Download Chang A., Boots R., Henderson R., Hodges P. 2005 Case

Reduced Inspiratory Muscle Endurance
Following Successful Weaning From
Prolonged Mechanical Ventilation
Angela T. Chang, Robert J. Boots, Michael G. Brown, Jennifer Paratz
and Paul W. Hodges
Chest 2005;128;553-559
DOI 10.1378/chest.128.2.553
The online version of this article, along with updated information
and services can be found online on the World Wide Web at:
http://chestjournal.org/cgi/content/abstract/128/2/553
CHEST is the official journal of the American College of Chest
Physicians. It has been published monthly since 1935. Copyright 2007
by the American College of Chest Physicians, 3300 Dundee Road,
Northbrook IL 60062. All rights reserved. No part of this article or PDF
may be reproduced or distributed without the prior written permission
of the copyright holder
(http://www.chestjournal.org/misc/reprints.shtml). ISSN: 0012-3692.
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians
Reduced Inspiratory Muscle Endurance
Following Successful Weaning From
Prolonged Mechanical Ventilation*
Angela T. Chang, PhD; Robert J. Boots, MBBS; Michael G. Brown, MAppSc;
Jennifer Paratz, PhD; and Paul W. Hodges, PhD
Study objectives: Respiratory muscle weakness and decreased endurance have been demonstrated following mechanical ventilation. However, its relationship to the duration of mechanical
ventilation is not known. The aim of this study was to assess respiratory muscle endurance and its
relationship to the duration of mechanical ventilation.
Design: Prospective study.
Setting: Tertiary teaching hospital ICU.
Patients: Twenty subjects were recruited for the study who had received mechanical ventilation
for > 48 h and had been discharged from the ICU.
Measurements: FEV1, FVC, and maximal inspiratory pressure (PImax) at functional residual
capacity were recorded. The PImax attained following resisted inspiration at 30% of the initial
PImax for 2 min was recorded, and the fatigue resistance index (FRI) [PImax final/PImax initial]
was calculated. The duration of ICU length of stay (ICULOS), duration of mechanical ventilation
(MVD), duration of weaning (WD), and Charlson comorbidities score (CCS) were also recorded.
Relationships between fatigue and other parameters were analyzed using the Spearman correlations (␳).
Results: Subjects were admitted to the ICU for a mean duration of 7.7 days (SD, 3.7 days) and
required mechanical ventilation for a mean duration of 4.6 days (SD, 2.5 days). The mean FRI was
0.88 (SD, 0.13), indicating a 12% fall in PImax, and was negatively correlated with MVD
(r ⴝ ⴚ0.65; p ⴝ 0.007). No correlations were found between the FRI and FEV1, FVC, ICULOS,
WD, or CCS.
Conclusions: Patients who had received mechanical ventilation for > 48 h have reduced
inspiratory muscle endurance that worsens with the duration of mechanical ventilation and is
present following successful weaning. These data suggest that patients needing prolonged
mechanical ventilation are at risk of respiratory muscle fatigue and may benefit from respiratory
muscle training.
(CHEST 2005; 128:553–559)
Key words: fatigue; inspiratory muscle; mechanical ventilation
Abbreviations: APACHE ⫽ acute physiology and chronic health evaluation; CCS ⫽ Charlson comorbidity score;
CMV ⫽ controlled mandatory ventilation; FRC ⫽ functional residual capacity; FRI ⫽ fatigue resistance index;
ICULOS ⫽ ICU length of stay; MVD ⫽ duration of mechanical ventilation; NMBA ⫽ neuromuscular blocking agent;
Pimax ⫽ maximal inspiratory pressure; RPE ⫽ rate of perceived exertion
percent of all patients admitted to the
T hirty-nine
ICU receive mechanical ventilation. Mechanical
1
ventilation is most commonly used in the management of patients with acute respiratory failure1 as it
*From the Division of Physiotherapy (Drs. Chang and Hodges),
The University of Queensland, St. Lucia, QLD, Australia; Departments of Intensive Care Medicine (Dr. Boots) and Women’s
Thoracic Medicine (Mr. Brown), Royal Brisbane Hospital, Brisbane, QLD, Australia; and Cardiopulmonary Research Centre
(Dr. Paratz), Alfred Hospital/La Trobe University, Melbourne,
VIC, Australia.
