Brian K. Ross, M.D., Ph.D.
Associate Professor of Anesthesiology
University of Washington, Seattle, WA 98195
bkross@u.washington.edu
Because many of the intraoperative manipulations performed
by anesthesiologists in the conduct of an anesthetic focus on
the respiratory system (e.g., assessing adequacy of patient
ventilation, gas exchange, acid-base balance, delivery of volatile
and inhalational agents), it is important for anesthesia providers
to understand how aging affects the respiratory system. Such
knowledge is becoming increasingly important as the U.S. population
ages and this aged population presents more often for surgery.
Knowledge of the age-related decrease in pulmonary capacity,
combined with an understanding of the effects of the anesthetic
process, will aid the practitioner in selecting appropriate
supportive and prophylactic measures before and after surgery
in the aged patient. With such information in hand, nonagenarians
and even centenarians should not be denied either elective or
emergency surgery for fear of respiratory limitations.
Characterizing the affect of the normal aging process on the
respiratory system is a complex concept as it is difficult to
separate the changes associated with age from those attributable
to diseases of the aged. In fact, age-related disease has far
more impact on the respiratory system and the conduct of an
anesthetic than do age-related respiratory changes. This discussion
will focus on those respiratory changes that can be attributable
to age alone.
The respiratory system can provide a young adult with adequate
gas exchange at many times beyond resting requirements even
in the face of both major reductions in pulmonary function (i.e.,
a 40 - 50 percent loss of maximal ventilation), as well as a
significant increases in metabolic rate (e.g., a doubling of
metabolic rate, as in severe fever). The magnitude of this reserve
will easily see an otherwise physically fit patient through
the convalescence of a major procedure even if complicated by
major pulmonary morbidity without pulmonary mortality. However,
aging inexorably reduces the capacity of all pulmonary functions.
Complicating our understanding of this process is the fact that
the rate of loss of function is extremely variable among persons
of the same chronological age. However, there are four hallmarks
of the aging process: 1) a decline in elasticity of the bony
thorax, 2) a loss of muscle mass with weakening of the muscles
of respiration and reduced mechanical advantage, 3) a decrease
in alveolar gas exchange surface and 4) a decrease in central
nervous system responsiveness, which have anatomical, mechanical
and functional consequences. There is very little information
in the literature as to whether pulmonary mechanics under anesthesia
are influenced by age.
There are a number of striking anatomic changes which occur
in the respiratory system with age. As a consequence of a generalized
loss of all muscular and neural elements (muscle fibers, mucosal
receptors, nerve fibers, etc.), laryngeal structures undergo
a slow but continual decline in function. Protective reflexes
involved in the regulation of coughing and swallowing are diminished.
The end result is chronic pulmonary inflammation from repeated
aspirations with frequent contamination of the lower airway
with oral and gastric organisms.
With aging, the larger and more central airways increase in
diameter, as noted by an increase in anatomic and physiologic
dead space. The trachea and large bronchi increase in size about
10 percent from youth to old age. However, expiratory flow and
resistance to gas flow in the large airways changes with little
or no physiological consequence. Beyond age 40, the diameter
of the small airways, not privileged to have cartilaginous support,
decreases significantly. Despite the decrease, overall airway
resistance does not appear to increase significantly. There
is a small but measurable increase in dead space. Further out
in the lung there are more functional changes. Elastic elements
of the lung parenchyma are lost with age. The distal orders
of respiratory bronchioles dilate as do alveolar ducts. The
alveoli become dilated, Kohn's pores become more numerous and
larger, and fine parenchymal tissue is lost with a loss of tethering
support. The end result is the smaller distal airways with a
tendency to early collapse, dilated alveolar ducts and fewer
gas exchange surfaces. These changes are manifest functionally
by air trapping, increased closing capacity, frequency-dependent
compliance and gas exchange problems.
A combination of factors alters the mechanical function of
the lung with age. These include: 1) a decrease in motor power
as a consequence of fewer muscle fibers and a decrease mechanical
advantage, 2) an increase in parenchymal compliance decreasing
elastic recoil of the lungs and ultimately a change in structure
and function of the chest wall due to a loss of intervertebral
spaces, and 3) a stiffening of the chest wall from changes in
ribs, sternum and articular cartilages making the chest less
expansible.
