SciELO - Scientific Electronic Library Online

vol.51 issue6Preoperative assessment and preparation of coronary artery disease patients for surgeryErratum author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Services on Demand




Related links


Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.51 no.6 Campinas Dec. 2001 



Mechanical ventilatory management in adult respiratory distress syndrome*


Propuestas en ventilación mecánica en la síndrome de angustia respiratoria



José Otávio Costa Auler Junior, M.D.I; Fernando Bliacheriene, M.D.II; Erika Miyoshi, M.D.III; Cláudia Regina Fernandes, M.D.IV

IProfessor Titular da Disciplina de Anestesiologia do Departamento de Cirurgia da FMUSP
IIME do CET da Disciplina de Anestesiologia da FMUSP
IIIMédica Assistente da Divisão de Anestesia do HC-FMUSP
IVMédica Assistente do Serviço de Anestesia do InCor-FMUSP





BACKGROUND AND OBJECTIVES: This article's objective is to summarize published ARDS ventilation strategies. This is very important since mechanical ventilation as a therapeutic measure has been under constant evaluation and many articles have been published on it.
CONTENTS: This is a 29 articles and one book review selected from a keyword search in MEDLINE.
CONCLUSIONS: Despite of the great number of articles published on ARDS, most of them suggest a so-called 'lung-protection' strategy based on low tidal volume and high PEEP levels. Other adjuvant measures would be serial thoracic computerized tomography, PaO2 adjustments, nitric oxide inhalation, prone position and ECMO.

Key Words: DISEASE: adult respiratory distress syndrome; VENTILATION: mechanical ventilation


JUSTIFICATIVA Y OBJETIVOS: El objetivo de este artículo es ofrecer al lector un resumen de las normas ya consagradas por la literatura a respecto de la estrategia actual del manoseo de la ventilación durante la Síndrome de la Angustia Respiratoria Aguda (SARA). Esto es de fundamental importancia, ya que la ventilación mecánica, como medida terapéutica, ha estado bajo constante revisión, muchos artículos han sido publicados a este respecto.
CONTENIDO: Este trabajo contiene la revisión de 29 artículos y un libro, seleccionados a partir de la pesquisa de palabras-claves realizada en el MEDLINE.
CONCLUSIONES: Mucho se ha publicado a respecto de ventilación en SARA, sin embargo, la tendencia es para una estrategia de protección pulmonar tomando como base el bajo volumen corriente y altos niveles de PEEP. Otras medidas de ayuda serian tomografías computadorizadas seriadas de tórax, ajuste de PaO2, inhalación de óxido nítrico, posición prono y ECMO (extracorporeal membrane oxygenation).




Discussing new advances in mechanical ventilation is a hard task, since several articles have been published on the subject in recent years. In addition to general anesthesia, mechanical ventilation is mostly applied to respiratory failure intensive care. Most available studies talk about advice, different techniques and new ventilatory strategies especially related to mechanical ventilation in Acute Respiratory Distress Syndrome patients (ARDS), meaning that we are far away from a consensus. Part of the progress seen in mechanical ventilation is due to microprocessed ventilators which allow for several functions, such as pulmonary mechanical evaluation at bedside, real time data and trend charts1,2. In the operating room, the recent introduction of workstations with microprocessed ventilators provides the anesthesiologist with new facilities to monitor pulmonary ventilation of anesthetized patients. Added to the accurate respiratory mechanical monitoring, there is a potential for the use of microprocessed ventilators in perioperative research, thus opening a new and fascinating field. The recent recognition of ARDS diffuse lung damage and its permanent clinical effects has allowed for the appearance of new ventilatory techniques with potential to improve gas exchanges while minimizing noxious ventilation effects. This shows that mechanical ventilation as a therapeutic modality has been submitted to important revaluations because it may support, damage or protect acutely damaged lungs. So, it is of paramount importance to review the literature dealing with ARDS patients, aiming at updating other aspects of pulmonary protection strategies.

This article aimed to supply the reader with a summary of widely accepted standards for ventilation during ARDS.



