Novel aspects of pulmonary mechanics in intensive care
2003; Elsevier BV; Volume: 91; Issue: 1 Linguagem: Inglês
10.1093/bja/aeg146
ISSN1471-6771
Autores Tópico(s)Airway Management and Intubation Techniques
ResumoThis review of the mechanical properties of the respiratory system is related to ventilator practice. As virtually all modern ventilators display traces of airway pressure (Paw), volume (V) and flow (V˙) the necessary information is immediately available with no additional effort. This review interprets the information contained in ventilator waveforms. The review concentrates on three aspects where measurements are most useful, namely: (i) the diagnosis and management of patients with injured lungs; (iii) patients with airways obstruction; and (iii) the assessment of respiratory motor output. We will outline the precision and accuracy of the derived variables, discuss their scientific basis and review how decisions based on these measurements improve patient outcomes. We give a personal perspective even if it means taking sides in debates on controversial issues. (For a full discussion of classic respiratory system mechanics the reader is referred to refs 6Bates JHT Assessment of mechanics.in: Lenfant C Marini JJ Slutsky AS Physiological Basis of Ventilatory Support. Lung Biology in Health and Disease Series, Chapter 7. Vol 118. Marcel Dekker, Inc., New York1998: 231-256Google Scholar and 47Loring SH Mechanics of the Lung and Chest Wall.in: Lenfant C Marini JJ Slutsky AS Physiological Basis of Ventilatory Support. Lung Biology in Health and Disease series, Chapter 5. Vol 118. Marcel Dekker, Inc., New York1998: 177-205Google Scholar). Classic respiratory mechanics is based on Newtonian physics as expressed in the equation of motion. The respiratory system is considered to be a resistive and elastic element in series. Any pressure applied to it is either stored as elastic pressure (Pel) or dissipated as resistive pressure (Pres) P(t)=Pel(t)+Pres(t)(1) where t indicates a particular time. In its simplest interpretation the elastic element represents lungs and chest wall, while the resistive element represents ventilator tubing, tracheal tube and airways (we will discuss the pitfalls and limitations of this simplistic model in the context of the specific applications). It follows that during inflation of the relaxed respiratory system Pel can be approximated by alveolar pressure (Palv) and Pres by the difference between proximal airway pressure (Paw) and Palv. Pel(t)=Palv(t)(2) and Pres(t)=Paw(t) – Palv(t)(3) If flow is zero then Palv equilibrates with Paw so that Pel can be estimated from airway occlusion pressure. This is how a static recoil pressure–volume curve measurement is made. As Pel is a function of volume and Pres a function of flow Equation 1 can be rewritten as P(t)=Po+EV(t)+RV˙(t)(4) where Po is the elastic recoil pressure at relaxed end-expiration. In the clinical literature Po is often referred to as total PEEP. The constants E and R denote respiratory elastance and resistance and are the factors that scale volume and flow to yield Pel and Pres, respectively. Clinicians are more likely to use the term compliance (C), which is the inverse of E. During relaxed expiration, flow is generated by Palv (relative to Paw), in that it is determined by the elastic recoil of the respiratory system and by the properties of the resistive element (i.e. properties of airway, tracheal tube and equipment). As both determinants vary with lung volume, so must passive expiratory flow. In normal lungs expiratory flow varies approximately linearly with volume and decreases exponentially with time. Rearranging Equation 4 shows that the slope of the passive expiratory volume flow relationship equals R/E (or R*C), which has the units of time. This quantity is the time constant of the respiratory system and defines the time it takes for the elastic element to passively empty approximately 63% of its contents. Inspection of linearity and slope of the expiratory flow–volume curve can be useful when a diagnosis of airway or tracheal tube obstruction is suspected (see page 85). The realization that the physical stress of mechanical ventilation can damage lungs or may amplify