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Anesthesiol Clin. Author manuscript; available in PMC 2016 September 01.
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Published in final edited form as:

Anesthesiol Clin. 2015 September ; 33(3): 447–456. doi:10.1016/j.anclin.2015.05.003.

Physiology Considerations in the Geriatric Patient

Bret D. Alvis, M.D. [Assistant Professor of Anesthesiology and Critical Care] and
Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN/USA;
Contribution: Dr. Alvis performed literature review, prepared manuscript, and approved final
manuscript

Christopher G. Hughes, M.D. [Associate Professor of Anesthesiology and Critical Care

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Medicine]
Department of Anesthesiology, Division of Critical Care Medicine, Vanderbilt University School of
Medicine, Nashville, TN/USA; Mailing Address: 1211 21st Ave South, 526 MAB, Nashville, TN
37212; Contribution: Dr. Hughes performed literature review, prepared manuscript, and approved
final manuscript
Bret D. Alvis: [email protected]; Christopher G. Hughes: [email protected]

Synopsis
A person’s physiology is ever-changing at the structural, functional, and molecular levels as they
age, and every major organ system experiences physiologic change with time. The changes to the
nervous system result mostly in cognitive impairments, the cardiovascular system result in higher
blood pressures with lower cardiac output, the respiratory system result in a reduction of arterial
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oxyhemoglobin, the gastrointestinal system result in delayed gastric emptying with a reduction of
hepatic metabolism, and the renal system experiences a diminished glomerular filtration rate. All
these changes are variable from patient to patient; however, combined, they create a complex
physiological condition. This unique physiology must be taken into consideration for a geriatric
patient undergoing general anesthesia.

Keywords
Geriatric; Physiology; Cardiovascular aging; Neurological aging; Aging

Introduction
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A person’s physiology is a complex, ever-changing state with aging-related changes

occurring at the structural, functional, and molecular levels.1 The process of aging is
complex and multifactorial with multiple hypotheses broadly categorized into either the

Conflicts of Interest: None.

Disclosure Statement: Dr. Hughes is supported by National Institutes of Health HL111111, R03AG045085 (Bethesda, Maryland,
USA) and Jahnigen Career Development Award sponsored by the American Geriatrics Society (New York, New York, USA.
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our
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‘programmed’ theory or the ‘error’ theory. 1 The ‘programmed’ theory states that delineated
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biological alterations in homeostatic state and natural defense will occur over time.1 The
‘error’ theory focuses on free radical accumulation secondary to reactive oxygen species
generated during mitochondrial energy production, causing oxidative damage to DNA,
protein, and lipids.1 No matter the theory, aging is defined as the normal progressive decline
in function and ability to respond to intrinsic (e.g., catecholamines, inflammation) or
extrinsic (e.g., infection, surgery) stimuli.2

A patients’ age is a strong correlate of risk of morbidity and mortality.3 For non-cardiac
surgery, 30-day mortality is expected to increase by a factor of 1.35 per decade of age.3 Age
itself is also an independent risk factor for a long list of diseases, injuries, hospitalization,
length of hospitalization, and adverse drug reactions,4 and almost every organ system is
affected by aging. We will therefore examine the most recent evidence and understanding of
how aging affects the major organ systems.
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Nervous System
The aging brain is accompanied by a change in structure, function, and metabolism (Figure
1).5 The volume and weight of the brain declines at a rate of approximately 5% per decade
after age 40.6 Once the brain is 70 years old, the rate of decline is thought to increase.6 The
changes in neuronal volume and affected areas may be related to gender.6 Brain atrophy
starts earlier in men but is more rapid in women once it has started.5 There are longitudinal
studies using MRI imaging and reviews of cross sectional studies that show the prefrontal
cortex as the most affected region of neuronal cell death.6 The medial temporal lobes are
also very sensitive to age,5 and additional areas also include the cerebellar vermis, cerebellar
hemispheres, and hippocampus.6
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Upon analysis of post-mortem brains, there is a greater loss of white matter than grey matter
with aging,7 and granular degeneration of myelinated axons is observed regularly by the age
of 40.7 Neuronal cell death is believed to be the main reason for the loss of grey matter;
whether this is the only reason, however, is unclear.6 There may be additional changes in
dendritic arbour, spines, and synapses, with dendritic sprouting occurring to help maintain a
similar number of synapses and compensating for any cell death.6

