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1 Laboratoire de Médecine
Aérospatiale, ABSTRACT Beaumont, Maurice, Damien Lejeune, Henri Marotte, Alain
Harf, and Frédéric Lofaso. Effects of chest wall
counterpressures on lung mechanics under high levels of CPAP in humans.
J. Appl. Physiol. 83(2): 591-598, 1997.
continuous positive airway pressure; +Gz tolerance; positive pressure
breathing; lung volumes; pattern of breathing; respiratory muscle
activity
INTRODUCTION TO IMPROVE THE ABILITY of combat aircraft pilots to
tolerate the physiological disturbances induced by accelerations with gravitoinertial forces acting from head to foot
(+Gz acceleration), counterpressure applied around the abdomen and the lower limbs by
inflating anti-G pants was proposed more than 10 years ago (9).
However, this failed to prevent hemodynamic disturbances with loss of
consciousness when pilots were subjected to the rapid onset (>8
+Gz/s) and sustained accelerations
observed with agile combat aircraft (27). Positive pressure breathing
applied as continuous positive airway pressure (CPAP) has been proposed
as an additional protection against such accelerations because positive intrathoracic pressure is transmitted to the vascular system, increasing systemic arterial pressure even when cardiac output is
decreased (6, 8, 30). CPAP can be applied at levels of up to 90 cmH2O at 9 +Gz (11). Higher levels
(110-120 cmH2O) can be used
to protect pilots against acute hypoxia after accidental cockpit
decompression at altitudes of up to 20 km (5). Application of CPAP
levels above 35-45 cmH2O
requires use of a chest garment inflated at the same pressure to avoid
excessive expansion of the lungs and rib cage (1).
To our knowledge, the effects on ventilatory mechanics of CPAP
protocols presently used in aeronautics [CPAP with thoracic (TCP)
and abdominal/lower limb counterpressures (ACP)] have not yet
been described. The purpose of our study was to determine the changes
in end-expiratory volume (EEV) and the activity of respiratory muscles
induced by short periods of CPAP up to 40 cmH2O with or without TCP
and/or ACP in humans. We hypothesized that in the absence of
counterpressure the ventilatory pattern would be characterized by
active expiration and passive inspiration to limit lung expansion but
that application of TCP and/or ACP would restore inspiratory
activity and reduce expiratory efforts. To check this hypothesis, we
assessed the specific and synergistic effects of TCP and ACP on
respiratory muscle activity and lung volumes.
METHODS Six healthy adults [4 men and 2 women; age 36 ± 5 (SD) yr;
height 175 ± 7 cm; weight 72 ± 12 kg] volunteered for
this study. All were naive to the purpose of the study. The
experimental protocol was approved by the Human Ethics Committee of the
Henri Mondor Hospital, Créteil, France. All subjects underwent a
medical evaluation before participation. Four had prior experience with
CPAP up to at least 60 cmH2O.
Furthermore, all study subjects attended a training session with the
pressurized equipment a few days before the experiment. This session
consisted of 3-min periods of CPAP at breathing pressures of 10, 20, 30, and 40 cmH2O with a 5-min recovery time between each period.
Experimental Setup
We assessed the respective effects of thoracic (TCP) and
abdominal/lower limb (ACP) counterpressures on end-expiratory volume
(EEV) and respiratory muscle activity in humans breathing at 40 cmH2O of continuous positive
airway pressure (CPAP). Expiratory activity was evaluated on the basis of the inspiratory drop in gastric pressure (
Pga) from its maximal end-expiratory level, whereas inspiratory activity was evaluated on the
basis of the transdiaphragmatic pressure-time product (PTPdi). CPAP
induced hyperventilation (+320%) and only a 28% increase in EEV
because of a high level of expiratory activity (Pga = 24 ± 5 cmH2O), contrasting with a
reduction in PTPdi from 17 ± 2 to 9 ± 7 cmH2O · s
1 · cycle1
during 0 and 40 cmH2O of CPAP,
respectively. When ACP, TCP, or both were added, hyperventilation
decreased and PTPdi increased (19 ± 5, 21 ± 5, and 35 ± 7 cmH2O · s1 · cycle1,
respectively), whereas Pga decreased (19 ± 6, 9 ± 4, and 2 ± 2 cmH2O, respectively). We
concluded that during high-level CPAP, TCP and ACP limit lung
hyperinflation and expiratory muscle activity and restore diaphragmatic
activity.
Fig. 1.
Subject wearing anti-G pants and pressurized jerkin.
[View Larger Version of this Image (105K GIF file)]
Table 1.
