pCO2

We want them to be in the middle of the road.

Same thing I believe holds true for our end tidal or our PCO2.

And I turned patients' vent rates up to 26 and felt really good about that 23 value for my PCO2 in the ICU.

And guess what? That harmed people.

The right spot, as of today, best evidence is somewhere in the middle to low normal,

The pathophysiology of this and its management is an essential part of neurophysiology.

You should be able to explain graphs relating to cerebral autoregulation, the effects of PCO2 and PO2 on cerebral blood flow, and the Monroe-Kelly hypothesis.

Also note that whilst historically an ICP of over 20 has been considered pathological, more recent guidance from the Brain Trauma Foundation has suggested that those of over 22 should be treated.

To minimise your learning trauma on this subject, Rachel.

Patients with moderate or severe TBI often require intubation.

Ketamine is now considered an appropriate induction agent for TBI, and this is discussed further in our ketamine episode.

Neuroprotective measures include nurse at 30 degrees head up, avoid tight tube ties which impede venous drainage, avoid hypoxia, PO2 greater than 13 kPa, and aim for normocarbia, PCO2 4.5 to 5 kPa.

Avoid high PEEP, or peak in spiritual pressures, as raised intrathoracic pressure impedes cerebral venous drainage.

That was less than ideal.

And, uh, his PCO2 was, um, 85.

And, uh, I, you know, I think that might've been why we're working by the way, when we actually did a core temp.

And this is one of my other pet peeves, right? Vitals are actually vital.

But I think what it hammers home is that all that initial volume that you inspired that you didn't get rid of, that's just dead space, right? So whatever little air gets in and out, like that 10%, you know, that's just like this like dead space ventilation.

You know what I mean? when we intubate patients with asthma and we allow them to like really decompress, very quickly their PCO2 gets better, right? It's like not, it's not like, it's not a getting rid of the PCO2 issue from like a lung perspective, like from a lung and alveolar capillary interface perspective.

It's an issue of like actually moving the gas out because they've been breathing so fast for so long, they've trapped a bunch of air and their effective alveolar ventilation, remember alveolar ventilation and sort of like total minute ventilation are two different things.

Your total minute ventilation is your alveolar ventilation and your dead space ventilation.

It's too hard because it becomes like a clinical bedside gestalt type thing.

But let's say you've got a gas and the pH was like seven or something.

And the PCO2 is like, you know, 70 or 80 or whatever.

I think the natural inclination is to want to like, you know, ventilate the patient a little bit faster, right? Or something like that.

Respiratory rate is 6, and the patient is on room air at a C-level destination.

And the patient's PaCO2 is 80, and the patient's PaO2 is 50.

Now, before blaming the lungs, which mechanism best fits this patient's respiratory numbers? Is it A, VQ mismatch? B, hypoventilation? C, intrapulmonary shunt? Or D, diffusion limitation?

This is a great question, and the correct answer is going to be B, hypoventilation.

Now, when you use the alveolar gas equation to calculate the oxygen available in the alveolus, on room air at sea level, inspired oxygen contributes about 150 millimeters of mercury.

Now, when you take that 150 and you subtract the PaCO2 divided by the respiratory quotient, which as many of us know is 0.8, alveolar oxygen is therefore about 50 because it's 150 minus 100, which is going to be 50.

And measured arterial oxygen is also 50.

So the AA gradient in hypoventilation is is essentially zero.

You should be reassessing your patients within 30 to 60 minutes to gauge for improvement or worsening, right? If they're breathing more comfortably with a reduced respiratory rate, reduced accessory muscle use, they look more comfortable.

These are all good signs that they're responding, okay? If they're oxygenating better and their pH is getting better and their PCO2 is getting better, these are all good, objective, quantitative signs that they are oxygenating and ventilating better, that the BPAP is working.

But if they're more tachypneic, their CO2 is going up, they have worsening acidemia, their oxygenation is getting worse, their mental status is starting to go, they can't tolerate the mask, we really should be considering it.

intubating these patients and putting them on mechanical ventilation.

EPAP primarily affects oxygenation and alveolar recruitment like we talked about.

The pressure support that also contributes to ventilation is the IPAP minus the EPAP because that's the true delta of inspiratory pressure that they're getting with each breath.

Increasing IPAP improves tidal volume and reduces PCO2, assuming that that creates better tidal volume and is within the confines of safety.

Increasing EPAP improves oxygenation through recruitment and improved FRC.

On the basic metabolic panel, carbon dioxide is an indirect measure of bicarbonate, which tells us about acid-base balance.

So don't confuse this with the PaCO2, which is a direct measure of carbon dioxide and obtainable from the ABG.

Elevated CO2 levels in the serum are associated with metabolic alkalosis and severe vomiting and diarrhea, while decreased levels are associated with metabolic acidosis, renal failure, and diabetic ketoacidosis, of course, among others.

I'm just pulling out a few common examples.

The pH had to be under 7.3.

The base deficit had to be at least four, and the PCO2 couldn’t be much above normal.

So this was mainly a metabolic problem, not a breathing one.

So a true metabolic acidosis, not just a low bicarbonate on the morning labs.

In the most severe acidemia, a pH of 7.1 or lower, there was a hint of lower mortality, a hint from a subgroup.

So back to that 2:00 in the morning call.

Our take? First, look at the whole gas, the pH and the PCO2, not just the bicarbonate.

Which is exactly how the trial picked its patients.