This study was supported by a Ludwig Engel Grant-in-Aid
(Australian Lung Foundation) and by the Royal Brisbane Hospital Research Foundation. Dr. Hodges was supported by the
National Health and Medical Research Council of Australia, and
Dr. Chang was supported by the Sir Robert Menzies Scholarship
for the Allied Health Sciences.
www.chestjournal.org
reduces the work of breathing and diaphragm activity.2 However, prolonged mechanical ventilation promotes respiratory muscle weakness3– 6 in the absence
of critical illness and is localized to the respiratory
muscles.4 The degree of weakness has been related
to the duration of mechanical ventilation6,7 and has
Manuscript received August 14, 2004; revision accepted January
21, 2005.
Reproduction of this article is prohibited without written permission
from the American College of Chest Physicians (www.chestjournal.
org/misc/reprints.shtml).
Correspondence to: Angela T. Chang, PhD, BPhty (Hons), Division of Physiotherapy, The University of Queensland, St. Lucia,
QLD 4072, Australia; e-mail: [email protected]
CHEST / 128 / 2 / AUGUST, 2005
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians
553
been suggested as a possible cause of delayed weaning from mechanical ventilation.8,9
Prolonged mechanical ventilation has been defined as mechanical ventilation for ⬎ 48 h.10 As
mechanical ventilation during this period is most
For editorial comment see page 481
likely due to the primary condition of the patient or
to early complications of underlying illness, it is
unlikely that patients will recover quickly following
⬎ 48 h of mechanical ventilation.11 Although controlled mandatory ventilation (CMV) for longer than
this period of time has reduced diaphragm strength
in animal models,3– 6 the effect on muscle fatigue
appears to be more complex.
There have been inconsistent reports of the effect
of up to 5 days of CMV on diaphragm endurance,
and studies have reported no change,4,5 decreased
endurance,12 or an improvement in diaphragm endurance.13 However, this variability may be due, at
least in part, to the shorter period of mechanical
ventilation, with larger changes seen in patients
receiving mechanical ventilation for ⬎ 7 days.13 Preliminary work by Anzueto et al3 has indicated that
periods of CMV for 11 days reduced diaphragm
endurance time by 45%. However, the relationship
between the endurance of the diaphragm and other
inspiratory muscles and the duration of mechanical
ventilation was not examined. In addition, the above
studies were all undertaken in animals that were not
critically ill and ventilated with CMV only. Although
these models provide insight into the effects of
mechanical ventilation on the respiratory muscles,
further investigation into respiratory muscle fatigue
in critically ill patients is needed to design preventative interventions. The aims of this study were as
follows: (1) to assess the inspiratory muscle endurance following successful weaning and discharge
from the ICU; and (2) to study the relationship
between respiratory muscle endurance and mechanical ventilation duration.
Materials and Methods
Subjects
Twenty subjects (9 women) with a mean age of 62 years (SD,
16 years) who had received mechanical ventilation (using synchronized intermittent mandatory ventilation and/or biphasic
positive airway pressure ventilation, where the latter is a subtype
of pressure-controlled ventilation14) for ⱖ 48 h were recruited for
the study from the institutional ICU (Table 1). Subjects were
enrolled as consecutive patients admitted to the ICU who met
the selection criteria. All study subjects were alert and cooperative, and had been discharged from the ICU for 24 h. Subjects
were excluded if they had experienced a cerebrovascular acci-
dent, had a head or spinal cord injury, had preexisting diaphragm
palsy, neuropathy, or myopathy, had unstable ischemic heart
disease, ischemic changes, or arrhythmias on an echocardiogram,
had a temperature of ⬎ 37.8°C except for systemic inflammatory
response syndrome, had experienced thoracic trauma or burns to
the thorax, required a fraction of inspired oxygen of ⬎ 30%, or
were unable to be transported by wheelchair to the laboratory.
Written informed consent was obtained from the subject, with
ethical clearance from the institutional human medical research
ethics committee. All procedures were conducted in accordance
with the Declaration of Helsinki.