The following keywords were searched: mechanical ventilation, adult respiratory distress syndrome (ARDS), positive end expiratory pressure (PEEP), pulmonary injury, pressure and volume controlled mechanical ventilation related to ventilator-induced pulmonary injury, "volutrauma", pulmonary hyperinflation and strategies for pulmonary protection during mechanical ventilation. The research was based on data of the last ten years obtained from MEDLINE (National Library Medicine). The book and the 29 articles discussed in this review were selected according to their impact on medical literature and scientific community.



According to Vasilyev et at. mortality rate of ARDS patients is high, varying from 45% to 66%3. Due to the different etiologies of ARDS, there is no treatment for a specific etiology. So, current management is ventilatory and symptomatic support with maintenance of oxygenation and prevention of mechanical ventilation-induced pulmonary lesions, such as barotrauma and oxygen toxicity. However, although ventilatory support through mechanical ventilation being vital for ARDS, its mode and parameter adjustments are still under discussion, according to Kacmarek et al.4. Hickling et al. suggest that low volume and limited pressure ventilation with permissive hypercapnia has resulted in lower ARDS mortality5. Only three prospective, controlled and randomized studies were published in recent years comparing mechanical ventilation strategies which may cause more or less pulmonary tissue stretch in ARDS patients6-8. These studies are based on a hypothesis tested in a similar way, but their results are seemingly conflicting. There are, however, two major differences among such important studies. The first and fundamental difference is the PEEP level. In the study by Amato et al.8, PEEP level variation initially applied to the treated group was significantly higher than the control group. The second difference is the plateau pressure which, in Amato's study, was above 35 cmH2O in the control group while in the other studies such parameter was kept in lower levels. Lower pressure and PEEP levels in Brochard's6 and Stewart's7 studies are due to the fact that PEEP was below the inflexion point of the pressure-volume curve, what explains different results between treatment and control groups as compared to Amato's study.

