Eur Respir J 1997; 10: 2847–2852
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Copyright ©ERS Journals Ltd 1997
European Respiratory Journal
ISSN 0903 - 1936
Influence of noninvasive positive pressure ventilation on
inspiratory muscle activity in obese subjects
W. Pankow, N. Hijjeh, F. Schüttler, T. Penzel, H.F. Becker, J.-H. Peter, P .v. Wichert
In most patients with OSA hypercapnic and hypoxae-
mic episodes exclusively occur during sleep. In contrast,
in a subgroup of grossly obese subjects hypoxaemia
and hypercapnia persists throughout the daytime. This
condition is commonly defined as obesity hypoventila-
tion syndrome (OHS), if there is no additional intrinsic
lung disease. Nasal continuous positive airway pressure
(nCPAP) has been effectively used to prevent pharyngeal
narrowing during sleep in patients with obstructive sleep
apnoea (OSA) and even patients with OHS may respond
to this treatment . In some patients with OHS, however,
nCPAP has proved to be ineffective in correcting hyper-
capnia and hypoxia both during sleep and wakefulness.
In these cases, noninvasive positive pressure ventilation
(NPPV) was found to be superior in terms of correction of
nocturnal and daytime blood gases [2–4].
Recently, beneficial effects of NPPV have been shown
in morbidly obese subjects undergoing abdominal surgery
. Compared to a control group the prophylactic use of
NPPV with bi-level positive airway pressure (BiPAP)
postoperatively reduced pulmonary dysfunction after gas-
troplasty and accelerated reestablishment of preoperative
The mechanism, by which nocturnal NPPV improves
the patients clinical condition in OHS is probably com-
plex and might be related to a more physiological sleep
architecture, correction of blood gas abnormalities and
respiratory muscle unloading. The improvement of venti-
latory function in the postoperative restrictive syndrome
might also be multifactorial.
Unloading of the respiratory muscles with NPPV has
been reported in chest wall restriction due to kyphoscolio-
sis , but no systematic investigation exists in patients
with massive obesity. We hypothesized that unloading
of the respiratory muscles might be achieved by NPPV
in massive obesity and that this effect could contribute to
Influence of noninvasive positive pressure ventilation on inspiratory muscle activity in
obese subjects. W. Pankow, N. Hijjeh, F. Schüttler, T. Penzel, H.F. Becker, J.-H. Peter, P.v.
Wichert. ERS Journals Ltd 1997.
ABSTRACT: Noninvasive positive pressure ventilation (NPPV) can improve ventila-
tion in obese subjects during the postoperative period after abdominal surgery. Com-
pared to nasal continuous positive airway pressure (nCPAP), NPPV was superior in
correcting blood gas abnormalities both during the night-time and during the day-
time in a subgroup of patients with the obesity hypoventilation syndrome (OHS).
However, as it is unknown, if and to what extent NPPV can unload the respiratory
muscles in the face of the increased impedance of the respiratory system in obesity,
this is what was investigated.
Eighteen obese subjects with a body mass index Š40 kg·m-2 were investigated dur-
ing the daytime, which included five healthy controls (simple obesity (SO)), seven
patients with obstructive sleep apnoea (OSA) and six patients with the obesity hypov-
entilation syndrome (OHS). Assisted PPV was performed with bi-level positive air-
way pressure (BiPAP), applied via a face mask. Inspiratory positive airway pressure
(IPAP) was set to 1.2 or 1.6 kPa and expiratory positive airway pressure (EPAP) was
set to 0.5 kPa. Inspiratory muscle activity was measured as diaphragmatic pressure
time product (PTPdi).
Comparison of spontaneous breathing with BiPAP ventilation showed no signifi-
cant difference in breathing pattern, although there was a tendency towards an
increase in tidal volume (VT) in all three groups and a decrease in respiratory fre-
quency (f R) in patients with OSA and OHS. End-tidal carbon dioxide (PET,CO2) with
BiPAP was unchanged in SO and OSA, but was decreased in OHS. In contrast,
inspiratory muscle activity was reduced by at least 40% in each group. This was indi-
cated by a decrease in PTPdi with BiPAP 1.2/0.5 kPa from mean±SD 39±5 to 20±9 kPa·s
(p<0.05) in SO, from 42±7 to 21±8 kPa·s (p<0.05) in OSA, and from 64±20 to 38±17
kPa·s (p<0.05) in OHS. With BiPAP 1.6/0.5 kPa, PTPdi was further reduced to 17±6
kPa·s in SO, and to 17±6 kPa·s in OSA, but not in OHS (40±22 kPa·s).