non-physical injury mechanisms has generated renewed interest in the mechanics of injured lungs.21Dreyfuss D Saumon G Ventilator-induced lung injury: lessons from experimental studies.Am J Respir Crit Care Med. 1998; 157: 294-323Crossref PubMed Scopus (1871) Google Scholar Publications on this topic have increased exponentially in the last decade (Fig. 1). An International Consensus Conference held in 1993 defined acute lung injury (ALI) and adult respiratory distress syndrome (ARDS) as conditions characterized by abnormal pulmonary gas exchange in the presence of bilateral pulmonary infiltrates.10Bernard GR Artigas A Brigham KL et al.Report of the American-European consensus conference on ARDS: definitions, mechanisms, relevant outcomes and clinical trial coordination. The Consensus Committee.Am J Respir Crit Care Med. 1994; 149: 818-824Crossref PubMed Scopus (5301) Google Scholar These features are non-specific, and must be related to the clinical setting and not attributed to left heart failure. ALI and ARDS differ only with respect to the severity of the gas exchange impairment and have a wide variety of causes. Irrespective of cause, injured lungs have an abnormal barrier function. The pulmonary capillaries are leaky and the alveolar epithelial cells cannot clear water and solute from the alveolar space properly,11Berthiaume Y Folkesson HG Matthay MA Lung edema clearance: 20 years of progress: invited review: alveolar edema fluid clearance in the injured lung.J Appl Physiol. 2002; 93: 2207-2213Crossref PubMed Scopus (103) Google Scholar with important consequences for the mechanical properties of the lung. Injury and oedema increase pulmonary elastance and resistance.23Eissa NT Ranieri VM Corbeil C et al.Analysis of behavior of the respiratory system in ARDS patients: effects of flow volume and time.J Appl Physiol. 1991; 70: 2719-2729Crossref PubMed Scopus (2) Google Scholar 84Tantucci J Corbeil C Chassé M et al.Flow and volume dependence of respiratory system resistance in patients with adult respiratory distress syndrome.Am Rev Respir Dis. 1992; 145: 355-360Crossref PubMed Google Scholar Numerous mechanisms have been proposed to explain this. Presently the most popular one is the ‘baby lung’ concept: alveolar flooding causes ‘collapse’ of the dependent lung so the greater lung elastance reflects the reduced number and smaller volume of near normal, non-dependent, and recruitable units.28Gattinoni L D'Andrea Ll Pelosi P Vitale G Fumagalli R Regional effects and mechanism of positive end expiratory pressure in early adult respiratory distress syndrome.JAMA. 1993; 269: 2122-2127Crossref PubMed Scopus (390) Google Scholar Other proposed mechanisms include increased surface tension by inactivation of surfactant,80Spragg RG Lewis JF Pathology of the surfactant system of a mature lung: Second San Diego Conference.Am J Resir Crit Care Med. 2001; 163: 280-282Crossref PubMed Scopus (14) Google Scholar airway block by air–liquid interfaces and bubble formation in small airways,16Cook CD Mead J Schreiner GL Frank NR Craig JM Pulmonary mechanics during induced pulmonary edema in anesthetized dogs.J Appl Physiol. 1959; 14: 177-186Crossref PubMed Scopus (83) Google Scholar 18Delaunois L Sergysels R Martin RR Acute effects on airways mechanics of pulmonary edema induced by intravenous oleic acid in dogs.Bull Eur Physiopath Respir. 1980; 16: 47-55PubMed Google Scholar 54Martynowicz MA Minor TA Walters BJ Hubmayr RD Regional expansion of oleic acid-injured lungs.Am J Respir Crit Care Med. 1999; 160: 250-258Crossref PubMed Scopus (125) Google Scholar 92Wilson TA Anafi RC Hubmayr RD Mechanics of edematous lungs.J Appl Physiol. 2001; 90: 2088-2093PubMed Google Scholar reflex-broncho-constriction,15Chung KF Keyes SJ Morgan BM Jones PW Snashall PD Mechanisms of airway narrowing in acute pulmonary edema in dogs: influence of the vagus and lung volume.Clin Sci. 1983; 65: 289-296Crossref PubMed Scopus (21) Google Scholar 19Derks CM D'Hollander AA Jacobovitz-Derks D Gas exchange and respiratory mechanics in moderate and severe pulmonary oedema in dogs.Bull Eur Physiopath Respir. 