Download The Respiratory Muscles

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Clinical Science (1985)68,l-10
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EDITORIAL REVIEW
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The respiratory muscles
MALCOLM GREEN A N D J O H N MOXHAM
Brompron and King’s College Hospitals, London
Introduction
Structure
The respiratory muscles provide the motive power
for breathing. Despite this central role in ventilation their physiology has been relatively neglected,
perhaps partly because of the complexity of their
function, and the difficulties of studying them.
However, in the last decade, there has been considerable increase in interest, and a number of new
concepts have arisen [l-31.
It is now appreciated that the translation of
central nervous output into ventilation requires a
sophisticated integration of the respiratory
muscles, which have to subserve the requirements
of posture and body movement, simultaneously
with breathing. The importance of the shape
(configuration) of the respiratory system to
muscle action has been emphasized. Analysis has
shown that the functions of the diaphragm are
complex: it is anatomically and embryologically
derived from two muscles, and these parts may
have different physiological actions. The abdominal muscles appear to be not only powerful
muscles of expiration, but also facilitate inspiration. Both internal and external intercostal
muscles now seem to be inspiratory at low lung
volumes and expiratory at high lung volumes. Like
all skeletal muscles the respiratory muscles are
capable of fatigue after heavy loads. It is increasingly believed that respiratory muscle fatigue
may play an important part in the pathogenesis
of respiratory failure, and part of the value of
artificial ventilation may lie in resting the respiratory muscles.
The respiratory muscles comprise the
diaphragm, the intercostal muscles, the abdominal
muscles, and the so-called ‘accessory’ muscles
including the sternomastoid and scalene muscles.
However, probably all of the muscles of the
trunk and neck can be recruited as respiratory
muscles under heavy loads.
The respiratory muscles are all skeletal (‘voluntary’)
muscles, consisting of motor units innervated by
a-motor neurones derived from anterior horn cells
in the spinal column down to L.2. The accessory,
intercostal and abdominal muscles are well
supplied with muscle spindles, tendon organs and
Paccinian corpuscles, providing an anatomical basis
for sensory input from these muscles [l]. The
diaphragm contains relatively fewer sensory endorgans, and there appear to be more tendon
organs than muscle spindles [4]. There are, however, afferent fibres in the phrenic nerve of the cat,
and afferent traffic has been recorded. The paucity
of end-organs may reflect the tendency of the
diaphragm to contract uniformly so that relatively
few organs are necessary to sample accurately its
functions [5].The main purpose of the diaphragm
is to generate pressure differences, and the
relatively greater number of tendon organs may
reflect this, since tendon organs can sensitively
reflect physiological contraction of muscle fibres
Correspondence: Dr Malcolm Green, Brompton
Hospital, Fulham Road, London SW3 6HP.
PI.
The respiratory muscles contain a mixture of
type 1 (slow twitch, oxygen dependent, fatigue
resistant fibres) and type 2 (fast twitch fibres,
most of which fatigue quickly, using glycolytic
energy stores) in approximately the same proportion as limb skeletal muscles. In man the
diaphragm contains about 55% of type 1 and 45%
of type 2 fibres, although the number of studies is
small and there appears to be variability between
subjects [6]. The physiological attributes and
size of fibres can be altered by suitable training
and detraining programmes in animals [7].
Physiology
The respiratory muscles including the diaphragm
appear to have physiological properties similar to
the other skeletal muscles; they generate maximum force at resting length, and the force falls off
as length diminishes: the length-tension relation-
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M. Green and J. Moxharn
ship. The diaphragm shows the same property
studied both in vitro [8] and in vivo [9, lo].
It also tends to become less curved as it shortens,
thus generating less pressure across it, by the
Laplace relation [ l l ] . This is probably a small
effect in normal subjects but may become significant in hyperinflation. The most important
consequence is that lung volume influences the
pressures the diaphragm can generate, being maximal when it is longest, and most curved, at low
lung volumes.