The tendency of the lung to assume a larger resting volume
and the limitations imposed by a stiffer chest wall plus a decrease
in motor power result in a change in the components of the total
lung capacity. Vital capacity declines progressively with age.
As a rough rule of thumb, there is a linear loss of 5 to 20
percent of functional ability per decade, which may be helpful
in comparing an elderly patient's current capacity against normal
values. From age 20, vital capacity (VC) decreases progressively
(-20 to -30 ml/yr) whereas residual volume (RV) increases (+10
to +20 ml/yr). In fact, the ratio of RV to TLC increases from
25 percent at 20 years of age to about 40 percent in a 70-year-old
man, which gives the chest wall a somewhat barrel-like appearance.
It is interesting that the decrease in elastic recoil of the
lungs and progressive stiffening of the chest wall serendipitously
counteract each other with no net significant change in absolute
FRC. The total lung capacity (TLC) grows with age until puberty,
where it reaches an average value of 6 to 7 liters, after which
a slow loss of volume begins. With the age-related loss in total
lung capacity (TLC), plus the very modest increase in FRC, the
ratio of FRC to TLC tends to increase with age.
The reduction in motor power of the accessory muscles of breathing
as well as the decreased expansion of the chest wall cause the
dynamic lung volumes and capacities to decrease progressively
with age (e.g., FEV1). The FEV1 decreases with age by about
27 ml/yr in men but by only 22 ml/yr in women. However, the
percent change in the two sexes is similar because men start
off with higher absolute values of these measurements.
There is a clear age-related increase in the closing volume
(CV) and closing capacity (CC). In childhood and youth, the
closing capacity remains well within the expiratory reserve
volume. Over time it progressively enlarges, encroaching on
the tidal volume in the 60-year-old. Both the CV and CC also
increase with recumbency, a common position perioperatively.
During active breathing, closing pressure in young subjects
is about -1.25 cm H20 pressure, and opening pressure is +2.5
cm H20, the difference being attributable to hysteresis. The
values for closing pressure (CP) and opening pressure (OP) in
subjects aged 65-75 years are 0 and 4.5 cm H20, respectively.
The higher values for both CP and OP will decrease the elderly
patient's ability to keep some ventilated areas open and to
re-open those areas that have collapsed.
The pressure-volume curve of an older lung is similar in shape,
but shifted upward and to the left; in other words, the aged
lung possesses less elastic recoil. This change in compliance
is quite regional rather than being evenly distributed across
the lung. The effect is to slow passive exhalation in some lung
areas while other lung areas empty normally. The dynamic lung
compliance (compliance measured during active breathing) becomes
more frequency dependent with age. Thus as breathing rate increases,
lung expansion becomes less effective particularly in some areas,
thereby increasing the maldistribution of ventilation to perfusion.
Also, in older subjects the pressure across basal lung units
may be positive rather than subatmospheric. During quiet breathing,
inspired gases will preferentially go to the more distensible
upper lung units leading to an uneven distribution of gases.
However, these variably compliant lung areas are surrounded
by a thoracic cage that has become stiffer; the stiffness of
the older chest wall overshadows the lesser elastic recoil of
the lung and the anesthesiologist may perceive a less compliant
respiratory system.
The functional, or gas exchange capability, of the aged lung
is affected by the anatomical and mechanical changes of age.
The efficiency of alveolar gas exchange decreases progressively
with age for a number of reasons. Alveolar surface area decreases
with age from about 75 m2 at age 20 years to about 60 m2 at
age 70 years.
Although blood volume does not change with age, the quantity
of blood present in the pulmonary circulation at any given instant
does decrease with age. There is also evidence that the distribution
of pulmonary blood flow changes with aging. The change in blood
flow, combined with the altered distribution of inspired gas,
promotes even more V/Q mismatching. Alveolar dead space, which
is a good index of the distribution of pulmonary blood flow,
increases with age. The increased V/Q mismatch plus the increased
alveolar dead space adversely affect the aged patient's blood
gas values.
Arterial blood gases become integral components in the interpretation
of lung function during anesthesia. There are reference values
available to aid in the interpretation of arterial blood gases
in middle-aged and elderly persons (40-70 yr). The normal alveolar
oxygen tension PAO2 is fairly constant from infancy to senescence.
A number of studies have demonstrated the mean PaO2 declines
from 95 ± 2 mmHg at age 20 to 73 ± 5 at age 75
years. This decline in arterial oxygen tension is modest: approximately
0.4 mmHg/year. After age 75, however, PaO2 stays relatively
constant at approximately 73 mmHg.
