Background

Sensitization of mechanosensitive afferents, which contribute to the exercise pressor reflex (EPR) has been recognized as a characteristic of patients with heart failure (HF), however, the hemodynamic implications of this hypersensitivity are unclear.

Objectives

The present study utilized passive leg movement (PLM) and intrathecal injection of fentanyl to blunt the afferent portion of this reflex arc to better understand the role of the mechanoreflex on central and peripheral hemodynamics in HF.

Methods

Femoral blood flow (FBF), mean arterial pressure (MAP), femoral vascular conductance (FVC), heart rate (HR), stroke volume (SV), cardiac output (CO), ventilation (V E), and muscle oxygenation of the vastus lateralis, were assessed in 10 NYHA class II HF patients at baseline and during 3-min of PLM both with fentanyl and without (control).

Results

Fentanyl had no effect on baseline measures, but increased (p< 0.05, control vs. fentanyl) the peak PLM-induced change in FBF (493±155 vs. 804±198 ΔmL/min), and FVC (4.7±2 vs. 8.5±3 ΔmL/min/mmHg), while norepinephrine spillover (103±19 vs. 58±17% Δ), and retrograde FBF (371±115 vs. 260±68 ΔmL/min) tended to be reduced (p< 0.10). Additionally, fentanyl administration resulted in greater PLM-induced increases in muscle oxygenation, suggestive of increased microvascular perfusion. Fentanyl had no effect on the V E, MAP, HR, SV, or CO response to PLM.

Conclusions

Although movement-induced central hemodynamics were unchanged by afferent blockade, peripheral hemodynamic responses were significantly enhanced. Thus, in patients with HF a heightened mechanoreflex appears to augment peripheral sympathetic vasoconstriction in response to movement, a phenomenon that may contribute to exercise intolerance in this population.