This is a favourite topic of CICM examiners. The following past paper SAQs involve the ventilation of ARDS:

In brief summary:

Initial ventilator strategy:

Additional ventilator manoeuvres to improve oxygenation:

Ventilator strategies to manage refractory hypoxia


    Which mode of ventilation should I choose?

    Well, to be honest, it doesn’t really matter. In Question 20 from the second paper of 2014, the college recommends one "use a mode with which one is familiar".

    Lets say you have set a pressure control mode. You will still be able to get the desired volume, nine times out of ten. Similarly, if you set up a volume control mode, you will still keep your peak airway pressure under 28-30 cmH2O. Overall, historically intensivists tend to prefer pressure control ventilation over volume control when it comes to ARDS.

    If lung compliance appears to be poor, one could also consider decreasing the I:E ratio (eg. to 1:1.5, 1:1 or even 2:1). However one does this with the knowledge that the benefit seems to be largely theoretical and manipulating the I:E ratio does not seem to improve survival, even though it may improve oxygenation.

    Lung protective ventilation : choosing a tidal volume and respiratory rate.

    The ARDS network group of investigators published the results of the ARMA trial in 2000, which remains among the best-known studies in ICU literature. The group randomised patients to be ventilated with either 6ml/kg or 12ml/kg tidal volumes; the mortality difference was 31% vs 40% in favour of the smaller volumes. A subsequent meta-analysis has confirmed this mortality reduction.

    In this fashion, a 70kg person is ventilated with volumes of around 350-400ml, at a rate of 16 breaths per minute. The discomfort of breathing in such an unnaturally shallow way requires more sedation than would otherwise be required with conventional ventilation.

    One starts at 8ml/kg of predicted body weight; over the following few hours one adjusts this down to 6ml/kg, while increasing the respiratory rate. The maximum plateau pressure is maintained around 30cmH2O, although 28cmH2O may be a more sensible limit.

    Among the downsides of this strategy, the generally well tolerated respiratory acidosis is only one. Some authors have wondered whether some of the beneficial effect of lung protective ventilation may actually be the result of auto-PEEP, which develops when a higher respiratory rate is used. Others have questioned the influence of the increased sedation requirements; however these do not seem to be a constant feature- you only need deep sedation of the first day or so. Furthermore, it is probably unwise to extrapolate this strategy to patients with normal lungs.

    In summary, the key issues are:

    • Tidal volume factors into minute volume, and determines CO2 removal
    • Tidal volume also determines the degree of lung inflation and recruitment of atelectatic lung
    • Adequate tidal volumes are important in ensuring patient comfort and decreasing sedation requirements
    • Low tidal volume (6ml/kg) works well for ARDS patients, prevents volutrauma and improves survival; however its disadvantages are hypercapnea and need for higher levels of sedation.
    • As a ventilation strategy, there is no advantage to its use in patients whose lungs have a normal compliance
    • In fact in patients with normal lung compliance low tidal volumes may lead to atelectasis and deterioration of gas exchange

    Open lung ventilation: choosing the "ideal" PEEP setting

    The “open lung” is the welcoming term used to describe a state in which all available alveoli are aerated throughout the ventilatory cycle. I suppose the opposite would be “closed lung” ventilation, where the alveoli are all collapsed. The aim of this approach is to reduce the trauma induced by constant collapse and reinflation of alveoli, the so-called “cyclic atelectasis” which is thought to be a major cause of lung injury in ARDS ventilation. There are two trials, and though both show promise, each is hobbled by problems with methodology, not the least of which is an unusually high institutional mortality from ARDS, the tendency to use Brazilian patients with leptospirosis, and the tendency to ventilate the control group with high volumes. Thankfully, even though the benefit is uncertain, there at least seems to be no real harm in this ventilation strategy.

    The use of open lung ventilation rests in setting the PEEP around 2cmH2O above the “critical opening pressure”, the PEEP at which the majority of alveoli remain inflated at end expiration. The problem with this is obviously the finding of that critical opening pressure. ARDS is a heterogenous condition, and for any given PEEP there will always be lung units which are overdistended, and others which are collapsing on expiration.

