Air emboli are reported to enter the cardiovascular system during cardiac surgery despite air-bubble filters in the arterial line of the cardiopulmonary bypass (CPB). A potential association with stroke, covert cerebral insults and cognitive decline after cardiac surgery has been hypothesized. Although most of the previous studies failed to prove it, this hypothesis cannot be rejected because the situation in the operating room (OR) is multifactorial and complex. Therefore, rigorous and standardized protocols are needed to investigate sources, patterns, as well as effective quantity and volume of air embolism.We hereby present our protocol in detail for systematic data collection as a standard quality control measure at our center, where air bubbles in the cardiopulmonary bypass circuit are measured by a commercial bubble counter. We also show a preview of the type of information that can be obtained for future analysis. The eventual aim is to determine a potential association between air emboli and adverse postoperative outcomes, as well as to identify major sources of air bubbles generation and in the long run to find effective prevention strategies.
Background Gaseous micro-embolism (GME) occurring during contemporary open heart surgery is poorly studied. Current understanding of the biological impact of cardiac surgery focuses on the surgical aggression itself together with contact activation of inflammatory cascades by the extracorporeal circulation (ECC), both promoting various degrees of a systemic inflammatory response syndrome (SIRS). Methods and Findings We prospectively collected data on GME in the ECC circuit according to a quality control protocol during a 12-month period at our institution. Bubbles were measured means of a last generation multi-channel ultrasound measuring unit (BCC300, Gampt GmbH, Meerseburg, Germany) upstream of the arterial line filter. For analysis, bubbles were separated in three size categories: small (S) (10-40 μm), medium (M) (41-200 μm) and large (L) (201-2000 μm). Small bubbles were considered as noise and excluded. A total of 58 out of 70 open heart procedures were included in the final evaluation performed on 58 patients (45 males, 13 females, mean age 66 +/- 9 years). Patient baseline data, type of procedure and perfusion data were retrieved. Preoperative treatment with beta-blockers, ACE-inhibitors, calcium-antagonists and statins was considered. Postoperative SIRS was identified according to modified SIRS and qSOFA criteria. A variably high amount of GME was detected (mean count 847 +/- 2560), we focused on M-sized GME (mean count 820 +/- 2546, mean volume 233 +/- 730 nL). A total of 22 patients (38%) developed SIRS. To account for differences between patient groups (SIRS- / SIRS+) propensity score (PS) matching was performed on the presence of M-bubbles at or above the 75th percentile (count and volume). The impact of such GME on the development of SIRS was statistically highly significant, as shown by the corresponding average treatment effects (ATE). Conclusions Significant GME was associated with postoperative SIRS after cardiac surgery in our setting. This novel finding warrants further confirmation.
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