Mean pressures measured in the mask, and anti-G jerkin and pants
CPAP,
cmH2O
Pmask
Pj
PP
Control
1.0 ± 0.1
0
0.2 ± 0.0
0
0
10
9.9 ± 0.1
9.5 ± 0.5
180.0 ± 1.0
20
19.7 ± 0.5
19.0 ± 0.5
202.0 ± 1.0
30
29.6 ± 1.0
29.0 ± 0.5
219.0 ± 1.0
40
40.0 ± 0.8
39.0 ± 0.5
240.0 ± 1.0
Values are means ± SE expressed in cmH2O; n = 6 subjects. Pmask, pressure measured in mask; Pj,
pressure measured in jerkin; PP, pressure measured in
pants. Control, without pressurized equipment; from 0 to 40 cmH2O continuous positive airway pressure (CPAP), with
pressurized suit. For CPAP of 10 cmH2O, PP = 161 + 1.97 * Pmask (r = 0.99;
P < 0.001).
Experimental Protocol and Data Analysis
Respective effects of TCP and ACP on lung mechanics at 40 cmH2O of CPAP. We evaluated the respective effects of TCP and ACP on EEV, respiratory pattern, and respiratory muscle activities at 40 cmH2O of CPAP. Four tests were performed in each subject with different types of counterpressure [no counterpressure (0CP), ACP, TCP, TCP+ACP]. During each test, measurements were performed during two periods, at two different levels of CPAP, i.e., 0 (control) and 40 cmH2O. The sequence of administration of the different types of counterpressure was randomized. Duration of each of the eight measurement periods was 4 min. The subject was allowed 2 min for familiarization with the setup, which was sufficient for all measured variables to achieve the steady state. Measurements during the last 2 min were used for the analysis, except for EEV, which was measured after the 4-min CPAP period. After each period, the subjects rested for at least 10 min. All measurements in a given subject were completed within ~2 h 30 min. Expiratory muscle activity was evaluated as previously described (23, 26) from the changes in Pga. On the Pga tracing, we measured the decrease from the maximal end-expiratory level to the minimal value (Pga). Figure 2 illustrates this
measurement in a representative subject breathing at 40 cmH2O of CPAP with TCP. In this
subject, most of the inspiratory effort was associated with a rise in
Pga and an increase in abdominal cross-sectional area, indicating
shortening and descent of the diaphragm. Relaxation of the diaphragm
during expiration resulted in a fall in Pga and a decrease in abdominal
diameter. After this early expiratory phase, however, Pga started to
rise again until the end of expiration, whereas abdominal diameter
continued to decrease. From the end-expiratory value, Pga then dropped
(i.e., Pga), whereas abdominal cross-sectional area increased. This
pattern clearly indicates expiratory contraction of the abdominal
muscles, and the increase in Pga during the expiratory phase of the
breathing cycle was taken as a reflection of the direct mechanical
effect of this contraction.
Diaphragmatic muscle activity was evaluated from the changes in transdiaphragmatic pressure (Pdi). Pdi pressure-time product (PTPdi) was used as an estimate of the metabolic work or the oxygen consumption of the diaphragm (28). We computed PTPdi as the area subtended by the Pdi above the end-expiratory baseline divided by inspiratory time (TI), as described previously (28). To assign variations in Pga to variations in expiratory activity, changes in Vrc and Vab were measured as described above. From the flow tracings, we measured TI, expiratory time (TE), respiratory frequency, and minute ventilation (
) as the product of
respiratory frequency times VT.
From the Finapres recordings, we measured HR, SBP, and DBP during
inspiration and expiration.
Statistics
All data were analyzed with commercially available software (PCSM plus, Deltasoft, Grenoble, France) by using a two-way (CPAP, type of counterpressure) analysis of variance. The critical significance level of P was set at 0.05. Post hoc comparisons were performed by using a Newman-Keuls test or a Student's t-test to determine differences in physiological responses to the CPAP or to equipment conditions.RESULTS
Pressures Measured in the Aeronautical Mask, Jerkin, and Pants
Pressures measured in the different parts of the equipment for each CPAP level are shown in Table 1. As expected, Pmask and Pj values were similar to CPAP levels. ACP was set at much higher levels determined on the basis of the CPAP level, according to the following two relationships that are used in French aircraft: CPAP = 18 * Gz (>4 +Gz) and ACP = 70 * Gz (>2 +Gz).Respective Effects of TCP and ACP on Lung Mechanics at 40 cmH2O of CPAP
All subjects felt more comfortable with TCP and/or ACP than with 0CP.Absolute end-expiratory Pes and Pga measured at 40 cmH2O of CPAP in all counterpressure conditions are shown in Table 2. Figure 3 shows the respective effects of TCP and ACP on EEV at 40 cmH2O of CPAP. With 0CP, EEV increased by only 28% over the functional residual capacity (FRC; P < 0.05). This change in EEV was abolished by the presence of either TCP or ACP (+7 and +3% over FRC, respectively; not significant). EEV decreased by 5% below FRC with TCP+ACP.
