Key result
Increasing concentrations of nitrous oxide gradually attenuated the pressor response to endotracheal intubation without affecting the tachycardiac response, while enhancing plasma norepinephrine increases.
Why the study?
Does nitrous oxide attenuate the cardiovascular response to endotracheal intubation in ASA I patients undergoing general anesthesia?
Population
100 ASA I patients (aged 35-60 yr) undergoing general anesthesia and endotracheal intubation
Comparison
Nitrous oxide in oxygen at concentrations of… vs 0% nitrous oxide in oxygen (control group)
Design
RCT, assigned randomly
Follow-up
up to 5 min after intubation
Authors
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Nitrous oxide may blunt hypertensive response during intubation in ASA I patients; extends RCT evidence on its differential hemodynamic and norepinephrine effects.
RCT (n=80)
Randomly assigned
No
Does nitrous oxide attenuate the cardiovascular response to endotracheal intubation in ASA I patients undergoing general anesthesia?
Nitrous oxide attenuates the pressor response but not the tachycardiac response to endotracheal intubation, while enhancing plasma norepinephrine increases.
Jeong et al. (2003) conducted an RCT in Patients undergoing general anesthesia and endotracheal intubation (n=80). Nitrous oxide vs. 0% N2O (oxygen only) was evaluated on Cardiovascular response (systolic arterial pressure and heart rate) to intubation. Increasing concentrations of nitrous oxide gradually attenuated the pressor response to endotracheal intubation without affecting the tachycardiac response, while enhancing plasma norepinephrine increases.
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