Measurements
Spirometry: Measurements of the subject’s FVC and FEV1
were measured using a spirometer (Compact; Vitalograph; Lenexa, KS) in accordance with American Thoracic Society guidelines.15
Inspiratory Muscle Strength: The maximal inspiratory pressure
(Pimax) was recorded at functional residual capacity (FRC) using
a two-way valve with two inflatable balloon valves (model 5600;
Hans Rudolph; Kansas City, MO) attached to a flanged mouthpiece (n ⫽ 19) via a bacterial/viral filter (RJ and VK Bird Pty Ltd;
Middlepark, VIC, Australia). Two inductance plethysmography
(Respitrace; Non-Invasive Measuring Systems; North Bay Village, FL) bands were placed at the level of the nipple and
umbilicus to measure chest expansion and to monitor the repeatability of FRC to within 150 mL or 10% of chest wall motion
observed during an isovolume maneuver.
Demographic Details: Measurements of the duration of mechanical ventilation (MVD) [in days] and weaning duration (WD)
[in hours], which was defined as the time from the initiation of
the first spontaneous breathing trial using either continuous
positive airway pressure and pressure support or T-piece trials
until extubation, and the ICU length of stay (ICULOS) were
recorded from the subject’s medical records. In addition, demographic information, including primary ICU admission diagnosis,
medical history, the degree of comorbidity quantified via the
Charlson comorbidity score (CCS),16 and the use of corticosteroids and neuromuscular blocking agents (NMBAs), were recorded. The subject’s severity of acute injury was assessed with
the acute physiology and chronic health evaluation (APACHE) II
score within 24 h of ICU admission.
Procedure: Data were recorded in two sessions. Spirometry
(FEV1 and FVC) was measured in the first session. Pimax and
endurance measurements were made during a second session to
minimize fatigue. Spirometry was performed with subjects in a
high sitting position. For one subject with a tracheostomy, an
attachment was used. Prior to inspiratory muscle testing, pressure
transducers and inductance plethysmographs were calibrated.
Inductance plethysmography bands were placed around the
subject’s torso with the subject seated. The subject was instructed
to breathe through the inspiratory valve via the mouthpiece/
attachment, and the inspired volume was measured by a respiratory mechanics monitor (Ventrak; Novametrix; Wallingford,
CT) attached at the inspiratory port. An isovolume maneuver was
used to calibrate the inductance plethysmography bands.17 During testing, the subject’s heart rate and pulse oximetric saturation
were monitored via a pulse oximeter.
Subjects exhaled to FRC. The balloon valves were then
inflated, and the subject inhaled maximally for 4 s as the Pimax
was recorded (solid-state differential pressure transducer, model
LX06015D; Sensym; Milipitas, CA). The balloons were then
deflated. Data were collected via a data acquisition system
(model ML795 PowerLab; ADInstruments; Castle Hill, NSW,
Australia) and were analyzed using specific software (Chart;
ADInstruments).
554
Clinical Investigations in Critical Care
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians
www.chestjournal.org
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians
CHEST / 128 / 2 / AUGUST, 2005
555
(L) Pneumothorax
Hematemesis, PR bleed
Colonic surgery for cancer
Pancreatitis, peritonitis
CAP, renal failure
Sepsis
25% burns
Abdoperineal resection
Aortic dissection
Hemihepatectomy
Pneumonia, tricuspid valve
endocarditis
Splenectomy
Respiratory failure, scleroderma
(L) Lower lobe pneumonia
Aspiration pneumonia
Pneumonia, acute renal failure
Abdominal aortic aneurysm repair
Total colectomy and ileostomy
