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Welcome back to the tasty morsels of critical care podcast.
Today we are going to talk about triggering on the ventilator. Now given the ubiquity of the word “triggering” in contemporary discourse I must confess that i do find it quite “triggering” to walk up to a vent and see the pressure support set at 11 or some other horror show like a PEEP of 7… I mean, who would do such a thing. But let me clear we are talking about a very different type of triggering.
If i was on a ventilator and somewhat engaged in the process of respiration at least at a brainstem level, I would feel a much more content if the ventilator cycled to inspiration whenever I requested it to. Indeed I would also find myself greatly contented if said ventilator did not randomly produce new inspirations any time it detected the slightest change in airway pressure. All of this is dependant on ventilator triggering.
Let’s start with the basics, the ventilator can be triggered to cycle to inspiration in a number of ways:
- time (in the case of mandatory ventilation, in fairness this is not really a trigger as the patient has no input)
- pressure trigger. The patient must produce enough negative pressure in the circuit to trigger the vent
- flow. The patient must produce a certain amount of inspiratory flow in the circuit to trigger the vent
My experience has been overwhelmingly with the ubiquitous servo ventilators found in many ICUs in Ireland. On the servo-i when you scroll through the menus you’ll see a dial for trigger. This dial is defaulted to flow trigger with a dimensionless number from 1-10 based on a proprietary software from Maquet. The more clockwise you turn the knob the lower the flow in the circuit the patient has to generate and therefore the easier it is to trigger inspiration. Swing it all the way right for the poor GBS patient who struggles to trigger. As the dial is turned left (or anticlockwise) then the trigger will magically switch to a pressure trigger with actual numbers in cm H20. These define the negative pressure in the circuit that has to be generated before the vent will trigger a breath. Thus flow triggers are easier for the patient and pressure triggers harder.
But when would you ever want to make the trigger harder for the patient? Typically it’s not actually that you want to make it harder for the patient, it’s more that you want to avoid autotriggering. A good example of auto triggering is commonly seen in the patient who has become dead by neurological criteria. The story at handover will typically be a devastating brain injury with some haemodynamic instability and loss of pupilary and cough reflexes but the trainee notes that brain death cannot have occurred because they are still triggering the vent. In this scenario it is quite common for the ventilatory to be auto triggering due to the minor fluctuations of flow within the circuit caused by the substantial cardiac oscillations of the hyperdynamic circulation of the person undergoing brain death. Simply switching from a flow trigger to a pressure trigger typically eliminates these auto triggers. Alternate sources of auto triggering can be the big air leaks of a bronchopleural fistula or a water logged circuit with a meniscus of rained out water oscillating back and forth in the tubing.
Failure of triggering is very common. In this scenario there has been a neurological trigger that may have even initiated some diaphragmatic contraction but it was missed by the ventilator. An oesophageal balloon is probably the gold standard here and you can use it to see if a negative deflection on the balloon is matched by a breath.
In the absence of a balloon (and aren’t we all?) we have to use some surrogates. It’s hard to detect but in some patients you can see a -ve deflection in the pressure waverform that is not matched by a breath. This may be the patient trying to trigger but failing. The flow waveform is similar but this time we’re looking for a +ve deflection of the expiratory slope. There are some nice pictures in the multiple references at the end of the post.
While it may seem inconceivable to many there is always the option of actually examining the patient. A hand on the sternocleidomastoid or tummy might make patient generated effort easier to recognise.
Intrinsic PEEP or gas trapping is one of the commonest causes of a failed trigger. Let’s say a COPD patient is emerging from propofol and fentanyl induced haze of 3 or 4 days on the vent for pneumonia. They are transitioning to a spontaneous mode as their respiratory drive increases. Unfortunately their obstructive lung disease is still an issue and the expiratory flow has not returned to zero before they try and take their next breath. Air is still exiting their body at a certain flow and pressure so they need to generate enough flow and pressure to reverse this gas in the circuit in order for gas flow to move from expiratory to inspiratory limb to allow the vent to recognize a trigger. You can often see this as artefact in the flow waveform.
There is an interesting technology called NAVA or Neurally Adjusted Ventilatory Assist . This involves a fancy NG tube that is placed in the distal oesophagus and picks up electrical signals from the diaphragm. This is then connected to the vent and allows the vent to know with a high degree of precision when the diaphragm is contracting and match the beginning of the breath to this. So even if the diaphragm is weak and ineffective the NAVA can pick up on the neural signal to breathe. Like most such things it’s been tricky to bring to widespread practice and trials showing signficant benefit are sparse.
Moving on from failed triggers there are 2 more concepts to discuss. 1) double triggering 2) reverse triggering. These can look quite similar at times and are often mistaken from each other but are quite distinct. Double triggering can be seen when neural inspiration is longer than mechanical inspiration; in other words the patient wants to take a really long drawn out breath in but the vent for any number of reasons has cycled to expiration before the patient was finished. This will be particularly common in partially controlled mode of vent where you’ve tried to set a small and “safe” tidal volume but the patients brainstem is having none of it.
The second one, reverse triggering is much more recently described and can be really quite subtle. It is usually seen in deeply sedated patients undergoing a control mode of ventilation. In this scenario the vent triggers the breath itself based on the set program. During the mandatory breath the diaphragm is activated and so as soon as the mandatory breath is over the vent senses the diagphrgm induced flow change and cycles into inspiration again. If you have something like NAVA or an oesophageal balloon you can see the diaphragmatic activation on the trace. Without one of these it can look almost like a hiccup. In addition look for a mandatory breath followed by a triggered breath during the expiratory phase.
As always this is by no means a comprehensive review of triggering but hopefully a little intro to some potential very examinable topics.
– Georgopoulos, D. & Roussos, C. Control of breathing in mechanically ventilated patients. Eur Respir J 9, 2151–2160 (1996).
– Good lecture on triggering from Brochard at the Toronto course
– Dres, M., Rittayamai, N. & Brochard, L. Monitoring patient–ventilator asynchrony. Curr Opin Crit Care 22, 246–253 (2016).
– Artigas, R. M. et al. Reverse Triggering Dyssynchrony 24 h after Initiation of Mechanical Ventilation. Anesthesiology 134, 760–769 (2021).
– Oto, B., Annesi, J. & Foley, R. J. Patient–ventilator dyssynchrony in the intensive care unit: A practical approach to diagnosis and management. Anaesth Intens Care 49, 86–97 (2021). [images above]