Pulse Rate Changes and Antagonism to Neuromuscular Blockade by Dose-Related Neostigmine and Atropine.
10.4097/kjae.1984.17.1.42
- Author:
Young Hoo MIN
1
;
Young Taek KIM
;
Jae Hyun SUH
;
Se Ung CHON
Author Information
1. Department of Anesthesiology, Catholic Medical College, Seoul, Korea.
- Publication Type:Original Article ; Randomized Controlled Trial
- MeSH:
Anesthesia;
Anesthesia, General;
Atropine*;
Blood Pressure;
Bradycardia;
Diazepam;
Electrocardiography;
Halothane;
Heart Rate*;
Humans;
Intubation;
Neostigmine*;
Neuromuscular Blockade*;
Oxygen;
Pancuronium;
Preanesthetic Medication;
Succinylcholine;
Thiopental
- From:Korean Journal of Anesthesiology
1984;17(1):42-46
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Neostigmine, an antagonist of the competitive muscle relaxants, is the reversal agent most commonly used clinically. Neostigmine produce a vagotonic effect causing bradycardia. For this reason, it has always been advocated that it shoud be blocked by anticholinergic drugs. Earlier clinical studies had demonstrated dose of atropine and neostigmine require to reverse the neuromuscular block and to prevent bradycardia. Several authors recommended titrating the amount neostigmine and atropine to a specific end point, but adequate dose was not established. Therefore, this study were designated to compare the heart rate changes and recovery index followed by dose related neostigmine and atropine. Forty patients undergoing general anesthesia were randomly divided in neostigmine 30ug/mg-atropine 15ug/kg(group A) and neostigmine 40ug/kg-atropine 15ug/kg(group B) group. All patients are received atropine 0.01mg/kg and valium 0.18mg/kg for preanesthetic medications. Anesthesia was induced with thiopental sodium 4~5mg/kg, followed by succinylcholine 1mg/kg to facilitate the intubation. Anesthesia was maintained with 50% N2O in oxygen with 1% halothane. In all patients following induction of anesthesia, neuromuscular block was monitored continuously throughout the study. Pancuronium was administered, as a bolus, in a dose of 0.04mg/kg with increment of 0.02mg/kg, when necessary, to depress the T4/T2 ratio less than 10%. When muscle twitch activity, following pancuronium administration, had recovered spontaneously to 20% of T4/T2 ratio, each dose of atropine and neoatigmine was given. Heart rate counted from the ECG tracing and blood pressure was checked for 30 minutes after injection. Recovery index was calculated. The results were as follows. 1) In group A, maximal increase of pulse rate by intravenous atropine was 23.3+/-4.79%, maximal decrease of pulse rate was 22.6+/-11.50% within 12.2+/-6.07 minutes. Recovery index was 7.5+/-4.82minutes. 2) In group B, maximal increase of pulse rate by intravenous atropine was 13.5+/-10.08%, Maximal decrease of pulse rate was 29.9+/-8.30% within 10.9+/-2.81 minutes. Recovery index was 6.3+/-3.95 minutes. 3) In A and B group, neuromuscular blockade induced by pancuronium 0.04mg/kg was adequately recovered by neostigmine 30~40 ug/kg in all cases. 4) Severe bradycardia was developed after mixed injection of atropine 15ug/kg to neostigmine 30~40 ug/kg in A and B group.
