Professional Documents
Culture Documents
1998 - Geriatric Respiratory Medicine
1998 - Geriatric Respiratory Medicine
Geriatric
Carolyn H. Welsh, MD
monia;
Abbreviations: ATS
eases
adults.
in which the
treatment
are
Pulmonary Function
in the
Elderly
maximum oxygen
consumption
complicated
by a number of issues. First, it is often
difficult to ascertain whether the
loss of respiratory
function is due to aging itself or is due to respiratoiy
illness, smoking, or protracted industrial or environ
mental exposure. Second, elderly patients are more
to have concurrent illnesses or deconditioning
likely
that may directly or indirectly influence pulmonary
function. Nevertheless, it has been established that
even in the healthy elderly population, pulmonary
function deteriorates with age.78 In the following
sections, we will review the anatomical and physio
logic
changes in the respiratory system that occur as
a result of senescence.
Reviews
Structural
of Respiration
lungs with
the
thoracic
and
muscles
also
age,
cage
respiratory
Chest
wall
decreases
due
change.
compliancecalcification of interto
age-associated kyphoscoliosis,
costal cartilages, and arthritis of the cos tovertebral
joints. This increased rigidity of the thoracic cage
leads to a greater contribution to breathing from the
diaphragm and abdominal muscles and a lesser
contribution from thoracic muscles. The prevalence
of diaphragmatic defects, resulting in the loss of
continuity of the diaphragm, also increases with
age.18 How these defects in the diaphragm relate to
the diminution of diaphragm strength with age, as
measured by the maximum transdiaphragmatic pres
sure with either maximal sniff or cervical magnetic
In addition to alterations noted in the
predispose
elderly patients to respiratory fatigue in
illnesses that require high minute ventilation.
Although expiration is mainly a passive process,
the lateral internal intercostal muscles also actively
contract during expiration and may be important in
nonventilatory activities such as coughing and sneez
ing. In contrast to the preservation of diaphragmatic
muscle mass with
these
intercostal
age,
"expiratoiy
area,
a progressive decrease
the vital capacity
due to: (1) increased stiffness of the chest wall; (2)
loss of elastic recoil of the lung; and (3) decreased
force generated by the respiratory muscles.7 Due to
the same mechanisms, there is an increase in the
residual volume such that the total lung capacity
(TLC) remains fairly constant (Fig 1). The functional
residual capacity (FRC) also increases with age,
although to a lesser degree because this increase is
counteracted slightly by a stiffening of the chest
wall.23 The site at which the small airways begin to
close during expiration may shift more distally in the
airways; as a consequence, the airways close at a
smaller exhaled tidal volume, thus increasing the
volume. The closing volume begins to exceed
closing
the supine FRC at about 44 years of age, and to
exceed the sitting FRC at approximately 65 years of
age.24 The significance of this is that the terminal
bronchioles close in the dependent parts of the lung
during tidal breathing, thus contributing to the re
duced arterial oxygen tension found in elderly
people.
In a study of > 400 subjects aged 70 years or
older living at home in a nonmining town in South
Wales, Burr et al25 showed that there was a progres
sive decline in FEVX and FVC with age, independent
of smoking or environmental exposure. Although
these cross-sectional data do not necessarily apply to
a given individual because subjects with low FEVX
and FVC may not survive into older age, they do
suggest that in a relatively healthy population spiro
metric functions decline with age.25 It has been
estimated that FEVX decreases by 30 niL/yr in men
CHEST / 114 / 6 / DECEMBER, 18
1705
VC'
VC
FRC
FRC
NORMAL
LUNG
AGED
LUNG
Exercise
and
Ventilatory Response
Elderly
in the
chitis than
1,000.66'67 Several
1708
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diagno
subjects.81
chitis than
1,000.66'67 Several
1708
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diagno
subjects.81
Older pa
possibly, the overuse of P2-agonists.5-96'97
tients with asthma (those > 65 years of age) have
been shown to be more likely than younger patients
with asthma (those < 40 years of age) to have a
prolonged period of exacerbative
symptoms before
This
being
hospitalized.98
delay, likely due to the
reduced awareness of bronchoconstriction by the
makes objective measurements of the sever
elderly,
of
airflow
limitation such as with a peak flowmeter
ity
especially important.5-83 Physician bias in assessing
the severity of asthma may also contribute to underIn a study comparing clinical and functional
therapy.
