Can't intubate, can't ventilate: is "rescue reversal" a pipe-dream?

Stefanutto et al. in this issue of Anesthesia & Analgesia continue the long quest to develop an optimal anesthetic induction protocol. A technique that assures good-to-excellent conditions for tracheal intubation upon loss of consciousness, yet assures that if “can’t intubate, can’t ventilate” (CICV) conditions are encountered, then adequate spontaneous ventilatory exchange will recover before significant arterial oxygen desaturation supervenes. In healthy patients, apneic intervals of 5 to 7 minutes may elapse before desaturation ( 90% arterial saturation) following preoxygenation in the presence of a patent airway, although in patients with decreased functional residual capacity or venous admixture, this interval may be significantly shorter. The protocol of Stefanutto et al. was designed so that their subjects retained the greatest chance of maintaining oxygenation during propofol/opioid-induced apnea: they received optimal preoxygenation (end-tidal oxygen 90%), and a tightly fitted facemask with insufflated oxygen flow at 6 L/min was kept in place. Assuming a patent airway, the authors’ subjects thus benefited from some degree of “apneic oxygenation. ” The authors chose to avoid the use of succinylcholine to facilitate intubation because there is convincing evidence that significant arterial hemoglobin desaturation may take place before recovery of adequate respiratory mechanics occurs after a traditional “intubating dose” of this relaxant. For example, Heier et al. were able to demonstrate that, after induction with thiopental and succinylcholine (no opioid), spontaneous recovery from succinylcholine-induced apnea frequently did not occur quickly enough to prevent arterial desaturation. The present authors hypothesized that perhaps substituting a short-acting opioid in lieu of succinylcholine might result in a shorter apneic interval. In the present investigation, they studied an induction dose of propofol (2.0 mg/kg) combined with 2 different doses of remifentanil. The first dose they selected, remifentanil 2 g/kg, resulted in arterial hemoglobin saturations 80% in one-third of subjects, although it offered acceptable intubating conditions in 11 of 12 subjects. This time course of respiratory depression and resulting arterial desaturation is consistent with remifentanil’s pharmacokinetic/pharmacodynamic profile. In another session, they reduced the dose of remifentanil to 1.5 g/kg and successfully shortened the apnea time by approximately 1 minute, but 4 of 12 subjects had unacceptable conditions for tracheal intubation. The present study thus demonstrates the limitations of a relaxant-free intubation technique using what are certainly only modest doses of propofol and remifentanil. As pointed out by Sneyd and O’Sullivan, in the absence of a good clinical reason for doing so, “attempting tracheal intubation without a neuromuscular blocking agent represents substitution of an inferior technique for one with greater efficacy. ” In the “real world” of unexpected CICV, a patent airway by definition would not be present, and the adequacy of preoxygenation may be questionable. Thus, the study by Stefanutto et al. probably represents a “best case” scenario. Nevertheless, the arterial O2 saturations in 14 of 24 subjects decreased to 90% at some point. Actual patients would likely experience a faster onset of arterial oxygen desaturation during apnea than the present authors observed. An induction sequence designed to facilitate tracheal intubation ideally should do more than simply induce hypnosis and abet mechanical placement of the endotracheal tube. It should also ensure reflex suppression and cardiovascular stability. Thus, significant reductions in the authors’ doses of propofol/opioid may not be realistic. In young, healthy subjects, perhaps the propofol dosage could be decreased to 1.5 mg/kg, but doses less than remifentanil 1.0 g/kg or fentanyl 2 g/kg are unlikely to suppress the hemodynamic response to intubation. Thus, it appears that muscle relaxant-facilitated intubation is here to stay. An ideal neuromuscular blocker used for intubation should have fast onset and either rapid elimination or the potential for prompt and complete antagonism of its effect. Succinylcholine is still the “gold standard” in this regard. After a 1 mg/kg dose, succinylcholine establishes complete block at the adductor pollicis in 70 20 seconds and first twitch (T1) height recovers to 10% of control in approximately 6 minutes and to 25% of control in 7 minutes. Diaphragmatic recovery takes place approximately 2 minutes earlier, and 50% recovery of this muscle’s strength is seen in 5 to 6 minutes. These data correlate nicely with From the *Department of Anesthesiology, Weill Cornell Medical College, New York, New York; and †Department of Anesthesia, Kyoto University Graduate School of Medicine, Kyoto, Japan.