Mechanisms underlying air aspiration in patients undergoing left atrial catheterization

Air embolism in patients undergoing percutaneous interventions requiring access to the left atrium (LA) represents a potentially fatal complication. Here we tested if a decline in LA pressures following sedation represents an important mechanistic link underlying air intrusion into the LA.

Left atrial pressures were measured in 26 consecutive patients (49 +/- 14 years; 27% male), who underwent percutaneous atrial septal occlusion for persistent foramen ovale or secundum atrial septal defects. Patients either received sedation by propofol allowing for guidance by transesophageal echocardiography (n = 13) or underwent occluder implantation without sedation and under fluoroscopic control only (n = 13). Whereas mean expiratory LA pressures remained unchanged in either group, sedation provoked a marked decline in the mean inspiratory LA pressure as compared to non-sedated patients (Delta p 6.9 +/- 8.6 mm Hg vs. 0.1 +/- 1.2 mm Hg in nonsedated patients, P < 0.001). Ex vivo experiments evaluating the air-tightness of different sheaths in response to negative pressures revealed air aspiration at -13.4 +/- 1.2 mm Hg of suction in all cases, once a guide wire was inserted.

Negative LA pressures in conjunction with air-leaking sheaths are identified as potentially important factors for air intrusion into the LA with the patient's sedation being a primary risk factor to lower LA pressure levels. The results advocate close monitoring of LA pressures during intervention, prevention of airway collapse and protection of LA sheaths from communication with the atmosphere, during procedures under sedation.