features of elderly vs younger patients with asthma,
older patients had a larger than predicted decrease
in pulmonary function even though physician-as
sessed severity was similar in both groups.80 A less
pronounced tachycardia and pulsus paradox in the
elderly patient with acute asthma than in younger
patients with asthma, despite similar airway obstruc
tion and blood
lull clinicians
gas abnormalities, may
elderly
determining the prognosis of asthma because of the
greater prevalence of other diseases coincident to, or
complicated by, asthma in the elderly. In a 7-year
longitudinal study of 24 elderly patients with asthma
older than 70 years of age, corticosteroid depen
dency remained in most patients (21 of 24), and
complications of therapy were common, including
diabetes mellitus, systemic hypertension, and various
infections.99 In the 11 patients who
life-threatening
died in the follow-up period, most from a "cardiac"
cause, the baseline FEVX was not predictive of
deaths from asthma or from all causes.
Therapy of Asthma in the Elderly
Asthma therapy in the elderly is similar to that for
younger individuals and should generally follow the
step care recommendations of the National Asthma
Education Program,96 beginning with the inhalation
of
on a relief basis for
1709
hyperreactivity58'99-106
In the elderly patient with asthma, therapeutic
regimens should be carefully individualized for sev
eral reasons. First, there is a higher incidence of
adverse drug reactions due to altered drug metabo
lism and elimination. Second, medications used to
treat concomitant diseases can lead to multiple drug
interactions or can precipitate asthma exacerbations.
Third, there may be noncompliance with medica
tions due to financial, neuropsychiatric, or physically
disabling disorders such as arthritis. Last, coexisting
disorders that are more prevalent in the elderly and
that may exacerbate asthma include chronic aspira
tion and gastroesophageal reflux.107-108 The use of
inhaled (32-agonists is relatively safe in the elderly,
systemic absorption can lead to
although evenandmild
muscle
tremor. Because asthma and
tachycardia
cardiovascular disease frequently coexist in the el
derly, the treatment of one has the potential to
exacerbate the symptoms of the other. For example,
crisis, cardiac ischemia, and dysrhythhypertensive
mias may be precipitated by the subcutaneous ad
ministration of epinephrine or terbutaline, but there
may be less of a chance of precipitation with inhaled
P2-agonists. In cardiac patients on digoxin or on
drugs that may prolong the QT interval, (32-agonistinduced hypokalemia and QT prolongation may lead
to life-threatening dysrhythmias.106 Theophylline
metabolism may be decreased by congestive heart
failure, by chronic liver disease, or by the concomi
tant use of medications such as cimetidine, calcium
channel blockers, erythromycin, fluoroquinolones,
and allopurinol, which can lead to toxic levels of
theophylline.
Theophylline may also cause urinary
retention in older men83 and may increase the risk of
developingisatrial tachyarrhythmias.109
Although the
ophylline generally not recommended for treat
ment of acute asthma if P2-agonists and corticoste
roids are used properly,110 long-acting theophylline
may be a useful adjunctive agent for the patient with
difficult-to-control nocturnal asthma.111 The
of
array
adverse effects of corticosteroids are well known and
1710
symptoms
in the
Elderly
COPD, defined
sema, is
features of the
our
discussion
therapeutic
on
the salient
armamentarium.
By
Reviews
since ciga
largely preventable
risk
factor.
