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1 Newborn Services, This study investigated factors
contributing to differences between mean alveolar pressure
(
high-frequency ventilation; gas trapping; lung volume; mean airway
pressure
THE POSSIBILITY THAT GAS TRAPPING may occur during
high-frequency oscillatory ventilation (HFOV) has been a source of
concern for many years. This concern has been heightened by perceived similarities with conventional mechanical ventilation, where it is well
recognized that gas trapping can occur at high ventilator rates (17,
18, 20).
During conventional mechanical ventilation (CMV), the time required for
pressure to equilibrate between the alveolar space and the patient's
airway, and thus for inspiration or expiration to be complete, is
determined by the time constant, which is the product of compliance (C)
and resistance (R) of the respiratory system. Because expiratory
resistance is commonly up to fourfold greater than inspiratory
resistance (17), application of rapid ventilator rates during CMV may
easily compromise expiration. Gas trapping results, with elevation of
alveolar pressure above airway pressure at end expiration, in a
phenomenon commonly referred to as inadvertent positive end-expiratory
pressure (3, 17, 20). To minimize the risk of this problem occurring
during CMV at rapid rates, inspiratory-to-expiratory time (I/E) ratios
of at least 1:2 are commonly employed.
Extrapolation of the principles underlying choice of I/E ratio for CMV
has lead many authorities to also recommend the use of I/E ratios of at
least 1:2 for HFOV, with the same intent of avoiding gas trapping and
the associated dangers of hyperinflation, air leak, and cardiovascular
compromise. The extent to which gas trapping occurs during HFOV,
elevating mean alveolar pressure ( To date, there has been no quantitative description of the effect of
oscillatory ventilator settings and mechanical characteristics of the
lung on the difference ( Experiments were performed on the lungs of four adult rabbits and an in
vitro model of the intubated newborn respiratory system. Animal
experiments were performed in accordance with the guidelines of the
Australian National Health and Medical Research Council and with the
approval of the Animal Ethics Committees of Monash Medical Centre and
Monash University (approval no. A9452).
Lung Models
Rabbit lung model.
Four adult New Zealand White rabbits (body weight, 4.0 ± 1.8 kg)
were administered a lethal dose of pentobarbital sodium (160 mg/kg) and
intubated through a tracheostomy with an 11-cm-long, 3.0-mm-ID
endotracheal tube (ETT) (Portex, UK). Intermittent positive pressure
ventilation of the lungs (peak inspiratory pressure = 15
cmH2O; end-expiratory pressure = 5 cmH2O;
rate = 30 breaths/min; and inspiratory time = 0.7 s) was initiated
with a Humming II ventilator (Senko Medical Instrument Manufacturing,
Japan) and maintained until the completion of surgical procedures when
HFOV was commenced with a SensorMedics 3100 high-frequency oscillator. To measure alveolar pressure (PA) by the alveolar capsule
technique (12, 13), a right thoracotomy was performed and a small
plastic capsule glued (Supaglue, Selleys Chemical, Australia) to the
exposed anterolateral surface of the right middle (n = 3) or
right lower (n = 1) lobe of the lung. The pleural surface
enclosed within the capsule was punctured in five places with a
23-gauge needle inserted to a uniform depth (2 mm). The capsule opening
was then sealed by inserting the tip of a Micron MP15 pressure
transducer (Micron Instruments), which was carefully supported to exert
minimal pressure on the underlying lung.
