
Clinical Window Educational Program
is sponsored by GE Healthcare

Clinical Window Web Journal
complies with the
HON code standard for
trustworthy health information:
verify
here.
Educational collaboration:

Clinical Window
is main sponsor for this concise, textbook style website of anaesthesiology
|
 |
 |
 |
|
Issue
24, June 2008
Airway
Suction and Lung Spirometry
|
Alveolar P/V curves reflecting regional lung
mechanics
Prof. Ola Stenqvist MD |
Prof.
Ola Stenqvist, MD, PhD
Dept of Anaesthesiology and Intensive Care
Sahlgrenska University Hospital
Gothenburg, Sweden
|
Correspondence: Prof. Ola Stenqvist, MD. Gothenburg,
Sweden. (E-mail and other contact info can be obtained from CWWJ’s
Editor-in-Chief).
Key Words: Lung Function, regional lung mechanics, mechanical
ventilation, dynostatic algorithm, Spirodynamics
Running title: Regional lung mechanics.
Clinical Window Web Journal #24: Alveolar P/V curves reflecting regional
lung mechanics (June 2008). ISSN 1795-6269. [www.clinicalwindow.net]
P/V –curve as the
gold standard
The static P/V-curve has been regarded as the gold standard tool for assessment
of the mechanical properties of the lung. On this curve, a lower inflection
point (LIP) can, in some patients, be detected and, in most patients,
an upper inflection point (UIP) can be seen. The most common interpretation
of the LIP and the UIP is that LIP represents the point where alveoli
collapse at end of expiration and reopen at start of inspiration. On the
other hand, UIP represents the pressure above which alveoli become over-distended.
To avoid cyclic closing and opening and over-distension of alveoli, ventilation
should be performed with pressures between the LIP and UIP, where the
compliance of the lungs is highest.
The background of LIP is much more complex and various hypotheses have
been promoted. In anesthesia, absorption atelectasis could be the cause
of LIP. Gattinoni and coworkers have proposed that the weight of the edematous
ALI/ARDS lung results in a superimposed pressure, increasing vertically,
causing a collapse of the most dorsal lung parts (1, 2). The LIP should,
according to this, be the pressure that is high enough to counteract the
threshold opening pressure and the superimposed pressure. This hypothesis
has been further analyzed in a mathematical model by Hickling (3), who
describes a continuous recruitment process during inflation. Hubmayr (4)
has argued against this interpretation and favors a hypothesis whereby
the LIP is caused by a gas/fluid interface in flooded lung parts.
Lung size vs. compliance
In the lung mechanics literature, the focus has been on the pressure level
of LIP, but very little is mentioned about the volume where LIP is positioned.
Clinical data are scarce, but from published figures of P/V curves (5,
6, 7), the volume can be estimated to lie between 50 and 150 ml. Compliance
below the LIP can be estimated to be 5 -20 ml/cmH2O, based on these figures.
In this context, it is important to realize that compliance is closely
related to the size of the lung. Thus, if you apply pressure control ventilation
to either a mouse or an elephant, with a pressure that results in normocapnia
in a normal size human, you will have normocapnia in both of these animals,
as the compliance of the elephant lung is enormous and that of the mouse
is very low.
Gattinoni has promoted the baby lung concept, where the ALI/ARDS patient
is supposed to have a part of the lung collapsed and the rest –
a small but supposedly healthy lung – a “baby lung”
that is quite normal (8). This dichotomic view of the ALI/ARDS lung may
be questioned, as it is most likely that the best parts of the lung are
also to some extent affected, with a lowered compliance as the result.
When a pressure volume curve for such a lung is obtained, the compliance
below the LIP will be low, representing compliance of the baby lung. The
compliance of this baby lung will be dependent on its size; the smaller
the baby lung, the lower the compliance. As the inflation continues and
more alveoli are recruited, compliance will increase until alveoli at
the very bottom of the lung with very low compliance are recruited, seen
as an upper inflection point.
