SummaryThe Airtraq Ò Laryngoscope is a novel intubation device which allows visualisation of the vocal cords without alignment of the oral, pharyngeal and tracheal axes. We compared the Airtraq Ò with the Macintosh laryngoscope in simulated easy and difficult laryngoscopy. Twenty-five anaesthetists were allowed up to three attempts to intubate the trachea in each of three laryngoscopy scenarios using a Laerdal Ò Intubation Trainer followed by five scenarios using a Laerdal SimMan Ò Manikin. Each anaesthetist then performed tracheal intubation of the normal airway a second time to characterise the learning curve. In the simulated easy laryngoscopy scenarios, there was no difference between the Airtraq Ò and the Macintosh in success of tracheal intubation. The time taken to intubate at the end of the protocol was significantly lower using the Airtraq Ò

SummaryDirect laryngoscopic tracheal intubation is taught to many healthcare professionals as it is a potentially lifesaving procedure. However, it is a difficult skill to acquire and maintain, and, of concern, the consequences of poorly performed intubation attempts are potentially serious. The Airtraq Ò Laryngoscope is a novel intubation device which may possess advantages over conventional direct laryngoscopes for use by novice personnel. We conducted a prospective trial with 40 medical students who had no prior airway management experience. Following brief didactic instruction, each participant took turns in performing laryngoscopy and intubation using the Macintosh and Airtraq devices under direct supervision. Each student was allowed up to three attempts to intubate in three laryngoscopy scenarios using a Laerdal Ò Intubation Trainer and one scenario in a Laerdal Ò SimMan Ò Manikin. They then performed tracheal intubation of the normal airway a second time to characterise the learning curve for each device. The Airtraq provided superior intubating conditions, resulting in greater success of intubation, particularly in the difficult laryngoscopy scenarios. In both easy and simulated difficult laryngoscopy scenarios, the Airtraq decreased the duration of intubation attempts, reduced the number of optimisation manoeuvres required, and reduced the potential for dental trauma. The Airtraq device showed a rapid learning curve and the students found it significantly easier to use. The Airtraq appears to be a superior device for novice personnel to acquire the skills of tracheal intubation.

Background: Hypercapnic acidosis exerts protective effects in acute lung injury but may also slow cellular repair. These effects may be mediated via inhibition of nuclear factor-kB (NF-kB), a pivotal transcriptional regulator in inflammation and repair. Objectives: To determine the effects of hypercapnic acidosis in pulmonary epithelial wound repair, to elucidate the role of NF-kB and to examine the mechanisms by which these effects are mediated. Methods: Confluent small airway epithelial cell, human bronchial epithelial cell and type II alveolar A549 cell monolayers were subjected to wound injury under conditions of hypercapnic acidosis (pH 7.0, carbon dioxide tension (PCO 2 ) 11 kPa) or normocapnia (pH 7.37, PCO 2 5.5 kPa) and the rate of healing determined. Subsequent experiments investigated the role of hypercapnia versus acidosis and elucidated the role of NF-kB and mitogenactivated protein kinases. The roles of cellular mitosis versus migration and of matrix metalloproteinases in mediating these effects were then determined. Results: Hypercapnic acidosis reduced wound closure (mean (SD) 33 (6.3)% vs 64 (5.9)%, p,0.01) and reduced activation of NF-kB compared with normocapnia. Buffering of the acidosis did not alter this inhibitory effect. Prior inhibition of NF-kB activation occluded the effect of hypercapnic acidosis. Inhibition of ERK, JNK and P38 did not modulate wound healing. Hypercapnic acidosis reduced epithelial cell migration but did not alter mitosis, and reduced matrix metalloproteinase-1 while increasing concentrations of tissue inhibitor of metalloproteinase-2. Conclusions: Hypercapnic acidosis inhibits pulmonary epithelial wound healing by reducing cell migration via an NF-kB dependent mechanism that may involve alterations in matrix metalloproteinase activity.

Hypercapnic acidosis attenuated ventilation-induced lung injury independent of injury severity and decreased mechanical stretch-induced epithelial injury and death, via a nuclear factor-κB-dependent mechanism.