In humans there is a normal amount of relative hypoxemia due
to shunt, diffusion block and ventilation/perfusion mismatch.
Age and anesthesia worsens hypoxia mostly by increasing ventilation/perfusion
maldistribution. We also know this can be made more prominent
by pulmonary disease, the effects of aging and the application
of mechanical ventilation.
The efficiency of vascular distensibility and recruitment decreases
with age. The increasingly rigid pulmonary vasculature probably
blunts the hypoxic pulmonary vasoconstrictor (HPV) reflex. The
loss of physical support of surrounding pulmonary elastic tissue
surrounding both the small airways and pulmonary vessels may
be a contributing factor. Thus the ability of the aged lung
to respond to altered ventilation/perfusion matching is compromised.
Finally, it is important to recognize that the ventilatory
response to hypercapnia and hypoxia is blunted in the elderly
patient. The ventilatory response (change in minute ventilation)
in the healthy aged patient (70-year-old) to either a hypercapnic
or hypoxic stimulus is half that seen in the 25-year-old.
In summary, the aged lungs have some but certainly not all of
the features of chronic obstructive lung disease, e.g., increased
RV and RV/TLC, reduced VC and FEV1 plus a compliance that worsens
as breathing rate increases. The fact that older patients have
some of the features of chronic obstructive pulmonary disease
(COPD) should not imply that they should be considered as having
COPD, however.
What does all of this mean to the clinician expected to provide
anesthesia for the aged patient? An increase in ventilation
during hypoxia and hypercapnia is a useful clinical sign and
also a homeostatic response. The fact that these responses are
blunted in older subjects indicates that simple clinical observation
of ventilatory frequency and chest movement with breathing may
not be an accurate manifestation of the ventilatory stimulus
to an aged patient. The clinician should also realize that,
together with these age-related decreases in reserve in the
awake state, the ventilatory responses to hypercapnea are reduced
by narcotic premedication and by thiopentone and narcotic and
inhalational anesthetics in a dose-related manner.
Aged patients may be hypoxemic during normal spontaneous ventilation
postoperatively because of the mechanical changes of the aged
lung and chest wall.. The risk is increased by the supine position
and by the use of narcotic analgesics in an age group that already
has blunted ventilatory reflexes to hypoxia and hypercapnia.
Any residual anesthetic will also exert an additive effect.
The elimination of narcotics and muscle relaxants may be delayed
due to the impaired renal function in older patients. The effects
of large volumes of crystalloid infusion may manifest in the
recovery room.
Older subjects are less able to increase and maintain ventilation
at high levels than young adults during periods of increased
demand for oxygen. Ventilatory muscle fatigue is quite likely
to occur early due to the altered physiology of voluntary muscle.
It seems reasonable to assume that older patients will develop
ventilatory inadequacy earlier for any given ventilatory load.
The subjective feature of ventilatory inadequacy is dyspnea.
The anesthetic technique and agents are of less importance
than the degree of preparedness and the acumen of the anesthesiologist.
In the aged the strategies are the same: increasing FIO2 as
necessary while remembering that oxygen toxicity is a concern.
Large tidal volumes are useful until circulatory impediment
and barotrauma become a concern. Aging limits the effectiveness
of each of these therapeutic interventions.
Finally, one should remember that, overall, the age-related
changes of the respiratory system essentially consists of a
mix of restrictive and obstructive lung disease. The whole picture
and how these changes impact the aged patient may not be apparent
immediately after surgery, but the changes may become maximally
manifest any time during the first 2 to 3 days after the operation.
References:
Smith TC. Respiratory system: aging, adversity, and anesthesia.
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Wilkins, Baltimore, 1997, pp 85-99
Wahba WM. Influence of aging on lung function - clinical significance
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Cerveri I, Zoia MC, Fanfulla F, et al. Reference values of arterial
oxygen tension in the middle-aged and elderly. Am J Resp Crit
Care Med 1995;152:934-941
Close G, Woodson GE. Common upper airway disorders in the elderly
and their management. Geriatrics 1989;44:67-72
Leopold DA, Bartoshuk L, Doty RL, et al. Aging of the upper
airway and the senses of taste and smell. Otolaryngol Head Neck
Surg 1989;100:287-289