Why the study?
Does induction of anaesthesia with halothane alter cardiovascular hemodynamics in infants and children?
Does induction of anaesthesia with halothane alter cardiovascular hemodynamics in infants and children?
Deep halothane anaesthesia for intubation in infants and children is tolerated but causes significant reductions in cardiac output, myocardial contractility, and blood pressure.
Answers are grounded in this paper and cite their sources.
Supports hemodynamic monitoring with halothane induction in infants and children; leaves open comparative safety versus modern agents.
Cardiac output, blood pressure and heart rate were measured with noninvasive techniques before, during and after induction of anaesthesia with halothane and after intubation in unpremedicated infants and in diazepam-atropine premedicated children presenting for elective surgery. Cardiac output was measured with pulsed doppler echocardiography. Left ventricular shortening fraction was estimated with M-mode echocardiography during induction. Induction with halothane in infants caused significant decrements in blood pressure, cardiac index, stroke volume index and significant depression of left ventricular shortening fraction. Induction with halothane in diazepam-atropine premedicated children caused a significant increase in heart rate but significant decreases in blood pressure, stroke volume index and left ventricular shortening fraction while cardiac index decreased slightly. Intubation in infants caused a mild increase in heart rate compared with pre-induction values but blood pressure, cardiac index and stroke volume index remained below pre-induction values. Intubation in diazepam-atropine premedicated children caused significant increases in heart rate and cardiac index, and a non-significant increase in blood pressure but stroke volume index remained significantly below pre-induction values. Healthy infants and children tolerate induction of anaesthesia with halothane to a depth to permit intubation but large reductions in cardiac output and myocardial contractility are expected with subsequent reductions in blood pressure.
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Tibballs et al. (1988) studied this question.
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