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Clinical Images

A Life-Saving Procedure for Treatment of Massive Pulmonary
Air Embolism

Mohamad Ali Ostovan, MD and Amir Aslani, MD
August 2007

 

Case report. A 65-year-old female with a history of repeated episodes of syncope was admitted for permanent pacemaker implantation due to sick sinus syndrome. A 9 Fr peel-away sheath, which is devoid of a hemostatic valve, was inserted. During ventricular lead implantation, the patient took a very deep inspiration followed immediately by extreme bradycardia of 30 beats/minute and a drop in blood pressure from 110/70 to 70/50 mmHg. On fluoroscopy, a large air embolus was detected in the main pulmonary trunk (Figure 1). Head-down positioning was not successful and the patient developed cardiopulmonary arrest. Intubation was done and precordial thumb with cardiac massage was started. Unfortunately, these maneuvers were not successful (Figure 2). Therefore, an 8 Fr right Judkins guide catheter was inserted into the main pulmonary artery via the left femoral vein and suction was performed by a 50 cc syringe (Figure 3). Immediately, the patient recovered and her hemodynamics stabilized. A permanent pacemaker was inserted and the patient was discharged 2 days later. The influx of air into the vasculature (air embolism) may result in significant morbidity and may be fatal. Air embolism can involve either the venous or arterial vasculature. Venous embolism occurs when air is introduced into the central venous system and embolizes to the right heart or pulmonary arterial system. Arterial embolism results from the entry of gas into the left heart chambers, as with paradoxical venous embolism across an intracardiac shunt, during cardiac surgery, or directly into the arteries of the systemic circulation, such as during decompression barotraumas, or penetrating trauma involving an artery.

 

Since venous air embolism is typically iatrogenic and may be associated with procedures performed in both medical and surgical specialties, it is important for clinicians to be aware of themechanisms, diagnosis, and management of venous air embolism associated with central venous access procedures. The physiologic effects of venous air embolism are similar to that of pulmonary embolism of any etiology: (1) elevated pulmonary artery and right ventricular pressures; (2) increased ventilation perfusion mismatch; (3) intrapulmonary shunting; and (4) increased alveolar dead space (all resulting in arterial hypoxemia and hypercapnia). The acute changes in right ventricular pressure result in right ventricular strain, which may lead to right heart failure, systemic circulatory collapse due to decreased cardiac output, right ventricular ischemia, arrhythmia and even death. The degree of physiological impairment depends on the volume of air, rate of air embolism, the type of gas (e.g., room air, carbon dioxide or nitrous oxide) and the position of the patient when the embolism occurs.1

 

Fatal air embolism has been documented with air influx of 1 cm3/kg per second.2 The true incidence of air embolism is unknown because of the nonspecific nature of signs and symptoms as well as difficulty in documenting the diagnosis. Risk factors for air embolism related to central venous catheter procedures include large-caliber catheters, low central venous pressure and inability for the patient to lie in a supine or Trendelenberg position. Because of the lack of specific signs and symptoms of venous air embolism, a high index of suspicion is necessary to establish the diagnosis. Transthoracic and transesophageal echocardiography are highly sensitive for ongoing air embolization or for visualization of trapped air in the heart.3 Magnetic resonance imaging and computed tomography scans can also confirm the diagnosis.4 Invasive pulmonary artery pressure measurement, pulse oximetry and physical examination have much lower sensitivities in diagnosing venous air embolism.3 Treatment of air embolism includes hemodynamic support, adequate supplementation of inspired oxygen and prevention of further air entry into the circulation. Previous studies have shown that left lateral decubitus positioning may be effective by allowing air to move toward the right ventricular apex, thereby relieving the obstruction of the pulmonary outflow tract.5,6 Permanent pacemaker implantation may be associated with either acute or late complications. Pulmonary air embolism, pneumothorax, venous or arterial bleeding, cardiac arrhythmia and myocardial perforation are potential risks of the procedure.7,8 We present an unusual case of massive pulmonary air embolism and cardiopulmonary arrest during permanent pacemaker implantation in which precordial thumb, cardiac massage and head-down position were not successful, and air suctioning with a large-lumen guide catheter was effective and life-saving.

References

1. Souders JE. Pulmonary air embolism. J Clin Monit Comput 2000;16:375–383.

2. Lucas CE, Irani F. Air embolus via subclavian catheter. N Engl J Med 1969;281:966–967.

3. Dudney TM, Elliott CG. Pulmonary embolism from amniotic fluid, fat, and air. Prog Cardiovasc Dis 1994;36:447–474.

4. Teichgraber UKM, Benter T. Air embolism after the insertion of a central venous catheter. N Engl J Med 2004;350:e17.

5. Durant TM, Oppenheimer MJ. Pulmonary (venous) air embolism. Am Heart J 1947;33:269–281.

6. Ericsson J, Gottlieb J, Sweet R. Closed-chest cardiac massage in the treatment of venous air embolism. N Engl J Med 1964;270:1353–1354.

7. Turgeman Y, Antonelli D, Atar S, Rosenfeld T. Massive transient pulmonary air embolism during pacemaker implantation under mild sedation: An unrecognized hazard of snoring. Pacing Clin Electrophysiol 2004;27:684–685.

8. Zeft HJ, Harley A, Whalen RE, McIntosh HD. Pulmonary air embolism during insertion of a permanent transvenous cardiac pacemaker. Circulation 1967;36:456–459.


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