Tasty Morsels of Critical Care 040 | Respiratory Monitoring

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Welcome back to the tasty morsels of critical care podcast.

With extreme brevity we are going to try and cover Oh’s Manual Chapter 38 on respiratory monitoring. This is something of a hodge podge i must admit. I’ll start by looking at the lung mechanics section.

The first useful point is that the pressures recorded by the vent are usually interpreted as reflecting the compliance of the lungs when in fact they often are significantly impacted by the chest wall, most commonly in the case of obesity. The oesophageal balloon is probably our best way round this as it gives a fairly accurate surrogate for pleural pressure. There is some data supporting the use of an oesophageal ballon to guide PEEP titration by calculating transpleural pressure (PEEP – oesophageal pressure) and typically you end up on a higher PEEP in the obese patient than you would have otherwise. This is all theoretical for me as these devices have not been available to me throughout my training and the outcome data for their use has not been supportive but all the smart ventilator people talk about it when they give lectures.

Talking of PEEP, one of the things we have to look for is intrinsic PEEP, sometimes called auto-PEEP, sometimes called dynamic hyperinflation. Intrinsic PEEP adds to the work of inspiration, with additional effort needed to overcome the additional +ve pressure within the lungs. We most commonly measure this with the end inspiratory expiratory hold (as Dean points out, I misspoke and of course means end expiratory hold). The number generated here is the static intrinsic PEEP which should be distinguished from its cousin – dynamic intrinsic PEEP.

Dynamic intrinsic PEEP instead reflects the pressure change needed to initiate inflation of the lungs. Oh describes a way to measure it while pointing out its complextity as you need oesophageal and even gastric balloons to appropriately quantify it. All this is to say dynamix intrinsic PEEP exists and it’s tricky to measure.

in the same chapter we have patient-ventilator asynchrony and we are bemoaned for missing it. Oh describes this as most commonly caused by a failure of triggering and notes that the best way to pick it up is to look for deflections on an oesophageal balloon that are not followed by a breath from the vent. When you don’t have a balloon then you’re stuck with looking at the patient and the vent waveforms. Note deflections in the pressure waveform are much less sensitive for asynchrony than changes in the flow waveform.

Autotriggering, defined as initiation of breath without patient effort, comes in a few flavours with, cardiac oscillations and hiccups being well known examples.

One important concept to think of is that of matching the length of inspiration from the vent with the length of inspiration that the body wants. This is described as mechanical inspiratory time vs neural inspiratory time. Where the mechanical time is shorter than the neural time then the body is not getting the breath it wants either in terms of the duration or the flow of gas it wants. As a result the body triggers the next breath very shortly after the completion of the first. Occasionally the mechanical breath can be longer than the neural breath and as a result the lungs are passively inflated rather than assisted or supported.

Following on from this we have a few methods of measuring neuromuscular function. Firstly we have the P0.1 or the airway occlusion pressure. (I had this wrong, the P0.1 and airway occlusion pressure are distinct entities.) The P0.1 measures the negative pressure generated in the first 100ms of inspiration. In the spontaneously breathing patient on a support mode this gives you some idea of the work of breathing or respiratory drive. A normal value is somewhere in the 1-5cmH20 range and I have used this as a means of checking if the patient is working harder than I’d like in a PS mode.

The Toronto group has recently published on using the occlusion pressure as an alternative method that measures the “swing in airway pressure generated by respiratory muscle effort under assisted ventilation when the airway is briefly occluded”. You can see why they use detalPocc as a surrogate. Personally I would just call it the occlusion pressure but that is of course not very specific. This is done on someone breathing in a spontaneous mode. An expiratory hold is applied randomly and the negative pressure deflection as the patient inhales against a closed valve is measured. This number is the occlusion pressure. In their study they used the oesophageal balloon and some methodological wizardry to see how this occlusion pressure weighed up agains things like Pmus (the pressure generated by the respiratory muscles) and  the transpleural driving pressure. Overall they conclude that the occlusion pressure is a good surrogate for the presence of badness in these numbers while not being able to quantify them. This has relevance as we commonly sit back and relax when a patient goes on a PS mode and the peak and driving pressures go from bad numbers to good numbers. However there may well be adverse “dynamic lung stress” that is going on unmeasured unless you use this nifty little move to look for it. I suspect many of us do this automatically by eye balling the patient and their sterno cleido mastoids and their overall work of breathing. Even looking at how negative the swing on the pressure trace is before the vent kicks in is some kind of surrogate for this. What we do about this I am not entirely sure but I am now worried about patients even when they’re in a pressure support mode. Thanks a lot Toronto…

Another interesting way of monitoring NM function is to look at the electrical function of the diaphragm. A modified NG tube is placed with a sensor that picks up electrical activation of the diaphragm and uses this to trigger the vent. I have used this a grand total of once and found it intriguing but of little use in the n = 1 case series.

If you were still looking for other things to place in an SAQ on monitoring the vented patient then a mention of diaphragmatic ultrasound is worth throwing in. Basically you can visualise the diaphragm fairly well and use its observed thickening as a way of predicting various things about ventilated patients. It remains as far as i can tell a fairly niche application of PoCUS.

Finally I would like to point you to a site called RTMaven.com that comes out of the group in Toronto.  This has some wonderful respiratory monitoring calculators with some nice videos on how to perform the particular moves on our beloved servo-i vents. Highly recommended.

References

Oh’s Manual Chapter 38

Telias I, Damiani F, Brochard L. The airway occlusion pressure (P0.1) to monitor respiratory drive during mechanical ventilation: increasing awareness of a not-so-new problem. Intensive Care Med. 2018 Sep;44(9):1532-1535. doi: 10.1007/s00134-018-5045-8. Epub 2018 Jan 19. PMID: 29350241.

Conti G, Antonelli M, Arzano S, Gasparetto A. Measurement of occlusion pressures in critically ill patients. Crit Care. 1997;1(3):89-93. doi: 10.1186/cc110. PMID: 11094467; PMCID: PMC137221.

RTMaven.com