Experimental studies, such as Tsuno et al.9, Dreyfuss et al10, Kolobow et al11 and Parker et al.12, have shown that different animal species with normal lungs presented severe tissue injuries when ventilated with high inspiratory pressures. Barotrauma is defined as air leakage from alveolar spaces and is one of the noxious effects of mechanical ventilation on the lungs. Added to those major events, subtle morphologic pulmonary changes may result from mechanical ventilation, especially when high airway pressures and volumes are used. Pulmonary edema, or ventilator-induced injury, is a consequence of endothelial and epithelial patency increase. Severe ultra-structural damages have been reported as noxious effects of excessive pulmonary inflation. Histological findings in damaged lungs of animals submitted to mechanical ventilation were atelectasis, congestion and edema9-12. Various studies suggest that microvascular patency changes are major determinants of pulmonary edema, and Webb & Tierney have speculated that the hydrostatic mechanism was the major responsible for edema during high pressure peaks in mechanical ventilation13. West et al. suggested that ventilator-induced edema could not only have a hydrostatic origin, but could also be associated to patency changes due to capillary vessels dysfunction or failure14. A study by Slutsk & Tremblay has shown that inadequate ventilation patterns not only cause pulmonary injury but also multiple organ dysfunctions: tidal volume and airway pressure inducing hyperdistension with inadequate PEEP levels could result in increased pulmonary cytokines which may result in a systemic increase, thus favoring multiple organ failure15. Several animal studies with ventilator-induced pulmonary injury have observed that the major determinant for such injuries was the volume of air at the end of inspiration16. Since it is difficult to measure pulmonary volume in the clinical practice, it is recommended that transpulmonary peak pressure in patients with decreased pulmonary compliance should be limited and estimated through end inspiratory plateau pressure measured at bedside. Dreyfuss et al. were able to isolate two factors - inspiratory pressure and tidal volume - and have proposed that pulmonary injury is more related to excessive volume than to excessive pressure. These authors have carved the word "volutrauma" to define pulmonary injuries caused by excessive pulmonary stretch17. Airway pressure limitation needed to ventilate patients with acute pulmonary injury, as suggested, could lead to hypercarbia. Systematic and acute tidal volume decrease in low compliance lungs, even necessary, is arguable. If high inspiratory pressures have been blamed for pulmonary injuries, on the other hand, too low airway pressures associated to low tidal volumes may worsen pulmonary injury. There are some evidences that unstable alveolar units could be damaged by repeated openings and closings during ventilation. This hypothesis is based on the maintenance of an open lung, that is, after alveolar recruiting, PEEP should be maintained during the whole ventilatory cycle18, aiming at avoiding a new collapse, as shown by Lachmann. According to Benito et al., PEEP above the corresponding pressure for the closing volume (inflexion point) has been associated to marked short-circuit decrease19. Muscedere et al. have shown that the correct PEEP application may prevent additional injuries by keeping the alveoli open20. Gattinoni et al. have shown through computerized tomography that PEEP was able to promote marked pulmonary collapse fraction decrease during mechanical ventilation in ARDS patients21. Currently it may be stated that injuries similar to those caused by ventilators in animals may also be seen in humans22, as shown by Rouby et al. The magnitude of pulmonary stretch necessary to establish a parenchymal injury in humans and the impact of volume or pressure limited ventilation on clinical results are yet to be defined. During mechanical ventilation in acute pulmonary injury, the technique of lung protection combined with CO2 extracorporeal removal was hystorically shown by Gattinoni et al. and decreased ARDS mortality from 90% to 51%. Gattinoni's technique consists in maintaining "lung rest" using ventilation with an extremely low minute volume by decreasing both tidal volume and respiratory rate, while waiting for the possible lung parenchyma recovery23. The lung protection strategy proposed by Hickling et al. has shown that limiting tidal volume and inflation pressures has caused hypercapnia in ARDS patients, but resulted in a lower mortality rate24. Additional clinical results, even with a small number of patients, have suggested that inspiratory pressure limitation could improve survival of mechanically ventilated ARDS patients. Amato et al.'s hypothesis is that pulmonary injury is a result of regional hyperinflation of pulmonary units and is related to increased volume and pressure and to the cyclic alveolar opening and closing with a consequent shearing injury and allowing for lung areas to collapse at the end of expiration25. Two major multicentric studies have then tried to apply the tidal volume decrease concept. None of them, however, could show a benefit in survival rate with tidal volume decrease adjusted to plateau pressure of approximately 25 cmH2O, as compared to the conventional strategy where normocapnia is obtained with plateau pressure below 35 cmH2O6,7. The main point of Stwart's study is the report of relatively low pressures in the control group as compared to the limited ventilation group. The value (mean of 28 cmH2O) is considerably below the limit of 35 cmH2O recommended by the ACCP Consensus Conference26. On the other hand, Amato et al. suggested that lungs may be protected by volume and inflation pressure limitation with PEEP levels enough to prevent most alveolar units to collapse at the end of expiration. This strategy was associated to a significant survival improvement in 28 days, but no survival improvement was seen for hospital discharge. Major ventilatory strategy in Amato's study was based on the individual selection of the ideal PEEP, 2 cmH2O above inflexion point, associated to pressure and volume limitation8. This is a point on the P.V. curve above which there is a sudden increase in pulmonary volume due to alveolar recruiting. The major difficulty is the accurate Pressure-Volume curve measurement to determine the ideal PEEP, because it requires time and experience on part of the professional and patient's deep sedation and neuromuscular paralysis. On the other hand, the static P-V curve used to estimate the inflexion point as proposed by Amato's group, is not usually adopted by most ICUs. Available clinical data suggest that limited ventilation, volume and pressure strategies are not significantly beneficial for ARDS patients, except when combined to PEEP adjusted above the inflexion point, as proposed by Amato.

Simultaneously, the consequence of deep respiratory acidosis, present in several major ventilatory restriction episodes, and its clinical results were not completely explained by the literature27, as observed by Meade.

With regards to non ventilatory therapy, the benefit of the prolonged use of low dose glucocorticoids in late ARDS patients was suggested in a recent randomized study by Meduri et al.28.