The force developed by skeletal muscles also
falls off as the speed of shortening increases. It has
been confirmed that the respiratory muscles also
show this force-velocity relationship [12]. Thus as
respiratory rate and depth increases the velocity
of muscle shortening increases, and force
generated for a given neural output falls. The
respiratory muscles have similar time courses of
pressure development [13, 141 and of relaxation
[ 151 as do limb muscles.
The diaphragm
Anatomically the diaphragm consists of two main
parts, inserted into the central tendinous dome.
The larger (costal) part originates over the inner
surfaces of the six lowest ribs and cartilages.
These fibres initially run directly upwards, parallel
and ‘apposed’ to the inner surface of the rib cage.
This ‘area of apposition’ represents up to onethird of the surface area of the rib cage at end
expiration, but diminishes during inspiration [ 161.
Both the origins and insertions of these costal
fibres are mobile, and potentially move with
respiration. By contrast the lumbar (crural)
portion has its origins on the second to fourth
lumbar vertebrae and associated ligaments, which
do not move with respiration.
Contraction of the diaphragm has several
effects [2, 16-19] (Fig. 1).
(1) The central dome of the diaphragm
descends with little change in its shape, peeling
the muscular fibres from the inner surface of the
rib cage along the area of apposition [lo]. This
tends to cause a fall in pleural pressure and an
increase in lung volume (inspiration).
(2) Contraction of the diaphragm causes an
increase in abdominal pressure. In the absence of
abdominal muscle contraction this causes the
anterior abdominal wall to move outwards. There
is also outward pressure exerted on the lower rib
cage through the area of apposition. This force is
inspiratory in direction and has been called the
‘appositional component’ [20].
(3) The costal fibres of the diaphragm tend to
lift the lower rib cage (insertional force). Because
force
m
i
a
p Appositional
p o s i
t Area
i o
of n
FIG. 1. Diagram to illustrate the actions of the
diaphragm. On contraction the dome descends and
abdominal pressure (Pab) rises. This expands the
lower rib cage via an ‘appositional force’ and
simultaneously the costal diaphragm elevates the
lower rib cage (‘insertional force’) with a resultant
force R. These actions cause a fall in pleural
pressure (Ppl), inspiration, and a tendency to
indrawing of the upper rib cage.
of the shape and articulations of the ribs, upward
movement also tends to cause forwards (pump
handle) and outward (bucket handle) motion,
particularly at low lung volumes. Since these fibres
of the diaphragm are mobile at both ends a
fulcrum is necessary to prevent mere descent of
the dome [(l) above]. This is provided by the
abdominal contents and anterior abdominal wall.
Removing the abdominal viscera in horses, dogs
and rabbits changes the result of costal diaphragm
contraction from expanding the lower rib cage to
contractingit [17, 18,211.
When the diaphragm acts in isolation it also
tends to have some expiratory components.
Patients with transection of the lower cervical cord
but intact phrenic nerve and diaphragm function
show paradoxical motion inwards of the upper
rib cage during inspiration [22,23]. This may also
be seen during spinal anaesthesia [24] and diaphragm pacing [25].
Different physiological functions of the two
parts of the diaphragm were proposed by Keith
in 1904 [26] and subsequently by Briscoe in 1920
[27] but these suggestions have been ignored until
recently. It has now been shown that the costal
part of the diaphragm is active whilst the crural
part is silent during vomiting, as might be expected
[281. De Troyer and colleagues have demonstrated
in dogs that both parts of the diaphragm cause an
increase in abdominal pressure and a fall in pleural
pressure..However, only the costal part has a direct
The respiratory muscles
inspiratory action on the rib cage by lifting the
lower ribs [l8, 291. There has been considerable
debate as to the relative contribution of the
direct effects of the diaphragm on the rib cage,
and its indirect effects via the abdominal and
pleural pressure [30-321. Goldman & Mead [33]
argued that the diaphragm expanded the rib cage
along its relaxed pressure-volume characteristic.
