There remains much confusion regarding the pathophysiology of pressure ulcers. Data indicate that the prevalence of pressure ulcers is increasing. The heel is unique in structure and well adapted to the task of shock absorption. However, it is often subject to prolonged pressure, which predisposes it to tissue breakdown, with attempts at reconstruction prone to failure. Four dissections were carried out of the heel region, which included removing each heel pad en bloc for histology. Seventeen arterial injection studies, 12 venous studies, and a combined arterial and venous study of the foot were performed. The results were correlated with clinical cases and previous research. The heel was found to be richly vascularized by a subdermal plexus and periosteal plexus with vessels traveling between the 2 within fibrous septa that connect the reticular dermis and periosteum of the calcaneus. These septa effectively create isolated compartments containing relatively avascular fat. A layer of panniculus carnosus muscle was observed in the subcutaneous tissue. It is likely that the metabolically active panniculus carnosus muscle is involved early in the course of pressure ulcers. Extensive pressure damage can be concealed by intact skin. Friction and shear are additional factors important in skin breakdown.