Ulrich et al.29 have built an algorhythm for ARDS additive therapies which includes: pressure controlled ventilation (< 35 cmH2O), PEEP from 12 to 50 cmH2O, permissive hypercapnia, nitric oxide inhalation, prone position and volume restriction, with the use of furosemide or continuous hemofiltration, and this set of measures was called conventional therapy. Treatment was considered successful when there was a 20% improvement in PaO2. In non responsive patients ECMO (extracorporeal membrane oxygenation) was installed. In addition, nitric oxide may be beneficial because this molecule is a potent endogenous vasodilator and, when inhaled, selectively decreases lung circulation pressure and improves oxygenation in ARDS patients. Prone position, also proposed, primarily promotes gas exchanges and short circuit improvement; however, more complex mechanisms seem to be involved. Lung injury severity was directly proportional to ECMO need without, however, being related to baseline PaO2 being survival directly related to ECMO time but not to ventilation time before ECMO. The use of this algorhythm, in this study, resulted in a general survival of 80% and 60% in patients submitted to ECMO. It should also be considered the early treatment of ARDS patients in highly specialized centers30.



ARDS patients' survival has increased in recent years and although the precise cause not being clear, a better knowledge of ARDS' pathophysiology and enhancements in mechanical ventilation and intensive care are necessary.

Based on recently published studies, the question is: should we transfer ARDS patients submitted to traditional ventilation to the "lung protection" strategy? Conventional ventilation is defined as tidal volume directed to normocapnia in a volume-controlled mode, random PEEP level and no control of airway inspiratory pressure peaks. However, based on clinical evidences, intensivists should be more liberal in the use of the limited pressure strategy. This strategy is based on tidal volume restriction coupled to high PEEP levels, because mechanical ventilation with low tidal volumes may collapse several lung alveoli. This may be prevented by PEEP above lower inflexion point of the pressure-volume curve, although the best way to reach such point is still to be discussed.

Other recommendations, although not totally agreed upon, are important. Serial thoracic computerized tomographies in patients under mechanical ventilation should be encouraged to check the presence of pulmonary recruitment and collapse under high PEEP levels. The specific mechanism of oxygen toxicity is still unknown, but it is desirable to adjust PaO2 for an adequate oxygen transport capacity, that is, above 90%. Finally, an important strategy is the multimodal management of the patient, using additive measures, such as nitric oxide inhalation, prone position, tracheal inflation with gas and ECMO.

According to current knowledge, a large number of clinical trials are in progress in several countries and it is possible that their results will definitively determine the benefits of protective ventilatory strategies with controlled pressure or volume in ARDS patients.



01. Sanborn W - Microprocessor based mechanical ventilation. Respir Care, 1993;38:72-109.         [ Links ]

02. Tobin MJ - Monitoring pressure, flow and volume during mechanical ventilation. Respir Care, 1993;37:1081-1096.         [ Links ]

03. Vasiley S, Schaap R, Mortensen JD - Hospital survival rate of patients with acute respiratory failure in modern respiratory intensive care units. An international multicenter prospective survey. Chest, 1995;107:1083-1088.         [ Links ]

04. Kacmarek RM, Chiche JD - Lung protective ventilatory strategies for ARDS - the data are convincing! Respir Care, 1998;43:724-727.         [ Links ]

05. Hickling KG, Henderson SJ, Jackson R - Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Med, 1990;16:372-377.         [ Links ]

06. Brochard L, Roudot Thoraval F et al - Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. Am J Respir Crit Care Med, 1998;158: 1831-1838.         [ Links ]

07. Stewart TW, Meade MO, Cook DJ et al - Evaluation of a ventilatory strategy to prevent barotrauma in patients at high risk for ARDS. N Engl J Med, 1998;338:355-361.         [ Links ]

08. Amato MBP, Barbas CV, Medeiros DM et al - Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med, 1998;338:347-354.         [ Links ]

09. Tsuno K, Prato P, Kolobow T - Acute lung injury from mechanical ventilation at moderately high airway pressures. J Appl Physiol, 1990;69:956-961.         [ Links ]

10. Dreyfuss D, Basset G, Soler P et al - Intermittent positive pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats. Am Rev Resp Dis, 1985; 132:880-884.         [ Links ]