Other risk
smoking
major
factors are less common. Alpha-one antitrypsin defi
ciency, detected in only 1 to 2% of persons with
COPD, and occupational exposures to mineral and
grain dusts can contribute to an accelerated loss of
the majority of smokers do not
lung function.121 As
there
is likely a yet unexplained,
develop COPD,
risk
multiple-factor genetic for COPD as well.
For COPD, therapy with proven impact on outcome
includes smoking cessation and oxygen therapy, when
medically indicated. It is never too late in the course of
a disease for a patient to stop smoking, as smoking
cessation slows the decline in lung function induced by
cigarettes.122-124 Smoking cessation also is associated
with lower
risk after 6 weeks as well as an
States,117 COPD
rette
is
is the
operative
1711
in the
Elderly
300,000
to
600,000
cases
are
pulmonary embolism
1712
may
breath and chest pain are attributed to other condi
tions that are prominent in the aged, including
COPD, angina, or congestive heart failure.158 For
elderly stroke patients who are at increased risk for
thromboembolism, neurological impairment may ob
scure the clinical presentation of pulmonaiy throm
boembolism. Second, due to a blunted perception of
that may occur with age,5-6 the elderly
dyspneawith
thromboembolism may delay seeking
patient
medical care or may mistakenly attribute dyspnea to
the effect of aging itself. In 37 subjects with PE who
were older than 64 years of age, only 1 had the classic
symptom triad of dyspnea, pleuritic chest pain, and
Reviews
which is used for detecting DVT, may yield falsepositive results in patients with congestive heart
failure.156 Fourth, ventilation-perfusion scans are
more difficult to interpret in the elderly. This diffi
is due both to the presence of comorbid
culty
illnesses that cause scan abnormalities and to the
slower clearance of radioaerosols even in aged nonsmokers without lung disease.160 Thus, in the face of
an indeterminate lung scan, a duplex ultrasound of
the lower extremities should be performed, and if it
is negative, a pulmonary angiography or helical CT
scan may be required to definitively diagnose or
exclude thromboemboli when clinical suspicion re
high.
for venous thromboem
Anticoagulation
therapyshown
has
to improve survival
which
been
bolism,
four-fold compared to no treatment, is the same for
young and older adults.161 In elderly patients with
marginal cardiopulmonary reserve due to preexisting
heart failure or COPD, a small embolus may have a
major adverse effect on hemodynamics or gas ex
a rapid achievement of therapeutic
change. Hence, with
heparin is especially important
anticoagulation
in this population to maximize therapeutic out
come.162 However, the risk of chronic anticoagula
tion with warfarin may be increased in the older
adult who, due to neurological impairment, may be
confused about medication dosing, which can lead to
over or under anticoagulation, or who falls and thus
is at increased risk for a bleeding-related complica
tion.163164 In addition, warfarin interacts with many
medications, including antibiotics,
commonly used oral
diabetic agents, hypolipemics,
anticonvulsants,
and
vitamins,
allopurinol. Most studies examining
the risk of bleeding while on warfarin fail to show a
correlation between age and bleeding risk except for
the "oldest old."165166 The duration of therapy has
traditionally been 3 to 6 months, but in patients with
a continued risk for thromboembolism, longer peri
ods of anticoagulation therapy may be required to
prevent the high probability of recurrence.150 For
the elderly patient with social issues or medical
disorders that preclude long-term anticoagulation
with a filter may be
therapy, vena caval interruption
a viable alternative in preventing immediate PE,
is associated with a
although this treatment likely
DVT.167
risk
of
later-onset
Although age per
higher
se is not a contraindication for thrombolytic therapy,
which is recommended for hemodynamically signif
with an increase
mains
Waning
and
Although a decline in the innatehas(neutrophil)
been
observed
immunity (lymphocytes)
specific