Along with a reduction of brain volume, there are cognitive changes associated with aging.
Memory declines are one such cognitive change, with decline in episodic memory being
most common.6 This type of memory is defined as ‘a form of memory in which information
is stored with mental tags, about where, when and how the information was picked up’ and
is thought to decline starting around the 4th and 5th decades onward.6
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Neurotransmitter changes also occur with age. Dopamine levels decline by around 10% per
decade starting in early adulthood.6 This decrease has been associated with declines in
cognitive and motor performance.6 Serotonin and brain derived neurotrophic factor levels
also decrease with age, and decreases in these neurotransmitters have been associated with
reduced synaptic plasticity regulation and neurogenesis.6 Monoamine oxidase, an important
substance in the homeostasis of neurotransmitter levels, increases with age and may liberate
free radicals from reactions that exceed inherent antioxidant reserves.6

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The blood-brain barrier protects the central nervous system from systemic insults through
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selective permeability. Increasing age is associated with increasing blood-brain barrier

permeability,8 thereby allowing inappropriate passage of mediators from the plasma into the
central nervous system. This likely results in an increased inflammatory response and
structural damage in the brain as well as altered patterns of neuronal activity by modulating
synthesis of neurotransmitters and changing expression of neurotransmitter receptors.9,10

Vascular distribution in the brain also changes every decade of life. Capillaries are densely
packed in areas of the brain that have higher processing demands, and these dense areas of
capillaries tend to decrease.7 Starting around the 5th decade of age, every decade of life
shows an increase in the degree and number of micro-vessel deformities.7 Cerebroarterial
change begins mostly in the intima with approximately 50% of the vessels showing intimal
thickening by the 4th decade and up to 80% by the 8th decade. 7 These changes are often the
precursors to arteriosclerosis which increases vascular resistance and decreases perfusion
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pressure, thereby compromising neurocognitive function.7 Studies using functional imaging

techniques to evaluate the effects of aging have found a reduction in cerebral metabolic rate
of oxygen consumption with decreased cerebral blood flow in grey matter but preservation
of blood flow to the white matter.7

With an aging population, there will be an increase in elderly patients having surgery.11
With this, the prevalence of postoperative cognitive disorders in the aging brain is likely to
increase.11 All the changes (Figure 1) seen in the brain increase the likelihood of post-
operative cognitive disorders including delirium in the acute setting and postoperative
cognitive dysfunction in the long term.11

Cardiovascular System
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The geriatric population tends to have higher blood pressures, similar heart rates and
ejection fractions, and lower left ventricular end-diastolic volumes, stroke volumes, and
cardiac outputs compared to younger populations (Figure 2).3 These aging-related changes
in the cardiovascular system primarily start with changes in connective tissues. Connective
tissue stiffens within the arteries, veins, and myocardium, causing them to become less
compliant.3 This stiffening is secondary to a cessation of elastin production in the 4th decade
of life.3 Also, collagen turnover is a slow process, and both elastin and collagen proteins
accumulate free radical damage over time.3 As elastin is damaged, it is then replaced with
less flexible collagen protein.3

Arterial stiffening leads to systolic hypertension, impaired impedance matching, and

myocardial hypertrophy.3,4 The stiffening within the aorta causes an increase in systolic
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blood pressure and a decrease diastolic pressure.3,4,12 The diminished diastolic pressure
leads to a decrease in coronary blood flow.12 Under normal circumstances, most of the
stroke volume is contained within the thoracic aorta; as the aorta stiffens, the pressure to
transfer this volume increases.3 Thus, chronically elevated left ventricular afterload leads to
left ventricular thickening.4 There is also an increase in impedance matching between the
declining strength of the myocardial contraction and the increases in pressure within the
aorta.3 When this pressure wave travels down the arterial tree, the wave will reflect off both