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
APPENDIX A
APPENDIX B
) and mean pressure at the
airway opening (
) during high-frequency
oscillatory ventilation (HFOV). The effect of the
inspiratory-to-expiratory time (I/E) ratio and amplitude of oscillation
on the magnitude of 
(
) was
examined by using the alveolar capsule technique in normal rabbit lungs
(n = 4) and an in vitro lung model. The effect of ventilator
frequency and endotracheal tube (ETT) diameter on
was further examined in the in vitro lung model at an I/E ratio of 1:2. In both lung models,
fell below
during HFOV when inspiratory time was
shorter than expiratory time. Under these conditions, differences
between inspiratory and expiratory flows, combined with the nonlinear
relationship between resistive pressure drop and flow in the ETT, are
the principal determinants of . In our
experiments, the magnitude of at each
combination of I/E, frequency, lung compliance, and ETT resistance
could be predicted from the difference between the mean squared
inspiratory and expiratory velocities in the ETT. These observations
provide an explanation for the measured differences in mean pressure
between the airway opening and the alveoli during HFOV and will assist
in the development of optimal strategies for the clinical application
of this technique.
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
APPENDIX A
APPENDIX B
) above mean airway opening
pressure (), remains controversial.
Various investigators have reported that global or regional measures of
may be the same (1, 5), higher
(1, 2, 5, 7, 13, 19, 21), or lower (13, 25) than
during HFOV. Differences in ventilator
settings including I/E ratio (13), (5),
ventilator amplitude (
Pao) (1), and the effects of regional factors
(1) and posture (1, 21) appear to account, at least in part, for these
disparate observations.
) between
and . This study was, therefore, undertaken to
systematically examine the interaction of key ventilatory parameters on
the magnitude of in the lungs of young
rabbits and in an in vitro lung model.
MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
APPENDIX A
APPENDIX B
1.
In vitro lung model.
To simulate the mechanical properties of the respiratory system of the
intubated human newborn infant suffering from hyaline membrane disease,
we employed a lung model comprising an 11-cm-long, 3.0-mm-ID ETT,
sealed into the neck of a 590-ml glass flask (see Fig.
1). The model had an adiabatic compliance C
of 0.4 ml/cmH2O and an R of 75 cmH2O · s · l1
[measured at a flow (V') = 0.1 l/s].
|
Measurement of Pressure
PA and pressure at the airway opening (Pao).
Pao was measured with a Micron MP15 pressure transducer (Micron
Instruments) via a sideport positioned immediately above the connection
to the ETT and perpendicular to the ventilator tubing. Pressure in the
interior of the in vitro lung model (PA) was also measured
with an MP15 transducer positioned at the end of an 11-cm-long, 12-gauge needle inserted into the glass flask. Similar measurements of
mean pressure were obtained when was
measured at other sites close to the airway opening and when
was determined at a variety of
sites within the glass flask (results not shown).
70 to +140 cmH2O. Transducer signals were amplified and low-pass filtered at 400 Hz
(Cyberamp 320, Axon Instruments), digitized at 1 kHz, and stored on a
personal computer by using data-acquisition software (Spike 2, Cambridge Electronic Design, UK).
Mean pressures.
Measurements of mean pressures were determined from the average of at
least 10 complete cycles of oscillation. The potential for errors
arising from differences in transducer calibration when determining
differences between and
was eliminated in the in vitro lung model
by measuring PA and Pao with the same transducer connected
either to the airway opening or to the interior of the lung. In the
rabbit lung, each transducer was carefully calibrated to the same gain.
Potential errors arising from zero drift were minimized by frequently
referencing each transducer to the same static pressure, achieved by
briefly reducing the amplitude of the pressure oscillation delivered by
the high-frequency ventilator to zero.
Amplitude of pressure oscillation at the airway opening Pao.
Reporting of the amplitude of pressure oscillation produced by the
SensorMedics 3100 at the airway opening is confounded by the
waveform's complex shape, which approximates to a square wave, upon
which are superimposed large-amplitude, damped oscillations at the
onset of both inspiration and expiration. Where observations were made
at various amplitudes, we have reported the amplitude displayed by the
ventilator. The ventilator internal pressure measurement provides a
damped estimate of the amplitude Pao, since the pressure transducer
is placed at the end of a 75-cm length of 3.5-mm-bore tubing attached
to the inspiratory limb of the ventilator circuit, 1 cm before the
patient's airway connection. Consequently, the Pao displayed by the
ventilator approximates the amplitude of the square-wave component of
the pressure waveform.