in the elderly, in many cases it is not clear whether
the defect is primary or secondary to an underlying
in
CHEST/114/6/DECEMBER, 1998
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1713
In a recent large
yearly vaccinations.175
> 65
of
old,
study elderly patients years it was shown
that vaccination against influenza is associated with a
in the hospitalization rate for
significant reduction
and
influenza
as well as for all acute and
pneumonia
chronic respiratoiy conditions.176 Furthermore, in
fluenza vaccination has been shown to reduce mor
tality by 40 to 50% from all causes during influenza
seasons, to be cost-effective, and to have no greater
adverse affects compared with placebo in the elder
tacts receive
>
consequences
pneumonia
respi
ratory
reserve,
1714
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pneu
moniae
in the
than other
causes
As a group,
for CAP,
management of pneumonia
poor
strong
is
1715
age
patients who
died and those who survived was 7.8 years.221 Fur
thermore, these investigators performed logistic re
gression analysis on 85 studies that reported the ages
between survivors and nonsurviviors and found that
the odds ratio of dying from pneumonia was 1.05 for
each 10-year increment in mean patient age. Thus,
increased age also has a direct association with
pneumonia mortality. In a prospective study of
> 10,000 persons older than 65 years of age, increas
ing age, diabetes mellitus, congestive heart failure,
and current cigarette smoking were all associated
with a two-fold increase in the risk of death from
pneumonia.226 In addition, both low mini-mental
status exam scores and an inability to perform the
activities of daily living are associated with an in
creased risk of death from pneumonia. In another
study examining the morbidity and mortality from
influenza and pneumonia, congestive heart failure,
COPD, renal insufficiency, diabetes, cancer, and age
all correlated with an increased risk of dying from
pneumonia.227 Radiographic progression of pneumo
nia, more commonly seen in the elderly, is also
associated with increased complications and mortal
ity 194,213
cardiopul
1716
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tations may
contribute
to
the increased
mortality
14,000
basic
outpatient care.212
Outpatient Treatment
/
60 years with
no co-morbid illness
<
(Macrolide
or
tetracycline
/ \
\
60 years and/or
co-morbid illness
>
Second- or third-
generation cephalosporin
or
inhibitor
p-lac-p-lactamase
or
antipseudomonal
antibiotic
TMP/SMX
+
macrolide
to
Inpatient Treatment
ing
A,
is
of deaths in institu
also leading
tionalized elderly individuals, associated with up to
50% mortality in bacteremic patients.238-241 Epide
and causative organisms in NHAP are suf
miology different
from CAP and thus will be consid
ficiently
ered separately here. The most likely risk factor for
NHAP is the presence of serious comorbid illnesses
seen with increased frequency in this group of
patients. These conditions may include: (1) underly
ing disorders that suppress immune function (eg,
diabetes, cirrhosis, malignancy, and malnutrition);
(2) increased bacterial colonization of the orophar
ynx, especially with Gram-negative organisms; (3)
such as nasogastric tubes,
therapeutic interventions
neutralization of gastric pH, or recent antibiotic use;
and (4) increased risk of aspiration due to dementia,
stroke, or cognitive effects from medications.242-244
In a prediction rule study that identified low- vs
high-risk
patients with pneumonia, patients with
NHAP automatically received a 10-point surcharge
a
infectious
cause
or
pathogenic.
However,
elderly patients
divided
1993, the empiric treatment of
between those patients with nonsevere illness and
those patients that have more severe illness for
whom hospitalization may be required.230 For the
former group, the empiric oral regimen may include
a
sulfamethoxazole or may include amoxacillin-clavulanic acid with or without a macrolide. For more
severe NHAP, empiric regimens include a fluoroor a second- or thirdquinolone plus penicillin with
or without a macro
generation cephalosporin
lide.
