1. Arteries stiffen with age, leading to faster propagation and reflection of the pulse pressure waveform. The reflected waveform augments the pressure at the aortic root. With increasing age, the reflected energy arrives progressively earlier in the cardiac cycle, shifting from early diastole to late systole. Thus, aging causes decreased diastolic and increased systolic pressure (and pulse pressure) and leads to ventricular thickening and prolonged ejection.

2. Slower myocardial relaxation and ventricular hypertrophy lead to late diastolic filling and diastolic dysfunction. Atrial contraction is important to maintain late filling.

3. Reduced venous capacitance decreases the “vascular reserve volume” available to buffer hemorrhage.

4. Reduced baroreceptor reflexes result from increased sympathetic tone, decreased parasympathetic tone, decreased baroreceptor sensitivity, and decreased responsiveness to β-adrenergic stimulation. Thus, hypotension occurs frequently with changes in volume, position, anesthetic depth, and regional anesthetic-induced sympathetic blockade.

5. Maximal heart rate decreases with age while stroke volume remains constant, but end-diastolic volume increases and ejection fraction decreases.

6. Maximal oxygen consumption decreases because of reductions in arteriovenous oxygen tension difference and cardiac output.

1. Parenchymal changes. Approximately 30% of alveolar wall tissue is lost between ages 20 and 80, diminishing elastic recoil and parenchymal traction that maintain airway patency. The loss produces the following changes:

a. Increased residual volume, closing volume, and functional residual capacity; decreased vital capacity and forced expiratory volume in first second (FEV₁).

b. Progressive mismatching of ventilation to perfusion, with an age-dependent decrease in arterial oxygen tension.

c. Increased physiologic dead space and reduced diffusing capacity.

2. Chest wall changes: multiple factors lead to a stiffer chest wall and respiratory muscle mass decreases.

3. Depressed ventilatory response to hypoxia and hypercarbia.

4. Decreased protective airway reflexes increase aspiration risk.

1. Progressive loss of neurons and decreased neurotransmitter activity contribute to decreased anesthetic requirements for all agents.

2. Cerebral autoregulatory responses to blood pressure, CO₂, and O₂ are maintained.

1. Serum creatinine remains stable with advancing age because age-associated decreases of creatinine clearance are offset by reduced
creatinine production from skeletal muscle. A normal creatinine level in the elderly should not be interpreted as an absence of renal impairment. For example, a healthy 80-year-old patient is expected to have half the creatinine clearance of a 20-year-old patient, even though they may have similar serum creatinine levels.

2. Progressive atrophy of renal parenchyma and sclerosis of vascular structures lead to diminished renal blood flow and glomerular filtration rate.

3. Reduced ability to correct alterations in electrolyte concentrations, intravascular volume, and free water.

4. Reduced glomerular filtration rate leads to delayed renal drug excretion.

1. Decreased liver mass and reduced portal and hepatic blood flows result in reduced hepatic drug clearance.

2. Cytochrome P-450 enzyme activity decreases with aging.

3. Phase 1 (oxidation and reduction) and phase 2 (conjugation) reactions may be depressed with aging.

1. Basal metabolism and heat production decrease because of skeletal muscle atrophy and variable replacement with adipose tissue.

2. The propensity for hypothermia increases because of blunted central thermoregulation and body compositional changes.

3. Decreases in muscle mass and total body water, coupled with increases in body fat, reduce the volume of distribution of water-soluble drugs and increase it for lipid-soluble drugs.

1. Protein binding of anesthetic drugs is reduced because of decreased levels of circulating serum protein—for example, albumin. Therefore, their pharmacologic effects are potentiated.

2. Reduction in blood volume, an increase in percentage of body fat, and decreases in hepatic and renal function result in prolonged elimination for drugs dependent on redistribution and/or elimination for termination of action thereby prolonging anesthetic effects.

1. The elderly brain is more sensitive to drugs. Reductions in neuronal density, cerebral blood flow, and oxygen consumption result in an age-related reduction in inhalation and intravenous anesthetic requirements.

2. Drug sensitivity varies with the type of drug. Responses to specific drugs are difficult to predict and may vary widely in the elderly. For example, catecholamines require higher doses for equivalent effects, and benzodiazepines exert greater effects in the elderly.

3. The rate of adverse drug reaction increases with age and with the number of drugs administered. This includes the increased occurrence of over sedation, excess respiratory depression, and altered mental status.

1. Age-related coexisting disease is a major predictor for perioperative mortality and serious morbidity. Age-related coexisting disease increases elderly patients’ risks for perioperative events such as:

a. Myocardial infarction

b. Congestive heart failure

c. Delirium

d. Stroke

e. Aspiration and pneumonia

f. Sepsis

g. Adverse drug reactions

h. Falls

i. Pressure sores

2. Age alone is a minor predictor for perioperative complications.

3. Assessment of health and functional status. A detailed history and physical examination are required, with emphasis on physical condition, ambulation, activities of daily living, preoperative living situation, and preexisting disabilities.

4. Preoperative testing. Testing should be based on coexisting disease and recommended guidelines (see Chapter 1). Recommended testing in elderly patients includes electrocardiogram, chest radiograph, complete blood count, electrolyte panel that includes blood urea nitrogen, creatinine, potassium (especially if the patient is receiving a diuretic), and glucose.