Infective exacerbation COPD
Fecal peritonitis
Diagnosis
6
5
10
4
4
7
8
4
9
8
4
4
6
7
16
5
12
6
8
14
14
6
3
4
4
4
2
2
5
3
7
5
2
3
4
5
10
3
7
2
3
7
10
5
MVD,
d
14
4
2
13
18
97
41
50
46
42
46
72
20
20
120
14
36
10
4
1
166
98
WD,
h
0.7
0.6
0.5
N
0.5
0.6
0.5
0.5
0.5
0.5
0.1
0.5
0.4
0.5
0.5
0.8
0.7
0.5
0.5
0.6
0.5
0.5
Highest
Fio2
8
10
10
N
5
10
5
5
5
7
2.4
5
7.5
7.5
5
8
10
5
5
12
5
5
Highest
PEEP,
cm H2O
None
Tracheostomy
None
None
None
None
None
None
None
None
None
None
None
None
None
None
None
None
None
None
Airway
7
9
7
8
4
4
13
16
4
7
3
3
3
7
7
7
7
9
6
2
10
11
Days
Post
0
4
1
3
3
1
1
2
2
4
0
1
6
0
5
0
0
3
0
2
2
CCS
17
39
22
17
23
19
21
26
16
21
7
23
25
23
23
35
11
7
14
14
24
20
APACHE
II Score
57
63
92
75
50
72
73
31
74
66
19
73
61
53
47
87
97
59
47
44
67
54
43
41
81
97
56
42
40
57
61
79
63
45
58
87
21
72
61
21
99
FVC, %
predicted
97
FEV1, %
predicted
NA
⫺ 33
NA
⫺ 15
⫺ 36
⫺9
⫺ 22
⫺ 30
⫺ 16
⫺ 18
⫺ 52
⫺ 81
NA
⫺ 25
⫺ 37
NA
⫺ 33
⫺ 29
⫺ 23
⫺ 27
⫺ 30
17
⫺ 95
NA
⫺ 35
⫺ 47
⫺ 12
⫺ 28
⫺ 28
⫺ 24
⫺ 31
⫺ 33
20
Pimax
Final,
cm H2O
⫺42
⫺ 40
⫺ 11
⫺ 22
⫺ 38
⫺ 11
⫺ 22
⫺ 33
⫺ 18
⫺ 25
⫺ 58
Pimax
Initial,
cm H2O
0.86
NA
0.72
0.79
NA
1.18
1.03
0.95
0.85†
0.88
0.13
NA
0.83
NA
0.68†
0.95
0.82†
1.00
0.91
0.89
0.72
0.90
FRI
*WD ⫽ weaning duration; Fio2 ⫽ fraction of inspired oxygen; PEEP ⫽ positive end-expiratory pressure; Days Post ⫽ days post-ICU discharge; PR ⫽ perirectal; CAP ⫽ community-acquired pneumonia;
NA ⫽ not applicable as subjects could not complete the inspiratory loading trial; M ⫽ male; F ⫽ female; N ⫽ details not available from mechanical notes.
†A Pimax of 0% was used during the endurance trial.
Mean
SD
68/M
62/F
89/M
60/F
69/F
72/M
85/M
73/F
58/F
61.5
16.2
60/F
52/M
72/F
41/F
62/F
42/F
52/M
87/M
49/M
51/M
26/M
Age/Sex
ICULOS,
d
Table 1—Demographics*
Subjects then breathed through an inspiratory resistance that
was equivalent to 30% of the initial Pimax (Threshold IMT
trainer; Respironics; Murrysville, PA), with further Pimax measurements made at 30-s intervals. This level of resistance was
selected as preliminary trials indicated that resistance equivalent
to 50% of Pimax resulted in severe dyspnea. If the subject was
not able to inspire at 30% of their Pimax, no resistance was
applied and Pimax measurements were repeated at 30-s intervals
for 2 min (n ⫽ 3). During the loading task, the rate of perceived
exertion (RPE) was recorded using a modified Borg scale (scale,
0 to 10),18 with testing ceasing if the RPE was ⱖ 7. If, at any time,
pulse oximetric saturation fell ⬎ 10% from initial values or to
⬍ 90%, the heart rate increased ⬎ 30 beats per minute, or there
was any other clinical deterioration, the testing ceased and
supplemental oxygen administered. Four subjects were unable to
complete the testing protocol. These subjects reported an RPE
score of ⱖ 7 before completion of the loading trial.
Data Analysis: The fatigue resistance index (FRI) is defined as
the final muscle strength following a fatiguing task divided by the
initial muscle strength19 and was calculated as the Pimax measured after a 2-min inspiratory loading protocol divided by the
initial Pimax.
Statistical Analysis: The change in Pimax following the fatigue
protocol was analyzed with a repeated-measures analysis of
variance. All relationships with FRI were analyzed using Spearman ␳ correlations. Kruskal-Wallis analysis was used for nonparametric variables. The relationship between long-term ventilation
and FRI, age, comorbidities, APACHE II score, and ICULOS
was assessed by division into subjects with MVD of ⱖ 7 days and
subjects with MVD of ⬍ 7 days. Subjects who were unable to
complete the inspiratory loading component (n ⫽ 4) were also
compared with subjects who completed the protocol (n ⫽ 16).
