Aging: Physiologic changes

All organ systems undergo physiologic changes with aging. From a cardiovascular standpoint, elderly patients have prolonged myocardial contraction and relaxation times (diastolic dysfunction), decreased arterial elasticity and compliance (increased SVR and PVR), decreased maximal heart rate, and decreased alpha1 and beta-adrenergic responsiveness (reduced chronotropic, inotropic, and baroreflex responsiveness) due to changes in autonomic function. Because of reduced cardiac output from diminished maximal heart rates, intravenous induction is prolonged due to increased time for the circulating drug to reach the brain. In contrast, inhalational induction is faster in older adults due to decreased anesthetic uptake from decreased cardiac output and a greater percentage of cardiac output going to the brain. Due to increased cardiac chamber stiffness (decreased ventricular compliance), elderly patients are volume dependent yet volume intolerant leading to a narrow range of end diastolic volume and pressure for optimal hemodynamics. Fibrosis of the sinoatrial node, normal pacemaker cell loss, and atrophy of conduction pathways lead to disturbances in cardiac rhythms and increased susceptibility to arrythmias.

From a respiratory standpoint, elderly patients have decreased lung volume surface area (increased anatomic and alveolar dead space and shunting), reduced gas exchange (increased alveolar-arterial oxygen gradient), reduced PaO₂ (leftward oxyhemoglobin curve shift), increased closing capacity greater than functional capacity leading to alveolar collapse during normal tidal volume breathing, reduced mucociliary clearance, and a less vigorous cough leading to increased risk of aspiration. The ventilatory responses to hypoxia and hypercapnia are markedly reduced increasing apnea/obstruction risk.

From a neurologic standpoint, cerebral autoregulation in response to ventilation and blood pressure changes remains intact. However, there is generalized atrophy of the CNS, which in part is responsible for the decreased MAC requirement by 4–6% each decade after the age of 40. Due to decreased blood flow to the subarachnoid space (slower absorption of anesthetic solutions), higher specific gravity and smaller CSF volumes leading to cephalad spread, and increased lumbar lordosis and thoracic kyphosis, elderly patients have higher levels of spinal anesthesia. Elderly patients also have changes in rhythmic physiologic processes such that normal electroencephalographic frequencies, circadian pattern of sleep, temperature, and plasma cortical levels are derailed. The impaired temperature regulation is in part due to decreased subcutaneous tissue.

Muscle mass decreases with aging, leading to impaired balance, increased insulin resistance, and decreased volume of distribution. The decrease in volume of distribution, in addition to decrease in liver blood flow and increased CNS sensitivity (pharmacodynamic changes), explains why opioids and benzodiazepines are more potent in the elderly, have high initial plasma levels, and have prolonged drug effects (e.g., midazolam half-life almost doubles in the elderly compared to younger patients).

Renal function declines along with renal mass, leading to decreased clearance, prolonged duration of action of renally-eliminated drugs, decreased ability to dilute urine and excrete acid load, and increased susceptibility to nephrotoxins. Similarly, drugs that are hepatically cleared have prolonged duration of action (eg, rocuronium) in the elderly. Colonic changes with aging include decreased motility leading to constipation. Finally, immunosenescence leads to a low inflammatory state as well as loss of regulation of inflammatory processes.