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Table 3 shows ,
respiratory rate, VT, and
changes in VT recruited from rib
cage and abdominal compartments
(Vrc/VT,
Vab/VT). At 40 cmH2O of CPAP with 0CP, there was
marked hyperventilation mainly because of an increase in
VT, with a predominant change in
thoracic volume. With TCP, the increase in
VT was limited, and changes in
Vrc and Vab did not differ from control. By contrast, the respiratory
rate increased and the CPAP-related hyperventilation persisted. ACP
alone had a significant effect on CPAP-related hyperventilation due to
a decrease in VT, whereas
respiratory rate not change. There was a further decrease in abdominal
contribution to VT with ACP
compared with 0CP. TCP+ACP had an additive effect on the CPAP-related
hyperventilation that was only increased by 30% vs. control, with a
VT that was not different from
control.
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Table 4 shows respiratory drive data (TI, TE, VT/TI, VT/TE). TI remained unchanged vs. control with CPAP levels up to 40 cmH2O under all counterpressure conditions except TCP+ACP, which was associated with an increase in TI. The increase in VT/TI due to CPAP with 0CP was limited by TCP and even more so by ACP and was even below control (not significant) with TCP+ACP. TE was decreased by CPAP under all counterpressure conditions.
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Figure 4 shows representative tracings from
a subject receiving CPAP under all counterpressure conditions studied.
With 0CP, no variations in Pdi were seen in five of the six study
subjects. Compared with 0CP, breathing with TCP+ACP was characterized
by a high Pdi and by a Pga signal indicating a considerably lower level
of expiratory muscle activity.
Figure 5 shows that during CPAP with
various conditions of counterpressure the PTPdi increased as changes in
Pga decreased, with a negative correlation
(r = 
0.71 ± 0.28, P < 0.05), indicating progressive
recruitment of the diaphragm as expiratory activity decreased. When
CPAP was applied with 0CP, PTPdi decreased. TCP or ACP returned PTPdi
to normal, and TCP+ACP increased PTPdi to a level above the control
value with no CPAP or with 0CP.
Pga; B). In addition PTPdi
was matched against Pga (C).
During CPAP, PTPdi was low with 0CP, normal with TCP or ACP, and high
with TCP+ACP, and there were significant differences between all types
of counterpressure (P < 0.05),
except between TCP and ACP. In addition, during CPAP, a significant
negative correlation was observed in the 6 subjects between PTPdi and
Pga (r = 0.71 ± 0.28, P < 0.05). 
, 
, 
, and star:
0CP, TCP, ACP, and TCP+ACP, respectively. 
, Control; solid symbols,
40 cmH2O of CPAP.
Respective Effects of TCP and ACP on Arterial Blood Pressures at 40 cmH2O of CPAP
Arterial SBP and DBP increased from control to 40 cmH2O of CPAP (Table 5). These increases were more marked when counterpressures were applied. The magnitude of the increase in SBP or DBP seen with TCP or ACP corresponded to the level of CPAP (30 mmHg). HR increased by ~30% from control to 40 cmH2O of CPAP in all counterpressure conditions except TCP+ACP, during which HR was identical to the control value (Table 5).
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DISCUSSION
Protection against +Gz accelerations is mainly obtained by inflation of anti-G pants to limit pooling of blood in the lower limbs and thereby improving venous blood return. Because the protection provided by anti-G pants against high levels of acceleration is often inadequate in agile fighters, CPAP has been suggested as a means of providing additional protection during accelerations above 4 +Gz because CPAP is known to increase arterial blood pressure (6). CPAP can be delivered at levels of up to 40 cmH2O during accelerations above 6 +Gz. To limit lung hyperinflation due to high-level CPAP, use of a pressurized jerkin has been proposed for flights in Mirage 2000 fighters. As shown in Table 1, ACP values were considerably higher than those for Pmask and TCP, as recommended in standard pressure schedules (11, 18, 29).
Numerous studies have demonstrated that high-level CPAP is associated with lung hyperinflation in healthy subjects (2, 3, 15, 22). In addition, the inspiratory workload was shared by the expiratory muscles, which forced the system below its equilibrium position (2, 15). When breathing against moderately high CPAP, many normal subjects strove to prevent or limit CPAP-induced chest distension (10).