1981; 17: 163-177PubMed Google Scholar pneumo-constriction caused by release of inflammatory mediators24Esbenshade AM Newman JH Lams PM Jolles H Brigham KL Respiratory failure after endotoxin infusion in sheep: lung mechanics and lung fluid balance.J Appl Physiol. 1982; 53: 967-976Crossref PubMed Scopus (132) Google Scholar and peribronchial oedema.18Delaunois L Sergysels R Martin RR Acute effects on airways mechanics of pulmonary edema induced by intravenous oleic acid in dogs.Bull Eur Physiopath Respir. 1980; 16: 47-55PubMed Google Scholar Two attributes of the injured lung explain its susceptibility to additional ventilator induced lung injury: (i) the number of alveoli that can expand during inspiration is decreased and (ii) the distribution of liquid and surface tension varies in distal airspaces and hence the local impedances to lung expansion are heterogeneous.5Bachofen H Schürch S Michel RP Weibel ER Experimental hydrostatic pulmonary edema in rabbit lungs: morphology.Am Rev Respir Dis. 1993; 147: 989-996Crossref PubMed Scopus (93) Google Scholar 42Hubmayr RD Perspective on lung injury and recruitment: a skeptical look at the opening and collapse story.Am J Respir Crit Care Med. 2002; 165: 1647-1653Crossref PubMed Scopus (264) Google Scholar The first attribute is the key abnormality in the ‘baby lung concept’.29Gattinoni L Pesenti A Avalli L et al.Pressure–volume curve of total respiratory system in acute respiratory failure: computed tomographic scan study.Am Rev Respir Dis. 1987; 136: 730-736Crossref PubMed Scopus (686) Google Scholar It explains the increased risk of lung injury from overdistension of aerated low impedance units. The second attribute, heterogeneity in regional impedances to lung expansion, has several consequences. One is a large shear stress between neighbouring, interdependent units that operate at different volumes. Tissue attachments between large aerated units and smaller neighbouring flooded or collapsed units carry a stress that is substantially greater than the average transpulmonary pressure.56Mead J Takashima T Leith D Stress distribution in lungs: a model of pulmonary elasticity.J Appl Physiol. 1970; 28: 596-603Crossref PubMed Scopus (1024) Google Scholar Another consequence is injury to small airways and alveolar ducts caused by their repeated opening and collapse,60Muscedere JG Mullen JB Gan K Slutsky AS Tidal ventilation at low airway pressures can augment lung injury.Am J Respir Crit Care Med. 1994; 149: 1327-1334Crossref PubMed Scopus (1041) Google Scholar 89Tremblay LN Slutsky AS Ventilator-induced injury: barotrauma and biotrauma.Proc Assoc Am Physician. 1998; 110: 482-488PubMed Google Scholar by energy dissipation during liquid bridge fracture or from the stress that is imposed on lining cells by the movement of air–liquid interfaces with respiration.30Gattinoni L Pelosi P Suter PM Pedoto A Vercesi P Lissoni A Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease: different syndromes?.Am J Respir Crit Care Med. 1998; 158: 3-11Crossref PubMed Scopus (718) Google Scholar 51Marini JJ Ventilator-induced airway dysfunction?.Am J Respir Crit Care Med. 2001; 163: 806-807Crossref PubMed Scopus (12) Google Scholar The relative contributions of these related injury mechanisms in different diseases is simply not known. Inferences from animal experiments with short-term endpoints are of interest but do not show which mechanism is important in which circumstance. Study of bubble and liquid flow in tubes, although constrained by simplifying assumptions (e.g. rigid tube of uniform diameter, smooth surface), are giving some quantitative data on this problem.12Bilek AM Dee KC Gaver 3rd, DP Mechanisms of surface-tension-induced epithelial cell damage in a model of pulmonary airway reopening.J Appl Physiol. 2003; 94: 770-783Crossref PubMed Scopus (275) Google Scholar 14Cassidy KJ Gavriely N Grotberg JB Liquid plug flow in straight and bifurcating tubes.J Biomech Eng. 2001; 123: 580-589Crossref PubMed Scopus (42) Google Scholar 30Gattinoni L Pelosi P Suter PM Pedoto A Vercesi P Lissoni A Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease: different syndromes?.Am J Respir Crit Care Med. 1998; 158: 3-11Crossref PubMed Scopus (718) Google Scholar Much literature now describes the static and dynamic pressure volume relationships of injured lungs, and the effects of interventions such as PEEP and recruitment manoeuvres.23Eissa NT Ranieri VM Corbeil C et al.Analysis of behavior of the respiratory system in ARDS patients: effects of flow volume and time.J Appl Physiol. 