Effects of three anesthetic induction techniques on heart rate variability

Abstract

Study Objective: To investigate the effects of different clinical induction techniques on heart rate variability (HRV). Design: Two studies are reported. Study 1 prospectively compared the effects of two induction techniques (tetomidate vs. thiopental sodium) known to have widely disparate effects on cardiovascular reflexes. Study 2 specifically investigated whether the vagotonic effects of sufentanil cause an increase in vagally mediated HRV. Setting: Elective surgery in a university-affiliated hospital. Patients: Study 1 : 18 ASA physical status I patients having minor surgery; Study 2: 10 ASA physical status III and IV patients having cardiac surgery. Interventions: In Study I, anesthesia was induced with either etomidate 0.3 mg/kg or thiopental sodium 4 mg/kg with 60% nitrous oxide in oxygen. In Study 2, anesthesia was induced with a sufentanil infusion (total dose 2.9 ± 0.2 μg/kg). Measurements and Main Results: The electrocardiogram-derived heart rate signal was subjected to power spectral analysis (similar to electroencephalographic analysis) to obtain measurements of (1) absolute HRV power [units of (beats per minute) 2] within defined frequency ranges (HRV LO = power between 0 and 0.125 Hz; HRV HI = power between 0.126 and 0.5 Hz; HRV TOT = HRV TOT = HRV LO + HRV HI) and (2) normalized HRV power (the percentage of total power) within these same frequency ranges [ e.g., %HRV HI = (HRV HI/HRV TOT × 100%]. In Study 1, both techniques caused large reductions in HRV TOT . The reduction caused by the thiopental sodium technique (−89% ± 2%) significantly exceeded that caused by the etomidate technique (−58% ± 13%, p < 0.02). In Study 2, sufentanil decreased absolute power measurements of vagally mediated HRV (−69 ± 12 change in HRV HI) but increased corresponding normalized measurements of vagally mediated HRV (90% ± 30% increase in %HRV HI). Conclusions: In Study 1, the greater reduction in HRV with the thiopental sodium technique provides evidence that the depressant effects of anesthetics on HRV are related in part to their effects on cardiovascular reflexes. However, the significant depression in HRV caused by the etomidate technique suggests that mechanisms other than baro-reflex depression (e.g., impaired consciousness) also are important in these depressant effects. In Study 2, the decrease in HRV HI caused by sufentanil documents that absolute power measurements of vagally mediated HRV are not correlated with changes in parasympathic tone during a potent opioid induction. This lack of a correlation may result from the decrease in total HRV observed with loss of consiousness. The increase in %HRV HI suggests that normalized measurements of HRV may still provide an index of changes in sympathetic-parasympathetic balance, even when total HRV is decreased following anesthetic administration.