Our data corroborate the findings from these studies, providing additional evidence that high-level CPAP without counterpressure in healthy subjects decreases the mechanical activity of the diaphragm and increases the expiratory activity of the abdominal muscles and that these changes fail to completely overcome lung hyperinflation. In addition, we observed that use of TCP+ACP during CPAP was effective in normalizing the lung EEV, reducing the expiratory activity of the abdominal muscles, and restoring the mechanical inspiratory activity of the diaphragm.
Methods Used To Estimate Respiratory Muscle Efforts
It has been previously demonstrated that, when expiratory activity is observed, abdominal muscles are responsible for most of this expiratory activity (23, 26). On the other hand, when performing expiratory efforts, normal humans cannot contract the abdominal muscles without also contracting the triangularis sterni, an important expiratory muscle of the rib cage (13). In this study, abdominal muscle activity was evaluated by measuring Pga changes during expiration. For technical reasons, including the use of CPAP and TCP, we were unable to use electromyography to assess the activity pattern of rib cage expiratory muscles. In addition, to separate inspiratory and expiratory activities of intercostal muscles, it would have been necessary to use needle or wire electrodes rather than surface electrodes. Although the contribution of thoracic expiratory muscles was not quantified in our study, we can assume that CPAP in our subjects increases the activity of all expiratory muscles.Mechanical diaphragmatic activity was evaluated on the basis of measurement of Pdi. Although we found a clear decrease in PTPdi with CPAP, the actual change in diaphragmatic activity was difficult to evaluate. Flattening of the diaphragm due to the increase in EEV that occurs during CPAP is known to decrease the pressure generated by the diaphragm for any given value of diaphragmatic tension (19, 25). This decrease in inspiratory performance with CPAP has been examined in detail by Agostoni (2), who found that Pdi became zero in conscious humans breathing at 30 cmH2O of CPAP, despite persistence of electrical diaphragmatic activity. Nevertheless, in our study the diaphragmatic force output decreased during CPAP with 0CP, whereas it increased when pulmonary overinflation was compensated for by either type of counterpressure studied.
Last, it could be argued that TCP during CPAP may restrict rib cage muscle action, thereby increasing the contribution of the diaphragm. However, the fact that ACP had an effect on PTPdi (Fig. 5) and EEV (Fig. 3) similar to that of TCP suggests that the increase in diaphragmatic contribution with TCP was due mainly to a reduction in overinflation.
Interpretation of Data
In keeping with a report by Ernsting (15), the ventilatory pattern observed during CPAP with 0CP was characterized by marked hyperventilation. It has been showed that instruction is important in determining the response of subjects to CPAP (19), suggesting that the stress induced by high-level CPAP may be a factor to explain hyperventilation. Nevertheless, our subjects were experienced in CPAP and were asked to remain relaxed during the tests. One explanation could be an increase in ventilatory demand due to a CPAP-induced fall in cardiac output (7), which follows the reduction in systemic venous return (20) and the increase in right ventricular afterload. Alternatively, the hyperventilation may have been produced by an increase in expiratory activity. We found that hyperventilation was reduced by the application of TCP and/or ACP, a finding compatible with either hemodynamics or a muscle hypothesis for hyperventilation.With regard to respiratory muscle activity, CPAP was associated with a high level of expiratory activity of the abdominal muscles (Fig. 5), a decrease in Pdi (Fig. 5), and an increase in EEV (Fig. 3), in keeping with other studies (2, 3, 15, 22, 24). As shown in Fig. 5, the mechanical inspiratory activity of the diaphragm during CPAP was inversely correlated with the mechanical activity of abdominal expiratory muscles, suggesting that during hyperinflation by CPAP the reduction in the mechanical inspiratory activity of the diaphragm was counterbalanced by an increase in the expiratory activity of the abdominal muscles, which stored elastic energy during expiration and released it at their relaxation, thereby assisting inspiratory muscles for the next inspiration (23-26). In our study, when CPAP was applied with 0CP, the increase in EEV was ~1 liter, corresponding to an effective elastance of 40 cmH2O/l, a value much too large to be accounted for by passive characteristics of the lungs and chest wall. This suggests that expiratory activity explained the relative small increase in EEV.