Hospital-Acquired Pneumonia
The incidence of hospital-acquired pneumonia
(HAP) increases significantly with age, and elderly
patients account for a disproportionate number of all
HAf' cases.249-250 In addition, HAP is also the leading
CHEST/114/6/DECEMBER, 1
in
1717
in the
Elderly
higher (234
years age to
who
are
older
95 years of age; in
than
patients
women, the rate drops from 40% to about 5%,
PPD reactivity in the nursing home is
respectively.261
and
to be due to more than simple
high appears
reactivation of disease.267 Potential explanations for
the high prevalence of positive skin test reactions in
nursing home residents include: the unrecognized
of TB in a closed environment; the early
spread
demise of the anergic patient; an improvement in
nutrition and general health in the patient after
admission; or a delayed or booster effect. In the
nursing home, much evidence suggests that TB is an
important and underrecognized nosocomial infec
tion.263 On admission to a nursing home, the rate of
PPD reactivity (initial test plus booster) is only 10 to
15%. However, higher rates of reactivity are found in
two step
tuberculin
skin test
non-reactor-
test yearly or ^
when an active
case is identified
Induration > 10 mm
or
recent converters
chest radiograph
\normal
recent converters or
abnormal
(see text)
least 3 drugs
1719
resistant case.279
Treatment for active TB in geriatric patients is the
same as for all adults.
resistance
TB is presently uncommon in elderly Americans, the
Although multidrug
immigration of people from areas with high rates of
multidrug resistance TB (eg, Southeast Asia and the
Philippines) will likely increase the number of such
cases in the elderly. Treatment regimens for sensi
tive strains include therapy for 2 months with isoni
azid, rifampin, pyrazinamide, and ethambutol, fol
lowed by 4 months of isoniazid and rifampin.
Therapy that is directly observed twice a week has
been advocated as an extremely important measure
to improve compliance with therapy and thus to
avoid the emergence of drug resistance.280
1720
with
Aging
Sleepto patterns
change with normal aging com
the patterns in young adults, and sleep
pared
disturbances are more common for the elderly.
to Dement et al,286 "the strongest and
According
most consistent factor affecting the pattern of sleep
across the night is age," although data to support this
for the oldest elderly, those above age 80, are scant.
At least 20 to 40% of all adults have sleep-related
Reviews
are
insomnias.286
abnormali
during sleep; they also noted that these
increasing age and obesity. Re
ported observations of the impact of aging on sleep
include the following. First, self-reports in the el
derly indicate increases with age in the difficulty of
both initiating and maintaining sleep, with more
frequent and early awakenings.288 These disruptions
result in more time in bed, despite less time asleep at
and more napping with increasing age. Sec
night,there
is more variability in sleep duration with
ond,
increased age. Thirty percent of adults sleep < 5 or
> 9 h/night. Persons who are outliers in sleep dura
tion are more common after age 64 and have an
associated increase in mortality,289 although there is
no evidence for causation of death by sleep disor
ders. Third, individuals 50 to 70 years old have
increased sleep latencies, ie, it takes them longer to
get to sleep than younger persons. Fourth, in labo
ratory testing, there is more frequent nocturnal
associated with more sleep fragmentation
awakening
and more stage 1, nonrestorative sleep. There are
more spontaneous nocturnal arousals and a four-fold
increase in time required to return to sleep. Fifth,
the amplitude of slow-wave sleep (stages 3 and 4
restorative sleep) markedly diminishes with age. The
amount of this slow-wave sleep also decreases. Sixth,
there is an age-related reduction in circadian rhythm
such as jet lag or
amplitude such that adjustments
in
shift
work
result
more
rotating
difficulty sleep
ing.290-291 These findings suggest a destabilization of
biological rhythm of the elderly compared to young
adults.
ties correlated with
1721
of OSA
particularly
mortality, which
elderly because the
seen with
uous
Sleep Disorders
in the
Elderly
1723
Uncorrectable PaC02
> 45 mm Hg not due to
Yes.
primary hypoventilation
Contraindication
to pneumonectomy
No
FEV1
>
Yes.
Acceptable pulmonary
operative risk
Yes.
Acceptable pulmonary
operative risk
tNo
Perfusion
lung scan
Predicted postoperative
FEV1 > 800 ml
or > 40% of normal
No
Unacceptable operative
improvement in symptoms.
1724
some
chemotherapeutic regimens,
assistance of
Nadia
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