Atrial Fibrillation: Sure, you can cardiovert it! But should you? (Part 2)

  In the first half of this post I emphasized a few points about AF. It can be triggered by a variety of non-cardiac sources - hypovolemia, alcohol, and especially sepsis can all exacerbate chronic AF, or provoke a new episode. You can cardiovert a hypotensive AF patient with any of those problems, and it might (might) fix the rhythm, but it would be unlikely to correct the underlying issue.

Need another example? Alright, how about AF and an ECG that suggests STEMI?
 
AF and proven STEMIs - first case
The examples above weren't actually hypotensive, but this last patient was. 

An elderly patient with a history of paroxysmal AF was transported by EMS for acute onset dyspnea, chest and abdominal pain. Things got more complicated when she arrested right upon arrival in the ED. 

Not the patient - this is me when the patient arrests 10 seconds after arrival.

 Fortunately, this meant that the patient got full, immediate, and successful resuscitation. The post-ROSC ECG, however, was concerning:

The patient had a pressure of 80/50 - what should the team have done next? If you say cardioversion, what would you have done if the first attempt didn't work? (or the second?)

(Also, does it help if you know that the prehospital ECG looked like this?)

Anything jumping out at you?

Well, you need a plan B in atrial fibrillation! In this case, the team decided not to re-shock a patient who had just regained their pulse, and who was apparently undergoing a STEMI. During emergent cardiac cath, a complete occlusion of their left anterior descending artery was found, and successfully stented.
 
AF and proven STEMIs - second case
I've talked about this case before, so I'll be brief. Midlle-aged woman, acute onset chest symptoms:

However, once the medic brought the rapid ventricular response (RVR) down a bit, and the symptoms improved a little, the computer message disappeared when the repeat ECG was obtained...

... but not the ST elevations, nor their apparent reciprocal changes. Her old ECG showed very normal inferior ST segments, supporting the diagnosis of an acute STEMI. During the emergent PCI, they found that an old stent in her RCA was 100% occluded.

On the other hand...
Some physicians are fairly skeptical about ST changes that are found in AF with RVR. As with other arrhythmias, you can end up with a variety of ST changes that resolve with the tachycardia. PSVT very commonly produces ST depressions, even in young folks with no heart disease. 

For example, despite the dramatic ST depressions (and aVR elevation!), this patient... 

ECG from a great case at EMS 12-Lead

 ... never had a troponin increase - no MI - and the ST segments normalized after cardioversion.

Stephen Smith, of Dr. Smith's ECG blog, also voices wariness about calling a STEMI in AF with RVR. He has a great case at his site that illustrates the lesson that, if the patient is losing units of blood from their GI tract, the cath lab is probably not the best first stop, even if the ECG computer is trying to tell you otherwise!

Pictured: Not a cath lab candidate.

So, when do you activate the cath lab? Do you wait to make the call until you've loaded the patient with diltiazem, or do you do it first thing? How long do you look for other causes, versus get everyone moving to the lab?

Ah, good question, and I wish I had some hard and fast answers. I don't know of any research that looks at this issue, and the experts can disagree. It's often going to depend on the clinical context, as well as evolutions in the ECG findings, echocardiograms, and comparisons with old ECGs - all of which are hard to do in the back of a rig!

The Bottom Line
This is a cornerstone of emergency medicine - if the rhythm is fast, and the patient is not doing well, and you think they are not doing well because of that rhythm, then the patient should be cardioverted. 

(Repeat - "they are not doing well because of that rhythm..." Important!)

This is clearly supported in our SHCGB protocols:

But we have seen in these posts a number of examples where cardioversion probably wouldn't have been effective, since the underlying medical issues needed treatment. Cardioversion isn't going to treat low magnesium, hypovolemia, and especially not sepsis!

Cardioversion for hemodynamically unstable AF is reasonable, but this isn't as "simple" as ventricular fibrillation. You need to consider the causes and aggressively treat them, and be ready with a "plan B."

Atrial Fibrillation: Sure, you can cardiovert it! But should you? (Part 1)

Some cardiac arrhythmias are exciting and fun for the prehospital provider. Ventricular fibrillation has, essentially, only one proven therapy, but needs a well-choreographed team to deliver it. Paroxysmal supraventricular tachycardia, on the other hand, has a far less dire prognosis, but the treatment is generally safe and dramatic - very satisfying for both the patient and provider!