Finally, the effect of inspiratory load during the fatigue task
(Pimax, 0% vs 30%, respectively) on FRI was analyzed. A total of
16 subjects were required to detect a correlation coefficient of
⬎ 0.6 and a 10% fall in Pimax with a power of 0.8 and a
significance of 0.05.
Figure 1. Relationship between FRI and mechanical ventilation.
The horizontal line denotes FRI ⫽ 1. All points below the line
denote decreased force-generating capacity (ie, fatigue), and all
points above the line denote increased force-generating capacity.
(␳ ⫽ 0.121; p ⫽ 0.66), inspiratory muscle strength
(␳ ⫽ 0.022; p ⫽ 0.94), or the use of NMBAs
(␳ ⫽ 0.392; p ⫽ 0.13).
Effect of Long-term Ventilation on FRI
Subjects who received mechanical ventilation for
ⱖ 7 days (n ⫽ 4) had a lower FRI compared to those
who received mechanical ventilation for ⬍ 7 days
(0.77 vs 0.92, respectively; p ⫽ 0.047; n ⫽ 16) [Fig
2]. Patients who received mechanical ventilation for
Results
Spirometry, Pimax, and demographic data are
shown in Table 1. The Pimax fell following the 2-min
inspiratory loading protocol from ⫺34.7 cm H2O
(SD, 19.6 cm H2O) to ⫺30.4 cm H2O (SD, 17.06 cm
H2O; p ⫽ 0.002). The mean FRI was 0.88 (SD,
0.13), representing a 12% fall in Pimax after the
loading protocol. There was no difference in any
parameter between subjects who completed the
inspiratory loading protocol (n ⫽ 16) and those who
did not complete it (n ⫽ 4; p ⬎ 0.05). There was no
difference in FRI between a fatigue load of 0%
Pimax (n ⫽ 3) and 30% Pimax (n ⫽ 13; p ⫽ 0.332).
Relationship Between FRI and Other Parameters
Greater fatigue (lower FRI) was related to longer
MVD (␳ ⫽ ⫺0.65; p ⫽ 0.007) [Fig 1]. There was no
relationship between FRI and FEV1 (␳ ⫽ 0.193;
p ⫽ 0.49), FVC (␳ ⫽ ⫺0.004; p ⫽ 0.99), age
(r ⫽ 0.344; p ⫽ 0.19), CCS (␳ ⫽ 0.262; p ⫽ 0.37),
APACHE II score (␳ ⫽ ⫺0.192; p ⫽ 0.49), ICULOS
(␳ ⫽ ⫺0.471; p ⫽ 0.07), time since ICU discharge
Figure 2. Change in Pimax after the loading trial. Top, A:
subject ventilated for ⬍ 7 days. Note that there is no change in
Pimax post-loading task at 30% of Pimax. Bottom, B: subject
received mechanical ventilation for ⱖ 7 days. Note the fall in
Pimax compared to initial levels.
556
Clinical Investigations in Critical Care
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians
a longer duration were younger (48.0 vs 64.9 years,
respectively; p ⫽ 0.023), had been admitted to the
ICU for a longer period of time (12.8 vs 6.5 days,
respectively; p ⫽ 0.007), and required weaning for
longer periods (16.3 vs 9.1 h, respectively;
p ⫽ 0.030). There was no difference in CCS
(p ⫽ 0.567) or APACHE II scores (p ⫽ 0.273) between groups.
Discussion
This is the first study to investigate the relationship
between the duration of mechanical ventilation and
inspiratory muscle endurance in patients who had
received mechanical ventilation in the ICU. The
results show that endurance is reduced with longer
periods of mechanical ventilation in patients who
were successfully weaned following mechanical ventilation for ⱖ 48 h. The effect on strength cannot be
determined, however, as absolute lung volume was
not recorded and FRC was standardized between
trials only. There was no correlation between inspiratory muscle endurance and other parameters, including APACHE II score, comorbidities, age, inspiratory muscle strength, administration of NMBAs,
or duration of ICU admission.
