The elderly patient

Physiology of aging Aging is a progressive physiological process characterized by “declining end organ reserve, decreased functional capacity, increasing imbalance of homeostatic mechanisms and an increasing incidence of pathologic processes” [1]. The effects of aging are particularly manifest in discrete organ systems: Central nervous system (CNS) Biochemical and structural changes have been described in the aging brain, but the exact mechanisms causing changes in functional reserve are unclear. Structurally, gray and white matter volume in the CNS decrease [2], but it is unclear whether the number of synapses present in the cortex is also altered. Older adults demonstrate increased sensitivity to anesthetic drugs, and increased risk of both perioperative delirium and postoperative cognitive dysfunction, likely due to decreases in brain reserve. Neuraxial structural changes include a reduced volume of cerebrospinal fluid, reduction of the epidural space, and increased dura permeability. The diameter and number of myelinated fibers in the dorsal and ventral nerve roots are reduced in older adults. Cardiovascular Cardiac structure and function is altered in older adults. Structural changes include a decrease in number of myocytes and left ventricular (LV) hypertrophy. These structural changes result in decreased contractility, increased myocardial stiffness, and increased ventricular filling pressures. Impairment of diastolic relaxation, which can occur as a result of LV hypertrophy, also leads to diastolic dysfunction in the aging heart. With diastolic dysfunction, echocardiography may demonstrate preserved or hyperdynamic LV systolic function but show characteristic changes in the pattern of flow through the mitral valve. Systolic dysfunction may also be present. Increased vascular stiffness is common with advancing age and leads to important secondary responses in the heart. With increased resistance in the vasculature, the velocity of pulse wave conduction down the vascular tree increases, and reflected pulse waves return to the heart at the end of ejection, resulting in increased cardiac afterload [3] and subsequent LV wall thickening, hypertrophy, and impaired diastolic filling [4].