Milwaukee Beers ≠ "well-choreographed team"

Unlike VF or PSVT, however, atrial fibrillation isn’t a fun rhythm to deal with, either in-hospital or prehospital, and there are many ways to screw up. Even the new edition of Nancy Caroline's Emergency Care in the Streets has little to say about management of atrial fibrillation, only mentioning that 

"Prehospital treatment of atrial fibrillation is rare because of the risks involved."

However, they don't describe those risks, or how to avoid them!

They are likely correct about the "rare" part - one study of atrial fibrillation treated by EMS backs this up - you just aren't likely to have a patient with atrial fibrillation that needs cardioversion or emergent diltiazem. On the other hand, atrial fibrillation is really common in EMS, and we should know a bit more about this. There are lots of recent articles and old insights about AF - how about we start with 4 things?

1. AF is often a symptom, not the disease

Some rhythms require treatment, regardless of the history or exam. In other words, sometimes we "treat the monitor."  AF is not like this.

Example: A medic recently brought us an older female with palpitations. Evidently this had started about 3 hours prior, and was just getting worse. She had been taking all her "heart pills," but had had some vomiting and diarrhea for the past day and a half. Her HR was 180, and she was somewhat hypotensive at 95/60. Her sat and RR were basically normal. 

A 12-lead was obtained:

ST-segment changes, rapid AF and hypotension - should the patient receive diliazem, metoprolol, or even cardiovert? These can the right answers for many rhythms with & without hypotension (e.g. VT, PSVT), but AF can be different.

The medic decided, based on the recent history of volume losses, that a fluid bolus should be tried. After 300 ml of NS he saw a change in heart rate, and recorded ECG #2:

The blood pressure settled out at 120s/70s, and the rest of transport was uneventful. She ended up getting some diltiazem in the ED, but it looked more like dehydration that caused her tachycardia, as well as impaired absorption of her medications.

This is very common - AF is often provoked or worsened by non-cardiac problems. A drinking binge can do it, and so can hyperthyroidism. A low magnesium, in some cases, may be responsible. Both a large pulmonary embolus (because of the right atrial strain), and an MI, may kick off AF. And as for alcohol...

2. Alcohol (too much or too little) and AF.
He was weak, had vomited at least 10 times that day, and couldn't stop shaking. This 40 y.o. man had stopped drinking 2 days ago, and had not done well since. The palpitations were the final straw, pushing him to come to the ED.

"Excuse me, did something crawl down your throat and die"
"It didn't die!"

His heart rate was bumping up over 200, but the ECG caught him at a relatively slow point:

His labs confirmed that he has dehydrated, with low levels of magnesium and potassium. His alcohol history, both the excess, and the abrupt cessation, also likely contributed to provoking a new-onset atrial fibrillation. 

He clearly didn't need cardioversion, but it also seemed premature to use diltiazem or metoprolol first. He received a liter of saline, some magnesium and potassium, as well as Valium for the withdrawal. This went a long way towards improving his heart rate, and he only needed a small dose of metoprolol after all that.

So, while he had atrial fibrillation, he had other medical issues (like the withdrawal) that were more important. This is actually pretty common - about 75% of patients who come to the emergency department who have AF on their ECG actually have a different primary diagnosis - the top three diagnoses are CHF, pneumonia, and chest pain. 

Patients with AF and an Alternative Primary Diagnosis in the ED

3. This is especially true for sepsis and AF.
I recently saw a patient brought in from a nursing home with AF at 170-180 bpm, as well as hypotension. Sorta looked like this:

LITFL

However, she also had a new history of a cough and altered mental status, although no documented fever. I decided to try a liter of saline first, rather than a bolus of diltiazem, thinking that the rapid ventricular response was due to pneumonia and metabolic stress. Fortunately, the bolus dropped the heart rate down to 110-120, and raised her BP. She was admitted to the ICU with a bad case of sepsis and pneumonia, no diltiazem or metoprolol needed.

This case was not unusual - it turns out there is a HUGE relationship between sepsis and AF. Some surprising facts:

• New-onset AF happens in > 6% of severe sepsis cases (or even 46%!)
• 14% of new-onset AF cases in the hospital occur during severe sepsis
• Mortality of patients w/ severe sepsis and new-onset AF is > 50%

AF & sepsis = bad news bears.

It isn't clear how AF should be treated in severe sepsis, besides treating the source of infection and supportive care. The use of rate-controlling medications (diltiazem and metoprolol) may "mask" the signs of sepsis, complicating the use of fluid boluses or pressors. Cardioversion with drugs or electricity pose their own hazards.