Decreased Inspiratory Muscle Endurance
Following Prolonged Ventilation
Although we have demonstrated that prolonged
mechanical ventilation is associated with reduced
inspiratory muscle endurance in patients who received mechanical ventilation for ⱖ 48 h, conflicting
findings have been reported in animal studies. No
change in diaphragm FRI was demonstrated by
Sassoon et al7 in rabbits following 72 h of CMV, and
by Yang et al20 in rats following CMV for 57.6 h. In
contrast, Capdevila et al12 reported a fall in diaphragm and intercostal FRI after 51 h of CMV in
rabbits, and Shanely et al13 found an increase in FRI
after CMV for 18 h in rats. However, the increased
endurance in the latter study may be due to the
shorter period of CMV and the resultant increased
oxidative capacity of the diaphragm.13 Conversely,
atrophy of the oxidative fibers may occur with prolonged periods of mechanical ventilation, leading to
decreased endurance.13 This was supported by the
negative relationship between MVD and FRI in the
present study.
The inspiratory muscle fatigue demonstrated in
the current study may be due to the longer period of
mechanical ventilation (mean duration, 110.4 h)
compared to those in the animal studies described
above. Interestingly, one study3 that investigated
long-term mechanical ventilation (11 days) in bawww.chestjournal.org
boons found decreased endurance of the diaphragm.
However, those data were preliminary findings as
only three animals were studied and no statistical
analysis was undertaken.
Reduced endurance of the inspiratory muscles
may be the cause rather than the outcome of longer
periods of mechanical ventilation.8,9 It is possible
that patients who required longer periods of mechanical ventilation may have had a preexisting
decrease in diaphragm endurance, which may have
contributed to the increased period of ventilation.
Whether the increased fatigability is the cause or the
effect of prolonged mechanical ventilation does not
compromise the importance of the findings and the
implications of these findings for rehabilitation.
The lower FRI in patients receiving mechanical
ventilation for ⱖ 7 days suggests that these patients
may not be able to meet respiratory demands with
the tasks associated with increased inspiratory load,
such as rehabilitation and the activities of daily living.
This may restrict a patient’s performance, as ventilatory limitations have been shown to limit function.
Possible Causes of Reduced Endurance
There are two main types of fatigue, central and
peripheral. Central fatigue is defined as a reduction
in the voluntary contraction force due to reduced
CNS output,21 and peripheral fatigue occurs due to
the failure of the neuromuscular junction or the
contractile component of muscle.22 Peripheral fatigue has been demonstrated to occur following
mechanical ventilation in animals, with both transmission fatigue (high-frequency) and contractile fatigue (low-frequency) present following CMV.4 – 6
However, the role of central fatigue is not yet known.
Although the present study demonstrates inspiratory
fatigue following mechanical ventilation in critically
ill patients, the separate central and peripheral contribution in the development of fatigue requires
further investigation.
Weakness and fatigue following mechanical ventilation may be a manifestation of conditions such as
critical illness polyneuropathy, critical illness myopathy, and disuse atrophy.23 In addition to these
conditions, the sustained use of medications such as
NMBAs or corticosteroids contributes to the development of weakness and fatigue23; however, their
effect on the contractile properties of respiratory
muscles in patients receiving mechanical ventilation
is not yet known. Regardless of the type of fatigue
and the possible mechanisms behind them, the
current study demonstrates that inspiratory muscle
fatigue is present in patients following prolonged
mechanical ventilation (ie, MVD for ⱖ 48 h) and was
not related to the use of NMBA in the current study.
CHEST / 128 / 2 / AUGUST, 2005
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians
557
Limitations
Due to the nature of the clinical population, it was
not possible to assess the patient’s initial FRI. It is
difficult to determine which patient will require
prolonged mechanical ventilation, and thus it is not
feasible to assess all patients prior to their ICU
admission. However, studies in healthy individuals
found no central or peripheral inspiratory muscle
fatigue following resisted breathing.24,25 Similarly,
stable patients with COPD have been shown26,27 to
inspire against 30% of Pimax for up to 30 min
without complication.
The follow-up period after discharge from the
ICU was variable in the current study, as subjects
were recruited when deemed clinically suitable to
undergo the spirometry and muscle strength tests by
their medical team. As the initial cause of ICU
admission and clinical course was variable, so too was
the follow-up period, with a mean duration of 7.2
days (SD, 3.5 days) post-ICU discharge, and this
reflects the heterogeneous patient population. Despite this variability, there was no effect of the length
of time since ICU discharge on FRI. This suggests
that the effect of mechanical ventilation on FRI is
not resolved following disconnection from the ventilator and may imply the need for specific intervention to improve the endurance capacity of the respiratory muscles.
