Vagal pathways and heart rate variability in recovery after caesarean delivery: a framework for multimodal autonomic-immune phenotyping

Recovery after caesarean delivery involves interacting inflammatory, autonomic, neuroendocrine, nociceptive and psychosocial processes. This Mini Review examines whether vagal pathways and heart rate variability (HRV) can provide a mechanistic and measurable framework for studying that recovery. The inflammatory reflex and cholinergic anti-inflammatory pathway offer a biological rationale: neural signals can restrain cytokine production through an autonomic-immune circuit that includes splenic sympathetic signalling, norepinephrine-responsive acetylcholine-producing T cells and the α7 nicotinic acetylcholine receptor (α7nAChR) on macrophages. However, the anatomy and relative vagal and sympathetic contributions to this circuit remain debated. HRV, particularly the root mean square of successive differences and high-frequency power under standardized recording conditions, indexes cardiac parasympathetic modulation rather than whole-body vagal activity or splenic anti-inflammatory output. Pregnancy is accompanied by substantial autonomic adaptation, and postpartum HRV follows a dynamic trajectory, but existing longitudinal data do not establish when individual values return to pre-pregnancy baselines. In obstetric anaesthesia, HRV has mainly been studied as a preoperative predictor of spinal anaesthesia-induced hypotension; evidence for serial HRV as a recovery measure remains limited. We therefore propose a testable framework in which standardized longitudinal HRV is paired with inflammatory biomarkers, patient-reported recovery and clinical milestones after caesarean delivery. Non-invasive interventions such as transcutaneous auricular vagus nerve stimulation, slow-paced breathing and HRV biofeedback are plausible probes of this framework, but their target engagement and clinical effects require rigorous sham-controlled evaluation. HRV should be treated as a candidate component of multimodal recovery phenotyping, not as a direct measure of the cholinergic anti-inflammatory pathway.