So, if your nursing home patient has new AF, think: Could this be sepsis?


To be continued!
So far these patients I've discussed haven't been terribly unstable. In my last example (to be posted soon!) I'll discuss a truly critical patient with paroxysmal AF, where cardioversion was not performed. I've already shown the ECG on the Mill Hill Ave Command Facebook page, but I'll share more elements, and how they relate to management.

Two ECGs - which goes to the cath lab?

A recent study suggests that a computer interpretation of the ECG can be extremely specific for diagnosing a STEMI; i.e. if the computer reads 

*** ACUTE MI  ***

you can take that to the bank.

This hasn't fit with my experience, and so I was very interested in Peter Canning's latest post, since it validated my suspicions. He found that the ECGs his system are acquiring show surprisingly poor sensitivity and specificity for STEMI, if you simply rely on the computer to diagnose. 

As an illustration of this point, I submit ECGs from 2 patients. 

(For more pairs of ECGs that show the problem with relying on the computer diagnosis of STEMI, click on the label "Paramedics need to read ECGs..." on the right.)

Case 1
Let's say that this was a middle-aged female, who started having substernal chest pain about 15 minutes ago. The EMS 12-lead shows:

Aside from diagnosing the patient as "borderline," anything else look suspicious?

Case 2
Again, a middle-aged female, this time with pleuritic chest pain and wheezing. An ECG obtained 5 minutes after arrival in the ED shows:

What's an appropriate next step? Call in the (cardiology) cavalry, or do a little sleuthing?

Call for a bat-stent? (source)

Resolution
If you look closely at  few of the leads, especially V3, you can see small spikes preceding the QRS. Since the computer hadn't seemed to notice, I adjusted the settings to recognize pacemakers. A second ECG then showed pretty much the same complexes, but a very different interpretation.

Fixed!

She turned out to have a fairly ordinary case of COPD.

How about case #1?

Evidently the patient was first transported to a non-PCI capable hospital. About 2 hours later she was on her way to a different hospital for an urgent cardiac catheterization. This gave EMS a unique opportunity to capture the evolution of the ECG over a time frame that we don't often find in urban/suburban EMS.

Frankly, I'm inclined to agree with the computer this time! But what did the computer "miss" on the first ECG?

Hyperacute T waves
As Peter found after analysis of his system's STEMIs, computers aren't good at recognizing the earliest sign of an MI on an ECG, the hyperacute T-wave. These are transient features, before the ST segment has had a chance to elevate, and EMS is in a unique position to find these on their initial ECG.

Stephen Smith has some great examples, some of which look very similar to case #2 here. For instance, this ECG was acquired by EMS, and was instrumental in suggesting ACS to the emergency physician:

Dr Smith's ECG Blog - 6/2011

Another case involved an anterior MI that was misdiagnosed as hyperkalemia because of the magnitude of the hyperacute T-waves:

Dr Smith's ECG Blog - 2/2009

Very similar to our patient #2!

The Bottom Line
For more teaching on hyperacute T-waves, follow the links above to the blogs written by Peter Canning or Dr Smith, or check out this review.

And remember - sometimes you have to treat the monitor, not just the patient. Just make sure you're not treating a mistaken computer!

The Chain of Survival - done right!

The American Heart Association has been using the phrase "chain of survival for years now. This imagery is used to emphasize the importance of an integrated response to a cardiac arrest. This is common sense - you and your gold patch aren't worth much if no one does CPR before you arrive. Or if no one even calls in the first place!

"He'll be okay!" - Source

We recently had a patient brought into the ED which beautifully illustrated this "chain" concept. And while this case did not get onto channel 12, it's a great example of what can be done when all the pieces work they way they should. I'll quote the AHA concept behind each link, and describe how it worked in that case.

1. Immediate recognition of cardiac arrest and activation of the emergency response system 
 Our patient, a 50-ish female, collapsed while at work. This was witnessed by her coworkers, fortunately, and 911 was immediately called.

2. Early CPR with an emphasis on chest compressions
Rather than waiting for EMS to arrive, or even having to be coached by 911 dispatchers, coworkers started CPR.

"They were doing quality CPR when we got there," recalled Christopher Lovell, the AMR paramedic who responded. "They knew what they were doing - probably had a medical response team at the company, from the way they were acting."

