary artery pressures. The mechanism of cardiovascular collapse in massive venous air embolism involves “air lock” resulting in obstruction of right ventricular outflow tract, pulmonary artery/arterioles, or pulmonary microcirculation. The smaller air bubbles trapped in the microcirculation can result in reactive vasoconstriction.¹⁰ These result in increased central venous pressure, right ventricular dysfunction and compromised left ventricular preload, resulting in profound systemic hypotension, hypoxia, and eventually cardiovascular collapse.^1,4,5

Many cases of venous air embolism are subclinical and do not result in negative outcomes. However, severe cases are characterized by cardiovascular collapse and/or acute vascular insufficiency of several specific organs, including but not limited to the brain, spinal cord, heart, and skin. Cardiovascular manifestations of venous air embolism includes dysrhythmias (tachyarrhythmias/bradycardias), “Mill wheel” murmur, hypotension, myocardial ischemia, nonspecific ST-segment and T-wave changes and/or evidence of right heart strain, pulmonary artery hypertension, increased central venous pressure, and circulatory shock/cardiovascular collapse.

In our patient, a ruptured Swan-Ganz catheter balloon resulted in introduction of air directly into the right ventricle, which resulted in occlusion of the already stenosed right ventricular outflow tract causing arrest of left heart filling, circulatory collapse, tachycardia, hypoxia, and ST elevation.
Arterial embolism as a complication of venous air embolism can occur through direct passage of air into the arterial system via anomalous structures such as an atrial septal defect or VSD, a patent foramen ovale, or pulmonary arterial-venous malformations. This can cause paradoxical embolization into the arterial tree.^1-4,7 In our patient, during intracardiac aspiration the air bubble fragmented into smaller bubbles and embolized into both pulmonary and systemic circulation (via large nonrestrictive VSD and overriding aorta), but the patient did not develop clinically significant neurologic deficits or other end-organ damage.

Laboratory tests are neither sensitive nor specific for the diagnosis of venous air embolism. The only indication for obtaining routine laboratory tests is to evaluate the associated end-organ injury resulting from air embolism. Arterial blood gas samples often show hypoxemia, hypercapnia, and metabolic acidosis secondary to right-to-left pulmonary shunting.

Management of venous air embolism, once suspected, includes identification of the source of air, prevention of further air entry (by clamping or disconnecting the circuit), a reduction in the volume of air entrained, and hemodynamic support. Any procedure posing a risk for venous air embolism, if in progress, should be aborted immediately once venous air embolism is suspected. Administer 100% O₂ 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. Immediately placing the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg position may help to prevent air from traveling through the right side of the heart into the pulmonary arteries, leading to right ventricular outflow obstruction (air lock).

Placement of a central venous catheter (multiorifice) or pulmonary artery catheter to attempt aspiration of air has been recommended in the literature.^1,4,10 When appropriately placed, it may be possible to aspirate approximately 50% of the entrained air with a right atrial catheter. In the event of circulatory collapse, cardiopulmonary resuscitation should be initiated to maintain cardiac output. Cardiopulmonary resuscitation may also serve to break large air bubbles into smaller ones and force air out of the right ventricle into the pulmonary vessels, thus improving cardiac output.¹⁰

Conclusion

Venous air embolism is a potentially life-threatening emergency demanding high index of suspicion, early diagnosis and appropriate institution of therapy. Catheter-related air embolism is dangerous especially in the setting of structural heart disease. Intracardiac aspiration of air embolism is effective and should be employed especially in the setting of hypotension and cardiovascular collapse.

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From the Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted April 23, 2012, provisional acceptance given May 7, 2012, final version accepted May 14, 2012.
Address for correspondence: Dr. Naveen Garg, MD, DM, FSCAI, FACC, Additional Professor, Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India. PIN 226014. Email: navgarg@sgpgi.ac.in