Reply to the “Letter to the Editor: Mind the gap: epistemology of heart rate variability”

Abstract

Dr. Frasch raises insightful points to be considered when measuring, interpreting, and designing experiments investigating the physiological origins of heart rate variability (HRV). Our focus arises directly from the clinical reality of fetal heart rate (FHR) analysis (6, 7). Labor inher-

Physiological control of fetal heart rate variability during labour: implications and controversies

“…The alternate use of both forms of parasympathetic blockade therefore controls for their potential individual indirect effects on autonomic activity. Both vagotomy and atropine had the same impact and essentially abolished visual and time-domain measures of FHRV between a short series of three UCOs (Lear et al 2020e). The similarity in responses also indicates that FHRV in this study was solely mediated via muscarinic receptors at the sinoatrial node.…”

“…The similarity in responses also indicates that FHRV in this study was solely mediated via muscarinic receptors at the sinoatrial node. Critically, RMSSD was reduced between UCOs compared with baseline levels, and visually there was no FHRV, demonstrating that the sympathetic neural contribution to FHRV was suppressed below baseline levels after even 1 × 1 min UCO, rather than merely being masked by increased parasympathetic activity (Lear et al 2020e).…”

“…This parasympathetic blockade study utilized a short series of three 1 min UCOs repeated every 5 min (Lear et al 2020e), which is well-tolerated by healthy fetal sheep. Our finding that the sympathetic contribution was suppressed even during this relatively low frequency of hypoxaemia strongly suggests that parasympathetic activity is the sole mediator of intrapartum FHRV once deep decelerations are present.…”

“…We therefore next tested the hypothesis that increased parasympathetic activity is the key mediator of FHRV during labour-like intermittent fetal hypoxia. In separate groups, parasympathetic blockade was achieved either by bilateral cervical vagotomy or by infusing the competitive, non-selective muscarinic acetylcholine receptor antagonist atropine sulphate (Lear et al 2020e).…”

Characteristics and physiological basis of falls in ventricular outputs after immediate cord clamping at delivery in preterm fetal lambs

“…That heart rate and arterial blood pressures did not increase during this phase may have been related to two factors. First, it is likely that the stimulatory actions of elevated concentrations of circulating catecholamines were countered by the parasympathetic activation occurring during fetal asphyxia (Galinsky et al 2014;Lear et al 2020d). Second, asphyxia appears to inhibit the chronotropic and pressor actions of circulating catecholamines in the immature circulation, particularly in the presence of acidaemia (Preziosi et al 1993).…”