Volume 55, Issue 7 p. 676-677
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Brainstem death and ventilator trigger settings

S. M. Willatts

S. M. Willatts

Consultant in Charge, Intensive Care Unit, Bristol Royal Infirmary, Bristol BS2 8HW, UK

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G. Drummond

G. Drummond

Senior Lecturer in Anaesthesia, Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, UK

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First published: 24 December 2001
Citations: 32
Dr S. M. Willatts


A patient with cerebral infarction was certified clinically brainstem dead. However, 4 h after the diagnosis of death, while the patient was being ventilated using the biphasic positive airway pressure mode, the ‘assist’ indicator light on the Drager Evita 2 ventilator illuminated intermittently. There was no evidence of spontaneous breathing. ‘Triggering’ was probably caused by a decrease in airway pressure in time with cardiac contraction. The trigger flow rate is crucial as factors other than the patient's inspiratory effort can initiate flow from the ventilator with very sensitive settings.

Case history

A 64-year-old male was admitted to hospital as an emergency after collapsing at home. He had a history of hypertension and recurrent headaches that were treated with atenolol and a serotonin antagonist, respectively. Over the previous 5 days, he had complained of an increasing occipital headache.

On admission to hospital, he was comatose with equal and sluggishly reacting pupils. There was no movement on his right side, minimal movement on his left, and both plantar responses were extensor. The cerebral computed tomography (CT) scan appeared normal and lumbar puncture yielded clear cerebrospinal fluid under increased pressure. The provisional diagnosis was cerebral infarction and he was transferred to another hospital for mechanical ventilation.

Four hours after transfer, the patient's pupils dilated and he became haemodynamically unstable with initially hypertension followed by hypotension. At this stage, a contrast-enhanced CT scan showed a large posterior fossa cerebral infarction.

Sedation was discontinued and 6 h later the patient fulfilled all the criteria for brainstem death testing [1]. Two sets of brainstem death tests were performed 1 h apart, and both unequivocally confirmed brainstem death. After the apnoea tests, the Paco2 increased to 12 kPa on the first occasion and 10 kPa on the second. The patient's relatives were willing for organ donation to proceed and the necessary procedures were started.

After the diagnosis of brainstem death, the patient was ventilated on a Drager Evita 2 ventilator using the biphasic positive airway pressure (BiPAP) mode. The ventilatory pattern was 10 breath.min−1 with biphasic pressures of 15 and 5 cmH2O and a 1 : 2 inspiratory to expiratory ratio. The flow rate was set to ‘fast rise’ and the trigger sensitivity left at its default setting of 1 l.min−1. Four hours later, the attendant nurse looking after the patient noticed the ‘assist’ indicator light on the ventilator illuminating intermittently. The ventilator appeared to be triggering at 2 breath.min−1. When the ventilator was set to ‘assisted breathing’ mode (pressure support ventilation) with 20 cmH2O assist and 5 cmH2O positive end expiratory pressure (PEEP) the patient received 23 breath.min−1 with each breath preceded by illumination of the ‘assist’ indicator light. When the ventilator was set to continuous positive airway pressure (CPAP) mode with no assist setting, there was no evidence of respiration. The nursing staff and transplant co-ordinator were understandably anxious and uncertain about this situation, despite reassurance from the consultant medical staff regarding the certain diagnosis of brainstem death. The patient was extubated. No respiratory activity was seen and asystole followed.


The Drager Evita 2 ventilator had been regularly serviced by the hospital's own medical engineering management department and was subsequently found by them and the manufacturer to be in perfect working condition. One of the advantages of the BiPAP mode is that it will allow the patient to breathe spontaneously. The ventilator has a pressure transducer to detect airway pressure changes. If the pressure in the breathing system decreases below the preset value, the ventilator delivers a compensatory flow to restore the preset airway pressure value. When set to an assisted breathing mode, a breath will be delivered when the compensatory flow delivered exceeds a certain threshold (in this case 1 l.min−1). The ‘inspiratory’ effort is displayed by illumination of the ‘assist’ light. After triggering, the ventilator then delivers gas flow according to the set ventilatory pattern.

The trigger flow rate is crucial. The minimum flow value (1 l.min−1) is very sensitive and factors other than the patient's inspiratory effort can generate sufficient flow or pressure change to exceed the trigger threshold. Such factors could include leaks in the breathing system, moving the patient or breathing system and movement of condensed water in the breathing system if a heated humidifier is in use.

However, we believe that triggering in this patient was caused by a decrease in airway pressure in time with cardiac contraction. At end-expiration, there is no respiratory flow in the airway and the ventilator maintains a constant pressure. During cardiac systole, blood leaves the thorax more rapidly than venous blood returns so that there is a net loss of blood volume from the thorax [2, 3]. This may decrease the airway pressure sufficiently to trigger the ventilator if the sensitivity is great. During expiration, the respiratory system empties by passive recoil and expiratory flow progressively decreases as the respiratory system empties. During expiration, cardiac contraction cannot decrease airway pressure below the values necessary to trigger the compensation flow.

At the time this problem arose, the patient's arterial blood pressure was 170/80 mmHg which is a relatively high pulse pressure and may reflect a large stroke volume. He was not receiving any inotropic medication. The heart rate was 98 beat.min−1 when his ‘respiratory rate’ was 23 breath.min−1, a ratio close to 4 : 1. This supports our hypothesis that during inspiration, a large stroke volume could initiate flow and thereby trigger mechanical ventilatory support.

This was the first time the staff on the unit had encountered these conditions and the consequence was loss of organs for donation. To manage patients with brainstem death properly, the characteristics of ventilators with trigger mechanisms must be clearly understood. It is not easy to explain these circumstances to nonintensive care clinicians or to relatives who may see the ‘inspiratory trigger’ light as a sign of an inspiratory attempt. We wish to draw this problem to the attention of doctors in intensive care so that they continue to be confident in their clinical judgement, and avoid alarm when these circumstances arise.


We wish to thank Drager UK and Dr Suzanne Ludgate of Medical Devices Agency for help and advice in the preparation of this case report. The patient's relatives received a full explanation of the events and agreed to publication.