The reason for elaborating on this point is that the relationship between
the size of the lung and compliance is fundamental for understanding the
P/V curve. If a healthy lung is divided into, for example, 5 vertical
parts with the same end expiratory size, and compliance is measured for
each of these parts of the lung, it would be a fifth of the total compliance
(Fig.1). If an ALI/ARDS lung with a lowered total compliance of 30 ml/cmH2O
is divided in the same way, the most ventral part would have the highest
compliance and the most dependent part the lowest compliance, because
of the superimposed pressure from the edematous tissue. The compliance
of these five parts would, when summed, result in a total compliance of
30 ml/cm H2O and could, if the superimposed pressure is increasing linearly,
be 10, 8, 6, 4 and 2 ml/cm H2O from top to bottom of the lung. If the
three most dependent compartments of the lung are collapsed, and the two
ventral compartments have the same properties, the total compliance would
only be 10 + 8 = 18 ml/cm H2O.

The path
of highest compliance
In ALI/ARDS, increased resistance is not a major factor; therefore, instead
of gas moving along the path of least resistance, we will see the gas
moving along the path of highest compliance.
Following the path of highest compliance, when inflation is started in
such a lung, the initial gas will naturally flow towards the non-dependent
lung with highest compliance (Fig. 2). Continuously during the inflation,
when pressure increases, the alveoli of this part of the lung will be
expanded. Prior to this, as pressure rises, gas will flow to more dorsal
parts of the lung, where compliance is lower. When the pressure is high
enough to inflate the most dorsal parts of the lung, the alveoli of the
most ventral parts are already stretched to their structural limits and
will not expand any further. This will result in the final part of the
P/V curve deflecting, as a sign of low compliance in the dependent part
of the lung, rather than a sign of over-distension of the ventral part
of the lung. The term over-distension is misleading, as the deflection
of the P/V curve indicates that pressure rises more than volume. If there
was true over-distension, i.e. the alveolar wall yielding to the pressure
(and finally bursting), the P/V curve would show an increase in compliance
instead of a decrease. The P/V curve of this lung will show a continuously
decreasing compliance as inflation proceeds and there will be no LIP,
as in this case, all 5 compartments of the lung were already open from
the start of the inflation.

Volume dependent compliance
Let us consider the behavior of the second example of a 5-compartment
lung, where the three most dependent compartments are collapsed during
an inflation (Fig. 3). In this case, the initial compliance will be 18
ml/cm H2O and, when the airway pressure is high enough to overcome the
superimposed pressure as well as the threshold opening pressure of the
mid compartment alveoli (the most non-dependent compartment of the three
collapsed compartments), compliance will increase by 6 ml/cm H2O, which
is the compliance of that very compartment. This sudden increase in compliance
will result in a LIP of the P/V curve. As the airway pressure increases
enough to open or recruit the two most dependent compartments, compliance
will further increase by 4 and 2 ml/cmH2O. When inflation proceeds, the
P/V-curve will show a continuous decrease in compliance, as in the above
example, where all five compartments were open from the start of inflation.
The changing of compliance along the P/V curve, i.e. volume dependent
compliance, indicates that different parts of the lung have different
properties. Normally, the regional differences are arranged along a vertical
axis, so that the highest compliance of the P/V curve represents the most
ventral parts of the lung and the lowest compliance the most dependent,
dorsal part of the lung. However, in singular cases, the regional differences
in mechanical properties of the lung occur more randomly. In any case,
whether regional differences in compliance are arranged vertically or
randomly, the volume dependent compliance of the P/V curve is a measurement
of these differences.

The pressure volume loop
So far, all references to P/V curves are static P/V curves, which are
rarely used in clinical practice. The most common lung mechanics monitoring
modality is the pressure volume loop, based on pressure and flow measured
in the ventilator or at the Y-piece. These dynamic loops are influenced
to a high degree by the endotracheal tube resistance, which distorts the
loop, resulting in a right shift of the inspiratory limb and a left shift
of the expiratory limb of the loop. A loop that represents the lung mechanics
more closely can be obtained by plotting the tracheal pressure versus
volume instead. The tracheal pressure can either be calculated from the
y-piece airway pressure and an algorithm for the endotracheal tube resistance
(9) or measured directly by insertion of a narrow pressure line through
the tube (10). From the tracheal pressure loop, an alveolar pressure volume
curve can be obtained by multiple linear regression analysis of the loop,
which is divided into six slices, where compliance is assumed to be constant
within each slice, for volume dependent compliance calculations (11).