Calculation of tidal volume (VT) and V'. In the in vitro lung model, VT was calculated by using the equation
|
(1) |
PA
is amplitude of oscillatory pressure waveform in the model lung,
P0 is atmospheric pressure, and 
is adiabatic gas
constant (1.4 for air). V' was calculated throughout the oscillatory
cycle by using numerical differentiation such that
|
(2) |
Experimental Protocols
In all experiments, HFOV was delivered by a SensorMedics 3100 high-frequency oscillator, operated in accordance with the manufacturer's instructions. All observations were made at a mean airway pressure of 10 cmH2O. in the rabbit lung
model.
Experiments were performed to test whether significant differences
between and
could be identified in the rabbit lung
model during HFOV and to investigate the effect of the I/E ratio on
these differences. By using a ventilator frequency of 15 Hz, the
magnitude of was determined at I/E
ratios of 1:1 and 1:2 across a range of Pao from a minimum of 10 cmH2O to a maximum of 90 cmH2O. Two
observations were made at each setting, and average values of
were determined for individual rabbits at each Pao and I/E ratio.
in the in vitro lung
model.
Experiments were performed to test whether differences between
and
could be identified in the in vitro lung model and to examine the independent effects of ventilator amplitude, frequency, and I/E ratio as well as the model lung compliance and ETT
resistance on those differences. The range of ventilator settings
examined and the characteristics of the lung model employed in each
protocol are summarized in Table 1.
Ventilator settings were changed in random sequence until triplicate
observations of and
had been made under each experimental
condition. Differences between
and were pooled to determine average
values for .
|
Statistical Analysis
Results are shown as means ± SE. Statistical analysis of the data derived from the rabbit experiments was complicated by the unequal number of measurements of obtained
across a range of ventilator amplitudes in each rabbit. A multilevel
modeling approach using a nested hierarchical design was employed
(statistical software MLn v 1.0a, Institute of Education, London, UK).
Constant variance was assumed. Two levels were employed in the analysis to account for differences between the observations of
made at different amplitudes (level
1) and between rabbits (level 2). Data at each I/E ratio
were assessed separately.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
APPENDIX A
APPENDIX B
|
|---|
in the Rabbit Lung
made during HFOV in
each of the rabbit lungs are illustrated in Fig.
2A. In the rabbit lung,
was not significantly different from
zero (maximum 0.8 ± 0.3 cmH2O) at an I/E ratio of
1:1. However, at an I/E ratio of 1:2, was substantially less than
, and the magnitude of
increased with the square of the
oscillatory pressure amplitude at the patient's airway to a maximum
value of 5.0 ± 0.2 cmH2O.
|
in the In Vitro Lung
Model
in the in vitro
lung was <1 cmH2O at an I/E ratio of 1:1 (Fig.
2B). In contrast to the rabbit lung, however,
was positive
(
), and
a statistically significant difference in
was demonstrable between models for
amplitudes in excess of 30 cmH2O. At an I/E ratio of 1:2,
was substantially less
than (maximum difference 6.6 ± 0.2
cmH2O), and the difference increased with increasing
amplitude in a similar manner to the rabbit lung.
Figure 3 illustrates the effect of changing
the amplitude, frequency, and I/E ratio of the ventilator and both the
ETT diameter and compliance of the lung model, on the magnitude of
. An increase in ventilator frequency
(Fig. 3A) at an I/E ratio of 1:2 or reduction of the
inspiratory time as a fraction of total cycle time (Fig. 3B)
caused to fall progressively below . Reduction in the resistance of the
lung model, by increasing ETT diameter, decreased
at a given VT (Fig.
