Key result
Nitrous oxide (75%) significantly attenuated the maximum systolic arterial blood pressure increase to endotracheal intubation compared to control (46 vs 65 mm Hg, P<0.05).
Why the study?
Does nitrous oxide modify the cardiovascular responses to tracheal intubation during general anesthesia in healthy patients?
RCT (n=100)
Randomly assigned
Does nitrous oxide modify the cardiovascular responses to tracheal intubation during general anesthesia in healthy patients?
Absolute Event Rate: 46% vs 65%
p-value: p=<0.05
Nitrous oxide suppresses the pressor response to endotracheal intubation despite augmenting norepinephrine concentrations.
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May blunt intubation pressor responses in healthy patients; extends RCT evidence on nitrous oxide hemodynamics.
Yoo et al. (2003) conducted an RCT in Healthy patients undergoing general anesthesia and tracheal intubation (n=100). Nitrous oxide (N2O) vs. 0% N2O in oxygen was evaluated on Maximum systolic arterial blood pressure changes after intubation (p=<0.05). Nitrous oxide (75%) significantly attenuated the maximum systolic arterial blood pressure increase to endotracheal intubation compared to control (46 vs 65 mm Hg, P<0.05).
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