The dynamic alveolar pressure
volume curve
We have selected to use another approach for obtaining an alveolar pressure
volume curve from direct tracheal pressure measurements: The dynostatic
algorithm. This algorithm is based on the assumption that inspiratory
and expiratory resistance of the airway is reasonably similar at the same
lung volume, during inspiration and expiration (12,13). The most prominent
feature of the dynamic alveolar pressure volume curve, which represents
the mechanic properties of the lung during on-going therapeutic ventilation,
is that compliance is lower than compliance of the static P/V curve of
the same patient. Also, if any LIP is present in the dynamic P/V curve
it is usually not very prominent. As well, the UIP is not an inflection
point, but rather a zone of decreasing compliance.
The reason for this difference in behavior of the lung during static and
dynamic conditions can probably be explained by the time factor playing
a more important role than expected. Thus, in five patients with acute
respiratory failure, we measured conventional quasistatic compliance and
FRC with a modified nitrogen washout/washin technique (14) at two different
PEEP levels. We found an increase in FRC close to 400 ml when PEEP was
increased 3 cm H2O. If conventional quasistatic compliance was used for
predicting the increase in FRC as a result of such a PEEP increase, the
FRC would only have increased by about 150 ml. The compliance of the lung,
calculated as the ?FRC/?PEEP, was twice as high as the conventional quasistatic
compliance. This indicates that the mechanical properties of the respiratory
system differ when subjected to fast and slow procedures. This is further
emphasized by the findings of a study on one lung lavaged piglet using
electric impedance tomography (15). Regional analysis of ventilation in
four ventral – dorsal compartments of the lung revealed that ventilation
in the two most dependent regions did not occur, even at the end of inspiration,
when the pressure was between 15 and 20 cm H2O. When the PEEP level was
increased to 15 cm H2O, there was ventilation in these regions already
from start of the inspiration at 15 cm H2O. Thus, although the peak pressure
was 20 cm H2O at ZEEP, and exceeded the 15 cm H2O level that was needed
to create tidal ventilation in the most dorsal region, such a tidal ventilation
was not seen.
There are several studies (16, 17) indicating that a low tidal volume
ventilation causes less damage to the alveoli than a high tidal volume.
The level of PEEP seems to have less impact on ventilator induced lung
injury, as long as it is not set at very low levels or at 0 cmH2O. The
reason for lung damage at low PEEP levels is most likely widespread, preferentially
dorsal, lung collapse. However, the upper inflection point of the static
or the dynamic P/V curve does not represent over-distension, but rather
recruitment of the most dorsal lung compartments with the lowest compliance,
during the last part of the inspiration, followed by the same alveoli
collapsing during the beginning of the expiration. During static measurements,
this occurs at a higher lung volume than during dynamic conditions. This
indicates that, in patients, it is important to monitor the lung mechanics
during prevailing conditions, in order to be able to set the ventilator
optimally.
Conclusions
> The compliance below the LIP, when present, is usually very
low, indicating that only a small lung volume is open when inspiration
starts.
> The LIP of a dynamic P/V curve is usually not very prominent, as
compared with the LIP of a static P/V curve.
> There is probably no LIP without partial lung collapse.
> The UIP is not a sign of over-distension, but rather a sign of low
compliant, dorsal lung parts being recruited at the end of the inspiration,
when the most compliant, ventral parts of the lung do not expand any further.
