M Carassiti1, A Mattei2, C M Pizzo2, N Vallone3, P Saccomandi3, E Schena3. 1. Unit of Anesthesia, Intensive Care and Pain Management, Department of Medicine m.carassiti@unicampus.it. 2. Unit of Anesthesia, Intensive Care and Pain Management, Department of Medicine. 3. Unit of Measurements and Biomedical Instrumentation, Center for Integrated Research, Università Campus Bio-Medico di Roma, Via Álvaro del Portillo 21, Rome 00128, Italy.
Abstract
BACKGROUND: Pressures (Pe) exerted by bronchial blockers on the inner wall of the bronchi may cause mucosal ischaemia. Our aims were as follows: (i) to compare the intracuff pressure (Pi) and Pe exerted by commercially available bronchial blockers in an in vitro and an ex vivo model; (ii) to investigate the influence of both the inflated intracuff volume and cuff diameter on Pe; and (iii) to estimate the minimal sealing volume (VSmin) and the corresponding Pe for each bronchial blocker studied. METHODS: The Pe exerted by seven commercial bronchial blockers was measured at different inflation volumes using a custom-designed system using in vitro and ex vivo animal models with two internal diameters (12 and 15 mm). RESULTS: In the same conditions, Pi was significantly lower than Pe (P<0.05), and Pe was higher in the in vitro model than in the ex vivo model. The Pe increased with the inflated volume, with use of the small-diameter model (P<0.05). Ex vivo models needed a higher minimal sealing volume than the in vitro models, and this volume increased with the diameter (e.g. the VSmin at a positive pressure of 25 cm H2O required a Pe ranging from 12 to 78 mm Hg on the 15 mm ex vivo model and from 66 to 110 mm Hg on the 12 mm ex vivo model). CONCLUSIONS: The Pi cannot be used to approximate Pe. The diameter of the model, the inflated volume, and the bronchial blocker design all influence Pe. A pressure higher than the critical ischaemic threshold (i.e. 25 mm Hg) was needed to prevent air leak around the cuff in the in vitro and ex vivo models.
BACKGROUND: Pressures (Pe) exerted by bronchial blockers on the inner wall of the bronchi may cause mucosal ischaemia. Our aims were as follows: (i) to compare the intracuff pressure (Pi) and Pe exerted by commercially available bronchial blockers in an in vitro and an ex vivo model; (ii) to investigate the influence of both the inflated intracuff volume and cuff diameter on Pe; and (iii) to estimate the minimal sealing volume (VSmin) and the corresponding Pe for each bronchial blocker studied. METHODS: The Pe exerted by seven commercial bronchial blockers was measured at different inflation volumes using a custom-designed system using in vitro and ex vivo animal models with two internal diameters (12 and 15 mm). RESULTS: In the same conditions, Pi was significantly lower than Pe (P<0.05), and Pe was higher in the in vitro model than in the ex vivo model. The Pe increased with the inflated volume, with use of the small-diameter model (P<0.05). Ex vivo models needed a higher minimal sealing volume than the in vitro models, and this volume increased with the diameter (e.g. the VSmin at a positive pressure of 25 cm H2O required a Pe ranging from 12 to 78 mm Hg on the 15 mm ex vivo model and from 66 to 110 mm Hg on the 12 mm ex vivo model). CONCLUSIONS: The Pi cannot be used to approximate Pe. The diameter of the model, the inflated volume, and the bronchial blocker design all influence Pe. A pressure higher than the critical ischaemic threshold (i.e. 25 mm Hg) was needed to prevent air leak around the cuff in the in vitro and ex vivo models.