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Open Access

What is a pressure–volume curve?

Critical Care200610:156

https://doi.org/10.1186/cc5002

Published: 10 August 2006

Abstract

The pressure–volume (PV) curve is a physiological tool proposed for diagnostic or monitoring purposes during mechanical ventilation of acute respiratory distress syndrome. The reduction in compliance measured by the PV curve and the different inflection points on the curve are considered interesting markers of the severity of and the levels of opening and closing pressures. Tracing a curve, however, may in itself influence the degree of opening or distension of the lung, and interpretation of the curve has to take this effect into account. In some individuals tracing the curve may even have moderate hemodynamic effects. Fortunately, on average, most of these effects are transient or negligible and do not invalidate the PV curve measurement.

Keywords

Acute Lung InjuryAcute Respiratory Distress SyndromeFunctional Residual CapacityAcute Respiratory Distress Syndrome PatientRecruitment Maneuver

The pressure–volume (PV) curve is a diagnostic or monitoring technique proposed soon after the initial description of acute respiratory distress syndrome (ARDS) [1]. The PV curve was really identified as a potentially important tool, however, by Matamis and colleagues [2], who described the relationship between alterations in respiratory mechanics and the stage of acute lung injury. The PV curve is usually traced from the elastic equilibrium lung volume that corresponds either to the functional residual capacity or to the end-expiratory lung volume. The end-expiratory lung volume can be greater than the residual capacity in the case of air trapping or of ventilation with positive end-expiratory pressure (PEEP).

The classic shape of the PV curve in ARDS patients is more or less sigmoidal, with a general slope (i.e. compliance of the respiratory system) that is markedly reduced compared with normal subjects. The curve is obtained by slowly insufflating the chest, either continuously or in a series of small steps [2, 3]. The PV curve is generally viewed as consisting of three segments separated by two inflection points; or, for other authors, it can also be described as a true sigmoid [4]. The first segment, characterized by low compliance, is separated from a more linear part of the curve by the lower inflection point. The intermediate segment can be considered linear and is used to measure the 'linear' compliance between the lower inflection point and the upper inflection point. Beyond the upper inflection point, the PV curve tends to flatten again.

The reduction in linear compliance measured by the PV curve is considered a hallmark of ARDS and is usually explained chiefly by the loss of aerated lung volume. Lung areas with a normal appearance on plain radiograph scans, however, show increases in lung tissue despite preserved aeration on computed tomography images, indicating that lung tissue alterations are diffuse in ARDS [5].

A weak but significant correlation between compliance and markers for collagen turnover was recently described [6], with a logarithmic pattern consistent with a model of collagen-dependent maximal distension. This model reflects the mechanical characteristics of elastin and collagen from freshly excised peripheral pulmonary parenchyma. The model suggests that, until collagen deposition reaches a threshold level, chord compliance is not influenced by or is only slightly influenced by collagen turnover. A reduction of chord compliance until around 30 ml/cmH2O is therefore essentially a result of a lung volume reduction. Compliance beyond this value may also be limited by collagen deposition, which at the cellular level is called the 'collagen-dependent maximal distension'. One can model the anatomical units of the fibrous skeleton of the lung as being made of extensible elastin and inextensible collagen, which are 'folded' in the lung resting position [7]. The limits of distension are dictated by the inextensible collagen fibers, which work as a 'stop-length' system. The significant correlation linking compliance to biological markers suggests that compliance may be also affected by alveolar remodeling.

The volume recruited by PEEP is usually assessed based on the static PV curve of the respiratory system. Alveolar recruitment leads to an upward shift along the volume axis of the PV curve with PEEP, compared with the curve with zero end-expiratory pressure, and is quantified as the volume increase with PEEP at the same elastic pressure [8, 9].

The technique used to perform the PV curve has been the subject of enormous attention. The three major questions regarding the technique are as follows. To what extent are the findings artifactual? What are the feasibility and the reproducibility of the different techniques? Does the measurement by itself affect the underlying physiology?