1991; 70: 2719-2729Crossref PubMed Scopus (2) Google Scholar 37Hermle G Mols G Zugel A et al.Intratidal compliance–volume curve as an alternative basis to adjust positive end-expiratory pressure: a study in isolated perfused rabbit lungs.Crit Care Med. 2002; 30: 1589-1597Crossref PubMed Scopus (19) Google Scholar 46Jonson B Richard JC 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: 1172-1178Crossref PubMed Scopus (297) Google Scholar 50Matamis 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: 58-66Abstract Full Text Full Text PDF PubMed Scopus (351) Google Scholar 53Martin-Lefèvre L Ricard JD Roupie E Dreyfuss D Saumon G Significance of the changes in the respiratory system pressure–volume curve during acute lung injury in rats.Am J Respir Crit Care Med. 2001; 164: 627-632Crossref PubMed Scopus (52) Google Scholar 55Martynowicz MA Walters BJ Hubmayr RD Mechanisms of recruitment in oleic acid injured lungs.J Appl Physiol. 2001; 90: 1744-1753PubMed Google Scholar 76Servillo G De Robertis E Maggiore S Lemaire F Brochard L Tufano R The upper inflection point on the pressure–volume curve.Intensive Care Med. 2002; 28: 842-849Crossref PubMed Scopus (20) Google Scholar 91Ward NS Lin DY Nelson DL et al.Successful determination of lower inflection point and maximal compliance in a population of patients with acute respiratory distress syndrome.Crit Care Med. 2002; 30: 963-968Crossref PubMed Scopus (35) Google Scholar A great deal of emphasis has been placed on methods and analytic approach,27Ganzert S Guttmann J Kersting K et al.Analysis of respiratory pressure–volume curves in intensive care medicine using inductive machine learning.Artif Intelligence Med. 2002; 26: 69-86Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar 36Harris SR Hess DR Venegas JG An objective analysis of the pressure–volume curve in the acute respiratory distress syndrome.Am J Resp Crit Care Med. 2000; 161: 432-439Crossref PubMed Scopus (153) Google Scholar 68Ranieri VM Giulani 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: 19-27Crossref PubMed Scopus (188) Google Scholar 72Rodriguez L Lemaire F Marquer B et al.A new simple method to perform pressure–volume curves obtained under quasi-static conditions during mechanical ventilation.Intensive Care Med. 1999; 25: 173-179Crossref PubMed Scopus (25) Google Scholar 77Servillo G Svantesson C Beydon L et al.Pressure–volume curves in acute respiratory failure. Automated low flow inflation versus occlusion.Am J Respir Crit Care Med. 1997; 155: 1629-1636Crossref PubMed Scopus (119) Google Scholar 94Younes M Webster K Kun J Roberts D Masiowski B A method for measuring passive elastance during proportional assist ventilation.Am J Respir Crit Care Med. 2001; 164: 50-60Crossref PubMed Scopus (101) Google Scholar but, there is little agreement how these measurements can be used clinically. The static respiratory system pressure–volume curve of patients with injured lungs has certain characteristics (Fig. 2): (i) an S-shaped inflation curve with an upper and lower inflection point (UIP and LIP, respectively); (ii) an increased recoil pressure at all lung volumes; and (iii) a reduced compliance defined by the slope of the inflation curve between LIP and UIP. For many years the pressure at LIP was regarded as the critical opening pressure of collapsed lung units and was considered a target of ‘best PEEP’. The pressure at UIP, in turn, was considered to indicate alveolar overdistension that should not be exceeded during mechanical ventilation.75Roupie E Dambrosio M Servillo G et al.Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome.Am J Resp Crit Care Med. 1995; 52: 121-128Crossref Scopus (278) Google Scholar These ideas have been challenged because most values from the PV curve have low specificity.42Hubmayr RD Perspective on lung injury and recruitment: a skeptical look at the opening and collapse story.Am J Respir Crit Care Med. 2002; 165: 1647-1653Crossref PubMed Scopus (264) Google Scholar 53Martin-Lefèvre L Ricard JD Roupie E Dreyfuss D Saumon G Significance of the changes in the respiratory system pressure–volume curve during acute lung injury in rats.Am J Respir Crit Care Med. 2001; 164: 627-632Crossref PubMed Scopus (52) Google Scholar For example, when lungs are rinsed with mineral oils to increase surface tension, the LIP is prominent even though the lung units are ‘open’, that is aerated.79Smith JC Stamenovic D Surface forces in lungs. I. Alveolar surface tension–lung volume relationships.J Appl Physiol. 1986; 60: 1341-1350PubMed Google Scholar 81Stamenovic D Smith JC Surface forces in lungs. II. Microstructural mechanics and lung stability.J Appl Physiol. 1986; 60: 1351-1357PubMed Google Scholar Similar characteristics are observed when saline filled lungs are inflated with air as happens during a newborn's first breath.4Avery ME The aeration of the lung at birth.in: Schaffer AJ The Lung and Its Disorders in the Newborn Infant. WB Saunders, Philadelphia, PA1968: 24-30Google Scholar Attention is now on oedema, airway liquid and interfacial phenomena as causes of increased ‘opening pressure’ and lung impedance.92Wilson TA Anafi RC Hubmayr RD Mechanics of edematous lungs.J Appl Physiol. 2001; 90: 2088-2093PubMed Google Scholar 53Martin-Lefèvre L Ricard JD Roupie E Dreyfuss D Saumon G Significance of the changes in the respiratory system pressure–volume curve during acute lung injury in rats.Am J Respir Crit Care Med. 2001; 164: 627-632Crossref PubMed Scopus (52) Google Scholar In some patients the LIP originates in the chest wall and not the lung.57Mergoni M Martelli A Volpi A Primavera S Zuccoli P Rossi A Impact of positive end-expiratory pressure on chest wall and lung pressure–volume curve in acute respiratory failure.Am J Respir Crit Care Med. 1997; 156: 846-854Crossref PubMed Scopus (140) Google Scholar This is likely in patients with small thoracic volumes because the chest wall PV curve is non-linear in the low volume range.67Ranieri VM Brienza N Santostasi S et al.Impairment of lung and chest wall mechanics in patients with acute respiratory distress syndrome: role of abdominal distention.Am J Respir Crit Care Med. 1997; 156: 1082-1091Crossref PubMed Scopus (257) Google Scholar Nevertheless, even in these patients the contribution of the chest wall to the pressure at LIP is quite small. Because the chest wall may generate PV artifacts, some have advocated oesophageal pressure measurement to guide management in patients with injured lungs. Advocates usually emphasize that even in recumbent patients the change in oesophageal pressure (ΔPoes) reflects the average change in lung surface pressure or pleural pressure (ΔPpl). However, support for this statement is from experiments on normal animals.34Gillespie DJ Lai YL Hyatt RE Comparison of esophageal and pleural pressures in the anaesthetized dog.J Appl Physiol. 1973; 35: 709-713PubMed Google Scholar Diseased lungs expand non-uniformly and non-uniform lung expansion is associated with non-uniform distributions of lung surface pressure.1Agostoni E Handbook of Physiology, The Respiratory System. Waverly Press, Baltimore, MD1986Google Scholar 43Hubmayr RD Margulies SS Effects of unilateral hyperinflation on the interpulmonary distribution of pleural pressure.J Appl Physiol. 1992; 73: 1650-1654PubMed Google Scholar 52Martin CJ Young AC Ishikawa K Regional lung mechanics in pulmonary disease.J Clin Invest. 1965; 44: 906-913Crossref PubMed Scopus (10) Google Scholar 62Pelosi P Goldner M McKibben A et al.Recruitment and derecruitment during acute respiratory failure: an experimental study.Am J Respir Crit Care Med. 2001; 164: 122-130Crossref PubMed Scopus (393) Google Scholar This means that the position of the oesophageal balloon at which ΔPoes mirrors ΔPpl varies greatly with posture, mode of breathing and with the pattern of respiratory muscle activation. In other words, in injured lungs the calibration of the device with an occlusion test7Bates JH Rossi A Milic-Emili J Analysis of the behavior of the respiratory system with constant inspiratory flow.J Appl Physiol. 