References
1. Gattinoni, D´Andrea, Pelosi, Vitale, Pesenti, Fumagalli. Regional
effects and mechanism of positive end-expiratory pressure in early adult
respiratory distress syndrome. JAMA 1993: 269: 2122
2. Gattinoni, Pelosi, Crotti, Valenza. Effects of positive end-expiratory
pressure on regional distribution of tidal volume and recruitment in adult
respiratory distress syndrome. Am J Respir Crit Care Med. 1995: 151: 1807
3. Hickling. Best compliance during a decremental, but not incremental,
positive end-expiratory pressure trial is related to open-lung positive
end-expiratory pressure. Am J Crit Care Med 2001: 163: 69
4. Hubmayr. Perspective on lung injury recruitment. Am J Crit Care Med
2002: 165: 1647
5. Gattinoni, Pesenti, Avalli, Rossi, Bombino. Pressure-volume curve of
total respiratory system in acute respiratory failure. Am J Respir Dis
1987: 136: 730
6. Masry, Kacmarek. Lung recruitment and the setting of PEEP in ALI/ARDS.
Yearbook of Intensive Care and Emergency Medicine. Springer. 2004: 444.
7. Mergoni, Martelli, Volpi, Primavera, Zuccoli, Rossi. Impact of positive
end-expiratory pressure on chest wall and lung pressure-volume curve in
acute respiratory failure. Am J Crit Care Med 1997: 156: 846
8. Gattinoni, Pesenti. The concept of "baby lung". Intens Care
Med 2005: 31: 776
9. Guttmann, Eberhard, Fabry, Bertschmann, Wolff. Continuous calculation
of intratracheal pressure in tracheally intubated patients. Anesthesiology
1993: 79: 503
10. Karason, Sondergaard, Lundin, Wiklund, Stenqvist. Direct tracheal
airway pressure measurements, essential for accurate and safe monitoring
of tracheal pressures. Acta Anaesthesiol Scand 2001: 45: 173
11. Mols, Brandes, Kessler, Lichtwarck-Aschoff, Loop, Geigert, Guttmann.
Volume-dependent compliance in ARDS: A proposal of a new diagnostic concept.
Intens Care Med 1999: 25: 1084
12. Karason, Sondergaard, Lundin, Wiklund, Stenqvist. A new method for
non-invasive, manoeuvre-free determination of “static” pressure-volume
curves during dynamic/therapeutic mechanical ventilation. Acta Anaesthesiol
Scand 2000: 44: 578
13. Sondergaard, Karason, Wiklund, Lundin, Stenqvist. Alveolar pressure
monitoring: an evaluation in a lung model and in patients with acute lung
injury. Intens Care Med 2003: 29: 955
14. Olegard, Söndergaard, Houltz, Lundin, Stenqvist. Estimation of
functional residual capacity at the bedside using standard monitoring
equipment: A modified nitrogen washout/washin technique requiring a small
change of the inspired oxygen fraction. Anesth Analg 2005: 101: 206
15. Frerichs, Dargaville, Dudykevvych, Rimensberger. Electrical impedance
tomography: a method for monitoring regional lung aeration and tidal volume
distribution? Intens Care Med 2003: 29: 2312
16. Amato, Barbas, Medeiros, Magaldi, Schettino, Lorenzi-Filho, Kairalla,
Deheinzelin, Munoz, Oliveira, Takagaki, Carvalho. Effect of a protective-ventilation
strategy on mortality in the acute respiratory distress syndrome. N Engl
J Med 1998: 338: 347
17. The Acute Respiratory Distress Syndrome Network. Ventilation with
lower tidal volumes as compared with traditional tidal volumes for acute
lung injury and the acute respiratory distress syndrome. N Engl J Med
2000: 342: 1301
Clinical Window Web Journal #24: Alveolar P/V curves reflecting regional
lung mechanics (June 2008). ISSN 1795-6269. [www.clinicalwindow.net]
© 2006-2008 GE Healthcare Finland Oy doing business
as GE Healthcare. All rights reserved. The copyright, any and all trademarks
and trade names and other intellectual property rights subsisting in or
used in connection with and related to this publication are, unless another
owner is specified, the property of GE Healthcare. No part of this publication
may be reproduced, stored in a retrieval system, or transmitted, in any
form or by any means, electronic, mechanical, photocopying, recording
or otherwise, without the prior written permission of GE Healthcare.
Last updated: 20
June 2008 |
 |
| Legal
notice |
© GE
Healthcare 2008
ISSN 1795-6269 (Web)
ISSN 1795-6277 (CD) |
Webmaster |
|
 |
|