We conclude that noninvasive assisted ventilation unloads the inspiratory muscles
in patients with gross obesity.
Eur Respir J 1997; 10: 2847–2852.
Dept of Internal Medicine, Schlafmed-
izinisches Labor, Medizinische Poliklinik,
Philipps-University, Marburg, Germany
Correspondence: W. Pankow
Innere Medizin III
Rudower Straβe 48
Keywords: Inspiratory muscles
noninvasive positive pressure ventilation
obesity hypoventilation syndrome
obstructive sleep apnoea
Received: April 17 1997
Accepted after revision September 30 1997
BiPAP is a registered trademark of Res-
pironics Inc, Murrysville, Pennsylvania,
W. PANKOW ET AL.
the beneficial clinical effects of NPPV in obese patients
who have an increased impedance of the respiratory sys-
tem due to morbid obesity. We therefore studied diaph-
ragmatic pressure time product (PTPdi) as an indicator of
diaphragmatic energy expenditure during short-term app-
lication of assisted NPPV using the BiPAP ventilator.
We studied eighteen subjects with marked obesity as
defined by a body mass index (BMI) Š40 kg·m-2. Fourteen
subjects had been admitted to our institution because of
suspected sleep apnoea. Six of these were hypercap-
nic (arterial carbon dioxide tension (Pa,CO2) >6.0 kPa (45
mmHg)) and had peripheral oedema indicating right heart
failure. All subjects reported loud and irregular snoring
and all except one reported excessive daytime sleepiness
(EDS). Four healthy obese volunteers without a history of
loud snoring or EDS were also studied. No subject had
complaints or clinical signs of chronic bronchitis or em-
Before measurements started, all subjects underwent
spirometric lung function testing and blood gas analysis.
Predicted values of lung function tests were those of the
European Coal and Steel Community (ECSC) . Stand-
ard polysomnography was also performed in all subjects.
The number of apnoeas and hypopnoeas divided by the
sleep-time in hours was used to calculate an apnoea plus
hypopnoea index (AHI). An AHI ð5 events·h-1 was con-
sidered normal . In the four obese volunteers and in one
otherwise healthy subject with suspected OSA, AHI was
ð5, while in all other subjects AHI was well above this
limit. Thus, there were three study groups: 1) five healthy
subjects with obesity (simple obesity (SO)); 2) seven nor-
mocapnic obese patients with obstructive sleep apnoea
(OSA); and 3) six hypercapnic obese patients with OSA
and right heart failure (obesity hypoventilation syndrome
(OHS)) . Tables 1 and 2 provide anthropometric data
and results of lung function and blood gas testing. All sub-
jects gave their informed consent prior to the study. The
study protocol was approved by the local Ethics Commit-
Oesophageal (Poes) and gastric pressures (Pga) were
measured using a catheter system with two piezoelectric
pressure transducers located on the tip and 20 cm proxi-
mal to the tip of the catheter (GaelTec, Dunvegan, Isle
of Skye, UK) . A face mask (Respironics Inc., Murrys-
ville, Pennsylvania, USA) was modified to accom-
modate this catheter system. The catheter was advanced
until both tranducers were located intragastrically and
then withdrawn until opposite phase directions appeared
during respiratory efforts, indicating placement of the Poes
transducer at the gastro-oesophageal junction. The cathe-
ter was then withdrawn another 8 to 13 cm until minimal
cardiac artifact was present and optimal correlations with-
in a 10% range of changes of mask pressure (ýPmask) and
oesophageal pressure (ýPoes) were recorded by means of
the occlusion method . The catheter was fixed to the
nose by elastic tape to prevent dislocation while different
body positions were assumed. Airflow (V ') was measured
with a variable orifice pneumotachograph (Bicore, Irvine,
CA, USA) attached to the face mask. A polyethylene
catheter was connected to a side-port of the face mask to
obtain mask pressure (Pmask). The pressure drop across
the pneumotachograph and Pmask was measured with Mic-
roswitch 163PCOlD36 and 143PC03D differential pres-
sure tranducers (Honeywell Inc., Freeport, Illnois, USA).
