EVIDENCE FOR A HEART RATE MECHANISM ASSOCIATED WITH TOLERANCE TO PROGRESSIVE CENTRAL HYPOVOLEMIA

Abstract

The tachycardia that accompanies reduced blood volume (e.g., hemorrhage) is associated with elevated sympathetic nerve activity and vagal withdrawal. Subjects with high tolerance (HT) to central hypovolemia display higher heart rates (HR) than low tolerant (LT) subjects. We tested the hypothesis that HT to central hypovolemia would be associated with higher HR, sympathetic activity and vagal withdrawal. Subjects were instrumented to record R‐R intervals (RRI) from ECG and beat‐by‐beat systolic arterial pressure (SAP) from a Finometer® during a progressive LBNP protocol taken to presyncope. Subjects with tolerance = 60 mmHg LBNP were classified as LT (n=31) while subjects who tolerated LBNP levels > 60 mmHg were classified as HT (n=76). The following calculations were performed: power spectral density in the high frequency for RRI (RRIHF; a surrogate of vagal activity that is inversely correlated with sympathetic activity) via fast Fourier transform and spontaneous baroreflex sensitivity (BRS) via RRI‐SAP down‐down sequences. At presyncope, higher (P < 0.001) HR in the HT group (120 ± 2 bpm) than the LT group (99 ± 3 bpm) was associated with lower BRS (HT = 1.7 ± 0.3 vs. LT = 5.7 ± 0.9 ms/mmHg; P = 0.006), and similar (P = 0.377) reductions in RRIHF. Our data support the hypothesis that higher HR associated with HT to progressive central hypovolemia appears to be mediated by sympathetic rather than vagal mechanisms. Similar RRIHF between groups in the presence of a higher BRS in the LT subjects suggests that a sympathetic mechanism for HT may reflect increased cardiac adrenoreceptor responsiveness rather than efferent nerve activity.