A Rare Case of Coronary Artery and Cerebral Air Embolism Associated with Catheterization and General Anesthesia

We report a rare case of coronary and cerebral air embolism (AE) following radiofrequency ablation (RFA) for ventricular premature beats (VPBs) combined with patent foramen ovale (PFO) closure. This study aims to highlight the role of anesthesia-induced negative pressure in the pathogenesis of AE. Case Presentation : A 67-year-old male was admitted due to palpitations. Twenty-four-hour Holter monitoring revealed 10,469 VPBs. Transthoracic and transesophageal echocardiography confirmed PFO with severe right-to-left shunt. The patient first underwent RFA under local anesthesia, followed by planned PFO closure under general anesthesia. After induction of general anesthesia, the patient developed bradycardia, junctional escape rhythm, and ST-segment elevation in leads Ⅱ and Ⅲ. Transesophageal echocardiography detected massive air bubbles in the left atrium, aorta, and inferior vena cava. Intraoperative monitoring showed a sudden decrease in end-tidal carbon dioxide (ETCO₂) from 35 mmHg to 28 mmHg (a reduction of 7 mmHg) and a drop in jugular bulb pressure (JBP) to -2 mmHg. Postoperative brain computed tomography (CT) and magnetic resonance imaging (MRI) demonstrated cerebral air accumulation and multiple small infarcts. Postoperative myocardial enzymes were significantly elevated. The patient was managed with antiepileptic drugs, neuroprotective agents, and supportive care. Discussion : AE is a life-threatening complication of cardiac interventional procedures. In this case, the key pathogenic factor was anesthesia-induced negative pressure: general anesthesia caused decreased central venous pressure (CVP) due to relative hypovolemia and increased intrathoracic negative pressure during laryngeal mask ventilation, creating a pressure gradient between the atmosphere and the vascular system ^1,2 . Additionally, the SL1 sheath with an indwelling guidewire exhibited reduced airtightness—when negative pressure falls below − 13.4 mmHg, air leakage may occur between the catheter sheath and guidewire, enabling air entry ³ . Our in vitro pressure testing of the SL1 sheath (conducted under standard laboratory conditions: 25°C, simulated physiological saline environment, n = 5 replicates) confirmed that the sheath-end cap assembly maintained integrity under negative pressure up to 54 kPa without a guidewire (exceeding the YY0450.1-2020 standard of 42 kPa), but only tolerated 16 kPa when a 0.035-inch guidewire (Biosense Webster) was inserted non-coaxially. PFO and iatrogenic atrial septal defect further facilitated paradoxical air embolism into the systemic circulation, leading to coronary and cerebral ischemia ⁴ . Anesthesia-induced negative pressure is closely associated with AE pathogenesis: changes in sympathetic tone after anesthesia induction (causing a mean 6.9 mmHg reduction in left atrial pressure ³ , switching from mechanical ventilation to spontaneous breathing, and body position adjustments during recovery can all expand the pressure gradient between veins and the atmosphere, promoting air aspiration ^2,3 . Conclusion : Anesthesia-induced negative pressure is a critical driver of AE in cardiac interventional procedures. Perioperative management should focus on maintaining CVP (5–15 cm H₂O) ^1,5 , optimizing sheath sealing (ensuring guidewire-catheter coaxiality), and closely monitoring for AE using transesophageal echocardiography (TEE) or precordial Doppler (PCD) with simultaneous tracking of JBP (> 0 mmHg) and ETCO₂ in patients with right-to-left shunts ^5,6 .