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the vessel walls and branch points, returning to the thoracic aorta.3 This pressure reflection
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creates a poor impedance match and causes more strain on the myocardium—serving as a
significant stimulus for myocyte hypertrophy.3

The combination of myocyte hypertrophy and elevated left ventricular afterload prolongs
myocardial contraction.4 This extended contraction leads to a delay in ventricular relaxation
and results in early diastolic filling rates declining by approximately 50% between the 2nd
and 8th decade.4 The end diastolic volume is typically preserved secondary to late diastolic
filling and becomes more reliant on atrial contribution for effective filling.4 Ventricular
myocardial stiffening and hypertrophy, therefore, render the heart dependent on atrial filling
pressures.3 It will also increase susceptibility to diastolic heart failure,3 for diastolic
dysfunction is a key factor in the development of heart failure with preserved ejection
fraction.13
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Venous stiffening with age decreases ability to buffer changes in blood volume and blood
distribution.3 Upwards of 80% of blood volume is stored within the venous network.3 This
reservoir, therefore, is important in maintaining a stable preload to the heart, and venous
stiffening will impair the ability to keep preload constant.3

Aging results in an increase in sympathetic nervous system activity and higher levels of
circulating norepinephrine, resulting in in an increase in arteriole constriction and systemic
vascular resistance.3 Evidence for this increase in norepinephrine include an increase in
norepinephrine release form nerve terminals, an increase in the percentage of norepinephrine
reaching the general circulation, and a decrease in the metabolism and reuptake.3

The myocardium’s beta-receptor is also affected with age. The response of the receptor to
stimulation is reduced, resulting in a decrease in heart rate and contractile response to
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hypotension, exercise, and catecholamines.3 This does not seem to be secondary to a decline
in the number of beta-receptors but rather a diminishment in the intracellular coupling with
adenylate cyclase.3 The diminished chronotropic and inotropic response of the heart to beta-
receptor stimulation changes the heart’s ability to respond to either intrinsic or exogenous
catecholamine stimulation.3 This beta-receptor limitation increases the dependence of the
Frank-Starling relationship to maintain cardiac output.3 Other changes in the cardiovascular
system include a diminished baroreflex stimulation, lower vagal nerve tone, and reduced
oxygen extraction.3 The impaired baroreflex system and vagal tone result in less heart rate
variability and ability to control a constant cardiac output.3

Endothelial dysfunction is a leading theory to the mechanism of vascular aging. Endothelial

function, including nitric oxide release, has vasoprotective and cardioprotective properties
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due to inhibition of platelet aggregation and inflammatory cell adhesion to endothelial cells,
disruption of pro-inflammatory cytokines, apoptosis inhibition, and tissue energy
metabolism regulation.12 There is considerable evidence published showing an increase in
reactive oxygen species within the heart and vasculature with age,14 and the accumulation of
oxidative stress results in altered nitric oxide production.12 Furthermore, there is also a
lower production of nitric oxide with age.12 These factors diminish the bioavailability of

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nitric oxide in the coronary and peripheral circulation in the elderly, resulting in impairment
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of flow in the microvasculature and increasing risk for organ dysfunction.12

The stiffening of the connective tissue, impaired impedance matching, the myocardial
hypertrophy, venous stiffening, increase in sympathetic nervous system, altered nitric oxide
production, and the diminished beta receptor response are the changes (Figure 2) in the
cardiovascular system that cause there to be more hypotension and greater blood pressure
lability during anesthesia in elderly patients versus young adults.3 This affects the depth and
type of anesthesia required and the sympathetic nervous system response to changes in
surgical stimulus and surgery in general.3

