Autotriggering of pressure support ventilation during general anaesthesia

Abstract

We are writing to report a complication of the use of patient-triggered, pressure support ventilation during general anaesthesia. This mode of spontaneous ventilation has been used for a long time in critical care but has only recently been introduced to general anaesthetic practice. A 61-year-old man underwent ureteroscopy under general anaesthesia induced with propofol and maintained using total intravenous anaesthesia with infusions of propofol and remifentanil. A size five laryngeal mask airway was inserted. A patient-triggered, pressure support ventilatory mode was chosen on the anaesthetic machine (Dräger Fabius, Dräger Medical UK Ltd, Hemel Hempstead, UK), with an inspiratory pressure of 12 cm H2O and a flow trigger of 2 l.min−1. The machine was set to deliver eight mandatory breaths per minute as the patient was unlikely to breath spontaneously on the remifentanil infusion. This mode of ventilation was chosen to allow the patient to take spontaneous breaths, when appropriate, without ‘fighting the ventilator’. It was also used to enable a smooth transition between apnoea and spontaneous ventilation. The patient appeared to start breathing immediately, with a spontaneous respiratory rate of 10 breaths per minute and tidal volumes of 500–540 ml. The end-tidal carbon dioxide was measured at 5.3 kPa. The patient was transferred to the operating theatre and surgery commenced. A few minutes later it was noted that the patient's respiratory rate had increased to 25 breaths per minute while tidal volumes remained at 500–540 ml. The end-tidal CO2 dropped to 4.5 kPa after a further few minutes. The heart rate and blood pressure remained stable. It was felt that the patient may not have been adequately anaesthetised and therefore the TIVA infusion was increased. This had no effect on the respiratory rate. The end-tidal CO2 continued to decrease (4.1 kPa). Since all the other clinical signs suggested that he was adequately anaesthetised, it was suspected that something was inappropriately triggering the ventilation. The flow trigger was increased to 3 l.min−1, with no effect. At the end of surgery the TIVA was discontinued and the pressure support was stopped. However, the patient did not make any respiratory effort. It was noted that cardiac pulsations could be felt in the bag connected to the circuit. He was commenced again on pressure support with the flow trigger set to 3 l.min−1. Ventilation started again with a respiratory rate of 25 breaths per minute and tidal volumes of 500–550 ml. It seems likely therefore that the patient's cardiac oscillations had been triggering the pressure support. His respiratory rate throughout surgery was 25 breaths per minute and his heart rate was 50 beats per minute, which suggests that the pressure support was being triggered by every other pulsation. We hand ventilated the patient until spontaneous ventilation returned. Shortly afterwards he was awake and the laryngeal mask was removed. We believe that this is the first description of cardiac oscillation triggering of the pressure support ventilation in patients during general anaesthesia. Anaesthetists are aware of the ability of cardiogenic pulsations to cause pressure or flow changes in a ventilatory circuit. This can be seen as small movements of the bag connected to the circuit or small oscillations in the capnograph trace. However, since the use of patient-triggered ventilation has only now become available to general anaesthetic practice, anaesthetists may not be aware of the existence of triggering due to cardiac oscillations. Triggering caused by cardiac oscillations is recognised in intensive care [1]. Flow triggering imposes less inspiratory workload than pressure triggering and is used more frequently [2]. The flow trigger is normally set at 2 l.min−1 but is occasionally too sensitive, leading to triggering of ventilatory support in mechanically ventilated patients [3]. This is known as autotriggering. Imanaka et al. report that patients with more dynamic circulations and lower respiratory resistance are more likely to autotrigger [1]. Increasing the trigger threshold may eliminate the problem. In our case increasing the threshold to 3 l.min−1 had no effect, and a higher threshold should have been set.