    The art and science of determining the optimal PEEP for open lung ventilation is discussed elsewhere. In brief, one can use the following strategies:

    Sensible bedside options

    • Keep PEEP at some arbitrary (high) value: higher levels of PEEP have been associated with improved survival on the basis of a meta-analysis (Briel et al, 2013).
    • Adjust depending on FiO2 (ARDSNet protocol) - in this protocol, worsening hypoxia is matched by an escalation of PEEP, from a PEEP of 5 cmH2O at 30% FiO2 to a PEEP of 22-24 at 100% FiO2.
    • Lower inflection point: the pressure-volume loop can be used to determine the "critical opening pressure" of the alveoli, and the PEEP set to something slightly above this. 
    • Maximal static compliance: the PEEP can be adjusted up or down to determine the maximal compliance; at the optimal PEEP, compliance will be maximal - and increasing the PEEP beyond this magical point will do little to improve the compliance.

    Experimental and research options

    • Intra-pulmonary shunt: if the patient already has a PA catheter with continuous SvO2 monitoring, one can adjust PEEP until the SvO2 reaches a maximum value. However, one would not insert a PA catheter purely for this purpose.
    • CT of the chest:  it is possible to determine the ideal PEEP by looking at repeated CT scans of the patients at different pressures. The exposure to radiation alone is enough to make this an undesiarable option, let alone the logistics.
    • Oesophageal balloon manometry: one may be able to measure pleural pressure using an oesophageal balloon, and therefore calculate the transpulmonary pressure. If it were not for the cumbersome nature of the measurements, this might be the gold standard for PEEP titration.
    • Electrical impedance tomography: the electrical resistance of the thorax should plateau at the point where all the recruitable alveoli are recruited (Long et al, 2015); one may even be able to assess the degree of ventilatory inhomogeneity (and how this changes with recruitment menoeuvres).

    High PEEP ventilation

    How high, you ask? There are three trials to examine: ALVEOLI, LOVS and EXPRESS. The findings have been complied into a nice meta-analysis. The high-PEEP groups averaged around 12-15 cmH2O; the low-PEEP groups had about 8-9 cmH2O. Though overall there was no in-hospital mortality benefit, the authors were forced to conclude that there seems to be a small (5%) mortality benefit for the most severe groups, i.e. those with a PaO2/FiO2 ratio less than 200.

    In short, the more severe your ARDS gets, the higher a PEEP you ought to use, up to a possible limit of around 15. Though the ARDSNet protocol goes all the way up to 24, one might consider stopping short of this value (indeed many ventilators stop at 20 cmH2O)

    Recruitment manoeuvres

    Typically, one performs one of these by applying a high pressure (say, 40cmH2O) for a short time (say, 40 seconds or so). One is immediately rewarded with hypotension, and possibly also pneumothorax. Oxygen saturation also drops- because the additional positive pressure is transmitted to the pulmonary arteries, suddenly doubling the pulmonary arterial pressure and causing a transient, frightening episode of right heart failure.

    Does this strategy improve survival? Probably not, according to this Cochrane review. But, it does improve oxygenation temporarily. On can see the benefit of recruitment manoeuvres in patients who have accidentally become disconnected from the ventilator.

    Neuromuscular junction blockers

    In our pursuit for control over ventilation physiology, we often grope around for the cisatracurium ampoule. The switching off of muscles has several benefits in ARDS.

    Firstly, the contribution of chest wall compliance to lung compliance is removed. One may find that ventilation at a desirably low plateau pressure is only possible while the patient is paralysed.

    Secondly, the whole-body oxygen demand is decreased (as there are no contracting muscles at work) and so oxygenation of the still-active organs is improved.

    Overall, this strategy (one study found)  leads to a sustained improvement in oxygenation.
    Of course, one cannot treat one’s muscle fibres as mere obstructive oxygen thieves, hanging parasitically from one’s skeleton. Sustained neuromuscular blockade has its disadvantages



    ARDS Definition Task Force. "Acute Respiratory Distress Syndrome." Jama307.23 (2012): 2526-2533.