It now appears, however, that the rib cage deforms
when intercostal activity is absent and that the
pressures applied are complex, depending at least
in part on the relative contributions of the two
parts of the diaphragm [34].
Intercostal muscles
The importance of the intercostal muscles in
stabilizing the rib cage and preventing paradoxical
motion of its parts has been mentioned above,
Even in quiet breathing in normal subjects they
appear to play a necessary role in ensuring coordinated movement of the whole of the rib cage
WI.
The parasternal intercostals elevate the ribs,
but tend to lower the sternum [35], and are active
during inspiration even in quiet breathing [36-381.
The external intercostal muscles run from the
lower surface of each rib anteriorly and inferiorly
to the upper surface of the rib below. The internal
intercostals by contrast run inferiorly and
posteriorly. On the basis of this anatomical
arrangement Hamberger concluded in 1727 [39]
that the external intercostal muscles were inspiratory since by their contraction each lower rib
was pulled upwards and backwards towards the
rib above it, thereby swinging outwards. Conversely the internal intercostal muscles pulled each
upper rib posteriorly, downwards, and inwards,
to cause expiration. Electromyographic studies
have shown that the external intercostals are active
during inspiration and internal intercostals during
expiration [36, 371. However, recently doubt
has been cast on Hamberger’s hypothesis by the
studies of De Troyer and colleagues who have:
shown in dogs that the action of the intercostal
muscles depends on lung volume [40]. At low lung
volumes both external and internal intercostal
muscles are inspiratory when they contract, and at
high lung volumes both groups are expiratory,
Since the uppermost and lowermost ribs are
mobile, there must be stabilization of the rib
cage for effective action by the intercostal
muscles. The scalene and sternomastoid muscles
stabilize the upper rib cage during inspiration, and
the abdominal muscles help fnate the lower rib
cage during expiration [35,41].
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Abdominal muscles
Contraction of these powerful muscles tends to
pull the rib cage inwards and downwards and to
push the abdominal contents upwards, elevating
the diaphragm. Both these actions cause expiration
and these muscles have generally been viewed as
purely expiratory [42]. However, their actions
now appear to have additional complexities
[20, 431. Thus contraction of the abdominal
muscles increases abdominal pressure. This, as
seen above (Fig. l), tends to expand the lower rib
cage through the area of apposition, an inspiratory
motion. Furthermore upward motion of the dome
of the diaphragm tends to stretch its costal fibres,
and thus to lift the lower rib cage, which is also in
an inspiratory direction. Theoretically, the net
effect of contraction of abdominal muscles would
depend on the relative importance of these factors,
and studies in dogs have shown a significant
inspiratory tendency, particularly of the external
oblique muscles [43].
The abdominal muscles also ensure that the
diaphragm returns to its resting length at endexpiration, so that it is best placed on its lengthtension characteristic for subsequent contraction
during inspiration [lo, 22, 441. The maintenance
of abdominal pressure by abdominal muscle contraction during inspiration serves as a fulcrum for
the costal diaphragm to elevate the lower ribs, so
that the abdominal muscles can be considered as
‘accessory muscles of inspiration’ [20].
The abdominal muscles are electrically silent
during quiet breathing when supine, but when
erect there is tonic activity which is greatest in the
lower abdomen [45]. This has been conceived as
entirely postural [37, 461. However, active contraction of the abdominal muscles during both
inspiration and expiration may play a role in both
phases of breathing, suggesting that this activity
may be partly ventilatory.
Accessory muscles
The most important of these are the scalene
muscles and the sternomastoids. Studies of the
scalenes using needle electrodes show that they
have inspiratory electrical activity even during
quiet breathing, so that they should probably be
viewed as muscles of normal inspiration rather
than ‘accessory muscles’ [41], acting to elevate, or
to prevent downward displacement of, the upper
rib cage during inspiration [351. These muscles
have increased activity during stimulated ventilation, in patients with lesions of the upper cervical
cord and in chronic airways obstruction [23,47].