It was not possible to use the same resistance for
the fatigue protocol across subjects. Three subjects
were not able to tolerate resistance equal to 30% of
their Pimax, and the fatigue protocol was performed
with no additional resistance. In these subjects,
Pimax measurements were repeated at 30-s intervals, and fatigue developed as a result of the repeated Pimax efforts. Despite the use of two different loads, the change in FRI was not related to the
applied load, and thus it appears that the minimal
load of the equipment itself was sufficient in these
subjects to demonstrate the reduction in inspiratory
muscle endurance.
Several patients (n ⫽ 4) were unable to complete
the 2-min inspiratory loading trial due to severe
dyspnea. These subjects were generally comparable
to those who completed the trial. Their inability to
tolerate the inspiratory loading trial may have been
related to severe inspiratory muscle weakness as two
subjects had a Pimax of ⬍ 13 cm H2O. One subject
was recruited following her third ICU admission,
and increased morbidity associated with readmission
to the ICU may have predisposed her to dyspnea. An
RPE of ⬎ 7 was reported in one subject following
resisted breathing at 50% of Pimax. This subject was
the first to participate in the study, and the results
led to the modification of the inspiratory loading to
30% of the initial Pimax.
A limitation of the analysis of long-term ventilation
(ⱖ 7 days) is that few subjects required ventilation
for this time (n ⫽ 4). This is representative of the
proportion of patients who experienced prolonged
mechanical ventilation in the ICU. These preliminary findings warrant further research in controlled
groups of subjects with short-term and long-term
ventilation to further investigate the effect of mechanical ventilation on FRI.
Clinical Implications
Patients who require prolonged mechanical ventilation (ie, MVD for ⱖ 48 h) may have reduced
endurance of the respiratory muscles following successful weaning, and this is more severe with increased periods of mechanical ventilation. Although
it is not known whether prolonged mechanical ventilation is a cause of inspiratory muscle fatigue or an
outcome, the presence of inspiratory muscle fatigue
in this population may increase the risk of respiratory
pump failure. Therefore, specific rehabilitation such
as inspiratory muscle training may be indicated to
improve inspiratory muscle endurance in this patient
population.
ACKNOWLEDGMENT: The authors would like to thank Anita
Brake and the Department of Thoracic Medicine at the Royal
Brisbane Hospital for their assistance with data collection.
References
1 Esteban A, Anzueto A, Alia I, et al. How is mechanical
ventilation employed in the intensive care unit? An international utilization review. Am J Respir Crit Care Med 2000;
161:1450 –1458
2 Brochard L, Harf A, Lorino H, et al. Inspiratory pressure
support prevents diaphragm fatigue during weaning from
mechanical ventilation. Am Rev Respir Dis 1989; 139:513–
521
3 Anzueto A, Peters JI, Tobin MJ, et al. Effects of prolonged
controlled mechanical ventilation of diaphragm function in
healthy adult baboons. Crit Care Med 1997; 25:1187–1190
4 Le Bourdelles G, Viires N, Boczkowski J, et al. Effects of
mechanical ventilation on diaphragmatic contractile properties in rats. Am J Respir Crit Care Med 1994; 149:1539 –1544
5 Radell PJ, Remahl S, Nichols DG, et al. Effects of prolonged
mechanical ventilation and inactivity on piglet diaphragm
function. Intensive Care Med 2002; 28:358 –364
6 Powers SK, Shanely RA, Coombes JS, et al. Mechanical
ventilation results in progressive contractile dysfunction in
the diaphragm. J Appl Physiol 2002; 92:1851–1858
7 Sassoon CS, Caiozzo VJ, Manka A, et al. Altered diaphragm
contractile properties with controlled mechanical ventilation.
J Appl Physiol 2002; 92:2585–2595
8 Yang KL, Tobin MJ. A prospective study of indexes predicting
the outcome of trials of weaning from mechanical ventilation.
