In the past several decades, there has been a dramatic increase in the percentage of the world's population that is elderly, defined as people 65 years or older. This trend is projected to continue to increase in the future.1 Understanding core principles of perioperative care of the elderly, particularly in the context of clinical pharmacology, will become increasingly more important for clinicians.
PHYSIOLOGIC CHANGES WITH AGING
As people age, there are important changes in physiology and response to pharmacologic interventions. Aging consists of the deterioration or loss of functional units (eg, neurons, nephrons, or alveoli) at the cellular, tissue, or organ level, as well as disruption of regulatory processes at the molecular level.2 Basal organ function, in the otherwise healthy individual, is relatively preserved with aging,3 but functional reserves and the ability to tolerate stress, such as occurs with anesthesia and surgery, declines significantly with age. However, with regard to organ function, wide intraindividual and interindividual variability does exist.4 That is, biologic age does not linearly correlate with physiologic or medical age. The geriatric population is unique in its physical and medical heterogeneity, which only increases with advancing age. Acute or chronic disease states, genetics, environmental, socioeconomic and likely countless other factors play into the rate or degree of organ function decline. Advanced age, nevertheless, has been shown by many studies to be an independent predictor of perioperative outcome (Table 25–1).
Table 25–1Physiologic changes with age and associated clinical consequences. |Favorite Table|Download (.pdf) Table 25–1 Physiologic changes with age and associated clinical consequences.
| ||Physiologic Changes With Age ||Consequences of Changes |
|Cardiovascular || |
Increased: systolic blood pressure, pulse pressure, sinoatrial node conduction time5
Decreased: LV compliance, β1-receptor response, heart rate,6 VO2 max (10% per decade between age 20 and 80),7 compliance of aorta and great arteries8
Increased: LV wall thickness, LV chamber size, LV mass, oxygen demand9
Decreased: chronotropic responses to noxious stimulus or β agonist, ability to compensatorily increase cardiac output
|Pulmonary || |
Increased: work of breathing, physiologic shunt, ventilation/perfusion mismatch, residual volume, closing capacity
Decreased: FEV1 (8%–10% per decade), chest wall compliance, vital capacity, respiratory muscle strength, maximal minute ventilation
Increased: propensity for hypoxemia, atelectasis
Decreased: functional reserve to deal with stresses of anesthesia/surgery, gas exchange, arterial oxygenation, respiratory mechanics
|Neurologic || |
Increased: enzymatic activity that leads to neuronal degradation
Decreased: brain mass, neurotransmitter synthesis, hypoxic drive, hypercarbic ventilatory drive
Increased: propensity for postoperative delirium, cognitive dysfunction (41% and 13% at 3 months)9
Additional risk factors include anticholinergics, opioids, preexisting cognitive impairment, blood urea nitrogen–to–creatine ration greater than 18, fever, blood loss, infections)
|Renal || |
Maintained: acid–base balance
Decreased: number of nephrons, renal mass, glomerular filtration rate and renal blood flow (30%–50% by age 70)
|Decreased: clearance of certain drugs, urine concentrating ability during water deprivation10 |
|Hepatic ||Decreased: hepatic ...|
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