Can capnography help the intubated trauma patient?

I had a conversation with a paramedic student recently, regarding a dyspneic patient who had either CHF or COPD. While I was explaining the utility of checking for JVD and other old-fashioned tests, she replied with "How about we just check the end-tidal CO2?" The dialogue about capnography continued something like this:

Paramedic: "The waveform might show some shark-fining, which would point to COPD, but if the nebs weren't working, and the patient looked shocky, you might worry that poor perfusion from CHF is producing a falsely low PetCO2, and you could start nitro."

Me: "After we intubate them, yellow means yes!"

I realized I wasn't contributing much to that discussion. 

Around the same time, I found a new study that looked at the use of end-tidal capnography to adjust ventilations for trauma patients, and the results were intriguing. So, in the interest of sounding smarter to the paramedic students, I plunged into the world of EMS capnography.

(Very) Brief review of capnography for EMS
People breath in oxygen, and breath out carbon dioxide. The level of carbon dioxide in the arterial blood is a very important number, and it's written as PaCO2, or the Partial pressure, in the artery, of CO2. Typically it runs around 35 - 45 mm Hg.

Google images - who knew?

This number is the one that counts when we're adjusting the rate or volume on a ventilator. Only problem is that we need to use a needle to draw an arterial blood gas (ABG), and then use a sizable machine to analyze the blood. It hurts too!

Of course, we breath out carbon dioxide, so we can also check the Partial pressure of CO2 as we breath out, especially the very last bit, at the end of the tide of airflow; the PetCO2. The point labeled "D" in the figure below marks the point at which PetCO2 is measured.

source

Usually the PaCO2 and the PetCO2 are pretty close to one another, and the arterial level is typically only 3-5 points higher than the end-tidal level. Another way to put it:

                   PaCO2 - PetCO2 ≤ 5 mm Hg

Well, usually that is ...

EMS and end-tidal capnography
EMS has been able to use capnography to do some important things. Rather than copy an extensive list, I'll turn this over to Peter Canning, over at Street Watch. He has compiled a list of the 10 Things Every Paramedic Should Know About Capnography, and it's a great focused summary. (Meaning, 90% of what I know comes from this article!). 

Of course, capnography can used to confirm intubation. It can also be used in cardiac arrest to check for ROSC, or assist in deciding on termination of efforts. Some evidence suggests that it has a role in diagnosing obstructive lung disease (asthma, COPD), as well as various other problems. 

First on his list, however, is its utility in monitoring ventilations, avoiding hypo- and hyperventilation. In the hospital, this is simple: If the PaCO2 from the ABG  is less than 35, the patient is being hyperventilated, and either the rate or the tidal volume needs to be decreased. With capnography, the numbers and waveform would look like this:

source

If the PaCO2 over 45, one of those parameters needs to be increased, because the patient is being hypoventilated. 

source

Because capnography is so much simpler and faster than using ABGs, it has been hoped that EMS could be able to modify ventilations just as well as in-hospital people can. So what does this recent study tell us about that potential?

"Utility of Prehospital Quantitative End Tidal CO2?"

Missouri EMS researchers wanted to test how well patients could be ventilated by EMS after intubation. They choose to focus on patients who had suffered either severe trauma or burns, and ended up with 160 patients (87% trauma, 13% burn-relate) who were transported to a level 1 trauma center. Overall, these were serious trauma cases - 75% had a GCS < 8 prior to intubation, and 1 out of 5 died in the hospital.

Paramedics had been trained in the use of end-tidal capnography to avoid hyper- or hypo-ventilation. During transport EMS recorded the PetCO2 levels, and adjusted the ventilations accordingly. Upon arrival to the ED, ventilations were maintained at the same rate and volume that EMS had used, and an ABG was obtained. The PaCO2 from this ABG was then analyzed against the end-tidal reading obtained during transport.

On average, the prehospital PetCO2 (34 mm Hg) was significantly lower than the ED PaCO2 (44 mm Hg); i.e. PaCO2 - PetCO2 = 10 mm Hg.  

This overall  difference between the PaCO2 and the PetCO2 only got larger when the sicker subsets of patients were examined. 

• Patients who died during hospitalization: PaCO2 - PetCO2 = 17 mm Hg.
• Patients with a pH < 7.2: PaCO2 - PetCO2 = 20 mm Hg.

So, were these results expected? What has the rest of the prehospital capnography literature showed? And how should we use capnography in the future?

FIrst, I'll review the studies that suggested that end-tidal capnography was potentially very accurate, and then I'll go over the studies that highlighted problems in applying it to the EMS patient population.


Studies that showed benefit of capnography
A 2003 helicopter study had suggested that capnography could help prevent hypoventilation in severely injured patients. Randomly assigned helicopter medics were able to use PetCO2 monitoring to adjust ventilation of intubated trauma patients, and ABGs were checked upon arrival to the trauma center. The patients were a mix of general poly-trauma, with high injury severity scores. The study suggested a big benefit - medics who had access to the ETCO2 monitor were far more likely to avoid hypoventilation and achieve normoventilation (although there was no change in hyperventilation).