The first question (artifactual findings) was related both to the technique (e.g. gas exchange occurring during a prolonged insufflation and deflation with the super-syringe technique [10]) and to the findings in general. Since the measurements are performed during static (or quasi-static) maneuvers, are we measuring phenomena that are relevant during mechanical ventilation (opening and closing of lung units) or is the observation related to the artificial derecruitment imposed by a prolonged expiration to functional residual capacity [11]? There is ample evidence that, during single expirations to lower PEEP values, a derecruitment occurs that becomes more and more pronounced at lower PEEP values, while recruitment continues up to 35–45 cmH2O during the following reinflation – but the whole picture may be very different during the course of mechanical ventilation from that during a single PV curve maneuver.

The second question (feasibility and reproducibility) has received relatively little attention, but research seems to indicate that the reproducibility is reasonably good [11, 12].

The final question is the object of investigation of the study by the group of Papazian in the present issue [13]. Many questions could be addressed regarding the influence of the PV curve measurement on the end-expiratory lung volume, hemodynamics and gas exchange. The authors produced PV curves with two different techniques in patients with acute lung injury and examined arterial blood gas changes in the 2 hours following recordings of each curve. The authors concluded that no significant (or substantial) influence existed on gas exchange in the group as a whole; this was far from true at an individual level, however, and changes occurred in different directions in terms of oxygenation or partial pressure of CO2. The PV curve is a kind of recruitment maneuver. The influence of this recruitment maneuver in many patients is again limited in terms of time and effect, but these effects may be larger than expected if the pressure used is markedly higher than the plateau pressure during the course of mechanical ventilation.

Among different patients, Papazian's group found sustained increases in PaO2, decreases in PaO2 and increases in PaCO2. Although it is difficult to speculate without having more precise data from these patients, several mechanisms can be at work explaining these effects. An increase in oxygenation may easily be explained by the reopening of some areas of the lungs, which were perfused but nonventilated; the increase in oxygenation could have occurred because these areas remained open after the maneuver. A sustained increase in lung volume after determining such PV curves has been observed [14]. A decrease in oxygenation may have resulted from adverse hemodynamic effects resulting in reduced mixed venous oxygen content, especially in patients with limited cardiorespiratory reserve. This may have been facilitated by hypovolemia and impediment to venous return, although this effect should not last long after the end of the maneuver. In patients with ARDS, the problem may be more at the right ventricular level, functioning on the edge of cardiac failure because of severe pulmonary hypertension. A recruitment maneuver can markedly increase the right ventricle afterload, can induce right ventricle dilation and can decrease left ventricular size and function. This was recently illustrated by Nielsen and colleagues [15]. The finding of an increased PaCO2 level may result from the same mechanism. It may also result from the reopening of nonperfused or poorly perfused previously collapsed alveoli. Finally, this finding may be explained by persisting overdistension after the maneuver, especially if some degree of hypovolemia was present, generating high ventilation–perfusion areas or non zone III of the lungs.

The merit of the study by Papazian's group is that it examines, in a systematic manner, the impact of a diagnostic or monitoring technique on the patient's underlying physiology. Studies like this are needed, especially in the intensive care unit setting, to more systematically address the impact of various diagnostic techniques on the underlying physiology or clinical course of patient. The PV curve acts like a recruitment maneuver, and the interpretation of the clinical management incorporating this tool must take this fact into account. Fortunately, as shown in this study, the observed effects of this maneuver are limited or insignificant in many, but not all, patients.

Abbreviations

ARDS = : 

acute respiratory distress syndrome

PEEP = : 

positive end-expiratory pressure

PV = : 

pressure–volume.

Declarations

Authors’ Affiliations

(1)
Réanimation Médicale, AP-HP, Hôpital Henri Mondor, Université Paris XII, INSERM U651, Créteil, France