As the variable orifice sensor produces a nonlinear differ-
ential pressure signal to airflow, linearization of this sig-
nal must be performed. A microcomputer constructed to
read the individual signal of the Bicore sensor (Bi-scope;
Sing Medical, Stäfa, Switzerland) was used to perform
this procedure. Dead space of the breathing assembly
when applied to the subject was approximately 150 mL.
Combined resistance of the face mask and the flow-sensor
when applied to the subject was measured as:
R = K1+K2V '
adapted from the Rohrer's equation
Pres = K1V '+K2V '2
where: Pres = resistive pressure (kPa), V ' = airflow (L·s-1),
K1 = coefficient of linear resistance, K2 = coefficient of
nonlinear resistance: K1 = 0.158, K2 = 0.016. A main-
stream infra-red capnograph (Novametrix Capnograph
7000; Novamterix Wallingford, Connecticut, USA) at-
tached to the pneumotachograph allowed continuous de-
termination of PET,CO2. Cardiac frequency (modified V2
Table 1. – Anthropometric data
Values are presented as mean±S D . M: male; F: female; BMI:
body mass index; S: smoking; ES: exsmoker; NS: nonsmoker;
SO: simple obesity; OSA: obstructive sleep apnoea; OHS: obes-
ity hypoventilation syndrome.
Table 2. – Lung function data and baseline blood gases
Values are presented as mean±S D . FVC: forced vital capacity; FEV1: forced expiratory volume in one second; ERV: expiratory reserve
volume; Pa,O2: arterial oxygen tension; Pa,CO2: arterial carbon dioxide tension; AHI: apnoea and hypopnoea index; % pred: percentage
of predicted value. For further definitions refer to table 1. 1 kPa = 7.52 mmHg.
RESPIRATORY MUSCLE UNLOADING IN OBESITY WITH NONINVASIVE VENTILATION
lead), blood pressure (Finapres; Ohmeda, Englewood, Co-
lorado, USA) and arterial oxygen saturation (Sa,O2) (Biox
3700 pulse oxymeter; Ohmeda, Boulder, USA) were also
continuously recorded. The signals of flow, pressure, car-
diac frequency and blood pressure were sampled at a rate
of 100 Hz and the Sa,O2 signal at a rate of 25 Hz, using a
computer data acquisition system with a built-in 12-bit
analogue-to-digital converter (Topas; constructed by our
group). The collected data were stored on optical disc for
subsequent analysis. All variables were also recorded on
a 16-channel strip chart recorder (Picker, München, Ger-
many) at a paper speed of 10 mm·s-1. The flow signal was
corrected for changes in gas temperature and gas compo-
sition. All pressure channels were calibrated using a water
Study protocol and data analysis
All investigations were performed in the morning at
least 2 h after breakfast. The face mask was firmly at-
tached. Performance of the occlusion test ensured that no
airleaks were present. Subjects were studied supine with
the upper part of the bed slightly elevated (10°) while
breathing spontaneously for 12 min each. Then pres-
sure support with BiPAP was initiated, starting with 1.2
kPa inspiratory positive airway pressure (IPAP) and then
switching to 1.6 kPa IPAP, while expiratory positive air-
way pressure (EPAP) was held constant at 0.5 kPa. Each
level of inspiratory assist was applied for 12 min. During
the course of the experiments subjects were instructed to
keep their eyes open in order to exclude the possibility
that they were falling asleep. To minimize airleaks the
mask was firmly tightened. During our experiments we
tried to minimize air leaks by firmly tightening the mask
and by subsequent repositioning if we noticed any leaks
around the mask with our fingertips. The absence of leaks
was continuously monitored from the flow signal tracing.