3. Rapid defibrillation
Even while the AMR unit was still enroute, the patient's coworkers were giving her every chance. They grabbed the AED available onsite, and they applied the pads, analyzed, and gave shock #1.

4. Effective advanced life support 
When the ALS unit arrived, they found the patient to be in VF, and gave shock #2. The VF continued, and they gave two more defibrillations before converting her into a sinus rhythm. Her blood pressure and oxygen saturation bounced back almost immediately, and they held off on intubating. A bolus of amiodarone was given to prevent VF recurrence, and they grabbed a 12-lead during transport:

Thoughts?

5. Integrated post–cardiac arrest care
EMS arrived in the ED with a patient who had great vitals (indeed, she has hypertensive), but who continued to have a poor mental status. She required RSI for intubation, while therapeutic hypothermia was started with ice bags. Her second ECG looked a lot like the first one:

After a detour for a head CT (She was oddly hypertensive for a post-cardiac arrest patient, raising suspicion that a subarachnoid or intercerebral hemorrhage had triggered the arrest. It happens.), cardiology swooped in to take her to the cath lab.

When I later got a chance to talk with the cardiologist who cathed the patient, he was thrilled to talk about the case. First of all, the infarct-related artery was not a surprise - a 100% occluded RCA.

But more importantly, the therapeutic hypothermia that we had started in the ED wasn't continued, but for all the right reasons. "By the time I had finished deploying the stent, she was moving around. We extubated her in the ICU, and she was talking to us an hour later!"

That's a good reason, we can all agree.

The Bottom Line
It's not just a catchy phrase or a silly graphic. The "chain of survival" works, and it depends on a robust, effective response from each link. 

'Cause even this guy needs the 4 other links!

When the STEMI disappears before you get to the ED!

So what do you do when your STEMI disappears? 

Spontaneous reperfusion (SR) is well-described in the cardiology literature. One moment you have a classic STEMI on the ECG, and the next you have nada. I wrote about just such a patient in a prior post. In that case, EMS had acquired this ECG in a patient with chest pain:

However, when her symptoms improved they ran a second ECG, and found:

This dramatic improvement suggests 2 questions. First, is this a good sign? Second, did the medics do anything (like oxygen, nitro, or aspirin) that could have caused the improvement?

Is this a good sign?
Yes.
 
In a 2008 study (Spontaneous reperfusion in ST-elevation myocardial infarction: comparison of angiographic and electrocardiographic assessments.), finding ≥ 70% resolution of ST elevation on the ECG was a very good sign, and predicted a far lower rate of bad things - mortality and re-infarct rates were 0% as illustrated in this graph:

SR = Spontaneous reperfusion

Other studies have also shown that  resolution of the ST elevation before PCI is associated with patent vessels before PCI, after PCI, and better outcomes overall. The table below gives you the numbers. (TIMI 3 flow = normal blood flow in the coronary artery, 0 = complete occlusion)

Source

Even if PCI was significantly delayed, the patients with SR in a 2008 study did very well. Only 8% of those patients had primary PCI (as opposed to 100% of the patients with persistent ST elevation. Again, check the graph:

A = PCI or lysis;  B = Primary PCI only

Onto the second question...

 

Do oxygen, aspirin, nitroglycerin, or morphine cause spontaneous reperfusion?

Hard to say. 

Although SR may occur in up to 15% of STEMIs, this isn't well-studied. One of the studies mentioned above (Relation of clinically defined spontaneous reperfusion to outcome in ST-elevation myocardial infarction) checked whether SR occured more often in patients who received aspirin or heparin from EMS or in the ED, and didn't find an association:

Dr Smith describes a STEMI case in which he felt that nitroglycerin had caused SR, and thus contributed to a delay in PCI. In his discussion he cites an abstract (copied below) from an EMS study, possibly the world's only clinical study on this topic. The brief version is that 6% of STEMI patients had partial or total SR in the period after NTG administration. Of course, it was retrospective, uncontrolled, etc. 

On top of that, it's hard to say if 6% is a high rate or not. Some researchers think the overall rate of SR in STEMI is about 15%, so 6% may actually be lower than expected.

Source

As for oxygen, there's no evidence of any sort, good or bad.

The Bottom Line
Although a good number of patients have serial ECGs that show resolution of ST elevations, we don't exactly know why. Although these patients appear to be at lower risk of complication, it is hardly zero risk. When in doubt, get ECGs early and often.



