Effects of three anesthetic induction techniques on heart rate variability

To investigate the effects of different clinical induction techniques on heart rate variability (HRV).

Two studies are reported. Study 1 prospectively compared the effects of two induction techniques (etomidate 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.

Elective surgery in a university-affiliated hospital.

Study 1: 18 ASA physical status I patients having minor surgery; Study 2: 10 ASA physical status III and IV patients having cardiac surgery.

In Study 1, 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 micrograms/kg).

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 (HRVLO = power between 0 and 0.125 Hz; HRVHI = power between 0.126 and 0.5 Hz; HRVTOT = HRVLO + HRVHI) and (2) normalized HRV power (the percentage of total power) within these same frequency ranges [e.g., %HRVHI = (HRVHI/HRVTOT) x 100%]. In Study 1, both techniques caused large reductions in HRVTOT. The reduction caused by the thiopental sodium technique (-89% +/- 2%) significantly exceeded that caused by the etomidate technique (-58% +/- 13%, p less than 0.02). In Study 2, sufentanil decreased absolute power measurements of vagally mediated HRV (-69 +/- 12 change in HRVHI) but increased corresponding normalized measurements of vagally mediated HRV (90% +/- 30% increase in %HRVHI).

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 baroreflex depression (e.g., impaired consciousness) also are important in these depressant effects. In Study 2, the decrease in HRVHI caused by sufentanil documents that absolute power measurements of vagally mediated HRV are not correlated with changes in parasympathetic tone during a potent opioid induction. This lack of a correlation may result from the decrease in total HRV observed with loss of consciousness. The increase in %HRVHI 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.