11. Kolobow T, Moretti MP, Fumagalli R et al - Severe impairment in lung function induced by high peak airway pressure during mechanical ventilation: an experimental study. Am Rev Resp Dis, 1987;135:312-315.         [ Links ]

12. Parker JC, Hernandez LA, Longenecker GL et al - Lung edema caused by high peak inspiratory pressure in dogs: role of increased microvascular filtration pressure and permeability. Am Rev Resp Dis, 1990;142:321-328.         [ Links ]

13. Webb HH, Tierney DF - Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflation pressures: protection by positive end expiratory pressure. Am Rev Resp Dis, 1974;110:556-565.         [ Links ]

14. West JB, Tsukimoto K, Mathieu-Costello O et al - Stress failure in pulmonary capillaries. J Appl Physiol, 1991;70:1731-1742.         [ Links ]

15. Slutsky A, Tremblay L - Multiple system organ failure: is mechanical ventilation a contributing factor? Am J Respir Crit Care Med, 1998;157:1721-1725.         [ Links ]

16. Dreyfuss D, Saumon G - Ventilation-Induced Injury, em: Tobin MJ - Principles and Practice of Mechanical Ventilation. New York: Mac-Graw Hill; 1994;793-811.         [ Links ]

17. Dreyfuss 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 Rev Resp Dis, 1988;137:1159-1164.         [ Links ]

18. Lachmann B - Open up the lung and keep the lung open. Intensive Care Med, 1992;18:319-321.         [ Links ]

19. Benito S, Lemaire F - Pulmonary pressure-volume relationship in acute respiratory distress syndrome in adults: role of positive end-expiratory pressure. J Crit Care, 1990;5:27-34.         [ Links ]

20. Muscedere JG, Mullen JBM, Gan K et al - Tidal ventilation at low airway pressures can augment lung injury. Am J Resp Crit Care Med, 1994;149:1327-1334.         [ Links ]

21. Gattinoni L, Pelosi P, Crotti S et al - Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome. Am J Resp Crit Care Med, 1995;151:1807-1814.         [ Links ]

22. Rouby JJ, Lherm T, Martin de Lassale E et al - Histologic aspects of pulmonary barotrauma in critically ill patients with acute respiratory failure. Intensive Care Med, 1993;19:383-389.         [ Links ]

23. Gattinoni L, Pesenti A, Masheroni D et al - Low-frequency positive-pressure ventilation with extracorporeal CO2 removal in severe acute respiratory failure. JAMA, 1986;256:881-886.         [ Links ]

24. Hickling KG, Walsh J, Henderson SJ et al - Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia: a prospective study. Crit Care Med, 1994;22:1568-1578.         [ Links ]

25. Amato MBP, Barbas CV, Medeiros DM et al - Beneficial effects of the lung approach with low distending pressures in the acute respiratory distress syndrome. Am J Respir Crit Care Med, 1995; 152:1835-1846.         [ Links ]

26. ACCP consensus conference. Mechanical Ventilation. Chest, 1994;106:656.         [ Links ]

27. Meade MO - An evidence based approach to pressure and volume-limited ventilation strategies. Crit Care Clin, 1998;14: 373-385.         [ Links ]

28. Meduri GU, Headley AS, Golden E et al - Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: A randomized controlled trial JAMA, 1998;280:159-165.         [ Links ]

29. Ullrich R, Lorber C, Roder G et al - Controlled airway pressure therapy, nitric oxide inhalation, prone position and extracorporeal membrane oxygenation (ECMO), as components, of an integrated approach to ARDS. Anesthesiology, 1999;91:1577-1586.         [ Links ]

30. Bigatello LM, Hurford NE, Pesenti A - Ventilatory management of severe acute respiratory failure for Y2K. Anesthesiology, 1999;91:1567-1570.         [ Links ]



Correspondence to
Dr. José Otávio Costa Auler Junior
Address: Instituto do Coração do Hospital das Clínicas da FMUSP
Av. Dr. Enéas Carvalho Aguiar, 44
ZIP: 05403-000 City: São Paulo, Brazil

Submitted for publication January 31, 2001
Accepted for publication May 2, 2001



* Received from Disciplina de Anestesiologia do Departamento de Cirurgia da Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, SP

Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License