Sly syndrome

Ventilatory modes employing different inspiratory flow patterns and inspiratory to expiratory ratios may alter lung strain in acute lung injury patients. To determine whether variations in lung strain existed between pressure-controlled, volume-controlled, and pressure-controlled inverse ratio modes of ventilation, we randomly applied each for 30 minutes in 18 acute lung injury patients, keeping tidal volume, respiratory rate, fractional inspired oxygen, and total positive end-expiratory pressure constant. After each mode, a multiple linear regression analysis of dynamic airway pressure and airflow was performed with a volume-dependent single compartment model of the equation of motion, and an index of nonlinear elastic behavior was calculated. In five additional patients, concurrent dynamic computerized axial tomography scanning at juxtadiaphragmatic and subcarinal levels was added. Although static mechanics, oxygenation, and hemodynamics were no different between pressure-controlled, volume-controlled, and pressure-controlled inverse ratio ventilation, we found significant differences in nonlinear behavior. This was least with pressure-controlled followed by volume-controlled ventilation, and pressure-controlled inverse ratio ventilation had the greatest nonlinear elastic behavior. Dynamic computerized axial tomography analysis revealed more overinflated units in the left subcarinal slice with pressure-controlled inverse ratio ventilation. Ventilator flow pattern and inspiratory to expiratory ratio independently influence lung strain in acute lung injury; however, further studies are needed to determine the biologic significance.

Keywords: acute respiratory distress syndrome; respiratory mechanics; nonlinear behavior, lung strain

Acute lung injury (ALI) results in an increase in the work of breathing and impairment of gas exchange that usually requires mechanical ventilation. However, the pathophysiology of ALI includes surfactant dysfunction, increased lung weight, and airspace collapse and consolidation, which predispose the lung to ventilation-induced lung injury (1). For example, mortality in patients with ALI is reduced by using small tidal volume (VT) ventilation (2), and protective ventilatory strategies using positive end-expiratory pressure (PEEP), recruitment maneuvers, surfactant replacement therapy, and varying VT may also reduce ventilation-induced lung injury (1). In general, these strategies aim to reduce ventilation-- induced lung injury by reducing sheer stress or lung strain (3).

The quasistatic volume-pressure curve and the static distending pressure of the respiratory system (plateau pressure [Pplat]) are the most commonly used measures of lung strain. However, the dynamic elastic distending pressure, which is composed of the static pressure, and the viscoelastic pressure will better reflect the volume-pressure relationships and end-- inspiratory pressure strain that are applied to the distal airspaces during mechanical ventilation (4, 5). The viscoelastic pressure is, in turn, composed of tissue viscance and the effects of time constant inequalities within the lung (6), which can lead to regional flow maldistribution.

When VT, PEEP, and inspiratory to expiratory ratio are constant compared with volume-controlled ventilation, pressure-controlled ventilation does not improve oxygenation or lower Pplat (7-9). In addition, when VT and total PEEP (PEEPtot) are constant, the inverse ratio ventilation at an inspiratory to expiratory ratio of 2:1 compared with 1:2 does not improve oxygenation or Pplat (7-10). However, the different inspiratory flow patterns and different inspiratory to expiratory ratios may alter the viscoelastic component of lung strain by altering the buildup of tissue resistance or the distribution of ventilation. Variation in the extent of nonlinear dynamic elastic volume-pressure behavior of the respiratory system will reflect the differences in viscoelastic strain between modes. To examine these issues, we used a volume-dependent single-compartment model to examine the extent of nonlinear dynamic volume-pressure relationships in 18 patients with ALT randomly receiving pressure-- controlled ventilation at an inspiratory to expiratory ratio of 1:2 and 2:1 (pressure-controlled inverse ratio ventilation) and volume-controlled ventilation at an inspiratory to expiratory ratio of 1:2 with PEEPtot, VT, and respiratory rate constant. To examine whether heterogeneity of regional ventilation contributed to differences in nonlinear volume-pressure behavior when these three modes of ventilation were applied, dynamic computerized axial tomography (CT) scans and dynamic volume-pressure relationships were examined in an additional five ALI patients.

METHODS

The local ethics committee approval for the study was granted (#26/ 97 and #94/01), and written informed consent was obtained from the patient's next of kin. Inclusion criteria were ALl as defined by the American European Consensus Conference criteria (11) and mechanical ventilation. Exclusion criteria were late ALI (greater than 5 days from onset), hemodynamic instability, and anticipated intolerance of transient PEEP removal. Demographic data (sex, height, and weight), Acute Physiology and Chronic Health Evaluation II score, etiologic factors, baseline ventilator settings, as set by the attending clinician before this study, and lung injury score (12) were recorded at inclusion.