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M. Green and J. Moxham
Configuration and lung volume
During inspiration the mechanical difficulty of
producing a negative pressure pump using only
contractile elements has been overcome by the
complex geometry and interactions of the respiratory muscles. The shape of the system has been
termed its configuration, and this importantly
determines the efficiency of ventilation. Configuration is closely, but not uniquely, related to
lung volume. As lung volume increases the respiratory muscles become less advantageously placed
for inspiration and more advantageously placed for
expiration. In normal subjects this appears to be an
important mechanism for maximizing the efficient
use of the muscles. However, it can have disadvantages in disease: airways obstruction leads to
hyperinflation, putting the inspiratory muscles at a
less advantageous configuration. By contrast
fibrotic lung diseases, causing a reduction of lung
size, tend to put the inspiratory muscles at a more
advantageous configuration so that they are better
placed to overcome the increased mechanical
load provided by the stiff lungs [48].
Modelling the respiratory muscles
A number of attempts have been made to model
the function of the respiratory muscles using
mechanical, electrical or pneumatic analogies [34].
A mechanical model, modified from these by
permission, is shown in Fig. 2.
Sterno-mastoids
Intercost
muscles
Rib cage
Abdominal
muscles
-
FIG. 2. Diagram to illustrate some of the respiratory muscle actions. This model shows the effect
of the two muscular parts of the diaphragm in
causing descent of the dome. The costal diaphragm
in addition elevates the rib cage. The role of the
intercostal muscles is not easily depicted: they
cause elevation or descent of the rib cage, depending partly on its initial position. The abdominal
contents are shown as a hydraulic system containing compressible fluid. Rise in abdominal
pressure (Pab) tends to stabilize the diaphragm
and expand the lower rib cage. The abdominal
muscles by relaxing can facilitate descent of the
diaphragm, and by contracting cause elevation of
the dome of the diaphragm. The scalenes and
sternomastoids fixate, or tend to elevate, the
upper rib cage.
Respiratory muscle fatigue
Patients with severe lung disease and hyperinflation have reduced force generating capacity of the
respiratory muscles. In contrast their ventilatory
requirements are increased. The muscles, particularly the inspiratory muscles, are subject to large
loads with every breath for prolonged periods and
with little opportunity for rest. Patients with
severe chronic airways obstruction have a high
neural output to the respiratory muscles [49]
comparable with that required to sustain near
maximum ventilation in normal subjects. This
combination of high drive and large loads for long
periods has led to the suggestion, by analogy
with limb muscles, that fatigue could develop in
the respiratory muscles and contribute to hypercapnic ventilatory failure [50].
Muscle fatigue can usefully be defined as the
inability to sustain the required force with continued contractions. This is a characteristic of limb
muscles and recent studies have demonstrated that
the respiratory muscies can also fatigue. Normal
subjects can sustain large respiratory loads for only
short periods. Thus the diaphragm cannot
maintain greater than 40% of its maximum
pressure with each breath indefinitely [Sl]. The
overall respiratory pressures that can be sustained
indefinitely are further reduced (i) by high lung
volumes when the muscles are shortened, (ii) as
mean inspiratory flow rates increase when there is
increased velocity of shortening, (iii) as breathing
frequency increases, (iv) as the proportion of the
time devoted to inspiration during each breath
rises with longer contraction of the inspiratory
muscles [52,53].
In spite of much research over recent years, the
precise cause of skeletal muscle fatigue is not clear;
indeed it is unlikely that a single cause is
responsible and it is probable that under different
circumstances a variety of factors can become
relevant. Reduced central neural drive, especially
The respiratoly muscles
during sustained maximum voluntary effort, may
be important [54]. However, for many contractions including the repetitive submaximal ones of
ventilation, an important aspect of fatigue is likely
to be reduced muscle contractility [55]. As
fatiguing exercise continues and contractility falls,
so central firing frequency increases to counteract
force loss, but eventually central frequency itself
falls despite the reduction in muscle tension. This
fall in firing frequency may represent an adaptation to peripheral fatigue that avoids excessive
ATP depletion and the onset of rigor.
