Instantaneous Time-Courses of Baroreflex Sensitivity, Sympathetic, and Vagal Activities in Response to Mueller Maneuver

Salvador Carrasco-Sosa and Alejandra Guillén-Mandujano
Universidad Autónoma Metropolitana-I


Abstract

Despite the clinical and physiological relevance of Mueller maneuver (MM), because it is the opposite respiratory strain of Valsalva maneuver, mimics obstructive sleep apnea effects, and is a therapeutic procedure used in cardiovascular diseases, its effects on the time-courses of baroreflex sensitivity (BRS), sympathetic and vagal activities have not been reported. Thus, we assessed, in 37 recordings of healthy volunteers, the effects provoked by MM (-40 mmHg, 20s) on the time-courses, estimated by a time-frequency distribution, of low-frequency components of RR (LFRR), systolic (LFSBP) and diastolic blood pressure (LFDBP); high-frequency component of RR (HFRR), BRS, computed by alpha index (√(LFRR/LFSBP)) and its coherence (BRSCO), obtained by cross time-frequency analysis. Ensemble averages of the indexes dynamics, relative to their control values, showed: increments of systolic (SBP) and diastolic blood pressure (DBP) -both after dropping in early phase II (IIE)-, LFSBP and LFDBP in late phase II (IIL) with a plateau that persists until early phase IV (IVE), and gradual recovery in late phase IV (IVL); decrement of RR in phases IIE, IIL and IVE, and increment in IVL; reductions of BRS (Table) and HFRR in phases IIE and IIL, followed by increments to a maximum in IVL; increment of LFRR/HFRR ratio in IIE and IIL and reduction in IVL (Table). In each phase, BRSCO was greater than 0.71 and most indexes' means were different (p<0.03) from their baseline. Our findings support that MM elicits, via baroreflex with reduced sensitivity, increments of cardiac and vasomotor sympathetic outflow and reduction of vagal activity in the strain, effects that provoke rise of SBP, DBP, and cardioacceleration, and, in the post-strain, greater elevations of SBP and DBP that, via baroreflex, now with augmented gain, cause gradual reduction of cardiac and vasomotor sympathetic activities and increment of vagal activity, leading to cardiodeceleration and arterial pressure recovery.