Anaesthesia and Critical Care, Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham, UK.
Anaesthesia and Critical Care, Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham, UK; Nottingham University Hospitals NHS Trust, Nottingham, UK.
Br J Anaesth. 2020 Jul;125(1):e69-e74. doi: 10.1016/j.bja.2020.01.004. Epub 2020 Jan 31.
During induction of general anaesthesia, patients frequently experience apnoea, which can lead to dangerous hypoxaemia. An obstructed upper airway can impede attempts to provide ventilation. Although unrelieved apnoea is rare, it continues to cause deaths. Clinical investigation of management strategies for such scenarios is effectively impossible because of ethical and practical considerations.
A population-representative cohort of 100 virtual (in silico) subjects was configured using a high-fidelity computational model of the pulmonary and cardiovascular systems. Each subject breathed 100% oxygen for 3 min and then became apnoeic, with an obstructed upper airway, during induction of general anaesthesia. Apnoea continued throughout the protocol. When arterial oxygen saturation (Sao) reached 20%, 40%, or 60%, airway obstruction was relieved. We examined the effect of varying supraglottic oxygen fraction (Fo) on the degree of passive re-oxygenation occurring without tidal ventilation.
Relief of airway obstruction during apnoea produced a single, passive inhalation (caused by intrathoracic hypobaric pressure) in all cases. The degree of re-oxygenation after airway opening was markedly influenced by the supraglottic Fo, with a supraglottic Fo of 100% providing significant and sustained re-oxygenation (post-rescue Pao 42.3 [4.4] kPa, when the airway rescue occurred after desaturation to Sao 60%).
Supraglottic oxygen supplementation before relieving upper airway obstruction improves the effectiveness of simulated airway rescue. Management strategies should be implemented to assure a substantially increased pharyngeal Fo during difficult airway management.
在全身麻醉诱导期间,患者经常会出现呼吸暂停,这可能导致危险的低氧血症。上呼吸道阻塞会妨碍通气尝试。尽管未缓解的呼吸暂停并不常见,但它仍会导致死亡。由于伦理和实际考虑,对这种情况的管理策略进行临床研究实际上是不可能的。
使用肺部和心血管系统的高保真计算模型,对 100 名虚拟(计算机模拟)受试者进行了代表性人群队列配置。每个受试者在全身麻醉诱导期间用 100%氧气呼吸 3 分钟,然后上呼吸道阻塞导致呼吸暂停。呼吸暂停在整个方案中持续进行。当动脉血氧饱和度(Sao)降至 20%、40%或 60%时,解除气道阻塞。我们检查了不同的上气道氧分数(Fo)对无潮气量通气时发生的被动再氧合程度的影响。
在呼吸暂停期间解除气道阻塞会在所有情况下产生单次被动吸入(由胸腔内低气压引起)。气道开放后的再氧合程度明显受到上气道 Fo 的影响,上气道 Fo 为 100% 可提供显著和持续的再氧合(气道抢救发生在 Sao 降至 60%后,抢救后 Pao 为 42.3[4.4]kPa)。
在上气道阻塞缓解前给予上气道氧补充可提高模拟气道抢救的效果。应实施管理策略,以确保在困难气道管理期间上咽部 Fo 显著增加。