3C), whereas a change in compliance had negligible effect
(Fig. 3D) until very low compliances were reached (<0.5
ml/cmH2O), after which fell
rapidly with decreasing compliance.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
APPENDIX A
APPENDIX B
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In common with several previous publications (1, 6, 19, 21), we found
evidence in this study that
may differ significantly from during HFOV
and that I/E ratio is a crucial determinant of whether such a
difference is present. The novel feature of our study is that it
represents the first systematic evaluation of the effects of individual
HFOV settings, and the influence of mechanical properties of the lung,
on the magnitude of differences between
and
. We found no evidence of significant gas
trapping
() at an
I/E ratio of 1:1. Rather, differences between
and
of sufficient magnitude to be of
potential clinical significance (
1 cmH2O) were seen only
at an I/E ratio of 1:2 and were opposite in sign
( < ). Interestingly, differences between and
(i.e., )
could be elicited even in a very simple in vitro lung model, where
their magnitude was very similar to that seen in whole rabbit lung
oscillated at comparable settings, suggesting that the ETT itself is
critical to the generation of .
Critique of Methods
Our in vitro and animal lung models were chosen because their mechanical properties resemble the human newborn infant's respiratory system. Thus the compliance of the in vitro model (0.4 ml/cmH2O) was comparable to that seen in severe hyaline membrane disease (13), a condition for which HFOV is commonly employed. We also used a range of ETTs (ID 2.5-3.5 mm) that spanned the range of sizes normally used for human newborn infants. However, although the total resistance of the intubated neonatal respiratory system has a significant contribution from the ETT (11), our in vitro model lacked conducting airways beyond the ETT, and its resistance must therefore have been less than that in the human newborn. Again, the rabbit was chosen as our whole lung model for its similarity in size and mechanical properties to the human newborn infant.Measurements of in the rabbit
lung were made with the alveolar capsule technique, which has been used
previously by several investigators to measure PA during
high-frequency ventilation (1, 11-13). This technique has been
demonstrated by Gerstmann and colleagues (13) to potentially
overestimate when capsule and
transducer are relatively heavy. We attempted to minimize this problem
in our experiments by carefully supporting the pressure transducer to
achieve a near-weightless condition. Whereas we cannot exclude the
presence of some residual effect, we note that by causing
overestimation of such an effect would have tended to lessen the
that we observed at an I/E ratio of 1:2. Employing a single alveolar
capsule, we were unable to examine whether any regional variation in
was present in our
experiments. However, when regional variation is present,
is usually lowest in the upper
lobe of the lung during HFOV (1, 13), and our choice of the middle or
lower lobe for alveolar capsule placement would again have tended to
give a minimum estimate of the magnitude of the
present at an I/E ratio of 1:2.
Although measurement of static pressure is relatively uncomplicated,
several investigators have previously noted that pressure measurements
in a moving stream of gas may underestimate the driving pressure
because of the Bernoulli effect (4, 8). In our measurement system, the
most likely pressure to be affected by a Bernoulli effect was
; however, the worst-case calculated dynamic pressure at that site was <0.1 cmH2O.
Difference Between
and
1
cmH2O) between and
in both the rabbit and in vitro lung
models at an I/E ratio of 1:1, several previous studies in dogs (21),
rabbits (13), and adult human subjects (19, 23) have each shown a
potential for to be significantly elevated above when HFOV
was employed at an I/E ratio of 1:1. A number of mechanisms have been
postulated to account for this effect, and each depends on the presence
of asymmetry between inspiratory and expiratory resistance. They include changes in airway caliber between inspiration and expiration (15) that may be particularly evident at low lung volumes (low ) and the effects of flow separation at
branch points in the airway (6). Bryan and Slutsky (5) have suggested,
however, that the elevation of
above , observed in the study of Saari and
colleagues (19) and that of Simon and co-workers (21), might
alternatively be explained by the development of "choke points"
that cause expiratory flow limitation at low
. In support of their hypothesis, they
found the level of to be the crucial
determinant of whether gas trapping occurred in normal or
surfactant-depleted rabbits given HFOV at an I/E ratio of 1:1.
