We appreciate the responses by Dr. Kopmen and by Dr. Adnet et al . to our article. 1Dr. Kopman raised the pertinent clinical question about what is the correct dose of succinylcholine necessary to facilitate tracheal intubation. We used 1 mg/kg of succinylcholine because that is the standard recommended dose. 2We did not devote much discussion to the question of dose because it was not a focus of our study. Dr. Kopman argues that smaller doses than 1 mg/kg are adequate for intubation because the ED 95 of succinylcholine is less than 0.3 mg/kg. 3This estimate of potency was obtained using the dorsal interosseous muscle of the hand, a muscle which is not as relevant to quality of tracheal intubation as are the laryngeal adductor muscles. In particular, the duration of action of succinylcholine at the laryngeal adductor muscles is several minutes shorter than at the intrinsic muscles of the hand. 4As a consequence, with small doses of succinylcholine recovery of the laryngeal adductors may occur so rapidly that the “window of opportunity” for tracheal intubation is very short. Consequently, delaying intubation may, in fact, lead to a diminished, not increased, chance of successful intubation. This may explain why a dose of 0.5 mg/kg results in worse conditions for intubation than a dose of 1.5 mg/kg. 5Dr. Kopman eloquently identifies the need for a definitive study on the relationship of dose of succinylcholine to timing and quality of tracheal intubation; we look forward to the results of such a study.
Regarding the comments by Dr. Adnet et al . on rapid-sequence intubation (RSI), our study did not address RSI nor call its safety into question. Our intent was solely to investigate the validity of a clinical belief, namely that recovery from succinylcholine occurs sufficiently rapidly to permit a margin of safety in airway management. We sought to replicate conditions in the “can't intubate and can't ventilate” situation, and while the incidence of this problem is low, the potential for a catastrophic outcome elevates its importance. In this situation, passive transfer of oxygen into the lungs will not take place, therefore, to approximate this circumstance we removed the oxygen mask from the subject's face. The argument by Adnet et al. that in the absence of ventilation, passive oxygenation will maintain hemoglobin saturation for 30 min is misleading. In the study they cite subjects had an endotracheal tube placed, and their lungs were ventilated with 100% oxygen for 30 min before apnea was induced. 6This does not resemble in any meaningful way the clinical situation of managing a difficult airway with a face mask in a paralyzed patient whose lungs cannot be effectively ventilated. In addition, in that study, during the time of passive oxygenation Paco2increased to between 130 and 250 mmHg and pH decreased to between 6.72 and 6.97. 6We believe we have provided important new information that clinicians can use in their decision-making processes, whether that is for an elective and uncomplicated or an emergent rapid-sequence intubation.