COPD: Is EMS Killing Patients with Oxygen? (2)

The Tasmanian Study
Disclosure - the lead author used to be my partner. We were both medics at the same two agencies (volunteer and hospital) in New Hampshire. He never seemed to run out of energy, and it doesn't seem like that's changing!

And since we're talking about Tasmania, we might as well get this out of the way...

Dr. Austin at work.

Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial was well done, especially for EMS research. It's unfortunate that the bar is so low in our corner of health care research, but Austin et al. are working to change that.

The study utilized an EMS service that covered both rural and urban settings, but transported to only one hospital. Paramedics were supposed to identify patients with "breathlessness and a history or risk of COPD," and enroll those patients that they suspected of having an acute exacerbation of COPD.

Most of the treatment was the usual stuff - salbutamol (aka albuterol), ipratropium, dexamethasone, etc. CPAP was not available. The only difference had to do with how oxygen got delivered.

Prior to treatment, patients were randomized to receive either titrated oxygen, delivered by nasal cannula to maintain a sat around 90%, or high-flow oxygen, administered by NRB mask.  Transports lasted an average of 45 minutes, and then the folks in the ED treated as they saw fit.

Before we look at the results, you have to understand two huge issues:

• Only about half of the patients had pre-existing COPD, as judged by a pulmonologist. There's no description of what the rest had. Perhaps many of them had a new diagnosis of COPD, while others where actually pneumonia or CHF with wheezing.
• There were a lot of protocol violations: 56% of the titrated-oxygen group got high-flow oxygen, while 21% of the high-flow group didn't get high-flow.

With those facts in mind, they found:

Note how the results are broken down by all patients versus only those patients with previously confirmed COPD. The most important result is that there's a 5% difference in mortality for all of the patients.

So, what's the problem? It seems to be pretty clear evidence that paramedics should be withholding oxygen in suspected COPD exacerbations, but there are a few reasons why we should be cautious in using these results on the streets tomorrow.

1. The results seem almost too remarkable to be true.
They show 5% increase in mortality between the high-flow and the titrated oxygen groups.  That's a "number needed to harm," or NNH, of 20. In other words, for every 20 patients you give a NRB to, 1 will die.

That's a really high number! Usually you have to do a lot of work in medicine to show that kind of effect. For example, you have to treat 20 STEMI patients with aspirin and streptokinase (versus placebos) to save one life.

And you know all that fuss about rushing the STEMI patient into the cath lab? We have to treat 50 STEMI patients with angioplasty (versus thrombolysis), to save 1 life.

Given this context, the result almost seems "too good to be true." Given that there is little randomized controlled data out there with similar results, and given the good-quality data that conflicts with it (as with the ICU studies described in the prior post), it is reasonable to be skeptical about the conclusions, and await validating data.

2. The oxygen therapy was brief.
The intervention only lasted during transport, on average about 45 minutes. Compare that with the Gomersall study in my last post, where patients in the ICU received higher levels of oxygen for 2 days. While certain brief EMS interventions can have important long-term consequences (defibrillation anyone?), the onus is on the authors to make the case that it was solely the EMS intervention that differed between the two treatment groups. They concede that it was difficult to isolate the effect of the EMS intervention, and state that:

"Unfortunately, collection of data on in-hospital management was beyond the scope of the study, so we cannot dissect the effect of prehospital and in-hospital oxygen administration."

3. Paramedics don't treat "confirmed" COPD
Although withholding oxygen in the cases of "confirmed" COPD looked very effective, the unfortunate truth is that paramedics apparently misidentified half of the patients as COPD.

Now, this may not be entirely true. