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Physiological changes in respiratory
function associated with ageing
To the Editor:
We read with interest the review of JANSSENS et al. [1]
entitled "Physiological changes in respiratory function asso-
ciated with ageing", more specifically the subheading devoted
to changes in arterial oxygenation and ventilation-perfusion
(V ©/Q ©) relationships. Although the seminal study of W
et al. [2] was addressed in full, it was a shame that they did not
discuss the more recent comprehensive work of our group in
this field [3]. We extensively investigated the distributions of
V ©/Q © ratios in 64 healthy individuals aged 18±71 yrs. The
principal findings of that study were: 1) that V ©/Q © imbalance,
but not increased intrapulmonary shunting, did increase with
age as previously expected; 2) that the increase over the span
of ~50 yrs was physiologically very small; 3) that most of the
variance in V ©/Q © mismatch in this cohort of subjects was not
due to ageing and remained unsettled; and 4) that the fall in
arterial partial pressure of oxygen (PO
) with age was also
quite small but was internally consistent with the V ©/Q ©
changes measured independently.
V ©/Q © relationships were characterized in most of these
healthy individuals by narrow distributions that widened
slightly with age together with a trivial shunt of <1% of the
cardiac output in 90% of cases. Both the second moments
(dispersions) of pulmonary blood flow (Log SDQ) and of
alveolar ventilation (Log SDV) increased by ~0.1 between
20±70 yrs. Accordingly, the dispersion of pulmonary perfu-
sion (Log SDQ) increased from 0.36±0.47, akin to a decrease
of oxygen tension in arterial blood (P
Only 10% of the total variance was attributed to age. A similar
amount was due to intrasubject variability, but none was due
to variations in other factors, such as forced expiratory volume
in one second (FEV
1), FEV1/forced vital capacity (FVC)
ratio, weight or height. We did not measure closing volume
and it is therefore likely that age could disturb V ©/Q ©
matching as a result of increases in closing volume. However,
since the latter mechanism is highly unlikely to influence V ©/
Q © relationships in young healthy individuals [4], and since
the variance of the dispersion of pulmonary blood flow was as
large amongst the subset of young as that of old individuals,
we would postulate that increased closing volume is not a
determinant factor of the variance in V ©/Q © homogeneity.
R. Rodriguez-Roisin*, F. Burgos*, J. Roca*, J.A.
*, R.M. Marrades*, P.D. Wagner
Servei de Pneumologia i Al.le
rgia Respirato
ria, Dept de
Medicina, Institut d©Investigacions Biome
diques August Pi i
Sunyer (IDIBAPS), Hospital Clõ
nic, Universitat de Barce-
lona, Barcelona, Spain. Dept of Medicine, University of
California, San Diego, La Jolla, CA, USA. Fax: 34 93
1. Janssens JP, Pache JC, Nicod LP. Physiological changes in
respiratory function associated with ageing. Eur Respir J
1999; 13: 197±205.
distributionsof ventilation-perfusion ratios in normal subjects
breathing air and 100% O
. J Clin Invest 1974; 54: 54±68.
3. Cardu
s J, Burgos F, Dõ
az O, et al. Increase in pulmonary
ventilation-perfusion inequality with age in healthy indivi-
duals. Am J Respir Crit Care Med 1997; 156: 648±653.
4. Buist AS, Ghezo H, Anthonisen NR, et al. Relationship
between the single-breath N
test and age, sex and smoking
habit in three North American cities. Am Rev Respir Dis
1979; 120: 305±318.
To the Editor:
With great interest, we read the review article by JANSSENS
et al. [1] concerning physiological changes in respiratory
function associated with ageing. The authors have summar-
ized in the abstract that "Physiological ageing of the lung is
associated with dilatation of alveoli, enlargement of air-
spaces, decrease in exchange surface area and loss of
supporting tissue for peripheral airways ("senile emphyse-
ma"), changes resulting in decreased static elastic recoil of
the lung and increased residual volume and functional
residual capacity". Although the functional and structural
alterations of the respiratory system with ageing were sophi-
sticatedly described in the article, we are not in agreement
with the authors that physiological ageing of the lung is
determined as the senile emphysema.
Because the airspace enlargement including ductectasia
and loss of elastic recoil of the lung are commonly inves-
tigated in aged humans without noxious insults [2±4], V
et al. [5, 6] proposed that the structural and functional
characteristics caused by isolated airspace enlargement seen
in the elderly as "senile lung (ageing lung)", were differen-
tiated from senile emphysema by the absence of alveolar
wall destruction. The ductectasia and airspace enlargement
without alveolar wall destruction was quantitatively assessed
by morphometric indices, e.g. mean linear intercept (MLI)
and destructive index (DI), while the loss of lung elastic
recoil was assessed by the left-sided shifts of pressure-vol-
ume curves of lungs and by the exponential equivalent K [7].
However, it is difficult in human lungs to separate the true
age effect, i.e., the physiological ageing effect, from the
cumulative environmental effects, i.e., the combination of
physiological and pathological ageing effects, since the hu-
man respiratory system is open to the environment, continu-
ously exposing the lung to a variety of pollutants. Although
senescence-accelerated mouse (SAM) is a good model to
investigate the differences between physiological ageing of
the lung, i.e., ageing lung or senile lung, and pathological
ageing of the lung, i.e., cigarette smoke-related airspace
enlargement [7±10], it has been reported that aged mice
under protected circumstances using a filter cage do not ex-
hibit the airspace enlargement or alveolar wall destruction
[11]. In contrast, several canine studies revealed that long-
term exposure to air pollutants at ambient levels might cause
bronchitis lesions and emphysematous lesions in dogs [12].
In humans, it has been suggested that cutaneous hypersensi-
tivity to common aeroallergens is a significant independent
predictor of subsequent decline of lung function among
middle-aged and older males with no history of asthma [13].
EYER et al. [14] also reported that neutrophil migration and
Eur Respir J 1999; 14: 1454±1457
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ERS Journals Ltd 1999
European Respiratory Journal
ISSN 0903-1936
low-grade inflammation existed in lower airways of many
clinically normal, older individuals. These results indicate
that long-term exposure to environmental pollution during
life-time, rather than age, plays an important role in the
development of airspace enlargement in later life. Thus, phy-
siological ageing should be named the senile lung or ageing
lung. "Senile emphysema" may be a condition of patholo-
gical ageing of the lung, since emphysema increases in
frequency with age and is found most frequently in patients
in the seventh decade [3, 15].
S. Teramoto, T. Matsuse, Y. Ouchi
Correspondence: S. Teramoto, Dept of Geriatric Medicine,
Faculty of Medicine, Tokyo University Hospital, 7-3-1-Hongo
Bunkyo-ku, Tokyo 113-8655, Japan. Fax: 81 358006530.
1. Janssens JP, Pache JC, Nicod LP. Physiological changes in
respiratory function associated with ageing. Eur Respir J
1999; 13: 197±205.
2. Chan ED, Welsh CH. Geriatric respiratory medicine. Chest
1998; 114: 1704±1733.
3. Thurlbeck WM. Chronic airflow obstruction. In: Pathology
of the lung. Thurlbeck WM, Churg AM, eds. New York,
Thieme Medical Publishers Inc., 1995; p.780±825.
4. Teramoto S, Matsuse T, Fukuchi Y, Ouchi Y. Influence of age
on the structure and function in respiratory system: special
reference to aged women. In: Facts, Research, and Inter-
vention in Gerontology. Kaiser FE, Nourhashemi F, Bertiere
MC, Ouhci Y, eds. Toulouse, France, Serdi Publisher, 1998;
pp. 145±155.
5. Verbeken EK, Cauberghs M, Mertens I, Clement J, Lau-
weryns JM, Van de Woestijne KP. The senile lung: com-
parison with normal and emphysematous lungs: 1. structural
aspects. Chest 1992; 101: 793±799.
6. Verbeken EK, Cauberghs M, Mertens I, Clement J, Lau-
weryns JM, Van de Woestijne KP. The senile lung: compa-
rison with normal and emphysematous lungs: 2 functional
aspects. Chest 1992; 101: 800±809.
7. Teramoto S, Fukuchi Y, Uejima Y, Teramoto K, Oka T,
Orimo H. A novel model of senile lung: senescence-acc-
elerated mouse (SAM). Am J Respir Crit Care Med 1994;
150: 234±244.
8. Teramoto S, Fukochi Y, Uejima Y, Teramoto K, Orimo H.
Biochemical characteristics of senescence-accelerated mouse
(SAM). Eur Respir J 1995; 8: 450±456.
9. Teramoto S, Uejima Y, Oka T, et al. Effects of chronic
cigarette smoke inhalation on the development of senile lung
in senescence-accelerated mouse. Res Exp Med 1997; 197:
10. Teramoto S, Fukuchi Y. Age-dependent changes in lung
structure and function in the senescence-accelerated mouse
(SAM): SAM-P/1 as a new model of senile hyperinflation of
lung. Am J Respir Crit Care Med 1997; 156: 1361.
11. Kawakami M, Paul JL, Thurlbeck WM. The effect of age on
lung structure in male BALB/cNNia inbred mice. Am J Anat
1984; 170: 1±21.
12. Heyder J, Takenaka S. Long-term canine exposure studies
with ambient air pollutants. Eur Respir J 1996; 9: 571±584.
13. Gottlieb DJ, Sparrow D, O©Connor GT, Weiss ST. Skin test
reactivity to common aeroallergens and decline of lung
function. The Normative Aging Study. Am J Respir Crit Care
Med 1996; 153: 561±566.
14. Meyer KC, Rosenthal NS, Soergel P, Peterson K. Neutrophils
and low-grade inflammation in the seemingly normal aging
human lungs. Mech Ageing Dev 1998; 104: 169±181.
15. Teramoto S, Fukuchi Y. Bullous emphysema. Curr Opin
Pulm Med 1995; 2: 90±96.
From the authors:
We read with interest the comments made by Rodriguez-
Roisin et al. as to the age-related changes in ventilation-
perfusion ratio (V ©/Q ©) heterogeneity and the implication of
increased closing volume (CV) as a possible explanation for
increased V ©/Q © heterogeneity in older healthy subjects.
Rodriguez-Roisin et al. refer to an excellent study analys-
ing, by the multiple inert gas technique changes in pulmo-
nary V ©/Q © inequality with age in 64 healthy individuals
aged 18±71 yrs [1].
The observation that the decrease in oxygen tension in
arterial blood (P
) with ageing is small is indeed consistent
with the observations of G
NARD et al. [2] and DECLAUX et
al. [3] who did not find any significant correlations between
age and changes in P
and suggest that normal values for
are in the range of 11.261.0 kPa (8467.5 mmHg;
SD) in healthy elderly subjects, which is well above
results obtained by previously published regression equa-
tions [4].
However, we have a few comments on the assertion that
increased CV is not a determinant factor in increased V ©/Q ©
heterogeneity in the elderly and on the data on which Rodri-
guez-Roisin et al. base their assumption: 1) The study referr-
ed to includes 64 patients of a mean age of 37614 yrs
SD); only our subjects (6%) are aged $60 yrs, the eld-
est being 71 and only 10 subjects are aged $55 yrs (15%).
These data are there-fore hardly representative of the physio-
logical changes in the respiratory system of elderly subjects,
which were the focus of our review [5]; 2) the proportion of
subjects with low V ©/Q © areas (>0.75% of cardiac output) is
75% for the small number of subjects aged $60 yrs (n=4),
versus 6.7% for those aged <60 yrs, suggesting an increase in
V ©/Q © mismatch in these "young" elderly subjects, although
this was not statistically significant; 3) the CV increases with
age; however, data published by L
EBLANC et al. [6] suggest
that the CV may equal the functional residual capacity (FRC)
only when subjects reach ~65 yrs of age (FRC - CV = 1.95 -
(0.036age (yrs)): in younger subjects, the increase in clos-
ing volume may not have a significant repercussion on V©/Q©
homogeneity; 4) the increase in CV with ageing is most
probably not linear; the increase in CV is accelerated after
the age of 50 yrs, and follows a curvilinear (exponential)
equation (DN
) = 0.85 +
0.0929 6 age - 6.302); this
emphasizes the importance of studying a large group of older
subjects to document the interaction between CV and V ©/Q ©
mismatch [7]; 5) C
RAPO et al. [8] suggests that the age-
associated anatomo-pathological modifications in small and
distal airways, which may affect and increase the CV, be-
come physiologically significant in much older individuals
than those studied by C
ARDUS et al. [1].
Based on available data, we believe therefore that in-
creased CV cannot presently be excluded as an explanation
for V ©/Q © mismatch in the old and very old; the answer to
this problem will necessitate studies similar to that published
by C
ARDUS et al. [1] including a larger population of older
subjects. Information extrapolated from studies including
younger adults may not reflect the physiological changes
which occur in the very old.
We agree with T
ERAMOTO et al. that the homogeneous
enlargement of alveolar ducts and airspaces, without signs of
inflammation or destruction described in our review [5]
should be considered as "senile lung" and not as "senile
emphysema". Whether the appearance of the characteristic
parenchymal alterations of the "senile lung" is related to a
low grade inflammation in the distal airways, as a reaction to
environmental pollutants, or is just the result of "wear and
tear" alterations in the collagen and elastin framework, warr-
ants further studies.
J.P. Janssens*, J.C. Pache
, L.P. Nicod
*Dept of Geriatrics,
Division of Pathology and
Division of
Lung Diseases, Geneva University Hospital, Route de Mon-
e, 1226, Tho
nex, Geneva, Switzerland. Fax: 41 223056115
1. Cardus J, Burgos F, Diaz O, et al. Increase in pulmonary
ventilation-perfusion inequality with age in healthy indivi-
duals. Am J Respir Crit Care Med 1997; 156: 648±653.
2. Gue
nard H, Marthan R. Pulmonary gas exchange in elderly
subjects. Eur Respir J 1996; 9: 2573±2577.
3. Delclaux B, Orcel B, Housset B, Whitelaw WA, Derenne J.
Arterial blood gases in elderly persons with chronic obstruc-
tive pulmonary disease (COPD). Eur Respir J 1994; 7: 856±
4. Hertle F, Georg R, Lange H. Die arteriellen Blutgaspart-
cke und ihre Beziehungen zu Alter und anthropo-
metrischen GroÈssen. Respiration 1971; 28: 1±30.
5. Janssens JP, Pache JP, Nicod LP. Physiological changes of
respiratory function associated with ageing. Eur Respir J
1999; 13: 197±205.
6. Leblanc P, Ruff F, Milic-Emili J. Effects of age and body
position on "airway closure" in man. J Appl Physiol 1970;
28: 448±451.
7. Sixt R, Bake B, OxhoÈj H. The single-breath N
test and
spirometry in healthy non-smoking males. Eur J Respir Dis
1984; 65: 296±304.
8. Crapo RO. The aging lung. In: Pulmonary disease in the
elderly patient. Mahler DA, ed. New York, USA, Marcel
Dekker Inc., 1993: pp. 1±21.
Postural drainage techniques and gas-
tro-oesophageal refkux in infants with
cystic fibrosis
To the Editor:
Recently PHILLIPS et al. [1] added to the body of knowledge
relating to gastro-oesophageal reflux (GOR) in cystic fibrosis
(CF). I noted with interest the high incidence of GOR (73%)
found in their study of 11 children with CF of <2.5 yrs. This
reinforces the sentiment that GOR is an important issue that
needs to be considered in the management of young children
with CF.
In their article, P
HILLIPS et al. [1] state that "holding the
baby: head downwards positioning for physiotherapy does
not cause gastro-oesophageal reflux". This is different to the
findings of three independent studies on this topic over the
past fifteen years [2±4]. I would like to comment on some of
the significant differences between the studies that may have
contributed to their different results and conclusions.
We studied 20 infants of <5.6 months newly diagnosed
with CF. Eighteen of the infants were <3 months, 15 of those
were #2 months; the other two were 4.4 and 5.6 months [4].
This large group of very young infants with CF is different to
the group of 11 infants and toddlers with CF aged up to 27
months of P
HILLIPS et al. [1].
They chose six positions, of which two positions were 208
head down lying on the left and right side and two positions
were 158 head down lying on the left and right side, both with
a quarter turn towards supine (the other two positions were
horizontal and head up). We studied four positions: supine
horizontal, prone with 30 head-down tilt and lying on the left
and right side with 308 head-down tilt. We studied those four
studied those four positions as they were what we were using
and teaching the parents of infants with CF at our clinic.
I noted with interest that the widely prescribed prone with
head down tilted position [5] was not included in the study of
HILLIPS et al. [1]. FOSTER et al. [2] found a mean oesophageal
pH of 2.8 during chest physiotherapy in the prone position in
their study of ten children with CF. The prone position was
associated with the lowest mean pH of the four standard
positions that they studied.
In considering the title of the study of P
HILLIPS et al. [1], I
was puzled by their acknowledgement that "in some infants it
is possible that the head-down tipped positions may worsen
GOR. Therefore, individual evaluation of physiotherapy is
recommended for infants undergoing lower oesophageal pH
monitoring in whom clearance of excess secretions is indi-
cated". Does this suggest that some of the 11 patients with CF
may have had episodes of GOR during chest physiotherapy?
What the study of P
HILLIPS et al. [1] may imply is that, first,
by excluding the prone head-down tilted position and reduc-
ing the angle of head-down tilt, the likelihood of increasing
episodes of reflux is reduced. Secondly, the older the infant
with CF, the lower the likelihood of increased episodes of
GOR during chest physiotherapy. Whether the prone position
should be used for infants with CF, by how much we need to
decrease the angle of head-down tilt and at what age in
infancy and early childhood GOR during chest physiotherapy
becomes less of an issue is open to debate and further
Newborn screening has resulted in the commencement of
daily chest physiotherapy in very young infants (often ~6±8
weeks of age) at many centres. There is substantial evidence
that there is a high incidence of gastro-oesophageal reflux in
infants with cystic fibrosis. I, therefore, believe that when pre-
scribing a chest physiotherapy regimen for infants with cystic
fibrosis, the unique infant differences compared to older pa-
tients should be considered, and further longer-term research
should be undertaken. The main objective is to provide chest
physiotherapy for infants with cystic fibrosis that is optimally
effective in terms of promoting clearance of pulmonary sec-
retions and that does not have iatrogenic effects. In the words
of O
RENSTEIN [6] "Respiratory disease may also provoke reflux
more indirectly by prompting the use of therapies that provoke
reflux. These therapies include . . . postural drainage.
B.M. Button
Physiotherapy Dept, The Alfred Hospital, P.O. Box 315,
Prahran, Victoria 181, Australia. Fax: 61 393491289.
From the authors:
We thank B.M. Button for showing interest in our study.
There are a number of reasons for the discrepancies between
our own [1] and previous studies [2±4]. In their abstract,
FOSTER et al. [2] conclude that chest physical therapy may
precipitate gastro-oesophageal reflux (GOR), but they do not
state whether the subjects were tipped; one position described
is "upright". V
ANDENPLAS et al. [3] investigated physiotherapy
using head-downwards positioning; however, each treatment
lasted 30 min and included the intermittent use of abdominal
thrusts and tracheal rubs to stimulate coughing. It is docu-
mented that the control subjects also suffered regurgitation
and vomiting during "physiotherapy". B
UTTON et al. [4] com-
pared a "standard" physiotherapy regimen (SPT) using tipped-
down positions with a "modified" regimen (MPT) excluding
all tipped postures. They concluded GOR was increased in the
SPT but not with the MPT, but, as T
pointed out, there was no significance difference in reflux
indices between the regimens, and, in the head-downwards
positions, acid refluxate was cleared faster.
In clinical practice, we assess each infant to determine
which segments of the lungs need clearing before treating. We
ensure, however, that, during the course of a day, all lobes are
treated and thus, in our study design, we included the lingula
and middle lobes, which other studies have not. The lateral
segments of the lower lobes were treated; prone head tilted
down was not indicated. Regarding the exact angle of head-
downwards tip in this age group, physiotherapy is most
frequently performed by parents/carers with the infant on a
pillow on the knees. The legs of the adult carer are positioned
to allow different tipped positions. No previous study
describes how the angle of tip was attained or indeed how
it was precisely maintained. Nor, in clinical practice, is it
likely to be measured by busy mothers in a home setting.
As with other studies, our own contains relatively small
numbers of children. In the group we studied, there was no
evidence that the head-down tipped position induced gastro-
oesophageal reflux in any infant. However, neither we nor
anyone else can exclude the possibility that there may be
individuals who were not in the study in whom this is not the
case. Our study does not "imply" anything; we concluded that,
in patients of this age, using standard techniques for chest
physiotherapy, head-down tilt does not cause gastro-oeso-
phageal reflux; indeed, it is in the sitting postural drainage
position that gastro-oesophageal is most likely. These postural
changes are compatible with physiological understanding. We
agree that extrapolation outside the specific conditions and
subjects of any study should be performed with caution, and
certainly what is needed is high quality research-based evid-
ence with proper statistical analysis, rather than mere "beliefs"
and "words".
G.E. Phillips, S.E. Pike, M. Rosenthal, A. Bush
Dept of Paediatric Respiratory Medicine, Royal Brompton
and Harefield Hospital Trust, Sydney Street, London SW3
6NP, UK. Fax: 44 2073518763.
1. Phillips GE, Pike SE, Rosenthal M, Bush A. Holding the
baby: head downwards positioning for physiotherapy does
not cause gastro-oesophageal reflux. Eur Respir J 1998; 12:
2. Foster AC, Voyles JB, Murphy SA. Twenty four hour pH
monitoring in children with cystic fibrosis: association of
chest physiotherapy to gastro-oesophageal reflux. Paediatr
Res 1983; 17: 188A.
3. Vandenplas Y, Diericx A, Blecker U, Lanciers S, Deneyer M.
Oesophageal pH monitoring data during chest physiotherapy.
J Paediatr Gastroenterol Nutr 1991; 13: 23±26.
4. Button BM, Heine RG, Catto-Smith A, Pheland PD, Olin-
sky A. Postural drainage and gastro-oesophageal reflux in
infants with cystic fibrosis. Arch Dis Child 1997; 76: 148±
5. Physiotherapy in the Treatment of Cystic Fibrosis (CF). Inter-
national Physiotherapy Group for Cystic Fibrosis Mucovis-
cidosis Association 1995. (Available from A. Ramos via email:
6. Orenstein SR. Respiratory complications of reflux disease in
infants. In: Stein MR, ed. Gastrooesophageal reflux disease
and airway disease. In: Lenfant C, exec.ed. Lung biology in
health and disease. Vol. 129: New York: Marcel Dekker,
1999: 269±284.
7. Taylor CJ, Threlfall D. Postural drainage techniques and
gastro-oesophageal reflux in cystic fibrosis. Lancet 1997;
349: 1567±1568.
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Simple Summary Idiopathic pulmonary fibrosis (IPF) presents a significant challenge. Despite extensive research, our understanding of its underlying causes remains limited. One intriguing hypothesis proposes that disruptions in mitochondrial functionality might play a role. Mitochondrial dysfunction is a recognized feature of the normal aging process, and parallels can be drawn to IPF, particularly within type 2 alveolar cells. This comprehensive review aims to unravel the various pathways of mitochondrial dysfunction observed in IPF. Furthermore, we explore potential therapeutic interventions designed to address this complex issue. Abstract Mitochondrial biology has always been a relevant field in chronic diseases such as fibrosis or cancer in different organs of the human body, not to mention the strong association between mitochondrial dysfunction and aging. With the development of new technologies and the emergence of new methodologies in the last few years, the role of mitochondria in pulmonary chronic diseases such as idiopathic pulmonary fibrosis (IPF) has taken an important position in the field. With this review, we will highlight the latest advances in mitochondrial research on pulmonary fibrosis, focusing on the role of the mitochondria in the aging lung, new proposals for mechanisms that support mitochondrial dysfunction as an important cause for IPF, mitochondrial dysfunction in different cell populations of the lung, and new proposals for treatment of the disease.
Introduction Long-term breathlessness is more common with age. However, in the oldest old (>85 years), little is known about the prevalence, or impact of breathlessness. We estimated breathlessness limiting exertion prevalence and explored (i) associated characteristics; and (ii) whether breathlessness limiting exertion explains clinical and social/functional outcomes. Methods Health and socio-demographic characteristics were extracted from the Newcastle 85+ Study cohort. Phase 1 (baseline) and follow-up data (18 months, Phase 2; 36 months, Phase 3; 60 months, Phase 4 after baseline) were examined using descriptive statistics and cross-sectional regression models. Results Eight hundred seventeen participants provided baseline breathlessness data (38.2% men; mean 84.5 years; SD 0.4). The proportions with any limitation of exertion, or severe limitation by breathlessness were 23% (95% confidence intervals (CIs) 20–25%) and 9% (95%CIs 7–11%) at baseline; 20% (16–25%) and 5% (3–8%) at Phase 4. Having more co-morbidities (odds ratio (OR) 1.34, 1.18–1.54; P < 0.001), or self-reported respiratory (OR 1.88, 1.25–2.82; P = 0.003) or cardiovascular disease (OR 2.38, 1.58–3.58; P < 0.001) were associated with breathlessness limiting exertion. Breathlessness severely limiting exertion was associated with poorer self-rated health (OR 0.50, 029–0.86; P = 0.012), depression (beta-coefficient 0.11, P = 0.001), increased primary care contacts (beta-co-efficient 0.13, P = 0.001) and number of nights in hospital (OR 1.81; 1.02–3.20; P = 0.042). Conclusions Breathlessness limiting exertion appears to become less prevalent over time due to death or withdrawal of participants with cardio-respiratory illness. Breathlessness severely limiting exertion had a wide range of service utilisation and wellbeing impacts.
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With the increasing number of elderly people in developed countries, physicians are often confronted with patients whose arterial oxygen tension, PaO2, is lower than that of normal young adults. The normal values predicted in the literature for very old individuals are generally extrapolated from younger subjects. The purpose of the present study was to obtain PaO2 values from a large population of elderly subjects with normal and obstructive ventilatory function. We measured arterial blood gases in 274 subjects, aged 65-100 yrs (mean 82 yrs), with chronic bronchitis and moderate airways obstruction (mean forced expiratory volume in one second (FEV1), 53% pred). Mean PaO2 was 10.0 +/- 1.4 kPa (75.2 +/- 10.8 mmHg) and mean arterial carbon dioxide tension (PaCO2) was 5.4 +/- 0.8 kPa (40.5 +/- 6.1 mmHg). Both PaO2 and PaCO2 were independent of age. Blood gas abnormalities were associated with airways obstruction: PaO2 was positively correlated to FEV1 and PaCo2 was negatively correlated to FEV1. PaO2 was 10.8 +/- 1.4 kPa (81.5 +/- 10.7 mmHg) in the patients with FEV1 > or = 90% predicted versus 9.5 +/- 1.3 kPa (71.5 +/- 10.1 mmHg) in those with FEV1 < or = 35% pred. These findings suggest that the predicted PaO2 extrapolated from younger normal values are often erroneously underestimated. It is probably more accurate to accept as normal a PaO2 of 10.6-11.3 kPa (80-85 mmHg) for all subjects over 65 yrs, irrespective of their age.
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Although important alterations in structure and function develop with age, the hypothesis that the lungs are capable of maintaining adequate gas exchange for the maximum human life span is generally accepted. This hypothesis was examined by measuring arterial oxygen and carbon dioxide tension (Pa,O2 and Pa,CO2) alveolo-arterial differences in oxygen and carbon dioxide tension (PA-a,O2 and Pa-A,CO2), steady state transfer capacity of the lung for carbon monoxide (TL,CO,ss) as well as the gas exchange ratio (R) in a series of 74 healthy subjects aged more than 68 yrs (69-104 yrs). In addition, Pa,O2 and Pa,CO2 were measured in a series of 55 young healthy subjects, who acted as controls. In the elderly subjects, except for TL,CO,ss, there was no significant correlation between any of the other variables and age. However, for a given Pa,CO2, Pa,O2 was always lower in the group of elderly subjects than in the group of young control subjects. TL,CO,ss, as well as TL,CO,ss/minute ventilation (V'k) ratio, was correlated with age, according to the following regression equations: TL,CO,ss (mL.min-1.kPa-1) = 126-0.90 x age (yrs), and TL,CO,ss/V'k (kPa-1 x 10(3)) = 13.5-0.085 x age, respectively. These results show that arterial oxygen tension did not decrease with age in this series of elderly subjects. However, the decrease in steady-state transfer capacity of the lungs for carbon monoxide with age indicates that oxygen transport could be diffusion-limited in elderly subjects, at least when oxygen consumption is increased.
The partial pressures of oxygen and carbon dioxide of the arterial blood were examined under strictly standardized conditions. The relationship of PaO2 to age was found as YR = -0.40 age + 96.2 and PaCO2 to age as YR = 0.03 age + 36.0. Furthermore, a correlation between PaCO2 and PaO2 could be calculated as YR = -0.073 PaO2 + 43.0. An estimation of PaO2 by biometrical data is given: YR= -0.39 age – 0.02 weight (kg) + 0.06 height (cm) + 85.9. The casual relations between blood partial pressures and age will be discussed in details.
Physiological ageing of the lung is associated with dilatation of alveoli, enlargement of airspaces, decrease in exchange surface area and loss of supporting tissue for peripheral airways (“senile emphysema”), changes resulting in decreased static elastic recoil of the lung and increased residual volume and functional residual capacity. Compliance of the chest wall diminishes, thereby increasing work of breathing when compared with younger subjects. Respiratory muscle strength also decreases with ageing, and is strongly correlated with nutritional status and cardiac index. Expiratory flow rates decrease with a characteristic alteration in the flow–volume curve suggesting small airway disease. The ventilation–perfusion ratio (V ′A/Q ′) heterogeneity increases, with low V ′A/Q ′ zones appearing as a result of premature closing of dependent airways. Carbon monoxide transfer decreases with age, reflecting mainly a loss of surface area. In spite of these changes, the respiratory system remains capable of maintaining adequate gas exchange at rest and during exertion during the entire lifespan, with only a slight decrease in arterial oxygen tension, and no significant change in arterial carbon dioxide tension. Ageing tends to diminish the reserve of the respiratory system in cases of acute disease. Decreased sensitivity of respiratory centres to hypoxia or hypercapnia results in a diminished ventilatory response in cases of heart failure, infection or aggravated airway obstruction. Furthermore, decreased perception bronchoconstriction and diminished physical activity may result in lesser awareness of the disease and delayed diagnosis.
Sixty-three infants, aged from 1 to 4 months, were examined for gastroesophageal reflux (GER) using esophageal pH monitoring. Thirty were examined because of chronic vomiting, 21 were healthy controls examined for GER as part of a screening program for sudden infant death syndrome, and 12 had an acute respiratory disease (RD). The 24-h pH monitoring data were within normal ranges in 26 infants (20 controls, 2 babies with emesis, and 4 with RD). Data were abnormal in 37 infants (1 control, 28 infants with emesis, and 8 with RD). All babies were submitted during a fasting awake period to a 30-min chest physiotherapy session. In the three groups studied, the incidence of GER episodes detected by the pH probe was significantly higher during physiotherapy if compared (a) to the calculated mean incidence during a 30-min period of the 24-h investigation or (b) to the incidence during a fasting awake period such as that during which the physiotherapy was given (p less than 0.001; Wilcoxon rank-sum test). We conclude that chest physiotherapy significantly increases GER incidence. We therefore propose restricting chest physiotherapy to fasting periods. These data add to the confusion that already exists regarding the possible causal relationship between (acid) GER and respiratory disease.
Healthy males (aged 30-70), who had never smoked, were studied. The 178 subjects were selected by systematic sampling from an urban population. Using the single-breath N2-washout test we measured the closing volume (CV) and the slope of the alveolar plateau (delta N2). A prediction equation for CV was produced by simple regression on age. delta N2 showed an accelerated increase with age above the age of 50. A curvilinear equation was established: delta N2 (%/1) = 0.85 + e0.0929 x A( yrs ) -6.302. Reference equations were also established for vital capacity (VC), forced expiratory volume in one second (FEV1) and FEV1 in per cent VC (FEV%) by means of linear multiple regression on age and height. The distribution of delta N2 was not homogenous throughout the age-range. As an upper limit of the reference range, we suggest 180% of the predicted value.
Gastro-oesophageal reflux is increased in cystic fibrosis and it is possible that postural drainage techniques may exacerbate reflux, potentially resulting in aspiration and further impairment of pulmonary function. To evaluate the effects of physiotherapy with head down tilt (standard physiotherapy, SPT) on gastroesophageal reflux and to compare this with physiotherapy without head down tilt (modified physiotherapy, MPT). Twenty (mean age 2.1 months) infants with cystic fibrosis underwent 30 hour oesophageal pH monitoring during which SPT and MPT were carried out for two sessions each on consecutive days. The number of reflux episodes per hour, but not their duration, was significantly increased during SPT compared with MPT (SPT 2.5 (0.4) v MPT 1.6 (0.3), p = 0.007) and to background (1.1 (0.)1, p = 0.0005). Fractional reflux time was also increased during SPT (11.7 (2.6)%) compared with background (6.9 (1.3)%) p = 0.03) but not compared with MPT (10.7 (2.7)%). There was no significant difference between MPT and background for number of reflux episodes, their duration, or fractional reflux time. SPT, but not MPT, was associated with a significant increase in gastro-oesophageal reflux in infants with cystic fibrosis.