1985; 58: 1840-1848Crossref PubMed Scopus (355) Google Scholar does not guarantee that the signal, that is ΔPoes, will represent ΔPpl under the conditions under which the actual measurements are made. Any concern about erroneous conclusions from oesophageal manometry in patients with ARDS is speculative because it is not possible to measure Ppl without artifact in humans. However, we cite two examples in support of our arguments. Rich and colleagues measured lung mechanics in prone dogs.71Rich CR Rehder K Knopp TJ Hyatt RE Halothane and enflurane anesthesia and respiratory mechanics in prone dogs.J Appl Physiol Respir Environ Exercise Physiol. 1979; 46: 646-653PubMed Google Scholar During inhalation anaesthesia they observed looping and inversions of dynamic PV loops that suggested negative pulmonary resistances. They attributed this artifact to a halothane-related inhibition of intercostal muscles, ribcage instability, and chest wall distortion that changed the topographical distribution of ΔPpl. Another example is the apparent large decrease in chest wall compliance of ARDS patients in the prone posture.63Pelosi P Tubiolo D Mascheroni D et al.Effects of the prone position on respiratory mechanics and gas exchange during acute lung injury.Am J Respir Crit Care Med. 1998; 157: 387-393Crossref PubMed Scopus (371) Google Scholar The investigators defined chest wall compliance (Cw) as the ratio of tidal volume to ΔPoes. In 15 of 16 supine patients the Cw estimate was larger than the predicted norm (reaching values up to 0.45 litre cm H2O−1) and decreased dramatically upon the assumption of the prone posture. This suggests that in the supine posture the oesophageal balloon is near flooded derecruited lung, which does not expand during mechanical ventilation and therefore does not generate a local pressure swing. Paraspinal lung recruitment associated with the assumption of the prone posture dramatically increases volume and ventilation of perioesophageal lung regions, leading to a much smaller estimate of Cw. While it is likely that some regions of the lungs approach their maximal volume at pressures near UIP,48Malbouisson LM Muller JC Constantin JM Lu Q Puybasset L Rouby JJ Computed tomography assessment of positive end-expiratory pressure-induced alveolar recruitment in patients with acute respiratory distress syndrome.Am J Respir Crit Care Med. 2001; 163: 1444-1450Crossref PubMed Scopus (239) Google Scholar 55Martynowicz MA Walters BJ Hubmayr RD Mechanisms of recruitment in oleic acid injured lungs.J Appl Physiol. 2001; 90: 1744-1753PubMed Google Scholar 74Rouby JJ Lu Q Goldstein I Selecting the right level of positive end-expiratory pressure in patients with acute respiratory distress syndrome.Am J Respir Crit Care Med. 2002; 165: 1182-1186Crossref PubMed Scopus (146) Google Scholar the evidence that ventilating patients in this way causes injury provided tidal volume is kept low is circumstantial.22Dreyfuss D Soler P Basset G et al.High inflation pressure pulmonary edema: respective effects of high airway pressure, high tidal volume and positive end expiratory pressure.Am J Resp Crit Care Med. 1988; 137: 1159-1164Crossref PubMed Scopus (1320) Google Scholar 69Ranieri VM Zhang H Mascia L et al.Pressure–time curve predicts minimally injurious ventilatory strategy in an isolated rat lung model.Anesthesiology. 2000; 93: 1320-1328Crossref PubMed Scopus (152) Google Scholar 75Roupie E Dambrosio M Servillo G et al.Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome.Am J Resp Crit Care Med. 1995; 52: 121-128Crossref Scopus (278) Google Scholar The pressures and volumes used to test this hypothesis in experimental animals were generally high and are nowadays rarely used in clinical practice. Therefore, the term overexpansion should be used with caution. We will return to this point in our discussion of clinical implications of mechanics measurements. The effects of injury on recoil and on compliance need not be related. This is because abnormal surfactants with increased minimal surface tension and impaired dynamic properties (adsorption, spreading, and compression) cannot cause an appropriate change in surface tension with lung volume.65Pison U Bock JC Pietschmann S Veit S Slama K The adult respiratory distress syndrome: pathophysiological concepts related to the pulmonary surfactant system.in: Robertson B Tauesch HW Lung Biology in Health and Disease. Vol 84: Surfactant Therapy for Lung Disease. Marcel Dekker, New York1995: 169-197Google Scholar 80Spragg RG Lewis JF Pathology of the surfactant system of a mature lung: Second San Diego Conference.Am J Resir Crit Care Med. 2001; 163: 280-282Crossref PubMed Scopus (14) Google Scholar As a result both recoil and compliance of aerated units with abnormal surfactants must increase,79Smith JC Stamenovic D Surface forces in lungs. I. Alveolar surface tension–lung volume relationships.J Appl Physiol. 