References

1. Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med 1998;157:294-323.

2. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome: the Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342:1301-1308.

3. Wirtz HR, Dobbs LG. The effects of mechanical forces on lung functions. Respir Physiol 2000;19:1-17.

4. Servillo G, Svantesson C, Beydon L, Roupie E, Brochard L, Lemaire F, Jonson B. Pressure-volume curves in acute respiratory failure: automated low flow inflation versus occlusion. Am J Respir Crit Care Med 1997;155:1629-1636.

5. Jonson B, Richard J-C, Straus C, Mancebo J, Lemaire F, Brochard F. Pressure-volume curves and compliance in acute lung injury: evidence for recruitment above the lower inflection point. Am J Respir Crit Care Med 1999;159:1172-1179.

6. Otis AB, McKerrow CB, Bartlett RA, Mead J, McIlroy MB, Selverstone NJ, Radford EP. Mechanical factors in distribution of ventilation. J Appl Physiol 1955;8:427-443.

7. Lessard MR, Guerot E, Lorino H, Lemaire F. Brochard L. Effects of pressure-controlled with different LE ratios versus volume-controlled ventilation on respiratory mechanics, gas exchange, and hemodynamics in patients with adult respiratory distress syndrome. Anesthesiology 1994:80:983-991.

8. Mang H, Kacmarek RM, Ritz R, Wilson RS, Kimball WP. Cardiorespiratory effects of volume- and pressure-controlled ventilation at various I/E ratios in an acute lung injury model. Am J Respir Crit Care Med 1995:151:731-736.

9. Zavala E, Ferrer M, Polese Cs, Masclans JR, Planas M, Milic-Emili J, Rodriguez-Roisin R, Roca J, Rossi A. Effect of inverse I:E ratio ventilation on pulmonary gas exchange in acute respiratory distress syndrome. Anesthesiology 1998;88:35-42.

10. Mercat A, Titriga M, Anguel N, Richard C, Teboul J-L. Inverse ratio

ventilation (I/E = 211) in acute respiratory distress syndrome: a sixhour controlled study. Am J Respir Crit Care Med 1997;155:1637-1642.

11. Bernard G, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, Lamy M, Legall JR, Morris A, Spragg R. The American-European Consensus Conference on ARDS: Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994; 149:818-824

12. Murray JF, Matthay MA, Luce JM, Flick MR. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis 1988; 138:720-723.

13. Bersten AD. Measurement of overinflation by multiple linear regression analysis in patients with acute lung injury. Eur Respir J 1998;12:526532.

14. Ranieri VM, Eissa NT, Corbeil C, Chasse M, Braidy J, Matar N, Milic-- Emili J. Effects of positive end-expiratory pressure on alveolar recruitment and gas exchange in patients with the adult respiratory distress syndrome. Am Rev Respir Dis 1991:144:544 551.

15. Kano S, Lanteri C, Duncan AW, Sly PD. Influence of nonlinearities on estimates of respiratory mechanics using multilinear regression analysis. J Appl Physiol 1994;77:1185-1197.

16. Vieira SRR, Puybasset L, Richecoeur J, Lu Q, Cluzel P, Gusman PB, Coriat P, Rouby JJ. A lung computed tomographic assessment of positive end-expiratory pressure-induced overdistension. Am. Respir Crit Care Med 1998;158:1571-1577.

17. Snedecor GW, Cochran WC. Statistical methods, 7th ed. Ames, IA: Iowa State University Press: 1980.

18. Mercat A, Graini L, Teboul J-L, Lenique F, Richard C. Cardiorespiratory effects of pressure-controlled ventilation with and without inverse ratio in the adult respiratory distress syndrome. Chest 1993;104:871-875.

19. Lanteri CJ, Kano S, Duncan AW, Sly PD. Changes in respiratory mechanics in children undergoing cardiopulmonary bypass. Am J Respir Crit Care Med 1995;152:1893-1900.

20. Peslin R, Felicio da Silva J, Chabot F, Duvivier C. Respiratory mechanics studied by multiple linear regression in unsedated ventilated patients. Eur Respir J 1992;5:871-878.

21. Peslin R, Gallina C, Saunier C, Duvivier C. Fourier analysis versus multiple linear regression analysis to analyse pressure-flow data during artificial ventilation. Eur Respir J 1994;7:2241-2245.