The various potential sources of asymmetry between expiratory and
inspiratory resistance (RE and RI,
respectively) outlined above each cause RE to
exceed RI, and, in turn, have the capacity to cause
to exceed
. None, however, explains the observations
made in our study where we saw minimal elevation of
above
at a 1:1 ratio in the in vitro lung and no elevation at all in the rabbit lung, where such sources of asymmetry
would have been most likely to be evident. The lack of evidence of
exceeding
may well be explained by the observation
made by Byran and Slutsky (5) that the level of
is a the crucial determinant of whether
gas trapping occurred in normal or surfactant-depleted rabbits given
HFOV at an I/E ratio of 1:1. Our studies employed a
of 10 cmH2O, which is well
above that employed in those earlier studies in which gas trapping was
seen (1, 6, 17, 25, 28) but is no higher than the minimum
commonly employed in the clinical setting.
By contrast, the striking finding in our study was that, at an I/E
ratio of 1:2, may fall
substantially below . Several years ago,
Gerstmann et al. (13) made a similar observation that the
average tracheal pressure may be less than during HFOV in the rabbit at an I/E ratio
of 1:2, and more recently Hatcher et al. (14) have found that
determined by airway occlusion
may be less than at an I/E ratio of 1:2. The lower value of compared
with may again be accounted for by
asymmetry between RE and RI, but requires the unusual situation to arise, whereby RI exceeds
RE, which is the converse of the relationship when
is higher than
. Our data provide evidence that
turbulence in the ETT, as first suggested by Gerstmann et al. (13), can
account for this phenomenon.
Turbulence and
In the simple circumstance of an I/E ratio of 1:1, the average
inspiratory flow 
must equal
the average expiratory flow 
,
and both the resistance and Pres during inspiration and
expiration will be equal. In our in vitro lung model at least, with no
airways beyond the ETT, we would therefore expect
to equal
. In contrast, at an I/E ratio of 1:2, the
average inspiratory flow must
be twice the average expiratory flow
, since it is sustained for
only half the time. As Pres depends on the square of V'
under turbulent flow conditions, the average 
will be four times
greater than the average
. The effect on
Pres of doubling inspiratory flow with respect to
expiratory flow will therefore exceed the countering effect on
Pres of expiratory time doubling, relative to inspiratory
time. Thus, at an I/E ratio of 1:2, the unusual circumstance whereby
RI is greater than RE arises, such that the
inspiratory Pres must exceed the expiratory Pres, with the inevitable consequence that
must fall below
in our in vitro lung model. In more
general terms, we can predict that, at any I/E ratio other than 1:1,
will deviate from
, and the magnitude of that deviation will be directly proportional to the difference between the mean squared inspiratory (
)
and expiratory velocities (
) in the
ETT (see APPENDIX A).
To test the capacity of this model to explain the magnitude of
in our in vitro lung model, we have
plotted each measurement of illustrated
in Fig. 3 against the corresponding difference between
and
which we
determined (knowing the in vitro lung compliance) by differentiating
the pressure change within the flask (see Fig. 4). The correlation between
and
( )
was very close (r2 = 0.95), suggesting that the
effect of turbulence could largely account for the
seen in our in vitro lung model.
Furthermore, the close similarity between the results obtained in the
in vitro lung model and those obtained in the rabbit strongly suggests that, even in the whole lung, events occurring in the ETT may be the
principal determinant of differences between
and
.
|
In deriving the relationship between
and we have
assumed that the values of k1 and
k2 during inspiration are equal to those during
expiration. Sly et al. (22) have published k1 and
k2 values measured during steady flow for a number
of ETT values ranging in size from 2.5 to 5.5 mm ID. Their observations
suggest that k1 and k2 during
expiration are slightly higher than during inspiration, by ~10%, in
agreement with differences in the inspiratory and expiratory ETT flow
profiles observed by Chang and Mortola (9). Such a small increase of
expiratory resistance relative to inspiratory resistance could account
for the small elevation of
above in our in vitro lung model at an
I/E ratio of 1:1. A further point of interest is that the calculated slope of the relationship between and
is 0.012,
which is in good agreement with the theoretically predicted slope
(0.013) calculated from the experimental data of Sly et al. (22)
(see APPENDIX A). Clearly, these conclusions are predicated
on the assumption that parameters measured from steady-flow experiments
are applicable in the high-frequency oscillation setting. Only further
experimental work directed at measuring k1 and
k2 during oscillatory flow can resolve this issue.