Only periods without or with minimal end-expiratory flow
shift from the zero line were analysed. BiPAP was applied
by means of a bi-level continuous high flow (120 L·min-1)
compressor-blower (BiPAP S/T- D; Respironics Inc.) set
in the spontaneous BiPAP-mode. The unit was attached to
the face mask distal to the capnograph with a special ex-
halation valve (Respironics whisper swivel valve, Res-
pironics Inc.), which provides a fixed leak during use.
Measurements were obtained from at least 10 consecu-
tive breaths during the last 2 min of each experimental
condition. Volume (V) was obtained by digital integration
of the flow signal. Duration of inspiration (tI) and expira-
tion (tE) was analysed from the flow tracing. Transdia-
phragmatic pressure (Pdi) was obtained electronically by
subtraction of Poes from Pga. Pdi at resting end-expiration
(functional residual capacity (FRC)) was used as the zero
reference point . PTPdi was obtained by electron-
ically integrating the area under the Pdi-curve over tI
 and calculated for 1 min (PTPdi) or for 1 L of ventila-
Comparisons between physiological data of unsup-
ported breathing and NPPV were made using the Wil-
coxon signed rank test. Error probability for significant
results was determined as p<0.05. All data are expressed
As shown in table 3, NPPV with BiPAP caused a
tendency to increased VT in all three groups. The f R
decreased in the patients with OSA and OHS, but not
in the SO subjects. This effect, however, was statis-
tically significant only in the OHS group. In line with
small changes in breathing pattern, Sa,O2 was slightly hig-
her and PET,CO2 slightly lower with each level of BiPAP
compared to unsupported breathing, while no differences
in cardiac frequency and blood pressure were detected
Table 3. – Influence of noninvasive positive pressure
ventilation on breathing pattern
f R breaths·min-1
V 'E L·min-1
f R breaths·min-1
V 'E L·min-1
f R breaths·min-1
V 'E L·min-1
Values are presented as mean±S D . BiPAP: bi-level positive air-
way pressure. VT: tidal volume; f R: respiratory frequency; V 'E:
minute ventilation; tI: inspiratory time; ttot: total breathing cycle
time; tI/ttot: duty cycle; *: p<0.05 versus baseline. For further
definitions refer to table 1.
Table 4. – Influence of noninvasive positive pressure
ventilation on blood gases, cardiac frequency (fC) and
f C beats·min-1
f C beats·min-1
f C beats·min-1
Values are presented as mean±S D . BiPAP: bi-level positive air-
ways pressure; Sa,O2: arterial oxygen saturation; PET,CO2: end-
tidal carbon dioxide pressure; BPsys: systolic blood pressure;
BPdia: diastolic blood pressure. *: p<0.05 versus baseline. For
further definitions refer to table 1. 1 kPa = 7.52 mmHg.
W. PANKOW ET AL.
As shown in table 3, NPPV with BiPAP caused a ten-
dency to increased VT in all three groups. The f R dec-
reased in the patients with OSA and OHS, but not in the
SO subjects. This effect, however, was statistically signi-
ficant only in the OHS group. In line with small changes
in breathing pattern, Sa,O2 was slightly higher and PET,CO2
slightly lower with each level of BiPAP compared to un-
supported breathing, while no differences in cardiac fre-
quency and blood pressure were detected (table 4).
Inspiratory muscle activity
During baseline breathing PTPdi and PTPdi/VT were
similar in SO and OSA, but were significantly (p<0.05)
higher in OHS (fig. 1a and b).
Tracings during unsupported breathing and during ass-
isted ventilation in one representative subject in figure 2
show that inspiratory muscle activity with BiPAP was
reduced. This is indicated by the reduction in pressure
Fig. 1. – Pressure-time products of the diaphragm (PTPdi): a) calculated for 1 min (PTPdi); b) calculated on a per breath basis for 1 L (PTPdi/tidal vol-
ume (VT)). ■: obesity hypoventilation syndrome; ●: obstructive sleep apnoea; ❍: simple obesity. BiPAP: bi-level positive airway pressure. *: p<0.05
compared to baseline.