The situation may be rather different when a
muscle is acutely subjected to an overwhelming
load. In this case there is likely to be a rapid fall
in local chemical energy supplies and a failure of
muscle excitation, an energy consuming process,
thereby causing a ‘catastrophic’ loss of force but
no further energy consumption [56]. During
respiratory failure both these patterns of fatigue
may operate. In patients with longstanding respiratory disease, due to chronic airways obstruction
or scoliosis, the central nervous system may
modify respiration in response to muscle fatigue
by changing the respiratory rate, inspiratory time
and mean inspiratory flow, thereby avoiding
critical depletion of chemical energy stores but
only at the expense of allowing hypoventilation
and hypercapnia. By contrast in severe acute
disease, as in life-threatening asthma, the overwhelming load on the respiratory muscles may
precipitate catastrophic force loss and acute
ventilatory failure.
Detection of fatigue
Detection of fatigue in the respiratory muscles is
difficult because there is no simple technique for
measuring their force generation. Therefore, less
direct techniques have been employed. Muscle
fatigue has been investigated by measuring the
frequency spectrum of the electromyogram
(EMG) [57]. When skeletal muscle generates a
tension that cannot be sustained there is an early
alteration in the EMG with reduction in high
frequency and increase in low frequency activity,
resulting in reduction in the EMG ‘high/low’
ratio. This has been used as a marker of muscle
fatigue and has been applied to the muscles of
respiration, particularly the diaphragm [58]. However, the cause of the shift in the power spectrum
is not known, nor is the relation of the EMG
change to force loss understood; for example,
after diaphragm and quadriceps fatigue the high/
low ratio returns to normal at a time when force
generation is still abnormal [59].
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With fatigue the speed of muscle characteristically slows. Recent work on the respiratory
muscles has examined the relaxation of the human
diaphragm measured from transdiaphragmatic
pressure during a maximal sniff. In normal subjects
the relaxation rate for the non-fatigued diaphragm
is similar to that of limb muscles and after prolonged inspiratory loading relaxation is slowed
[ 151. The investigation of respiratory muscle
relaxation rates may be possible in patients and
allow identification of fatigue clinically.
Some of the techniques used to study limb
muscle fatigue can also be applied to the respiratory muscles. Studies in resting hand and leg
muscles of the force produced by electrical
stimulation show a characteristic relationship of
stimulation frequency to force, described by the
frequency-force curve [60]. With fatigue the shape
of the curve is altered with a reduction in the
forces generated at high stimulation frequencies
(‘high frequency fatigue’) [61] and/or reduction
in the forces at low stimulation frequencies, less
than 30 Hz (‘low frequency fatigue’) [62]. In high
frequency fatigue there is defective muscular
excitation due either to neuromuscular junction
failure or to impaired depolarization of the muscle
cell membrane. This excitatory failure is associated
with a reduced EMG and is rapidly restored to
normal by rest. In low frequency fatigue excitation of the muscle cell membrane is normal and
the EMG is not diminished, but the force per
membrane action potential is reduced implying
impaired contractility of the muscle fibre itself.
This type of fatigue can be long lasting, sometimes
persisting for many hours. After prolonged
muscular activity, force generation at low frequencies may also be reduced by changes in
tendons which become more extensible [63].
Furthermore muscle shortening due to hyperinflation reduces forces at low frequencies to a
greater extent than at high frequencies [64].
Thus, a number of factors can shift the frequencyforce curve to the right and may be of particular
physiological importance because the firing
frequency of motor neurones during everyday
activities is low (5-30 Hz) [65]. Even during a
maximum voluntary contraction the motor
neurone firing frequency falls to below 30Hz
within a few seconds [66].
