Mechanical ventilatory management in adult respiratory distress syndrome

Abstracts

JUSTIFICATIVA E OBJETIVOS: O objetivo deste artigo é oferecer ao leitor um resumo das normas já consagradas pela literatura a respeito da estratégia atual do manuseio da ventilação durante a Síndrome da Angústia Respiratória Aguda (SARA). Isto é de fundamental importância, já que a ventilação mecânica, como medida terapêutica, tem estado sob constante revisão e muitos artigos têm sido publicados a este respeito. CONTEÚDO: Este trabalho contém a revisão de 29 artigos e um livro, selecionados a partir de pesquisa de palavras-chaves realizada no MEDLINE. CONCLUSÕES: Muito se tem publicado a respeito de ventilação em SARA, porém, tende-se para uma estratégia de proteção pulmonar baseada em baixo volume corrente e altos níveis de PEEP. Outras medidas adjuvantes seriam tomografias computadorizadas seriadas de tórax, ajuste de PaO2, inalação de óxido nítrico, posição prona e ECMO (extracorporeal membrane oxygenation).

DOENÇA; VENTILAÇÃO

REVIEW ARTICLE

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

Correspondence

SUMMARY

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

RESUMEN

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).

INTRODUCTION

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 charts^1,2. 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.

METHODS

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.

RESULTS AND DISCUSSION

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 patients^6-8. 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 edema^9-12. 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 cmH₂O^6,7. 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.

CONCLUSIONS

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.

REFERENCES

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*

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

Publication Dates

• Publication in this collection
  10 Nov 2010
• Date of issue
  Dec 2001

History

• Received
  31 Jan 2001
• Accepted
  02 May 2001