Airway management is one of the most time-critical interventions in intensive care. If any difficulty delays or prevents ideal airway management, the patient is exposed to severe risk. Most texts place heavy emphasis on the prediction of anatomical difficulties. Additionally, considerable focus is provided on the steps of physically placing an endotracheal tube.
However, the difficulties posed by a patient's underlying physiology is where many of the pitfalls lie in critical care airway management. The decision to intubate a patient emergently indicates that patient is in extremis, and so particular attention to the patient's physiologic reserve and potential response to induction options should hold equal importance in the process of intubation as technique and tools.
Upon the decision to intubate, it is crucial to assess the patient's physiologic reserve and, while preparing, take steps to optimize the patient's chances of making it through the intubation process without decompensation. This chapter outlines several key considerations in the approach to the physiology of the peri-intubation period in the crashing patient.
Broadly, the factors that lead to the difficult physiologic intubation can be broken down into three categories: hemodynamics, oxygenation, and pH (acidosis). When ignored, each can lead to devastating consequences. As airway texts gravitate towards acronyms, these factors can be encompassed by the mnemonic “HOp killers.”
A patient who is hypotensive prior to intubation is at high risk of further hemodynamic decompensation or cardiac arrest during the peri-intubation period.1–2 Cognizance of this risk and careful selection of induction agent can significantly impact a patient's likelihood of surviving the intubation. The highest priority is to keep the patient alive; all other concerns are secondary to this goal. Amnesia, analgesia, and a lack of awareness are imperative, but should not be prioritized above preserving hemodynamics until a definitive airway is in place.
Every induction agent will lower an already hypotensive patient's blood pressure due to the loss of the patient's catecholamine surge. During critical illness, the “fight or flight” mode supplies endogenous surges of catecholamines. Induction will blunt this surge as we shut off the central stress response. Preload, and therefore cardiac output, are further augmented by large tidal volumes generated by negative inspiratory force. The switch to positive pressure ventilation can reduce preload and worsen hypotension.
In the case of propofol, markedly reducing the dose of propofol by 90% can facilitate induction without causing such exaggerated hemodynamic effects. These reduced doses when administered to shock patients seem to still retain the central sedating effects of full doses.3,4
Etomidate intrinsically does not cause hemodynamic effects, but it does cause the same removal of catecholamine drive.5,6 As opposed to propofol, the dose of etomidate should not be reduced, and may even require a ...