1. To examine the contribution of paradoxical reflex forearm vasodilatation during unloading of cardiopulmonary baroreceptors to systemic haemodynamics, the responses of central and peripheral haemodynamics during lower-body negative pressure were measured in 24 patients with chronic congestive heart failure (New York Heart Association functional class II-IV) and were compared with those of 10 normal subjects.
2. Lower-body negative pressure of less than −20 mmHg caused a significant forearm vasoconstriction in normal subjects but not in patients with congestive heart failure. In the individual cases, however, eight patients (subgroup A) had a significant forearm vasoconstriction, whereas 10 patients (subgroup B) had a paradoxical forearm vasodilatation. The remaining six patients had a blunted forearm vascular response. Baseline pulmonary capillary wedge pressure (26 ± 3 versus 20 ± 1 mmHg, means ± SEM) and left ventricular wall stress in end-diastole (57 ± 6 versus 37 ± 4 g/cm2) were significantly (P <0.05) higher in subgroup B than in subgroup A.
3. During lower-body negative pressure of −20 mmHg, the plasma level of noradrenaline, systemic vascular resistance and cardiac index did not change significantly in subgroup A. In subgroup B, however, during this orthostatic stimulus systemic vascular resistance fell significantly from a baseline value of 2023 ± 109 to 1740 ± 110 dyns−1 cm−5 (P <0.01) and cardiac index increased significantly from a baseline value of 2.0 ± 0.1 to 2.5 ± 0.21 min−1 m−2 (P <0.01) despite there being no significant change in the plasma level of noradrenaline.
4. After treatment, a second bout of lower-body negative pressure was applied to seven patients in subgroup B. The forearm vascular response to the second bout of lower-body negative pressure was normalized.
5. These data suggest that the patients with more severe heart failure show a paradoxical forearm vasodilatation during mild lower-body negative pressure and that this altered cardiopulmonary baroreflex control of the circulation serves to improve the depressed cardiac performance.