The question here was to know whether chest wall counterpressure was effective in significantly limiting lung volume expansion, expiratory activity, and hyperventilation in subjects receiving CPAP. The "chest wall" includes all the parts of the body outside the lung that share the changes in volume of the lungs and can be divided into the rib cage and the abdomen (21). Each appears to move as a unit, with considerable independence of motion. For example, it is easy to expand the lung volume with either the rib cage or the abdomen and even to cause outward displacements of one of these units while one moves the other inward (21). We therefore elected to conduct separate evaluations of TCP, ACP, and total counterpressure.
TCP or ACP showed comparable efficacy in preventing increases in EEV to levels significantly above the control value (Fig. 3). In addition, either method returned the mechanical inspiratory activity of the diaphragm to a level similar to that during the control situation (no CPAP, 0CP) (Fig. 5). As expected, in addition to this similar effect on the diaphragm, ACP induced a dramatic reduction in abdominal compartment and, as a result, increased the changes in the rib cage compartment. Conversely, when TCP was applied, thoracic volume and Vab changes decreased and increased, respectively. Both modes of counterpressure induced a significant reduction in the expiratory activity of the abdominal muscles, although this reduction was larger with TCP than ACP. These data suggest that TCP may restore normal mechanical diaphragmatic activity and normal EEV with less expiratory activity compared with ACP. Because the ACP compartment was inflated at high pressures, the lesser efficacy of ACP compared with TCP was surprising. One explanation may be that compliance of the abdomen is lower than that of the rib cage (16). Alternatively, the straps placed on the abdomen to secure the TCP compartment to the chest may have increased the efficacy of TCP compared with ACP (see Fig. 1).
We observed an additive effect of TCP and ACP on volumes and respiratory muscle activities: total counterpressure provided a further increase in diaphragmatic activity and further decreases in expiratory activity, EEV, and hyperventilation, compared with TCP or ACP alone. This result is in agreement with the concept that the rib cage and the abdomen are functionally separate (21) and demonstrates that counterpressure is optimally efficient only if it is applied to both mobile parts of the chest wall. With TCP and ACP, the PTPdi was above the control value (no CPAP). This increase in Pdi was largely ascribable to the decrease in thoracoabdominal compliance. Therefore, for a given inspiratory diaphragmatic displacement, the diaphragm must develop a higher tension in the presence of CPAP with TCP+ACP than in the absence of CPAP. In addition, the enhanced diaphragmatic activity compared with control may have been due in part to the persistence of ~40% hyperventilation.
Arterial SBP and DBP increased from control to 40 cmH2O (30 mmHg) of CPAP. As previously reported, the magnitude of this increase was approximately one-half that of the CPAP level (14). A possible explanation is limitation of venous return, resulting in a decrease in cardiac output despite an increase in HR. Moreover, due to the elasticity of the lung, transmission of intra-alveolar pressure to the vessels was not total (6). In keeping with previous studies (1, 17), arterial blood pressures further increased with TCP or ACP. Interestingly, when either type of counterpressures was applied, the magnitude of the blood pressure increase was similar to the CPAP level (30 mmHg). Furthermore, TCP+ACP had an additive effect on SBP and DBP, which further increased by 10 mmHg compared with use of TCP or ACP alone. It has been established that TCP improves intrapulmonary-to-vascular pressure transmission, whereas ACP increases venous return and therefore the cardiac preload. These hemodynamic effects may counteract hypotension in subjects exposed to accelerations.
In this study, we demonstrated that respiratory and hemodynamic
disturbances observed with 40 cmH2O of CPAP, namely, increases in , lung volumes, expiratory muscle activity, and HR
were adequately counterbalanced by an additive effect of TCP and ACP.
We conclude that TCP and ACP limit lung hyperinflation and expiratory
muscle activity and restore diaphragmatic activity and that these
effects add to the limitation of CPAP-related hemodynamic disturbances provided by anti-G pants.
ACKNOWLEDGEMENTS
The authors are grateful to the subjects who volunteered for this study and to J. Bajolet, S. Canot, F. Guyard, G. Legrand, B. Louwagie, J. B. Marchetti, C. Nault, R. Vallet, and S. Voisembert for technical assistance.
FOOTNOTES
Address for reprint requests: F. Lofaso, Service de Physiologie-Explorations Fonctionnelles, Hôpital Henri Mondor, 94010 Créteil, France.
Received 26 December 1996; accepted in final form 8 April 1997.
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 F. Lofaso, M. P. d'Ortho, R. Fodil, C. Delclaux, A. Harf, and A. M. Lorino Abdominal Muscle Activity in Sleep Apnea During Continuous Positive Airway Pressure Titration Chest, August 1, 2001; 120(2): 390 - 396. [Abstract] [Full Text] [PDF]
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ABSTRACT
