Effects of support surface relief pressures on heel skin blood perfusion

Advances in Skin & Wound Care,  May/Jun 2003  by Mayrovitz, Harvey N,  Sims, Nancy,  Taylor, Martha C,  Dribin, Lori

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ABSTRACT

OBJECTIVE: To investigate the effect of pressure-relief magnitude on heel blood flow.

DESIGN: 12 healthy subjects (5 male, 7 female; 21 to 43 years of age) lay on a support surface for 50 minutes with 1 heel on the end cell of the support surface. Cell pressure was computer controlled to vary cyclically at 5-minute intervals between a constant 20 mm Hg during loading and 10, 5, and 0 mm Hg during off-loading. Heel skin blood perfusion was monitored by laser Doppler probes on the heel and foot dorsum. Average skin blood perfusion during each 10-minute cycle and the hyperemic response after pressure relief were determined absolutely and relative to baseline.

SETTING: University research center

RESULTS: An inverse relationship was found between relief pressure and heel skin blood perfusion over each pressurization-relief cycle and during the hyperemia phase. Full-cycle average skin blood perfusion associated with release to O, 5, and 10 mm Hg were 34.1 + or - 7.5 arbitrary units (AU), 26.4 + or - 7.5 AU, and 9.3 + or - 3.3 AU, respectively (P

CONCLUSIONS: The reduced average skin blood perfusion is attributable to blunting of hyperemia when relief pressure is too high. When it corresponded to an interface pressure near diastolic pressure, little, if any, functional pressure relief or hyperemia is realized. Suitable relief pressures are likely dependent on an individual's diastolic blood pressure and the net tissue forces acting on heel blood vessels. This suggests that lower blood pressures need lower pressure-relief levels. It is suspected that if depressed vascular responsiveness and/or diminished hyperemic reserve is also present, even lower relief pressures are needed.

Pressure ulcers due to sustained unrelieved or inadequately relieved pressure are an important clinical, humanitarian, and economic problem.1-3 Pressure-dependent blood flow changes play a major role in the skin breakdown process, with the greatest breakdown frequency at sites of bony prominences. The heel is particularly prone to such effects,4 in part because of its relatively lower resting blood perfusion level5 and higher amount of surface pressure when under load.6-9 Local blood flow decreases during heel loading5 and flow recovery after unloading are involved in the breakdown process.10-12

Previous work has shown that when the pressure supporting the heel was cycled at different rates, the average blood flow over complete cycles was significantly greater when the level of pressure was zero (full release) when compared with a nonzero-pressure value (partial release).13 However, because only 2 levels of pressure relief were investigated, the blood flow effects of intermediary levels of pressure relief are unknown. The present study sought to characterize the flow responses of the heel to 3 separate pressure-relief levels when the heel was supported with a uniform load magnitude and duration.

METHODS

Subjects

Twelve volunteers (7 female and 5 male), randomly drawn from the medical school student and staff population, were tested after signing an approved institutional review board consent form. All subjects were free of lower-extremity vascular disease verified by pretest ankle-brachial pressure indices (1.13 + or - 0.02 [mean + or - SEM]). None were taking medications that would impact vascular reactivity. Demographic features of the overall group were age, 29.8 + or - 3.1 years (range, 21 to 43 yr); height, 66.4 + or - 1.2 inches; and weight, 148 + or - 7 pounds (range, 125 to 195 lb). All subjects were normotensive, with systolic, diastolic, and mean blood pressures of 107 + or - 7 mm Hg, 67 + or - 2 mm Hg, and 80.3 + or - 2.6 mm Hg, respectively. No subject had diabetes or any other notable medical history.

Protocol and support patterns

Subjects lay on a support surface with their left heel positioned on the end cell. Pressure in the supporting cell was computer controlled and could be made to vary on a cyclic basis between a constant upper limit of 20 mm Hg and a variable lower limit of 10, 5, or 0 mm Hg (Figure 1). The overall test sequence was 50 minutes, during which time the dynamic pattern illustrated in Figure 1 was used. The first cyclic pattern was initiated after a baseline recording interval of 10 minutes, during which the heel was not loaded (0 mm Hg). Tests were conducted in a room with well-controlled ambient temperature. During the course of the experiments, room temperature varied from 23.6 + or - 0.5[degrees]C at the start of the tests to 23.9 + or - 0.5[degrees]C at the end.

Blood perfusion

Heel skin blood perfusion (SBF) was monitored with a laser Doppler probe affixed to the heel with tape and connected to a perfusion monitor (model BPM2; Vasamedics, Inc, St Paul, MN). The probe (P-440 Soflex; Vasamedics, Inc, St Paul, MN) is flat, thin, and has a large surface contact area. The probe was positioned where the heel made contact with the support surface. SBF was continuously monitored throughout the experimental sequence. A second probe was placed on the foot dorsum just proximal to the union of the great and second toe. The second probe monitored foot SBF and was connected to a second perfusion monitor of the same type. The foot SBF was used to judge if any systemic changes in SBF occurred during the experimental procedure. All laser Doppler data was acquired using a time constant setting of 1 second. Skin temperature was measured with a thermocouple on the foot. Average skin temperature of the group at the start of the experiment was 30.5 + or - 0.6[degrees]C and 30.2 + or - 0.7[degrees]C at the end, with no significant temporal changes detected. At the end of the procedure, the biologic zero of both laser Doppler measures were determined using a thigh cuff that was inflated to 40 mm Hg above systolic blood pressure for 2 minutes. The biologic zero value was subtracted from all laser Doppler raw values, which is standard procedure.14