Respiratory System
The lungs continue to develop throughout life, and maximal functional status is achieved in
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the early part of the 3rd decade, after which lung function gradually declines.15 Changes
with aging include alteration of the mechanical properties of the respiratory system,
reduction of arterial oxyhemoglobin saturation, and impaired response to hypoxia (Figure
3).15

The parenchyma of the lung under goes significant structural alterations with aging, with the
most important one being a reduction in number and crosslinks of elastic fibers resulting in a
reduction of elastic recoil.15–17 This creates inward forces that promote a decrease in lung
volumes at an average rate of between 0.1–0.2 cm H2O per year, and this decrease is most
pronounced after the 5th decade.15 Homogenous enlargement of the air spaces also causes a
reduction in alveolar surface area from 75 m2 to 30–60 cm2 by the age of 70—increasing
lung compliance and representing functional emphysema.15,17
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In addition to decreased elastic recoil, there is also a decrease in compliance with age due to
structural changes with intercostal muscles, joints, and rib vertebral articulations that
decrease compliance of the chest wall.15–18 Age-related development of osteoporosis results
in a reduction of height of the thoracic vertebrae causing further restriction.18 In addition, a
reduction of respiratory muscle mass may contribute to a decrease in the force produced by
the respiratory muscle activity.15 This loss of chest wall muscular function, however, does
decrease the outward force requirements such that the total lung capacity remains
unchanged.15,18

With these changes in the properties of the connective tissues, there are significant changes
to the mechanics of the lung. The functional residual capacity increases by 1–3% per
decade.15 The residual volume increases by 5–10% per decade.15 Because the total lung
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capacity remains unchanged, there is a decrease in vital capacity.15 This decrease in

physiological reserve increases geriatric patients’ vulnerability to infection and
impairment.16 After the age of 20 years, the vital capacity will decrease from 25% to 40%
by 70 years of age.15 There are progressive decreases in both forced vital capacity (14–30
mL per year) and forced expiratory volume in one second (23–32 mL per year).15 At the age
of 65, there is a decrease in FEV1 of approximately 38 mL per year.15 These changes can
make a normal FEV1/FVC ratio as low at 55% in the elderly.15

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Aging also affects gas exchange properties. Arterial oxygenation gradually declines with
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aging,15,17 likely secondary to an increase in ventilation/perfusion heterogeneity caused by a

decrease in alveolar surface area and the premature closure of small airways.15,16 To predict
the effect of age on arterial oxygenation, several equations have been proposed.15 Between
the ages of 40–75 years, the best equation that takes into account both PaCO2 and body
mass index (BMI) is: PaO2(mmHg)=143.6 − (0.39 x age) − (0.56 x BMI) − (0.57 x
PaCO2).15 Once over the age of 75 years, arterial oxygen tension does not correlate with
BMI and PaCO2 and instead remains stable at approximately 83 mm Hg.15

Elderly subjects will have a lower tidal volume and a higher respiratory rate than younger
subjects.15 There is an approximately 50% decrease in their response to hypoxia and
hypercapnia15 and a decrease in diffusion capacity of the lung.16 Increased ventilation is
often required to compensate for this decreased efficiency of gas exchange.15
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Along with these changes in the lung, there are important changes seen in the upper airway.
There is a loss of muscular pharyngeal support making the elderly more susceptible to upper
airway obstruction.15 There is also a decrease in respiratory effort in response to upper
airway occlusion.15 Protective mechanisms of coughing and swallowing also diminish with
time, making a geriatric individual more at risk for aspiration.15 A presumed explanation for
these changes includes peripheral differentiation along with decreased central nervous
system reflex activity.15

These changes in the respiratory system (Figure 3) contribute to the pulmonary

complications that can be seen post-anesthesia.15 The decrease in chest wall compliance
results in an increase in a geriatric patients work of breathing post-anesthesia.15 The changes
in lung mechanics will impair a geriatric patient’s gas exchange and the tendency for small
airway closure leading to atelectasis.15 Several studies have shown that age alone is a
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significant independent predictor of risk for perioperative pulmonary complications.15