    Esteban, Andrés, et al. "Prospective randomized trial comparing pressure-controlled ventilation and volume-controlled ventilation in ARDS." CHEST Journal 117.6 (2000): 1690-1696.
    Gainnier, Marc, et al. "Effect of neuromuscular blocking agents on gas exchange in patients presenting with acute respiratory distress syndrome*."Critical care medicine 32.1 (2004): 113-119.

    Watling, Sharon M., and Joseph F. Dasta. "Prolonged paralysis in intensive care unit patients after the use of neuromuscular blocking agents: a review of the literature." Critical care medicine 22.5 (1994): 884-893.

    Armstrong Jr, Bruce W., and Neil R. MacIntyre. "Pressure-controlled, inverse ratio ventilation that avoids air trapping in the adult respiratory distress syndrome." Critical care medicine 23.2 (1995): 279-285.

    Hodgson, Carol, et al. "Recruitment manoeuvres for adults with acute lung injury receiving mechanical ventilation." Cochrane Database Syst Rev 2.2 (2009).

    Zavala, Elizabeth et al.Effect of Inverse I: E Ratio Ventilation on Pulmonary Gas Exchange in Acute Respiratory Distress Syndrome Anesthesiology: January 1998 - Volume 88 - Issue 1 - p 35–42

    Brower RG, Lanken PN, MacIntyre N, et al; National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Higher versus lower positive endexpiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351(4):327-336.

    Meade MO, Cook DJ, Guyatt GH, et al; Lung Open Ventilation Study Investigators. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):637-645.

    Mercat A, Richard JC, Vielle B, et al; Expiratory Pressure (Express) Study Group. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646- 655.

    Briel, Matthias, et al. "Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome." JAMA: the journal of the American Medical Association 303.9 (2010): 865-873.

    De Campos, T. "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 Med342.18 (2000): 1302-130g.

    Putensen, Christian, et al. "Meta-analysis: ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury." Annals of internal medicine 151.8 (2009): 566-576.

    de Durante, Gabriella, et al. "ARDSNet lower tidal volume ventilatory strategy may generate intrinsic positive end-expiratory pressure in patients with acute respiratory distress syndrome." American journal of respiratory and critical care medicine 165.9 (2002): 1271-1274.

    Kahn, Jeremy M., et al. "Low tidal volume ventilation does not increase sedation use in patients with acute lung injury*." Critical care medicine 33.4 (2005): 766-771.

    Hodgson, Carol L., et al. "A randomised controlled trial of an open lung strategy with staircase recruitment, titrated PEEP and targeted low airway pressures in patients with acute respiratory distress syndrome." Crit Care 15.3 (2011): R133.

    MANCINI, MARCO, et al. "Mechanisms of pulmonary gas exchange improvement during a protective ventilatory strategy in acute respiratory distress syndrome." American journal of respiratory and critical care medicine 164.8 (2012).

    Amato, Marcelo Britto Passos, et al. "Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome." New England Journal of Medicine 338.6 (1998): 347-354.

    Chu, Eric K., Tom Whitehead, and Arthur S. Slutsky. "Effects of cyclic opening and closing at low-and high-volume ventilation on bronchoalveolar lavage cytokines*." Critical care medicine 32.1 (2004): 168-174.

    Amato, Marcelo BP, et al. "Driving pressure and survival in the acute respiratory distress syndrome." New England Journal of Medicine 372.8 (2015): 747-755.
    Guérin, Claude, et al. "Prone positioning in severe acute respiratory distress syndrome." New England Journal of Medicine 368.23 (2013): 2159-2168.
    Young D, et al. " High-frequency oscillation for ARDS". N Engl J Med 2013, 368:806-813
    Ferguson, Niall D., et al. "High-frequency oscillation in early acute respiratory distress syndrome." New England Journal of Medicine 368.9 (2013): 795-805.