Blood perfusion hyperaemia in response to graded loading of human heels assessed by laser-Doppler imaging.
Heel pressure ulcers are important clinical, humanitarian and economic problems arising in part from localized blood flow deficits during loading and inadequate flow recovery. Because there are few data available with regard to the intrinsic physiological responses of heel skin to pressure-induced ischaemia, the present study was undertaken to characterize the main features of the post-loading hyperaemic response. Laser-Doppler perfusion imaging was used to measure hyperaemia in 14 vascularly normal women who were subjected to sequential local heel loading with graded magnitudes (30-140 mmHg) and durations (2.5-20 min). Peak heel perfusion produced by local heating to 44 degrees C for 5 min was used as a comparison standard. All heel loads and durations resulted in hyperaemic responses, with the largest increase in peak response occurring between heel loads of 60 and 120 mmHg. During this transition, peak hyperaemia increased from about 32% to 79% of the local maximal microvascular vasodilatory capacity. Recovery times also increased with both load duration and magnitude, with the longest recovery time being about 7.5 min. Hyperaemic responses and recovery times were analytically dependent on the heel load pressure duration product, with evidence of suppression of the peak response at 1500 mmHg min and a levelling off of recovery time at higher pressure durations. These findings serve to characterize normal physiological perfusion responses to pressure-induced ischaemia at an anatomical site prone to pressure ulceration. The results suggest the possibility of a 'critical' heel loading, above which a near-maximum response is elicited and beyond which vasodilatory recovery potential is blunted.