Gastrointestinal System
Age-related changes occur along most of the gastrointestinal track (Figure 4). There is a
decrease in the amplitude of esophageal contractions and a decrease in the number of
peristaltic waves that occur with a standard swallow.19 When studied, there was found to be
an increase in the number of disordered contractions in the body of the esophagus.19
Geriatric individuals are also subject to prolonged gastric emptying.19 One study
demonstrated a standard mixed meal took double the time to empty when compared to
younger subjects.19 Thus, elderly patients are at higher risk for aspiration at anesthetic
induction or in the postoperative period. Gastric acid secretion decreases with age at both a
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basal rate and when fixed doses of exogenous gastrin are given to stimulate production.19
This is secondary to the development of atrophic gastritis that causes a decrease in secretion
of acid and intrinsic factor (not enough, however, to result in vitamin B-12 malabsorption
and pernicious anemia).19 Atrophic gastritis may affect calcium bioavailability because of a
limited ability to dissociate from food complexes.19

Pancreatic function does not seem to be diminished with age, for there does not seem to be
any diminished response to stimulation by secretin or cholecystokinin.19 The mucosal

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surface of the small intestine is slightly diminished in the aging human.19 Despite this, the
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ratio of mean surface area to volume of jejunal mucosa does not change with age.19

The liver does experience significant change with age (Figure 4). There is a reduction of
liver volume, ranging from 20–40% across the human lifespan.2,20 With the loss of volume,
there is also age-related decline in hepatic blood flow.2,20 The age-related loss of surfaced
endoplasmic reticulum causes a strong negative correlation between age and hepatic
microsomal Phase-I drug metabolizing activity.2,20 This decline in total capacity of the liver
to metabolize drugs can increase the incidence of adverse drug reactions.20 This decline can
be very variable, from drug to drug and from person to person.20

Renal and Volume Regulation System

Renal function declines related to age have been well documented within multiple
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geographic settings, patient populations, and using a wide range of methods and parameters
(Figure 5).21 There is a cumulative increase in patients with end stage renal disease with
increasing age.22 Age-related renal decline is affected by gender, with males more affected
than females secondary to increased damage from vascular changes and androgen
production.21 Aging causes both creatinine clearance and glomerular filtration rates to
decline, resulting in not only a sharp increase in chronic renal impairment and end-stage
renal failure but increased susceptibility to acute insults.21

Electrolyte homeostasis is also affected with age. There is a slower homeostatic

responsiveness to sodium changes and a decreased ability to maximally dilute or concentrate
urine.21,23 There is also a global impairment of movement of other electrolytes and ions
transport across the tubular epithelium.21
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There are significant changes to the renal vascular network in the geriatric population. This
includes a reduction in the actual and proportional renal blood flow with age.21 After the 4th
decade, there is a 10% decrease in renal blood flow with each decade thereafter.23 With this
diminished renal blood flow, there is an accompanied decrease in responsiveness and
autoregulation of volume status.21 The infrarenal arterial changes are similar to the systemic
changes—arteriolosclerosis, intimal and medial hypertrophy.21

There are also significant interstitial changes to an aging kidney. When looking at the size of
the kidney, it was found that they increase in size up to the 5th decade and then start to
decrease.21 This volume loss is thought to be due to tubule-interstitial changes including
infarction, scaring, and fibrosis, resulting in decreased clearance capabilities.21

The renin-angiotension-aldosterone system is also affected with age, resulting in substantial

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declines in plasma renin activity.24 The most significant decreases are found in the 6th
decade onward.24 Age has a greater effect on the decrease in plasma renin and aldosterone
level compared to angiotension II.24

The geriatric patient will have pharmacokinetic changes in the absorption, distribution,
metabolism, and excretion of anesthetic drugs.22 There is a reduction in systemic clearance
of drugs that are eliminated unchanged by the kidney due to age-related changes in