References

  1. Falke KJ, Pontoppidan H, Kumar A, Leith DE, Geffin B, Laver HB: Ventilation with positive end-expiratory pressure in acute lung disease. J Clin Invest 1972, 51: 2315-2323.PubMed CentralView ArticlePubMedGoogle Scholar
  2. Matamis D, Lemaire F, Harf A, Brun-Buisson C, Ansquer JC, Atlan G: Total respiratory pressure–volume curves in the adult respiratory distress syndrome. Chest 1984, 86: 58-66.View ArticlePubMedGoogle Scholar
  3. Jonson B, Richard J-C, Straus C, Mancebo J, Lemaire F, Brochard L: Pressure–volume curves and compliance in acute lung injury. Evidence of recruitment above the lower inflection point. Am J Respir Crit Care Med 1999, 159: 1172-1178.View ArticlePubMedGoogle Scholar
  4. Harris RS, Hess DR, Venegas JG: An objective analysis ofthe pressure–volume curve in the acute respiratory distress syndrome. Am J Respir Crit Care Med 2000, 161: 432-439.View ArticlePubMedGoogle Scholar
  5. Puybasset L, Cluzel P, Gusman P, Grenier P, Preteux F, Rouby J-J: Regional distribution of gas and tissue in ARDS. I consequences for lung morphology. Intensive Care Med 2000, 26: 857-869. 10.1007/s001340051274View ArticlePubMedGoogle Scholar
  6. Demoule A, Decailliot F, Jonson B, Christov C, Maitre B, Touqui L, Brochard L, Delclaux C: Relationship between pressure–volume curve and markers for collagen turn-over in early acute respiratory distress syndrome. Intensive Care Med 2006, 32: 413-420. 10.1007/s00134-005-0043-zView ArticlePubMedGoogle Scholar
  7. Gattinoni L, Pesenti A: The concept of 'baby lung'. Intensive Care Med 2005, 31: 776-784. 10.1007/s00134-005-2627-zView ArticlePubMedGoogle Scholar
  8. Jonson B, Svantesson C: Elastic pressure–volume curves: what information do they convey? Thorax 1999, 54: 82-87.PubMed CentralView ArticlePubMedGoogle Scholar
  9. Ranieri MV, Giuliani R, Fiore T, Dambrosio M, Milic-Emili J: Volume–pressure curve of the respiratory system predicts effects of PEEP in ARDS: 'occlusion' versus 'constant flow' technique. Am J Respir Crit Care Med 1994, 149: 19-27.View ArticlePubMedGoogle Scholar
  10. Gattinoni L, Mascheroni D, Basilico E, Foti G, Pesenti A, Avalli L: Volume/pressure curve of total respiratory system in paralysed patients: artefacts and correction factors. Intensive Care Med 1987, 13: 19-25. 10.1007/BF00263552View ArticlePubMedGoogle Scholar
  11. Brochard L: Pressure–volume curves. In Principles and Practice of Respiratory Monitoring. Edited by: Tobin MJ. New York: McGraw-Hill, Inc.; 1998:579-616.Google Scholar
  12. Mehta S, Stewart TE, MacDonald R, Hallett D, Banayan D, Lapinsky S, Slutsky A: Temporal change, reproducibility, and interobserver variability in pressure–volume curves in adults with acute lung injury and acute respiratory distress syndrome. Crit Care Med 2003, 31: 2118-2125. 10.1097/01.CCM.0000069342.00360.9FView ArticlePubMedGoogle Scholar
  13. Roch A, Forel JM, Demory D, Arnal JM, Donati S, Gainnier M, Papazian L: Generation of a single pulmonary pressure–volume curve does not durably affect oxygenation in ARDS patients. Crit Care 2006, 10: R85. 10.1186/cc4936PubMed CentralView ArticlePubMedGoogle Scholar
  14. Maggiore SM, Jonson B, Richard JC, Jaber S, Lemaire F, Brochard L: Alveolar derecruitment at decremental positive end-expiratory pressure levels in acute lung injury: comparison with the lower inflection point, oxygenation, and compliance. Am J Respir Crit Care Med 2001, 164: 795-801.View ArticlePubMedGoogle Scholar
  15. Nielsen J, Ostergaard M, Kjaergaard J, Tingleff J, Berthelsen PG, Nygard E, Larsson A: Lung recruitment maneuver depresses central hemodynamics in patients following cardiac surgery. Intensive Care Med 2005, 31: 1189-1194. 10.1007/s00134-005-2732-zView ArticlePubMedGoogle Scholar

Copyright

© BioMed Central Ltd 2006

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