*************************************************
Mahoney BD, Hildebrandt DA, Allegra P. 
Normalization of Diagnostic For STEMI Prehospital ECG with Nitroglycerin Therapy. 
Prehospital Emergency Care 2008;15:105, Abstract 24.
Hypothesis. The decision to take a patient for emergent reperfusion therapy is largely determined by an ECG diagnostic for ST Elevation Myocardial Infarction (STEMI). Hildebrandt et al have proven that  prehospital 12 Lead ECGs followed by an immediate call for reperfusion team mobilization reduce door to balloon times.We hypothesize that prehospital ECGs will normalize in some STEMI patients after  nitroglycerin (NTG)therapy or due to spontaneous reperfusion.  NTG therapy before an ECG, or the absence of a prehospital ECG capacity in some services may lead to missing the early diagnosis of STEMI thus delaying reperfusion therapy. 

Methods. A prospective analysis of consecutive adult patients  presenting to an urban/suburban two paramedic ambulance service fromJuly 15, 2006, to August 15, 2007, who have diagnostic ECGs for STEMI.  Paramedics managing a possible myocardial infarction patient were instructed to obtain rapidly an ECG prior to treatment with NTG. If the initial ECG was diagnostic for STEMI the paramedic called to mobilize the reperfusion team. A second ECG was done prior to arrival at the ED. The ECGs were later reviewed by emergency physicians and cardiologists who confirmed the presence of a diagnostic prehospital ECG and STEMI.  

Results. During the 13 month interval, 87 patients had an initial ECG that was diagnostic for STEMI. These patients received no NTG from the paramedics prior to obtaining the first ECG. An average of 16 minutes 42 seconds later, 3 patients had an ECG that was no longer diagnostic for STEMI and 3 had a partial normalization in their ECG that made diagnosis of STEMI more difficult. 

Conclusions. Prehospital ECGs diagnostic for STEMI can normalize or become nondiagnostic after NTG administration or due to spontaneous reperfusion or evolution. In the absence of a prehospital ECG, it is possible that 6 of 87 (7%) of STEMI patients in this study would have had reperfusion delayed due to a rapid change in their ECG. Limitations include no control group receiving NTG prior to the first ECG.

Hyperoxia during CPR associated with improved survival

There has been some great discussion on the web recently about the potential danger of hyperoxia. Mike McEvoy was interviewed on EMS 12-lead about the emergency and ICU evidence, and a vigorous discussion took place on EMTLIFE about the same topic. Rogue Medic weighed in as well, asking the question "How many hundreds of thousands of patient have we killed with oxygen and our refusal to require evidence of improved outcomes?" 

In the midst of this heated dialogue about reactive oxygen species, a recent study was published that may be an important addition to this discussion. 

The new paper
The study, "Increasing arterial oxygen partial pressure during cardiopulmonary resuscitation is associated with improved rates of hospital admission," was conducted in an Austrian EMS system. The ambulances are staffed with physicians, and are equipped with portable ABG analyzers as well. They retrospectively analyzed all non-trauma cardiac arrest calls over a 7-year span, and found 145 patients that had received ABG analysis of the PaO2 during the code. The ABGs were obtained after compressions, intubation, and 100% oxygen had been started. 

After dividing the patients into low, intermediate, and high levels of PaO2, they examined which patients had survived to hospital admission (HA), as well as the "cerebral performance category"(CPC) of the longer-term survivors. About half of the 145 cardiac arrest patients with an ABG had ROSC.

It turned out that patients with intermediate (61-300 mm Hg) or high (> 300 mm Hg) levels of PaO2 were incrementally more likely to survive to hospital admission. This positive association did not extend to showing a significant improvement in cerebral performance in survivors, however, despite a suggestive trend.

How does this fit with prior studies?
One retrospective study conducted in the ICU demonstrated an association between post-ROSC hyperoxia and increased mortality, while a similar trial showed no consistent association. No other trials have looked at pre-ROSC PaO2, however.

The accompanying editorial attempts to explain this seeming paradox - that hyperoxia pre-ROSC increases survial, but worsens survival post-ROSC - but I wonder if it is premature to try and reconcile these studies. Given all the known limitations of retrospectively-obtained data, and of this trial in particular, perhaps we should await controlled trials that more clearly define the role of oxygen levels and survival. As the authors note, "Reasons for the benefit of higher oxygen tensions during CPR can more easily be hypothesized than explained." Given the conflicting data, it might behoove us to proceed cautiously in modifying the targets for oxygen delivery in cardiac arrest.

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.