22. Rousselot JM, Peslin R, Duvivier C. Evaluation of the multiple linear regression method to monitor respiratory mechanics in ventilated neonates and young children. Pediatr Pulmonol 1992;13:161-168.

23. Wagers S, Lundblad L, Moriya HT, Bates JHT, Irvin CG. Nonlinearity of respiratory mechanics during bronchoconstriction in mice with airway inflammation. J Appi Physiol 2002;92:1802-1807.

24. Lutchen KR, Hantos Z, Petak F, Adamicza A, Suki B. Airway inhomoge

neities contribute to apparent lung tissue mechanics during constriction. J Appl Physiol 1996;80:1841-1849.

25. Jonson B, Beydon L, Brauer K, Mansson C, Valind S, Grytzell H. Mechanics of respiratory system in healthy anesthetized humans with emphasis on viscoelastic properties. J Appl Physiol 1993;75:132-140.

26. Beydon L, Svantesson C, Brauer K, Lemaire F, Jonson B. Respiratory mechanics in patients ventilated for critical lung disease. Eur Respir J 1996;9:262-273.

27. Rouby JJ, Lu Q, Goldstein I. Selecting the right level of positive endexpiratory pressure in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2002;165:1182-1186.

28. Gattinoni L, Caironi P, Pelosi P, Goodman LR. What has computed tomography taught us about the acute respiratory distress syndrome? Am J Respir Crit Care Med 2001;164:1701-1711.

29. Dambrosio M, Roupei E, Mollet JJ, Anaglde MC, Vasile N, Lemaire F, Brochard L. Effects of positive end-expiratory pressure and different tidal volumes on alveolar recruitment and hyperinflation. Anesthesiology 1997;87:495-503.

30. Vieira SRR, Puybasset L, Lu Q. Richecoeur, Cluzel P, Coriat P, Rouby J-J. A scanographic assessment of pulmonary morphology in acute lung injury: significance of the lower inflection point detected on the lung pressure-volume curve. Am J Respir Crit Care Med 1999;159: 1612-1623.

31. Malbouisson LM, Busch CJ, Puybasset L, Lu Q, Cluzel P, Rouby JJ. A role of the heart in the loss of aeration characterizing lower lobes in acute respiratory distress syndrome: the CT scan ARDS group. Am J Repir Crit Care Med 2000;161:2005 2012.

32. Ludwigs U, Klingstedt C, Bachrentz S, Wegenius G, Hedenstiena G. Volume-controlled inverse ratio ventilation in oleic acid induced lung injury: effects on gas exchange, hemodynamics, and computed tomographic density. Chest 1995;108:804-809.

33. Neumann P, Berglund JE, Andersson LG, Maripu E, Magnusson A, Hedenstierna G. Effects of inverse ratio ventilation and positive endexpiratory pressure in oleic acid-induced lung injury. Am J Respir Crit Care Med 2000;161:1537-1545.

34. Kacmarek R, Kirmse M, Nishimura M, Mang H, Kimball WR. The effects of applied vs. auto-PEEP on local lung unit pressure and volume in a four-unit lung model. Chest 1995;108:1073-1079.

35. Ranieri VM, Zhang H, Mascia L, Aubin M, Lin CY, Mullen J, Grasso S, Binnie M, Volgyesi G, Eng P, et al. Pressure-time curve predicts minimally injurious ventilatory strategy in an isolated rat lung model. Anesthesiology 2000;93:1320-1328.

36. Esteban A, Inmaculada A, Federico G, Raul DP, Gumersindo G, Blanco J. Prospective randomized trial comparing pressure-controlled ventilation and volume-controlled ventilation in ARDS: for the Spanish Lung Failure Collaborative Group. Chest 20(001;117:1690-1696.

Cyrus Edibam, Albert J. Rutten, Daniel V. Collins, and Andrew D. Bersten

Department of Critical Care Medicine, Flinders Medical Centre, Bedford Park, South Australia

(Received in original form December 21, 2000; accepted in final form November 12, 2002)

Supported by the National Health and Medical Research Council (grant #980451).

Correspondence and requests for reprints should be addressed to Andrew D. Bersten, Department of Critical Care Medicine, Flinders Medical Centre, Bedford Park, South Australia, 5042. E-mail: andrew.bersten@flinders.edu.au

This article has an online supplement, which is accessible from this issue's table of contents online at www.atsjournals.org

Am J Respir Crit Care Med Vol 167. pp 702-707, 2003

DOI: 10.1164/rccm.2012110

Internet address: www.atsjournals.org

Copyright American Thoracic Society Mar 1, 2003
Provided by ProQuest Information and Learning Company. All rights Reserved