Next, end-tidal CO2 was used to manage ventilations in a 2004 ground EMS study conducted in San Diego. The researchers enrolled 291 patients with severe head injury who had been intubated. Most of the patients had ventilation managed through standardized setting, but for about 1/2 of the patients the paramedics had ventilator management protocols that targeted a PetCO2 of 30-35 mm Hg, and avoided a PetCO2 < 25 mm Hg. As in the present study, the PaCO2 was confirmed by ABG after arrival at the ED. The use of the end-tidal capnography resulted in about 8% less hyperventilation.
 
Studies that suggested problems with it.
A 2005 study was conducted by a French EMS agency that uses specialist physicians, and uses ambulances equipped with ventilators, end-tidal capnography, and portable ABG analyzers as well. They looked at 100 patients that had been intubated over the course of 16 months, and examined how the PetCO2 levels corresponded to the PaCO2. An important note: only the PaCO2 values were used to adjust the vent. The patients were a mix of medical and trauma. They found that, even though, on average, the PaCO2 was the same as the PetCO2, there was significant variability in individual patients.

•  For 27% of the patients: PaCO2 - PetCO2 > 10 mm Hg
•  For 2% of the patients: PaCO2 - PetCO2 < -10 mm Hg

In other words, over a third of the patients would have been ventilated using false setting, had PetCO2 been used. In graph form:

An ED-based study from 2009, by Korean researchers, looked at 66 patients with severe head injury who had been intubated in the ED, and were mechanically ventilated. ABGs were obtained simultaneously with PetCO2 readings, and the paired values were compared. In general there was a good correlation between the two methods, and the PaCO2 exceeded the PetCO2 by less than 4 mm Hg, on average. However, this relationship broke down in the sicker patients; e.g. those with acidosis, greater injury scores, hypotension, or chest trauma.

A second 2009 trial conducted on 180 trauma patients who were intubated in the ED showed an extremely poor relationship between PaCO2 and PetCO2 obtained simultaneously. In the subset of patients with an isolated mild head injury the correlation was somewhat better. Noentheless, the authors concluded that: 

If the recommendations for ventilation to an PetCO2 of 35 mm Hg to 40 mm Hg were implemented in this population, 80% of patients would have a PaCO2 > 40 mm Hg and 30% would have a PaCO2 > 50 mm Hg.

Not good!

How to use the results of this new study.
Although these studies employed a variety of protocols (for example, different definitions of hyperventilation), 2 common threads  emerge. 

The first is that if the trauma is either mild, or limited to the head, then PetCO2 is probably an accurate surrogate for PaCO2, and can be used to modify ventilations. On the other hand, if a person has sustained trauma to multiple organ systems, or is showing any signs of shock, then the PetCO2 may (or may not) significantly underestimate the PaCO2 - there's no way to know. You're flying blind, vent-wise.

It turns out that this is sort of a common theme in using end-tidal capnography - it works best in patients with a single problem, but loses utility when the patient gets complex. Specifically, PetCO2 is no longer accurate when the patient has problems both with ventilation and perfusion.

Take asthma and CHF as another example. Both can present with hypoxia, true, but asthma usually only involves the lung, a ventilation problem. A number of studies have shown that certain qualitative aspects of the waveform - the "shark's fin" - may serve as a way to demonstrate improvement or worsening. 

Source

On the other hand, CHF can involve both the pulmonary and the cardiac systems, at the least. There can be a complex relationship between things that drive the PetCO2 down (like poor perfusion from systolic failure) and those that drive it up (such as impaired ventilation from coexistent COPD). 

With these complexities, it isn't at all clear how to use end-tidal capnography in CHF, despite the advice offered in some EMS magazines. The best research that described using capnography to diagnose CHF versus COPD/asthma comes from a single article in the Croatian Medical Journal. Not something to hang your hat on.

By way of contrast, you can use PetCO2 to predict the degree of metabolic acidosis in pediatric DKA (studies here and here), or in pediatric gastroenteritis. These are strictly problems of metabolic acidosis (which would be reflected in the PetCO2), while only in the rare extreme cases would perfusion be affected.

The Bottom Line
The current study is consistent with prior studies, and it appears that end-tidal capnography is not yet reliable enough to use in severely traumatized or burned patients. Using capnography in this population runs the risk of underestimating the PaCO2, leading to hypoventilation.

ResQ-Pod 2: The story, and device, continues...

ResQ-Pod 2: Pod Harder.

 This study caught my eye caught my eye because the lead author is Stephen Smith, the author of one of the best ECG blogs out there. He also writes for other blogs, and at least one EMS ECG blog follows his work. Dr Smith is, in short, the man.

 The study also caught my eye because it uses a retooled version on the ResQPOD, now called the ResQGARD. I know a lot of EMS folk swear by the ResQPOD, but the recent evidence has not proven its value. So, it's interesting to see "part 2" of the ResQPOD saga.

