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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
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Airway Suction and Lung Spirometry

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