Sympathetic responses of patients with congestive heart failure to cold pressor stimulus

Studies in patients with congestive heart failure (CHF) demonstrate blunting of sympathoexcitatory responses to baroreflex perturbation. Whereas experimental and limited clinical evidence suggests impairment of baroreflex mechanisms as the etiology of these attenuated responses, an alternative mechanism would be an inability of patients with CHF to increase sympathetic neural outflow above markedly elevated baseline levels. Hemodynamic and sympathetic neural responses (peroneal microneurography) were therefore compared of normal subjects (n = 10) and patients with CHF (n = 10) during the non-baroreflex sympathoexcitatory stimulus of the cold pressor test. The cold pressor stimulus produced increases in arterial pressure and heart rate in both groups. During hand immersion in ice water, normal subjects demonstrated significant increases in muscle sympathetic nerve activity expressed as burst frequency (20 ± 2 to 28 ± 3 bursts/min, p < 0.01), total integrated nerve activity (224 ± 41 to 342 ± 62 U/ min, p < 0.05), and total activity corrected for accompanying changes in heart rate (375 ± 81 to 538 ± 118 U/100 heart beats, p < 0.05). Similarly, despite elevated control levels of sympathetic activity, patients with CHF also demonstrated significant sympathoexcitatory responses to the cold pressor stimulus, with increases in muscle sympathetic nerve burst frequency (60 ± 7 to 67 ± 7 bursts/min, p < 0.01) total integrated nerve activity (818 ± 159 to 1,015 ± 191 U, p < 0.001), and total activity corrected for accompanying changes in heart rate (1,008 ± 178 to 1,173 ± 201 U/100 heart beats, p < 0.01). Thus, patients with CHF have a preserved capacity for sympathoexcitation despite markedly elevated levels of resting sympathetic activity.