A 50-year-old obese (BMI 51 kg/m2) woman was intubated on October 25, 2014 for acute respiratory distress syndrome due to septic shock from skin and soft tissues infection of the left leg. Because PaO2/FIO2 was 117 mmHg on PEEP, 13 cm H2O and FIO2 0.60, she was placed in the prone position for 16 h under continuous i.v. sedation and neuromuscular blockade. As oxygenation improved, prone positioning was not resumed and neuromuscular blockade and sedation were stopped on October 27 and 28, respectively. On October 31, while Ramsay score was 6, she exhibited a respiratory pattern suggesting patient–ventilator asynchrony. Arterial pH was 7.40 and PaCO2 43 mmHg. As an oesophageal balloon was in place since her admission to monitor esophageal pressure (Pes), airflow, Pes, and airway pressure were recorded (Fig. 1). Deflections of Pes systematically occurred after each mechanical breath, defining a typical pattern of reverse triggering. Only the third breath was not followed by Pes deflection. The peak-to-peak Pes rate was the same (24 cycles per minute) as the breathing frequency set at the ventilator. Accordingly, we did not resume sedation and just waited. Her breathing pattern remained the same for 24 h, then inspiratory efforts re-appeared allowing weaning that succeeded on November 11, 2014. She was discharged alive from the ICU on December 2, 2014. The clear implication of this case is that should Pes be not recorded sedation would have resumed.

Fig. 1
figure 1

From top to bottom, recording of flow, esophageal pressure (Pes), and airway pressure (Paw) over time during mechanical ventilation in volume controlled mode with the following settings: constant flow inflation 0.71 L/s, tidal volume 0.340 L, respiratory rate 24 breaths per minute, inspiratory time 0.60 s. All mechanical breaths but one are followed by downward deflection of esophageal pressure (vertical continuous lines). None of mechanical breaths is triggered by the inspiratory effort of the patient, but rather each mechanical breath triggers esophageal pressure. The rate of set breathing frequency at the ventilator and that of peak-to-peak esophageal pressure (horizontal double arrowed lines) are equal (24 breaths per minute). For the third breath, the oesophageal pressure is in phase with airway pressure (vertical dotted arrowed line) and its morphology is in accordance with chest wall inflation. It should be noted that peak Paw was a bit high (38 cm H2O), while plateau pressure of the respiratory system amounted to 23 cm H2O. Therefore, the main reason for peak Paw is increased resistive pressure due to high inspiratory flow. It would be important in further cases to look at the effect of changing inspiratory flow, and hence Paw on the occurrence of reverse triggering