Strong spontaneous inspiratory efforts can be difficult to control and prohibit protective mechanical ventilation. Instead of using deep sedation and neuromuscular blockade, the authors hypothesized that perineural administration of lidocaine around the phrenic nerve would reduce tidal volume (VT) and peak transpulmonary pressure in spontaneously breathing patients with acute respiratory distress syndrome.


An established animal model of acute respiratory distress syndrome with six female pigs was used in a proof-of-concept study. The authors then evaluated this technique in nine mechanically ventilated patients under pressure support exhibiting driving pressure greater than 15 cm H2O or VT greater than 10 ml/kg of predicted body weight. Esophageal and transpulmonary pressures, electrical activity of the diaphragm, and electrical impedance tomography were measured in pigs and patients. Ultrasound imaging and a nerve stimulator were used to identify the phrenic nerve, and perineural lidocaine was administered sequentially around the left and right phrenic nerves.


Results are presented as median [interquartile range, 25th to 75th percentiles]. In pigs, VT decreased from 7.4 ml/kg [7.2 to 8.4] to 5.9 ml/kg [5.5 to 6.6] (P < 0.001), as did peak transpulmonary pressure (25.8 cm H2O [20.2 to 27.2] to 17.7 cm H2O [13.8 to 18.8]; P < 0.001) and driving pressure (28.7 cm H2O [20.4 to 30.8] to 19.4 cm H2O [15.2 to 22.9]; P < 0.001). Ventilation in the most dependent part decreased from 29.3% [26.4 to 29.5] to 20.1% [15.3 to 20.8] (P < 0.001). In patients, VT decreased (8.2 ml/ kg [7.9 to 11.1] to 6.0 ml/ kg [5.7 to 6.7]; P < 0.001), as did driving pressure (24.7 cm H2O [20.4 to 34.5] to 18.4 cm H2O [16.8 to 20.7]; P < 0.001). Esophageal pressure, peak transpulmonary pressure, and electrical activity of the diaphragm also decreased. Dependent ventilation only slightly decreased from 11.5% [8.5 to 12.6] to 7.9% [5.3 to 8.6] (P = 0.005). Respiratory rate did not vary. Variables recovered 1 to 12.7 h [6.7 to 13.7] after phrenic nerve block.


Phrenic nerve block is feasible, lasts around 12 h, and reduces VT and driving pressure without changing respiratory rate in patients under assisted ventilation.

Editor’s Perspective
What We Already Know about This Topic
  • Excessive spontaneous inspiratory efforts potentially resulting in high tidal volumes in patients on mechanical ventilation for acute respiratory distress syndrome may exacerbate lung injury

  • Strategies to control such efforts without involving overly deep sedation or neuromuscular blockade may be beneficial

  • Phrenic nerve blockade with local anesthetics has seen limited use for select medical indications but has not been evaluated in the setting of acute lung injury

What This Article Tells Us That Is New
  • The authors evaluated the effects of phrenic nerve block in a porcine model of acute respiratory distress syndrome and in nine patients with excessive inspiratory effort with acute respiratory distress syndrome on mechanical ventilation by evaluating transdiaphragmatic pressures and electrical activity, as well as distribution of ventilation by electrical impedance tomography

  • In both groups, tidal volume, driving pressure, peak transpulmonary pressure, and electrical activity of the diaphragm decreased significantly with phrenic nerve block, with a slight decrease in dependent ventilation, while the respiratory rate was unchanged

  • Duration of the block was approximately 12 h

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