Welcome back to the tasty morsels of critical care podcast.
Oh Chapter 37 is dedicated to NIV in the ICU and is probably worth some time given that this is a common respiratory support both in the ICU and throughout the hospital.
Many of the benefits of NIV are similar to those seen with ventilation with the blue plastic tube through the vocal cords.For example you still get:
- positive airway pressure which recruits alveoli and improves oxygenation
- improved alveolar ventilation which improves minute volume and lowers CO2
- reduction in work of breathing as the machine is doing some of the work
- stabilisation of the chest wall eg in rib fractures
- reduction in transmural LV pressures acting as a sort of poor man’s IABP (more on that later)
The big advantage of course is that you get all the positives but avoid the blue plastic tube through the cords and all the hassle and complications that come with that.
But it’s not all unicorns and rose petals, the mask itself has a tendency to macerate the face over time and patients who are already feeling breathless and suffocating often don’t take kindly to having a plastic mask shoved over their face. Even if they do tolerate the mask it is frequently difficult to make a decent seal and maintain that lovely positive mean airway pressure that you’re looking for.
And while i did wax lyrical about the potential positives of positive pressure ventilation at the beginning of the post, it seems only fair to point out the negatives of positive pressure ventilation. It is clear that positive pressure ventilation is non physiological and is known to cause its own form of lung injury when applied through a plastic tube through the cords. The alveoli only see the pressure and care not which device it’s being delivered through, so there’s no good reason why NIV wouldn’t cause similar problems.
This of course brings up the unanswered and quite entertaining controversy over P-SILI or patient self induced lung injury that hit its zenith during the worst days of the COVID-19 pandemic. There were back and forth letters in the journals between some of the heaviest hitters in the ventilation world bouncing back and forth whether they actually believed self induced lung injury was a thing. Now this is not the post to explore it, but perhaps suffice to say that someone sitting with a resp rate of 30 for a week on 80% O2 and a PEEP of 10 on NIV may well be undergoing some of the same lung stress that any typical ventilated ARDS patient may be undergoing. NIV is not necessarily a free pass.
When it comes to modes, the names are, as ever, confusing and baffling. Overall they split into some kind of CPAP mode where airway pressure is constant throughout the respiratory cycle and a mode with pressure support set above the PEEP where the pressure increases above the baseline CPAP when the patient inspires. To make matters worse there’s no clear consensus in how the numbers are described. For example, our portable, single limb circuit, ward based NIV machines use the terminology EPAP and IPAP to describe the pressures with both numbers starting from zero. for example 10/5 would be a CPAP of 5 with an additional 5cmH2O pressure support whenever the patient expires. On an ICU vent this would be described as 5/5.
When would you reach for NIV over say one of the aforementioned blue plastic tubes through the cords? Well there are a number of now well established indications where it is entirely appropriate to try and temporise with NIV rather than just putting the tube in. I’ll give a brief summary of a few of them below:
Pulmonary oedema.
- the heart is poor, the lungs are wet and heavy and the sats are low. The patient is crying out for some CPAP. How might it help, let me count the ways.
- by increasing intrathoracic pressure you are decreasing the gradient of pressure between the low pressure at end disastole in the LV and the high pressure at end diastole in the aorta. As a result the LV has to do less work to pop open the AV and get blood moving forward to the aorta. This mechanism is somewhat akin (though probably not nearly as effective) to the afterload reduction with an IABP. hence the description of CPAP as the poor man’s balloon pump
- improving oxygenation by recruiting alveoli
- reducing work of breathing by giving a little boost as the chest wall tries to expand those wet and heavy lungs
- applying a little +ve hydrostatic pressure to the alveoli to get the fluid back into the vasculature where the furosemide can do its glorious work of diuresis.
- there is a clearly proven benefit for reducing intubations and improving oxygenation though the signal for mortality improvement is not as clear.
Exacerbations of COPD
- in this scenario the lungs are scarred and the airways constricted and obstructed. A minor sniffles can be enough to push them over the edge of respiratory failure and the CO2 is rising and the pH is falling and they do not have the respiratory reserve to up their work of breathing
- NIV, and in particular a mode with increased support during inspiration can improve the minute volume and clear the CO2 and wake them from their CO2 narcosis.
- This is a very well supported intervention with 14 or so RCTs showing benefit and an NNT to avoid intubation and death of 4 and 10 respectively .
Asthma
- now we have rapidly strayed into the evidence lite zone. It seems somewhat counterintuitive that a disease where the main issue is difficulty breathing out would be helped by adding positive pressure down the airway but it may be that the extrinsic PEEP is helping them overcome the intrinsic PEEP, or it could be that its reducing the work of breathing or it could be any number of potential arguable benefits. Still to be proven but commonly tried.
ARDS
- For a long time this was firmly in the controversial box and many would have argued that ARDS needs low volume low pressure ventilation, all of which we can not control in NIV. Meaningful trials were lacking. Then COVID came along and we all went mad with the old CPAP handing out CPAP masks with the coffee and dexamethasone on the morning ward round. Allowing that the bilateral infiltrates of COVID meet the definition of ARDS by any standard then it seems that NIV had found a role in the world of ARDS. That role and how far you might push CPAP before biting the bullet and tubing them remains to be defined. Yes I can keep this person going for 2 weeks on 90% FiO2 and a PEEP of 10 but is that really the best thing to do? There’s no sarcasm here, i really don’t know the answer to that…
Post extubation support
- so you’ve taken the tube out and they’re struggling, should you stick an NIV mask on or just put the tube back in? Again, data not exactly clear on that but it seems that if they’re failing extubation due to either pulmonary oedema or bronchospasm/COPD then it’s probably worth a go. hardly surprising seeing as they’re the two most solid indications we have already. If its’ not either of those then probably best just to put the tube back in.
Reading:
Oh’s Manual of intensive Care chapter 37