Clinical Implications
Although a substantial was only seen at
relatively high ventilator pressure amplitudes in these experiments, it
should be noted that the resistance of our in vitro lung model (75 cmH2O · s · l1)
was relatively low, compared with established values of resistance in
the intubated newborn infant with respiratory distress (120-380 cmH2O · s · l1)
(24). Given that our in vitro studies show that
increases with increased airway
resistance, it is likely that may reach
substantial levels at lower pressure amplitudes when an I/E of 1:2 is
used in the sick intubated newborn baby. Similarly, the resistance of
the ETT itself may be higher in the clinical setting, where its
interior is frequently coated with secretions. The development of
high-frequency ventilators with a capacity to deliver I/E ratios of 1:3
or more further increases the possibility of substantial
occurring even at relatively low amplitude.
Importantly, the pressure difference that arises across the ETT is a rapidly achieved, steady-state phenomenon. The main clinical consequence of this phenomenon, therefore, is that whenever the mechanical characteristics of the respiratory system or ventilator settings are altered, a new lung volume will result. The magnitude of such changes in lung volume will increase as I/E ratio moves away from 1:1. Our studies show that the adoption of I/E ratios approaching 1:1 might eliminate the fluctuations in lung volume, which might otherwise result from the pressure drop across the ETT. Where I/E ratios other than 1:1 are employed, the accurate measurement of flow across the ETT would provide a means of calculating the difference in mean pressure between the airway opening and the lung.
The optimization of lung volume has been a focus of clinical HFOV
strategies during the last decade. Common clinical practice involves
initial setting of 1-2
cmH2O higher than that employed during CMV, with increments
in being imposed until a substantial reduction in the inspired O2 fraction, necessary to
maintain normoxia, is achieved. To date, no data are available to
indicate the extent to which the required
in clinical practice for optimal lung recruitment may be related to the
I/E ratio employed.
Although HFOV is frequently employed in the premature infant with
hyaline membrane disease, which is a homogeneous lung disease, it is
also used to ventilate neonates with other forms of respiratory disease. In some cases, this might be associated with a degree of
ventilation inhomogeneity. Although it is likely that this scenario
might create small regional differences in
, the pros and cons of a
symmetric vs. asymmetric I/E ratio in the presence of conditions such
as pulmonary interstitial emphysema remain to be tested.
In conclusion, our observations of minimal difference between
and
at an I/E of 1:1, and the presence of a substantial difference at an I/E ratio of 1:2, call into question whether the common practice of employing an I/E ratio of 1:2 is the
optimal strategy for HFOV. Whereas it may be argued that the generated at an I/E ratio of 1:2 has
the advantage of offsetting any tendency toward gas trapping, either
due to expiratory flow limitation or reduced airway caliber in
expiration, this strategy is not without potential problems. Not only
does it create the potential for
to be substantially different
from the displayed by the machine, it
also creates the opportunity for changes in ventilator amplitude and
frequency, or in the size of the infant's ETT, to have quite
unanticipated and undesirable effects on
.