Electrical stimulation has been used to investigate the contractile properties of the respiratory
muscles and to detect fatigue. Crucially the
frequency-force curve of the sternomastoid and
the frequency-transdiaphragmatic pressure curve
of the diaphragm have the same shape as the
curves of other skeletal muscles [67, 681. In
normal subjects, inspiratory loading and sustained
M. Green and J. Moxharn
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maximum voluntary ventilation produces low
frequency fatigue both in the sternomastoid and
also in the diaphragm (Fig. 3). Furthermore,
patients with chronic airways obstruction who
voluntarily breathe maximally develop low frequency fatigue of the sternomastoid [69]. To date
it has not been possible to evaluate low frequency
fatigue of the diaphragm in these patients.
Although it is likely that low frequency fatigue
of the respiratory muscles is of clinical importance,
the detection of such fatigue in patients with
respiratory failure presents great difficulties.
During very brief maximum voluntary efforts
lasting less than 2 or 3 s motor neurone firing
frequencies are high so that force generation is
little affected by low frequency fatigue, probably
due to saturation of the interior of muscle fibres
with calcium ions [70]. Thus maximum respiratory pressures, peak expiratory flow rates and
forced vital capacity are not reduced [71]. Resting
ventilation is associated with lower neural firing
frequencies. Experimental data for the cat suggest
that during tidal breathing phrenic motor neurone
firing frequency is 10-15 Hz rising to 20-30 Hz
with COz stimulation [72]. Low frequency fatigue
might therefore cause an important fall in respira-
tory muscle force production not revealed by tests
of maximum effort. Consistent with this
suggestion is the observation that respiratory
muscle fatigue may cause a reduction in the
ventilatory response to carbon dioxide of normal
subjects [71].
In limb muscles, fatigue is most likely to
develop when contractions are each a large proportion of maximum force. During high force
contractions many limb muscles become ischaemic
[73] and metabolism is therefore anaerobic.
However, the blood supply of the diaphragm is
excellent and continues to rise with hyperventilation [74]. Despite this there could be poor oxygen
delivery at a cellular level, particularly when the
respiratory muscles contract throughout the
respiratory cycle, as may be the case in severe
asthma. The importance of oxygen delivery
appears to be -supported by the observation that
during loaded breathing the endurance of the
inspiratory muscles of normal subjects is decreased
by hypoxia [51]. However, the mechanism of this
effect is not clear and could be mediated via the
central nervous system or through a direct action
on peripheral muscle.
Therapy
0
20
40
60
80
100
Stimulation frequency (Hz)
FIG. 3. Frequency-pressure curves of the diaphragm. The phrenic nerve of a normal subject
was stimulated in the neck at increasing frequencies (abscissa) and the resultant transdiaphragmatic pressure (A) was measured with oesophageal
and gastric balloons and expressed as a percentage
of the maximum Pdi (ordinate). The subject then
fatigued his diaphragm by breathing through an
inspiratory resistance to exhaustion. After fatigue
(A) there was a characteristic shift of the curve
to the right.
Treatment of patients with respiratory disease
should take account of factors that can affect
respiratory muscle function. Adequate nutrition
is important to maintain muscle mass since wasting
causes weakness and predisposes to fatigue. In
wasting diseases the respiratory muscles atrophy
and pressure generation is impaired [75]. High
dose steroids commonly used in chest medicine
and known to cause skeletal muscle wasting could
produce respiratory muscle weakness in addition
to hypokalaemia.
It is possible to increase the strength and
endurance of muscle by appropriate training. It
is not known whether training renders muscle less
susceptible to low frequency fatigue, but training
for strength may raise the threshold for fatigue
and endurance training increases capillaries, mitochondria and oxidative enzymes. Maximum
respiratory pressures can be increased in normal
subjects by training [76] and specific training of
the respiratory muscles can improve ventilatory
performance of patients with cystic fibrosis,
quadriplegia and chronic airways obstruction
[77-791. However, respiratory muscle training is
difficult, the increases in strength may be only
small [80] and whether such training schedules
produce long term benefit remains uncertain.
