Chiumello Davide, Carlesso Eleonora, Cadringher Paolo, Caironi Pietro, Valenza Franco, Polli Federico, Tallarini Federica, Cozzi Paola, Cressoni Massimo, Colombo Angelo, Marini John J, Gattinoni Luciano
Dipartimento di Anestesia, Rianimazione, Intensiva e Subintensivae, Terapia del Dolore, Fondazione IRCCS, Ospedale Maggiore Policlinico Mangiagalli Regina Elena di Milano, Milan, Italy.
Am J Respir Crit Care Med. 2008 Aug 15;178(4):346-55. doi: 10.1164/rccm.200710-1589OC. Epub 2008 May 1.
Lung injury caused by a ventilator results from nonphysiologic lung stress (transpulmonary pressure) and strain (inflated volume to functional residual capacity ratio).
To determine whether plateau pressure and tidal volume are adequate surrogates for stress and strain, and to quantify the stress to strain relationship in patients and control subjects.
Nineteen postsurgical healthy patients (group 1), 11 patients with medical diseases (group 2), 26 patients with acute lung injury (group 3), and 24 patients with acute respiratory distress syndrome (group 4) underwent a positive end-expiratory pressure (PEEP) trial (5 and 15 cm H2O) with 6, 8, 10, and 12 ml/kg tidal volume.
Plateau airway pressure, lung and chest wall elastances, and lung stress and strain significantly increased from groups 1 to 4 and with increasing PEEP and tidal volume. Within each group, a given applied airway pressure produced largely variable stress due to the variability of the lung elastance to respiratory system elastance ratio (range, 0.33-0.95). Analogously, for the same applied tidal volume, the strain variability within subgroups was remarkable, due to the functional residual capacity variability. Therefore, low or high tidal volume, such as 6 and 12 ml/kg, respectively, could produce similar stress and strain in a remarkable fraction of patients in each subgroup. In contrast, the stress to strain ratio-that is, specific lung elastance-was similar throughout the subgroups (13.4 +/- 3.4, 12.6 +/- 3.0, 14.4 +/- 3.6, and 13.5 +/- 4.1 cm H2O for groups 1 through 4, respectively; P = 0.58) and did not change with PEEP and tidal volume.
Plateau pressure and tidal volume are inadequate surrogates for lung stress and strain. Clinical trial registered with www.clinicaltrials.gov (NCT 00143468).
呼吸机所致肺损伤源于非生理性肺应力(跨肺压)和应变(充气容积与功能残气量之比)。
确定平台压和潮气量是否为应力和应变的充分替代指标,并量化患者和对照受试者的应力与应变关系。
19例术后健康患者(第1组)、11例内科疾病患者(第2组)、26例急性肺损伤患者(第3组)和24例急性呼吸窘迫综合征患者(第4组)接受呼气末正压(PEEP)试验(5和15 cm H₂O),潮气量分别为6、8、10和12 ml/kg。
从第1组到第4组,随着PEEP和潮气量增加,平台气道压、肺和胸壁弹性、肺应力和应变显著增加。在每组中,由于肺弹性与呼吸系统弹性之比的变异性(范围为0.33 - 0.95),给定的气道压力产生的应力变化很大。类似地,对于相同的潮气量,由于功能残气量的变异性,亚组内的应变变异性也很显著。因此,低或高潮气量,如分别为6和12 ml/kg,在每个亚组的相当一部分患者中可产生相似的应力和应变。相比之下,应力与应变之比,即比肺弹性,在各亚组中相似(第1组至第4组分别为13.4 ± 3.4、12.6 ± 3.0、14.4 ± 3.6和13.5 ± 4.1 cm H₂O;P = 0.58),且不随PEEP和潮气量而改变。
平台压和潮气量并非肺应力和应变的充分替代指标。在www.clinicaltrials.gov注册的临床试验(NCT 00143468)。