N Engl J Med 1991; 324:1445–1450
558
Clinical Investigations in Critical Care
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians
9 Karpel JP, Aldrich TK. Respiratory failure and mechanical
ventilation: pathophysiology and methods of promoting weaning. Lung 1986; 164:309
10 Chelluri L, Rotondi A, Sirio C, et al. 2-Month mortality and
functional status of critically ill adult patients receiving prolonged mechanical ventilation. Chest 2002; 121:549 –558
11 Douglas SL, Daly BJ, Gordon N, et al. Survival and quality of
life: short-term versus long-term ventilator patients. Crit Care
Med 2002; 30:2655–2662
12 Capdevila X, Lopez S, Bernard N, et al. Effects of controlled
mechanical ventilation on respiratory muscle contractile
properties in rabbits. Intensive Care Med 2003; 29:103–110
13 Shanely RA, Coombes JS, Zergeroglu AM, et al. Shortduration mechanical ventilation enhances diaphragmatic fatigue resistance but impairs force production. Chest 2003;
123:195–201
14 Hormann C, Baum M, Putensen C, et al. Biphasic positive
airway pressure (BIPAP)–a new mode of ventilatory support.
Eur J Anaesthesiol 1994; 11:37– 42
15 ATS. Standardization of spirometry, 1994 update: American
Thoracic Society. Am J Respir Crit Care Med 1995; 152:
1107–1136
16 Charlson M, Szatrowski T, Peterson J, et al. Validation of a
combined comorbidity index. J Clin Epidemiol 1994; 47:
1245–1251
17 Chadha TS, Watson H, Birch S, et al. Validation of respiratory
inductive plethysmography using different calibration procedures. Am Rev Respir Dis 1982; 125:644 – 649
18 Borg GA. Psychophysical bases of perceived exertion. Med
Sci Sports Exerc 1982; 14:377–381
www.chestjournal.org
19 Duchateau J, Hainaut K. Electrical and mechanical changes
in immobilized human muscle. J Appl Physiol 1987; 62:2168 –
2173
20 Yang L, Luo J, Bourdon J, et al. Controlled mechanical
ventilation leads to remodeling of the rat diaphragm. Am J
Respir Crit Care Med 2002; 166:1135–1140
21 Bigland-Ritchie B, Jones DA, Hosking GP, et al. Central and
peripheral fatigue in sustained maximum voluntary contractions of human quadriceps muscle. Clin Sci Mol Med 1978;
54:609 – 614
22 Roussos C, Zakynthinos S. Fatigue of the respiratory muscles.
Intensive Care Med 1996; 22:134 –155
23 Hund E. Neurological complications of sepsis: critical illness
polyneuropathy and myopathy. J Neurol 2001; 248:929 –934
24 McKenzie DK, Allen GM, Butler JE, et al. Task failure with
lack of diaphragm fatigue during inspiratory resistive loading
in human subjects. J Appl Physiol 1997; 82:2011–2019
25 Gorman RB, McKenzie DK, Gandevia SC. Task failure,
breathing discomfort and CO2 accumulation without fatigue
during inspiratory resistive loading in humans. Respir Physiol
1999; 115:273–286
26 Nield MA. Inspiratory muscle training protocol using a
pressure threshold device: effect on dyspnea in chronic
obstructive pulmonary disease. Arch Phys Med Rehabil 1999;
80:100 –102
27 Lisboa C, Munoz V, Beroiza T, et al. Inspiratory muscle
training in chronic airflow limitation: comparison of two
different training loads with a threshold device. Eur Respir J
1994; 7:1266 –1274
CHEST / 128 / 2 / AUGUST, 2005
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians
559
Reduced Inspiratory Muscle Endurance Following Successful Weaning
From Prolonged Mechanical Ventilation
Angela T. Chang, Robert J. Boots, Michael G. Brown, Jennifer Paratz and
Paul W. Hodges
Chest 2005;128;553-559
DOI 10.1378/chest.128.2.553
This information is current as of April 9, 2008
Updated Information
& Services
Updated information and services, including
high-resolution figures, can be found at:
http://chestjournal.org/cgi/content/full/128/2/553
References
This article cites 27 articles, 11 of which you can access
for free at:
http://chestjournal.org/cgi/content/full/128/2/553#BIBL
Permissions & Licensing
Information about reproducing this article in parts
(figures, tables) or in its entirety can be found online at:
http://chestjournal.org/misc/reprints.shtml
Reprints
Information about ordering reprints can be found online:
http://chestjournal.org/misc/reprints.shtml
Email alerting service
Receive free email alerts when new articles cite this
article sign up in the box at the top right corner of the
online article.
Images in PowerPoint format Figures that appear in CHEST articles can be
downloaded for teaching purposes in PowerPoint slide
format. See any online article figure for directions.
Downloaded from chestjournal.org on April 9, 2008
Copyright © 2005 by American College of Chest Physicians