Repeated massive pulmonary air embolism during pacemaker implantation

Abstract

Pacemaker implantation is associated with the potential for various acute and late complications. Though they rarely occur, massive pulmonary air embolisms are lethal. We report the case of a 72-year old male with sick sinus syndrome who underwent permanent pacemaker implantation. Sedation was administered due to back pain with the resultant appearance of snoring. The procedure was complicated with repeated massive pulmonary air embolisms. The events occurred after the leads had been placed in the sheaths. The patient was successfully resuscitated with fluid challenge, O₂ supplement, vasopressor and catheter aspiration. This case illustrates that in a heavily sedated, snoring patient, the marked negative intrathoracic pressure can overcome the frictional resistance of air to being sucked into the gap between the lead body and sheath's wall. Careful manipulation alone is not enough to prevent pulmonary air embolisms. Aggressive treatment for upper airway obstruction is important. The use of a sheath with a haemostatic valve is strongly recommended if the upper airway obstruction cannot be treated adequately.

INTRODUCTION

Pacemaker implantation has the inherent potential for adverse events. Pneumothorax, haemothorax, lead dislodgement, cardiac perforation and arrhythmia can all occur during the procedure. Massive air embolisms are rare. Here, we report the case of a massive pulmonary air embolism (PAE) that occurred in a heavily sedated, snoring patient.

CASE REPORT

A 72-year old man with a history of hypertension was admitted because of symptomatic bradycardia–tachycardia syndrome. There was no history of chronic lung disease or sleep apnoea syndrome. He weighed 53 kg with a body weight index of 19.5 kg/m². Hydration with normal saline 500 ml/day was given for 2 days before the procedure. On preparation for pacemaker implantation, he could not maintain a supine position because of back pain. Sedation was administered for agitation and restlessness, and meperidine (25 mg, intramuscularly) and midazolam (5 mg, intravenously) were given initially. The treatment was changed to midazolam 2.5 mg intravenously two times with an interval of 10 min because of an inadequate sedation level. Deep sedation was achieved, and he appeared to be snoring. A left subclavian vein approach with an 18-gauge needle attached to a 10-ml syringe was used with venography guidance. The needle was inserted into the left subclavian vein, and successful entry was indicated by smooth aspiration of dark red blood. However, when the syringe was detached, no back flow of blood was noted. The J-tip guide wire was inserted through the needle and advanced to the inferior vena cava smoothly. For dual chamber pacing system, another wire was inserted via a separate subclavian puncture. Then, a 7-Fr peel-away sheath without the haemostatic valve was inserted via one wire. The sheath's orifice was occluded by a finger just until the ventricular lead (Medtronic CapsureFix Novus Model 5076 screw-in lead) was inserted. A hiss of air was heard that accompanied the deep inspiration of the patient despite the ventricular lead being placed in the superior vena cava through the sheath. Fluoroscopy showed a large air embolus in the main pulmonary trunk. A decrease in blood pressure from 130/80 to 70/56 mmHg was observed, which was associated with desaturation. O₂ saturation dropped from 100 to 90% on telemetry. Pinching of the neck of the sheath did not stop further entry of air. The sheath was withdrawn and peeled apart immediately. Left-sided tension pneumothorax was excluded by fluoroscopy. Fluid challenge, 100% O₂ supplement and vasopressor were administered. The right ventricular lead was stabilized first to provide back-up pacing in the case of bradycardia. A 6-Fr JR4 guide catheter was inserted via the right femoral vein for air aspiration. However, when the guide catheter reached the main pulmonary artery, most of the air had disappeared. The tip of the catheter was left in the main pulmonary trunk. After management, hypotension and desaturation resolved gradually. Subsequently, another 7-Fr sheath (also without the haemostatic valve) was introduced into the left subclavian vein, and the atrial lead (Medtronic CapSure SP Novus Model 5594 tined lead) was inserted at end inspiration. After insertion of the atrial lead, the orifice of the sheath was covered with wet gauze and pinched, but this was not effective because the same scenario was repeated. Air was sucked into the central vein and a large air embolus was noted in the pulmonary trunk again (Fig. 1). His blood pressure dropped again to 66/40 mmHg. Because the JR guide catheter had been placed in the main pulmonary trunk during the previous episode, air aspiration was performed immediately. Approximately 20 ml of air was aspirated via a syringe. No visible residual air in the pulmonary trunk was noted after aspiration (Fig. 2). Hypotension improved quickly after aspiration. The atrial lead was positioned at an adequate site, and the subsequent pacemaker implantation procedures were completed without incident. The patient was discharged uneventfully 2 days after the procedure.

Figure 1:

Large air embolus (white arrow) in the main pulmonary trunk with a 6-Fr guide catheter (black arrow) inserted. Aspiration was performed.

Figure 2:

Disappearance of the air embolus after catheter aspiration.

DISCUSSION

PAE occurs in a number of clinical situations, such as during the insertion and removal of central venous catheters [1, 2] and invasive surgical and medical procedures [3]. Pacemaker implantation was associated with the potential for various acute and late complications. PAE is rare but can be fatal if it occurs. It is especially risky in sedated snoring patients [4]. The appearance of snoring represents the development of upper airway obstruction and can be viewed as an alarm signal. The patency of the upper airway is determined by pharyngeal muscle tone competing against negative transmural pharyngeal pressures during inspiration. Sedative agents decrease pharyngeal muscle tone. The supine position used in operations makes airway collapse more likely because of posterior displacement of the tongue and soft palate. The inspiratory efforts against a collapsed airway generate marked negative intrathoracic pressures. The fluctuation in intrathoracic pressures during respiration is transmitted to the central veins and can produce a sucking force during inspiration. In our patient, sedation was necessary because of restlessness and back pain. Our goal was to achieve a moderate level of sedation because spontaneous ventilation may have been inadequate under deep sedation. However, sedation is a continuum, and it is not always possible to predict how a patient will respond to sedatives. Our patient's state progressed almost directly from minimal sedation to deep sedation despite the staged administration of the sedatives. Patients with a low intravascular volume are also at higher risk of developing PAE. When the needle is inserted into the left subclavian vein and no back flow of blood is noted after the syringe has been detached, it is a sign of inadequate volume status and/or it might reflect increased negative intrathoracic pressure during inspiration. Usually, PAE occurs after the venous sheath has been advanced into the central vein and just before the lead has been inserted [4, 5]. In our patient, PAE did not occur during this period. It occurred after the lead had been placed in the sheath. The excessive negative intrathoracic pressure overcame the frictional resistance of air to passing through the gap between the wall of the sheath and the lead. Hence, for a heavily sedated snoring patient, careful manipulation alone is not enough to prevent PAE during pacemaker implantation, particularly if it is concurrent with low-volume status; a special strategy is required. First, good preparation of patients is important, particularly with respect to volume status. Low-volume status should be corrected adequately. Secondly, management of the airway should be first completed. The nasopharyngeal airway is helpful for the relief of upper airway obstructions. As in patients with obstructive sleep apnoea, positive airway pressure therapy effectively splits open the airway and prevents its collapse; it eliminates the generation of marked negative intrathoracic pressure and can thus decrease the risk of PAE. The combined use of both strategies is reasonable. The use of a sheath with a haemostatic valve is strongly recommended if the upper airway obstruction cannot be treated adequately.

Conflict of interest: none declared.