Tasty Morsels of Critical Care 040 | Respiratory Monitoring
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 che...