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glomerular filtration rate and tubular function.22 There is also a higher incidence of chronic
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kidney disease; this fact, along with the diminished blood flow and changes to
autoregulation, leads to an increase in prevalence of perioperative acute kidney injury.21,22

Endocrine System
There is a decline in endocrine function with age that includes decreased tissue
responsiveness and a reduction in hormone secretion from peripheral glands (Figure 6).25
Examples include reductions in thyroxin (T4) and triiodothyronine (T3). Age also results in
a dampening of circadian hormonal and non-hormonal rhythms.25

Impaired glucose tolerance develops in over 50% of individuals older than 80 years of
age.26 There is a decrease in insulin production by beta cells, an increase in insulin
resistance related to poor diet, an increase in abdominal fat mass, and a decrease in lean
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body mass. These all contribute to the deterioration of glucose metabolism26 and make
elderly patients at higher risk of poor glycemic control in the perioperative setting.

Women typically experience menopause in the 6th decade of life when serum estradiol
concentrations are lower and follicle-stimulating hormone concentrations are higher than in
younger women.25 Luteinizing hormone does not change like follicle-stimulating
hormone.25 These changes, along with the fall of estrogen, increase the risk of
cardiovascular events, rapid loss of skeletal mass, vasomotor instability, psychological
symptoms, and atrophy of estrogen-responsive tissue.25

Male gonadal steroid production also changes with age – a change termed andropause.25
There is a marked decline in free testosterone levels from an increase in sex hormone-
binding globulin levels.25 The age of this decline is variable, and the physiological
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consequences are unclear.25 There is also a decline in total serum testosterone

concentrations due to a decrease in production rates as men age.25

Summary
No matter the mechanism, aging affects the physiology of every major organ system. The
nervous system experiences cognitive decline and volume loss. The cardiovascular system
changes result in lower cardiac output and higher blood pressures leading to significant
changes to the structure and function of the heart. The respiratory system changes lead to
impaired oxygenation, diminished ventilation/perfusion matching, and an increase risk of
atelectasis. The gastrointestinal system experiences a delay in emptying along with
diminished hepatic metabolism. The renal system changes result in a diminished glomerular
filtration rate and a diminished ability to control electrolyte hemostasis. The endocrine
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system results in hormonal changes that lead to variation in the patients’ condition.
Importantly, all these changes can have major effects on the perioperative course of a
geriatric patient, and anesthesia providers require an understanding of these changes and
how they will affect the management of their geriatric patients.

References
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2. Schmucker DL. Age-related changes in liver structure and function: Implications for disease?
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assessing pulmonary function. The journals of gerontology Series A, Biological sciences and
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19*. Russell RM. Changes in gastrointestinal function attributed to aging. The American journal of
clinical nutrition. 1992; 55:1203S–7S. [PubMed: 1590257]
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Key Points
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1. Changes in structure, function, metabolism, and blood flow in the aging brain
lead to cognitive impairments, most frequently episodic memory changes, and
an increased risk of delirium in the acute setting.

2. The geriatric population tends to have higher blood pressure with lower cardiac
output and diminished chronotropic and inotropic responses to beta-receptor
stimulation.

3. Respiratory aging results in changes to mechanical properties of the respiratory

system, reduction of arterial oxyhemoglobin saturation, and impaired response
to hypoxia.

4. Gastrointestinal changes with aging include altered esophageal motility, delayed

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gastric emptying, and reduction in hepatic metabolism.

5. There is a reduction in renal function with age, and changes also occur to the
endocrine system, including diminished tissue responsiveness and reduction in
hormone secretion from peripheral glands.
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Figure 1.
Changes in the neurological system with age
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Figure 2.
Changes in the cardiovascular system with age
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Figure 3.
Changes in the respiratory system with age
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Figure 4.
Changes in the gastrointestinal and hepatic system with age
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Figure 5.
Changes in the renal system with age
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Figure 6.
Changes in the endocrine system
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