BiPAP 1.2/0.5 kPa
BiPAP 1.6/0.5 kPa
Fig. 2. – Tracings obtained from a representative subject during: a) unsupported breathing; b) noninvasive positive pressure ventilation (NPPV) with
bi-level positive airways pressure (BiPAP) 1.2/0.5 kPa; and c) NPPV with BiPAP 1.6/0.5 kPa. Flow: airflow; Pmask: mask pressure; Poes: oesophageal
pressure; Pga: gastric pressure; Pdi: transdiaphragmatic pressure. Note, that with increasing levels of pressure support, tidal swings of Poes and Pdi are
reduced. This indicates transformation of breathing work from the patient to the ventilator. Note also, that end-expiratory Poes with BiPAP is slightly
increased. This might indicate increased functional residual capacity, induced by the positive end-expiratory pressure. See text for further details.
RESPIRATORY MUSCLE UNLOADING IN OBESITY WITH NONINVASIVE VENTILATION
swings of Poes and Pdi. Compared to unsupported breath-
ing PTPdi with BiPAP 1.2/0.5 kPa was reduced from 39±5
to 20±9 kPa·s (p<0.05) in SO, from 42±7 to 21±8 kPa·s
(p<0.05) in OSA, and from 64±20 to 38±17 (p<0.05) in
OHS. With BiPAP 1.6/0.5 kPa PTPdi was further reduced
to 17±6 kPa·s in SO, to 17±6 kPa·s in OSA, but not in
OHS (40±22 kPa·s) (fig. 1a). When PTPdi was calculated
on a per breath basis for 1 L of ventilation, comparable
results were obtained (fig. 1b).
This study shows that NPPV can unload the inspiratory
muscles of grossly obese subjects. We used inspira-
tory pressure assist limited to 1.6 kPa because otherwise
airleaks would have restricted the exact measurement of
airflow. Higher pressures might have further reduced res-
piratory muscle activity, but in our experience pressures of
more than 2.0 kPa are rarely tolerated and cannot be
applied with the ventilator used in this study. In a previous
investigation total muscle unloading was achieved with a
pressure support level of 3.0 kPa in intubated normal-
weight patients with respiratory failure . Therefore,
total respiratory muscle rest in obesity can certainly not be
achieved with noninvasive ventilation, since only limited
positive pressures can be applied via face masks to the
patient. The 46% reduction in diaphragmatic activity,
nevertheless, is more than we had expected in the face of
gross obesity in the patients of this investigation. In the
SO and OSA group we observed a further reduction in
PTPdi with BiPAP 1.6/0.5 kPa compared with BiPAP 1.2/
0.5 kPa, which, however, was not statistically significant.
In the OHS group there was no further reduction in PTPdi
with the higher pressure. However, due to the relatively
small number of patients and the small difference between
the two levels of BiPAP, it cannot be assumed that there
definitely is no further decrease in PTPdi with higher lev-
els of BiPAP.
With BiPAP we used an assisted mode of NPPV, that
combines CPAP and pressure support by setting different
levels of EPAP and IPAP. Since with pressure support the
patient controls inspiratory flow, f R and expiratory time to
some degree, the effect of mechanical ventilation is not
only dependent on the pressure support level, but also on
the patient-ventilator interaction . Depending on the
ventilatory drive, the patient can use the machine work
either to increase ventilation or reduce his own work of
breathing at a given level of ventilation or combine these
two effects. Because breathing pattern and PET,CO2
changed only slightly with BiPAP, it follows that the
respiratory controller gave a higher priority to muscle un-
loading. We observed, however, a tendency towards im-
proved ventilation. This could indicate, that ventilation is
normalized after a longer period of NPPV.
Breathing during our experiments was certainly stimu-
lated by rebreathing carbon dioxide from the high dead
space of the face mask. However, as this factor was kept
constant throughout the entire test, dead space should not
have influenced our results.
In obesity the increased abdominal load shifts the dia-
phragm in the upward direction, thereby decreasing expir-
atory reserve volume and FRC . As a result, obese
subjects breathe at low lung volumes along the very flat
portion of the already flattened pressure-volume curve.