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APPENDIX A |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
APPENDIX A
APPENDIX B
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The instantaneous pressure at the airway opening Pao is equal to the sum of the resistive and inertive pressure drops associated with the ETT (Pres and Pin, respectively) and the alveolar pressure PA
|
(A1) |
|
(A2) |
= 0 (see APPENDIX
B), and defining
Eq. A2 simplifies to
|
(A3) |
When using Rohrer's equation to represent the effects of turbulent
flow in the ETT, the 
for
inspiration (I) and expiration (E) is, respectively
|
(A4a) |
|
(A4b) |
over a complete cycle is
|
(A5) |
|
(A6) |
Assuming that k1I = k1E and,
further, that k2I = k2E = k2, and recognizing that
= 
Eqs. A3 and A6 yield
|
(A7) |
Finally, rewriting Eq. A7 in terms of flow velocity U in the ETT
|
(A8) |
and
is a straight
line through the origin with a negative slope of k2A2. Calculation of
k2A2, using averaged
k2 values derived from the inspiratory and
expiratory k2 data of Sly et al. (22) for a
10-cm-long ETT, gives 0.014, 0.013, and 0.011 for 2.5-, 3.0-, and 4.0-mm ETTs, respectively. The average calculated slope for the
three ETTs is 0.013, in excellent agreement with that deduced from
Fig. 4, which is 0.012.
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APPENDIX B |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
APPENDIX A
APPENDIX B
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The pressure drop Pin across the inertance (I) of the ETT is
|
(B1) |
Assuming I is invariant, the average Pin is, therefore
|
(B2) |
Evaluation of Eq. B2 gives
![<OVL>P<SUB>in</SUB></OVL> = <FR><NU>I</NU><DE><IT>T</IT></DE></FR> [V′(<IT>T</IT> ) − V′(0)]](/content/vol87/issue1/fulltext/407/img032.gif)
|
(B3) |
If flow is periodic, so that V'(T ) = V'(0), then
|
(B4) |
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ACKNOWLEDGEMENTS |
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We gratefully acknowledge the support of the SensorMedics Corporation for the loan of a SensorMedics 3100 ventilator, which made these investigations possible.
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FOOTNOTES |
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This study was supported by a Financial Services Foundation for Children Grant and the SW Shields Research Fellowship from the Royal Australasian College of Physicians. The authors also gratefully acknowledge the support of the Monash Medical Centre Newborn Services Special Purpose Fund for assistance in providing the additional support required for completion of these studies.
Address for reprint requests and other correspondence: J. Pillow, TVW Telethon Institute for Child Health Research, PO Box 855, West Perth 6872, Western Australia, Australia (E-mail: janep{at}ichr.uwa.edu.au).
Received 16 October 1998; accepted in final form 4 March 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
APPENDIX A
APPENDIX B
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1.
Allen, J.,
I. Frantz III,
and
J. Fredberg.
Heterogeneity of mean alveolar pressure during high-frequency oscillations.
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62:
223-228,
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Bancalari, A.,
T. Gerhardt,
E. Bancalari,
C. Suguihara,
D. Hehre,
L. Reifenberg,
and
R. Goldberg.
Gas trapping with high-frequency ventilation: jet versus oscillatory ventilation.
J. Pediatr.
110:
617-622,
1987[Medline].
3.
Bancalari, E.
Inadvertent positive end-expiratory pressure during mechanical ventilation.
J. Pediatr.
108:
567-569,
1986[Medline].
4.
Bates, J. H.,
P. D. Sly,
J. Sato,
B. L. Davey,
and
B. Suki.
Correcting for the Bernoulli effect in lateral pressure measurements.
Pediatr. Pulmonol.
12:
251-256,
1992[Medline].
5.
Bryan, A.,
and
A. Slutsky.
Long volume during high-frequency oscillation.
Am. Rev. Respir. Dis.
133:
928-930,
1986[Medline].
6.
Bush, E.,
D. Spahn,
P. Niederer,
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) and 1:2 (
). Each data point in A represents a single
observation of 
with different symbols
representing different animals. Each data point in B represents
mean ± SE at each amplitude and I/E ratio. In both lung models at
1:1, mean PA was not substantially different from mean Pao,
whereas at 1:2, mean PA was considerably lower than mean
Pao.
The effect of tidal volume (A
and C), % inspiratory time (B), and model lung
compliance (D) on the magnitude of
