Halothane and cardiac autonomic control in infants: assessment with quantitative respiratory sinus arrhythmia
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Updated: Nov 3, 2026

Quantitative Autonomic Testing
Published on: July 19, 2011
T F Oberlander1, C B Berde, J P Saul
1Department of Cardiology, Children's Hospital, Boston, Massachusetts 02115, USA.
Abstract:
In comparison to adults, infants undergoing halothane anesthesia have an increased incidence of clinically significant episodes of bradycardia, hypotension, and cardiac arrest. To examine potential cardiac autonomic regulatory mechanisms that may account for these observations, the relationship between respiratory activity and short-term variations of heart rate was quantified in 10 healthy term nonpremedicated infants (28.4 +/- 0.6 wk old) undergoing elective surgery with halothane and low caudal anesthesia. Quantitative respiratory activity, heart rate, and cuff blood pressure data were obtained during the preoperative awake period, and at three depths of halothane--1, 1.3, and 2.0 mean alveolar concentration (MAC). Time and frequency domain analyses were performed on two 2.2-min epochs of data from each condition to yield mean values, spectral measures of low (0.02-0.15 Hz) and high (0.15-0.80 Hz) frequency power (LF and HF), and the LF/HF ratio. The sympathetic (As) and parasympathetic (Ap) components of respiratory sinus arrhythmia were quantified using the transfer relations between respiration and heart rate to derive gain factors Ax and Ap, respectively. Mean heart rate, blood pressure, and respiratory activity all decreased with halothane exposure (p < 0.01), but did not differ by halothane dose. Similarly, LF, HF, LF/HF, and respiratory powers all decreased with halothane, but not between doses. When the effects of respiratory activity on heart rate were accounted for, As decreased at 1.3 and 2.0 MAC only, but Ap remained unchanged. Decreased LF and HF power suggests that halothane altered both sympathetic and parasympathetic heart rate control; however, when the ratio between LF and HF and the quantitative effects of respiration are accounted for, halothane appears to cause a reduction in respiratory related sympathetic heart rate control, without a significant change in parasympathetic control.
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