Because Part 1 worked out so well.

The ResQGARD works on the same general physiologic principle as the ResQPOD. It allows for normal, unimpeded exhalation, and does not provide any PEEP. During inhalation, however, it slightly increases the force required to draw in a breath. The actively expanding thorax normally acts as a sort of "suction" to also pull blood up from the belly, but with this added resistance to the air inflow, this "suction" effect is magnified.

And there is some animal and human data to back up the claims for usefulness in treating hypotension.

Red means more blood, I guess.

This device is evidently "cleared" by the FDA for treating "low blood circulation," and various studies have shown an ability to raise the blood pressure in, for example, blood-donors, or in other models of hypovolemia or hemorrhage. You can check out some background device in this article from Journal of Special Operations Medicine, the coolest journal that you aren't reading yet.

"Oh, is that JEMS you're reading? That's cute."

This trial had two parts. In the first part, the device was tested in a randomized, controlled, and blinded fashion in the emergency department for patients with hypotension due to various causes. The primary endpoint was the maximum change in SBP over the first 10 minutes after placement of the device. They enrolled 47 hypotensive patients. These patients ended up with diagnoses of dehydration, sepsis, or hemorrhage most of the time. You can see the average change in SBP in the table below, broken down by the cause of the hypotension.

When they looked at the overall results, they found that patients who had the real device had an average rise in SBP of 12.9 mmHg, while patients who got the sham device only had a rise of 5.9 mmHg, a difference of 7 mmHg. They tell us that the difference is statistically significant.

In the second part, the device was used by EMS, with no control therapy, in an unblinded manner. It's not much of a study, and they were really only looking at "feasability" of using the device by prehospital providers. They also had 47 patients in this arm of the study, and they determined that, yes, it was feasible to use, and that patients tolerated the device well.

It's hard to interpret the data on the change in blood pressure, etc., in part 2, since, as we saw in the results of the first part, the average blood pressure tended to go up with or without the device. The bar graph below shows that the pressure came up to a statistically significant degree, but it can't tell us if this was better than doin' nuthin'.

So, what can we take from this paper?

In the end, not much. Let me list the reasons why:

1. The difference in SBP is statistically significant, but unclear if clinically significant.
2. Some of the causes for hypotension have established, beneficial treatments.
3. Some of the causes require no treatment, and improve on their own.
4. The majority of the literature supporting the use of this device is written, in part, by the inventor of the device.

The average difference in systolic blood pressures was 7 mmHg, which is pretty small. How much do you care about raising the pressure by 7 points? In addition, it looks like almost everyone's pressure went up somewhat, with or without the device. Remember that 7 represents the average difference - some patients didn't improve much with the device, and some people had a big jump in pressure with the fake device!

In another article about the ResQGARD (or ITD-7) written by Smith, the authors present this table:

"Treatable" ≠ "Proven effective for"

Let's look at the causes they list. First off, heat stroke is about heat load and mental status - the primary treatment is cooling, and hypovolemia is usually not a significant component of the problem.

The proper treatment of true dehydration is, well, hydration. As for sepsis, while hypotension is a manifestation of the problem, there is a large amount of evidence that large amounts of IV fluids, delivered rapidly, saves lives. Simply raising the pressure through other means is not appropriate.

Regarding hemorrhage, there is a thicket of controversy about optimum treatment. While much of current practice emphasizes normalizing the blood pressure, a lot of evidence suggests that "permissive hypotension" may be the best (non-)treatment. Where the ResQGARD falls in this area is not clear at all.

Lastly, orthostatic hypotension is usually transient, and requires no intensive therapy; e.g. juice & cookies after blood donation.

Let me speak of the appearance of bias in the studies supporting the ResQGARD. The inventor of the device is Keith Lurie, a cardiologist. I have no doubt that he has aspirations to advance medical science and save lives. Unfortunately, as the inventor of the device in question, and the owner of the company that sells them, he has a vested interest in selling the device. And, while it's not the most expensive medical device out there, it costs real money.

Look at the references listed in the paper. Of the 23 studies that Smith et al. provide as references, 20 had Dr. Lurie as a co-author. That's a real conflict of interest. By way of example, check out this intervew that appeared with Dr. Lurie in an EMS blog. He had an interesting take in the failure of the ResQPOD to show an effect in the ROC trial.

Interviewer: "I think many of us who have been following the ResQPOD were surprised by the recent announcement by the National Institute of Health that the ROC PRIMED trial was stopping enrollment. ...  Considering that the ROC PRIMED trial was a prospective, multi-centered, randomized clinical trial with large enrollment, are you concerned about these results?

Dr. Lurie: "To directly answer your question, I am not concerned with the results, nor am I surprised."

To sum up: The ResQGARD appears to have a statically significant effect in hypotensive patients, but the clinical effect, as well as the appropriateness of this therapy, are unclear. I don't think any EMS service should be stocking up on these yet.