Background: Sensitization of mechanosensitive afferents, which contribute to the exercise pressor reflex, 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 used 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, femoral vascular conductance, HR, stroke volume, cardiac output, ventilation, and muscle oxygenation of the vastus lateralis were assessed in 10 patients with New York Heart Association class II HF at baseline and during 3 min of PLM both with fentanyl and without (control).
Results: Fentanyl had no effect on baseline measures but increased (control vs fentanyl, P < 0.05) the peak PLM-induced change in FBF (493 ± 155 vs 804 ± 198 ΔmL·min−1) and femoral vascular conductance (4.7 ± 2 vs 8.5 ± 3 ΔmL·min−1·mm Hg−1) while norepinephrine spillover (103% ± 19% vs 58% ± 17%Δ) and retrograde FBF (371 ± 115 vs 260 ± 68 ΔmL·min−1) tended to be reduced (P < 0.10). In addition, fentanyl administration resulted in greater PLM-induced increases in muscle oxygenation, suggestive of increased microvascular perfusion. Fentanyl had no effect on the ventilation, mean arterial pressure, HR, stroke volume, or cardiac output 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 seems to augment peripheral sympathetic vasoconstriction in response to movement, a phenomenon that may contribute to exercise intolerance in this population.
1Geriatric Research, Education, and Clinical Center, George E. Wahlen Department of Veteran Affairs Medical Center, Salt Lake City, UT; 2Department of Internal Medicine, University of Utah, Salt Lake City, UT; 3Health and Exercise Sciences Department, Skidmore College, Saratoga Springs, NY; 4Department of Exercise and Sport Science, University of Utah, Salt Lake City, UT; 5Department of Biomedical Sciences for Health, University of Milan, Milan, ITALY; 6Department of Kinesiology and Applied Physiology, University of Delaware, Newark, DE; and 7Department of Anesthesiology, University of Utah, Salt Lake City, UT
Address for correspondence: Stephen J. Ives, Ph.D., Health and Exercise Sciences Department, Skidmore College, 815 N. Broadway Saratoga Springs, NY 12866; E-mail: email@example.com.
Submitted for publication June 2015.
Accepted for publication September 2015.