With the low level of EPAP (0.5 kPa), we chose a ventila-
tor setting, which in an earlier study  effectively pre-
vented upper airway obstruction during sleep in patients
with OHS. In contrast to this study, our experiments were
performed in awake subjects. Here, CPAP might have in-
creased FRC. This is indicated by the increased end-
expiratory Poes (see fig. 2). With increased FRC tidal
breathing is performed along the steeper portion of the
compliance curve, so work of breathing is decreased. Thus,
in addition to pressure support, CPAP could have contri-
buted to the reduced diaphragmatic activity in our study.
Patients with OHS had a higher BMI than the OSA and
SO subjects. This might have led to lower expiratory
reserve volume and higher PTPdi in these patients. There
is evidence however, that the increased PTPdi is mainly
related to intrinsic factors associated with OHS. Lung
and chest wall compliance in OHS is lower and work of
breathing is increased compared with SO [17, 18]. This
difference is unexplained by differences of weight in the
two groups of subjects . In addition, OHS is character-
ized by persistent inadequate ventilatory compensation
for these extra loads [9, 19], a result of which is chronic
hypercapnia during the daytime. It is speculated that in
OHS the combination of obesity-related alterations of
chest wall and lung mechanics and increased inspiratory
load due to functional upper airway obstruction dur-
ing sleep may induce respiratory muscle fatigue . This
concept is supported by the observation that in some
patients with OHS nocturnal splinting of the upper airway
with nCPAP results in rapid normalization of daytime
blood gases .
In some patients, however, nCPAP is not sufficient
to prevent nocturnal hypoxaemia  and intermittent or
permanent NPPV is required. One study  and several
reports of small numbers of patients [4, 22] or case reports
[23, 24] have shown that nocturnal application of NPPV
can effectively improve blood gases in OHS. One of sev-
eral mechanisms also proposed to normalize ventilation
during the daytime is respiratory muscle rest . Other
mechanisms may add to these beneficial effects. These
include improvement of central respiratory drive, ventila-
tion of atelectatic lung areas with reduced ventilation-per-
fusion mismatch and improvement of sleep architecture.
A problem of this study might be that measurements
were performed during the daytime, while patients with
OHS are generally ventilated at night. Our hypothesis was
that NPPV can unload the respiratory muscles despite the
increased mechanical impedance of the respiratory sys-
tem. In obesity, work of breathing is increased as a result
of decreased lung and chest wall compliance [18, 25].
This factor is largely independent of the state of vigilance
and can therefore be studied during the daytime. Thus,
although we have not done our measurements at night, we
might hypothesize that our findings are also valid dur-
ing sleep. Still, this assumption needs confirmation.
Upper airway narrowing during sleep will cause addi-
tional muscle loading in OSA and OHS and sleep itself
alters respiratory drive, which is important in respect to
patient-ventilator interaction in modes of partial ventila-
tory support. Thus, although we think that muscle unload-
ing with BiPAP will be present during sleep, it cannot be
assumed that the settings of the ventilator used in the
present study will be equally effective in ventilating pat-
ients during sleep.
W. PANKOW ET AL.
The rationale to investigate different groups of subjects
with obesity was to show that respiratory muscle unload-
ing can be effectively performed in obesity irrespective of
additional problems like OSA or OHS. Most subjects with
SO as well as normocapnic OSA (treated with nCPAP)
will not experience problems associated with obesity-rel-
ated respiratory muscle load. It has been demonstrated,
however, that grossly obese patients have an increased risk
of respiratory complications in the perioperative period
[26–28], and that noninvasive mechanical ventilation can
improve the ventilatory function . We have now shown
that NPPV can provide partial respiratory muscle rest. We
suggest that this mechanism might have contributed to the
beneficial clinical effects of NPPV demonstrated in earlier
In summary, the data of this study show for the first
time that the diaphragm in extreme obesity and in the
obesity hypoventilation syndrome is unloaded, though not
completely rested with noninvasive positive pressure ven-
tilation. Improvement of the clinical condition shown in
earlier investigations might, in part, be due to this mecha-
nism. Our results also suggest that in acute respiratory
failure as a complication of obesity hypoventilation syn-
drome, or during the postoperative period, noninvasive
ventilation might be used as an alternative to invasive ven-
Acknowledgement: The authors would like to thank M.
Aarts for reviewing the English of the manuscript.
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