Abstract
BackgroundKetamine is a potent sedative drug that helps to maintain upper‐airway patency, due to its higher upper‐airway dilator muscular activity and higher level of duty cycle, as seen in rats. However, no clinical trials have tested passive upper‐airway collapsibility and changes in the inspiratory duty cycle against partial upper‐airway obstruction in humans. The present study evaluated both the passive mechanical upper‐airway collapsibility and compensatory response against acute partial upper‐airway obstruction using three different sedative drugs in a crossover trial.MethodsEight male volunteers entered this nonblinded, randomized crossover study. Upper‐airway collapsibility (passive critical closing pressure) and inspiratory duty cycle were measured under moderate sedation with ketamine, propofol, and dexmedetomidine. Propofol, dexmedetomidine, and ketamine anesthesia were induced to obtain adequate, same‐level sedation, with a BIS value of 50–70 and the OAA/S score of 2–3 and RASS score of −3.ResultsThe median passive critical closing pressure of 0.08 [−5.51 to 1.20] cm H2O was not significantly different compared to that of propofol sedation (−0.32 [−1.41 to −0.19] cm H2O) and of dexmedetomidine sedation (−0.28 [−0.95 to −0.03] cm H2O) (p = .045). The median passive R US for ketamine 54.35 [32.00 to 117.50] cm H2O/L/s was significantly higher than that for propofol 5.50 [2.475 to 19.60] cm H2O/L/s; (mean difference, 27.50; 95% CI 9.17 to 45.83) (p = .009) and for dexmedetomidine 19.25 [4.125 to 22.05] cm H2O/L/s; (mean difference, 22.88; 95% CI 4.67 to 41.09) (p = .021). The inspiratory duty cycle increased significantly as the inspiratory airflow decreased in passive conditions for each sedative drug, but behavior differed among the three sedative drugs.ConclusionOur findings demonstrate that ketamine sedation may have an advantage of both maintained passive upper‐airway collapsibility and a compensatory respiratory response, due to both increase in neuromuscular activity and the increased duty cycle, to acute partial upper‐airway obstruction.
Highlights
Upper airway obstruction during sedation can result from changes in either the passive structural properties of the pharynx or from disturbances in neuromuscular control (Ayuse, 2010, 2016; Ayuse et al, 2009; Hoshino et al, 2009; Kobayashi et al, 2011), similar to the mechanism in sleep (Patil et al, 2007; Schneider et al, 2009)
An Richmond Agitation-Sedation Scale (RASS) scale of −3 was confirmed for all three sedative drugs, indicating that comparable levels of moderate sedation were achieved with the value of average −3.0 ± 0.5 for propofol, −2.9 ± 0.4 for dexmedetomidine, and −2.8 ± 0.5 for ketamine
The median passive RUS for ketamine 54.35 [32.00 to 117.50] cm H2O/L/s was significantly higher than that for propofol 5.50 [2.475 to 19.60] cm H2O/L/s; (p = .009) and for dexmedetomidine 19.25 [4.125 to 22.05] cm H2O/L/s; (p = .021) (Figure 5)
Summary
Upper airway obstruction during sedation can result from changes in either the passive structural properties of the pharynx or from disturbances in neuromuscular control (Ayuse, 2010, 2016; Ayuse et al, 2009; Hoshino et al, 2009; Kobayashi et al, 2011), similar to the mechanism in sleep (Patil et al, 2007; Schneider et al, 2009). The protocols for sedation using propofol, dexmedetomidine, and ketamine are well established according to age, the magnitude of surgical invasion, and the site of the procedure, for maintaining safety in different clinical contexts Each of these drugs have different characteristics in terms of maintaining upper-airway patency during sedation. We hypothesized that at comparable levels of moderate sedation as assessed clinically, upper airway collapsibility is less with ketamine than that with propofol or dexmedetomidine To address this hypothesis, we examined passive upper-airway properties and timing responses to acute and sustained periods of airflow obstruction under ketamine, propofol, and dexmedetomidine sedation
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