Therapy directed at the underlying respiratory
disorder may reduce the load on the respiratory
The respiratoory muscles
muscles to a level that will not precipitate or
perpetuate fatigue. Delivery of oxygen to the
working muscle can be optimized by attention to
arterial 'oxygen tensions, haemoglobin levels and
cardiac output. Metabolic acidosis should be
corrected as well as other metabolic disturbances
known to cause muscle weakness such as hypophosphataemia, hypokalaemia and disorders of
calcium metabolism. Therapy that reduces overinflation may be particularly helpful by improving
chest wall geometry, length-tension characteristics
and restoring diaphragm curvature. Both low
frequency fatigue and muscle shortening can be
offset by an increase in motor neurone firing
frequency; thus respiratory stimulants may have a
short term therapeutic role. Conversely drugs
causing depression of the respiratory centre may
substantially impair ventilation.
Drugs that increase muscle twitch tension
would be particularly helpful, shifting the frequency-force curve to the left and improving force
generation at physiological firing frequencies
(Fig. 3). Furthermore, such a shift would diminish
the effect of low frequency fatigue and muscle
shortening. Xanthine-related drugs can improve
the contractile performance of skeletal muscle
studied in vitro [81] and aminophylline has been
reported to improve the force-generating
properties of the diaphragm in man [82]. However, studies in vivo of the effect of aminophylline
on the adductor pollicis muscle of the hand show
that twitch-tension, the frequency-force curve
and low frequency fatigue are not affected by this
drug at therapeutic concentrations [83]. Similarly
the transdiaphragmatic twitch pressure from
stimulation of the phrenic nerve of normal
subjects is not affected by intravenous aminophylline [84]. Thus, while the usefulness of aminophylline in respiratory disease is not in doubt, a
direct beneficial action on respiratory muscle
contractility remains unproven. 0-Receptor
agonists such as terbutaline and salbutamol may
enhance respiratory muscle contractility [85]. The
effect of terbutaline appears to be greater on
fatigued than fresh muscle. This may be due to the
slowing of muscle contraction and relaxation with
fatigue since terbutaline has a greater potentiating
effect on slow twitch than on fast twitch fibres.
In patients with progressive respiratory failure,
assisted ventilation may become necessary. If
fatigue is present, one benefit may be the total
resting of the respiratory muscles for sufficient
time for fatigue to resolve. It is also conceivable
that carefully selected patients can be helped by
patient-triggered positive pressure ventilators to
assist inspiration and reduce the workload of the
respiratory muscles, protect against fatigue and
7
thereby avoid the necessity of intubation and
mandatory ventilation. In patients with neuromuscular weakness, intermittent support by tank
and cuirass ventilation can be beneficial. Scoliosis
patients and those who have had thoracoplasties
in the past can be similarly helped by intermittent
assisted ventilation [86]. The mechanism whereby
such patients derive benefit is not certain but
resting the respiratory muscles may be an
important factor serving to avoid or reverse
fatigue. If this is so, efforts to rest the respiratory
muscles intermittently by using techniques that do
not require intubation may deserve careful reappraisal in patients with severe chronic airways
obstruction.
The clinical importance of respiratory muscle
fatigue is not yet clear and further progress must
depend on developing suitable techniques for its
detection. Only then will the relative contributions
of, for example, inadequate respiratory centre
output or reduced muscle contractility become
apparent. The many stages from central nervous
system output via respiratory muscle force generation to the production of appropriate ventilation
are of bewildering complexity. The process is one
of integration, both when functioning normally
and during ventilatory failure. Biological feedback
serves to modify overall function in response to
failure at any given level. Thus, in most cases of
respiratory failure to identify any single step as
the crucial weak link may be neither sensible nor
possible.
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M. Green and J. Moxham
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