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Echocardiographic evaluation of vagolytic effects of atropine sulfate during pediatric halothane anesthesia

H Horigome1, M Tsuji, M Yamashita

  • 1Department of Pediatrics, Ibaraki Children's Hospital, Mito, Japan.

Acta Paediatrica Japonica : Overseas Edition
|December 1, 1993
PubMed

Insights

Atropine sulfate effectively reversed halothane-induced bradycardia and hypotension in children. However, higher doses did not improve left ventricular function, indicating myocardial depression is not fully attenuated by vagolysis.

Area of Science:

  • Pediatric Anesthesiology
  • Cardiovascular Pharmacology
  • Pediatric Cardiology

Background:

  • Halothane anesthesia can induce cardiovascular depression in children, characterized by decreased heart rate, blood pressure, and left ventricular function.
  • Atropine sulfate is commonly used to counteract these effects, but its optimal dosage for pediatric patients remains debated.
  • Understanding the dose-dependent efficacy of atropine is crucial for managing anesthesia-related cardiovascular complications in children.

Purpose of the Study:

  • To investigate the antagonistic effects of atropine sulfate on halothane-induced cardiovascular depression in pediatric patients.
  • To determine if a higher dose of atropine sulfate is more effective in attenuating halothane-induced myocardial depression.
  • To evaluate the impact of different atropine sulfate dosages on cardiac function parameters.

Main Methods:

  • A randomized study involving 34 children (1-12 years) undergoing minor surgery.
  • M-mode echocardiography assessed left ventricular function (LVSF, LVEDD) at three time points: pre-induction, post-induction, and post-atropine administration.
  • Patients received either 0.01 mg/kg or 0.02 mg/kg of atropine sulfate, with comparisons made between groups and time points.

Main Results:

  • Halothane induction significantly decreased heart rate (HR), mean blood pressure (MBP), and left ventricular shortening fraction (LVSF), while increasing left ventricular end-diastolic dimension (LVEDD).
  • Atropine administration recovered HR and MBP, but LVSF and LVEDD remained unchanged, suggesting persistent myocardial depression.
  • No significant differences in cardiovascular parameters were observed between the 0.01 mg/kg and 0.02 mg/kg atropine groups, except for HR and mean velocity of circumferential fiber shortening (mVcf).

Conclusions:

  • Atropine sulfate effectively antagonizes halothane-induced bradycardia and hypotension in children.
  • The myocardial depression induced by halothane is not necessarily attenuated by vagolysis, irrespective of atropine dosage.
  • A lower dose of atropine sulfate (0.01 mg/kg) appears sufficient to counteract the immediate cardiovascular effects of halothane anesthesia in pediatric patients.

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