1986; 60: 1341-1350PubMed Google Scholar 81Stamenovic D Smith JC Surface forces in lungs. II. Microstructural mechanics and lung stability.J Appl Physiol. 1986; 60: 1351-1357PubMed Google Scholar 82Stamenovic D Smith JC Surface forces in lungs. III. Alveolar surface tension and elastic properties of lung parenchyma.J Appl Physiol. 1986; 60: 1358-1362PubMed Google Scholar while the compliance of flooded and collapsed units must be more or less zero. This is just one of many examples why it is difficult to draw inferences about specific mechanisms from static whole lung PV curves. This would only be possible if the small-scale distributions of regional elastances were known. In some patients there is a larger than anticipated recoil pressure difference between inflation and deflation, indicating PV hysteresis. There are several possible mechanisms for PV hysteresis: (i) the recruitment and derecruitment of lung units during the manoeuvre; (ii) the volume- and time-dependent molecular reorganization of surface active material which coats air–liquid interfaces in alveoli and conducting airways; (iii) stress relaxation and stress recovery of airways and lung parenchyma; (iv) spurious changes in lung volume on account of gas absorption during the PV measurement. The last is a well-described problem of the supersyringe technique.83Sydow M Burchardi H Zinserling J Ische H Crozier TA Weyland W Improved determination of static compliance by automated single volume steps in ventilated patients.Intensive Care Med. 1991; 17: 108-114Crossref PubMed Scopus (42) Google Scholar The clinical literature on ALI and ARDS has generally ignored mechanisms two and three and has attributed all volume- and time-related changes in PV characteristics to lung recruitment (i.e. the opening of previously closed units). While in injured lungs recruitment is undoubtedly an important cause of airway pressure and time-related changes in lung mechanics, it is certainly not the only one. In a series of classic papers Hildebrandt and colleagues studied the physiologic determinants of the PV loop.39Hildebrandt J Pressure–volume data of cat lung interpreted by a plastoelastic, linear viscoelastic model.J Appl Physiol. 1970; 28: 365-372PubMed Google Scholar In the normal lung, stress relaxation, stress recovery, and hysteresis are surfactant and surface tension phenomena, and they account for changes in lung volume with pressure and time. In other words ‘recruitment manoeuvres’ as they have been described in the critical care literature would be fully expected to alter volume and recoil of normal lungs by recruitment independent mechanisms. Compared with surface properties the fraction of elastic pressure that is lost because of tissue hysteresis is small.25Fredberg JJ Stamenovic D On the imperfect elasticity of the lung.J Appl Physiol. 1989; 67: 2408-2419PubMed Google Scholar However, it is not zero and as emphasized in studies of patients with asthma, can be an important source of relaxation in a lung which is actively constricted.59Mitzner W Brown RH Potential mechanism of hyperresponsive airways.Am J Respir Crit Care Med. 2000; 161: 1619-1623Crossref PubMed Scopus (27) Google Scholar The neglect of alternative mechanisms as explanations for PEEP induced changes in the volume of injured lungs is regrettable, because the reasoning behind the ‘open lung approach’ is largely based on putative benefits derived from recruitment. However, if PV measurements cannot distinguish between recruitment of new units and stress relaxation of already recruited units, then clinical decisions will be based on a mechanism (recruitment) that c
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