A patient with a driving pressure of 12 cm H 2O when tidal volume is 4 ml/kg will have a normalized elastance of 3 cm H 2O/ml/kg. A patient with a driving pressure of 12 cm H 2O when tidal volume is 6 ml/kg will have a normalized elastance value 2 cm H 2O/ml/kg. It is simply the driving pressure divided by the tidal volume (measured in ml/kg predicted body weight, as usual). Normalized respiratory system elastance is easy to compute and interpret. Because lung volume is also correlated to height, normalizing elastance to predicted body weight corrects for variations in height and the resulting value more specifically reflects variation in lung volume. Smaller ‘baby lungs’ have higher elastance (and lower compliance) due to atelectasis and consolidation and resulting lung volume loss. Why was respiratory system elastance normalized to predicted body weight?Įlastance (and compliance) are variables that reflect ‘baby lung’ volume. Additionally, low tidal volume can lead to atelectasis when PEEP is not set appropriately. Heavy sedation limits spontaneous breathing and patient mobility and is associated with delirium and long-term morbidity. Lowering tidal volume can result in breath-stacking dyssynchrony (which effectively increases tidal volume!). Heavy sedation or possible neuromuscular blocking agents may be required to prevent the patient from demanding higher tidal volume. We limit tidal volume with the assumption that it will reduce VILI, but it can introduce other possible issues. While low tidal volume of 6 ml/kg of PBW is physiologically ‘normal’, patients with increased respiratory drive may demand higher tidal volumes. What are the possible harms of using low tidal volume? Additionally, we considered the possibility of harm with using lower tidal volume in patients with low elastance. If driving pressure is the true cause of VILI then there should be a greater benefit to lowering tidal volume in patients with high elastance, and a lesser benefit in those with normal or low elastance. Using randomized trials allowed us to infer causation based on randomized treatment assignment. This comparison was made in previous randomized controlled trials varied based on respiratory system elastance. We aimed to do this by comparing the effect of lowering tidal volume on mortality between patients with lower respiratory system elastance (in whom driving pressures would be low) and patients with higher respiratory system elastance (in whom driving pressures from the same tidal volume would be high). We set out to resolve whether the real target for lung protection should be driving pressure or tidal volume. Goligher the following questions to elaborate on the key information provided by this study. Recommendations have additionally been made to use 6 ml/kg of predicted body weight as a standard setting due to the reason that ARDS can go unrecognized approximately 40% of the time.(1) It is possible that the driving pressure resulting from the tidal volume, not the tidal volume itself, determines the risk of lung injury and mortality in patients with ARDS.(2)Ī recent study published in the American Journal of Respiratory and Critical Care by Ewan Goligher and colleagues assessed the benefits of using a lower tidal volume strategy.(3) They investigated the relationship of tidal volume and driving pressure on mortality in an interesting and intuitive way using respiratory system elastance normalized to predicted body weight. The use of low tidal volume (4-8 ml/kg of predicted body weight) has been considered the default way to ventilate patients with acute respiratory distress syndrome (ARDS) to minimize ventilator-induced lung injury (VILI).
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