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Heart rate variations (HRV) result from moment-to-moment changes in sympathetic and parasympathetic activity in response to many conditions. These two neural inputs to the heart can be identified by analyzing power spectra of HRV for frequency components at the vasomotor (low-frequency [LF]) and the respiratory (high-frequency [HF]) rhythms. HRV analysis has been used successfully in humans to noninvasively evaluate the autonomic responses to specific maneuvers and drugs, as well as responses to more chronic preexisting pathologic conditions. The effects of an isolated "acute" withdrawal of sympathetic activity in humans, however, have not as yet been evaluated using an autoregressive (AR) technique. We examined HRV using this technique in a group of patients receiving subarachnoid block for abdominal surgery. The sensory levels achieved were within the range of those reported to interrupt sympathetic outflow to the heart. Electrocardiograms were recorded and subjected to AR analysis. AR analysis of HRV after spinal anesthesia revealed significant decreases in both dominant frequency components (LF and HF) that occur between 0.03 Hz and 0.5 Hz. These reductions coincided with blockade of cardiac sympathetic outflow after cephalad spread of the spinal block. The power spectra were almost abolished in patients with sensory blocks reaching T1-2. The decreases in amplitude of the LF and HF components, therefore, act as markers of diminished sympathetic and parasympathetic activity to the heart, while the ratio of LF:HF indicated that sympathovagal balance was predominantly maintained during most of the block.(ABSTRACT TRUNCATED AT 250 WORDS)

The interrelationship between drug-induced changes in heart rate and drug-induced alterations in ventricular automaticity was studied in dogs with intact conduction systems and dogs with surgically-induced complete heart block. The effects of epinephrine (0.5 microgram-kg-1-min-1) and propranolol (1.0 mg-kg-1) on ventricular automaticity were shown to be partially concealed by heart rate changes produced by these agents. Partial concealment of ventricular automaticity changes was shown to result from an alteration in the degree of overdrive suppression secondary to rate changes. Changes in the degree of overdrive suppression have a masking effect on drug-induced alterations in ventricular automaticity and only when the degree of suppression was held constant could the full extent of drug effects on ventricular automaticity be determined. Following vagal stimulation or rapid pacing, the rate of recovery from overdrive suppression as measured by the number of ventricular beats in 30 s was shown to be a dependable index of ventricular automaticity. It was concluded that determinations of drug effects on ventricular automaticity should take into account changes in heart rate produced by the drug. A method for determining ventricular automaticity is described which matches overdrive suppression during the control period to that during drug action in order to cancel out the influence of changes in heart rate on ventricular automaticity.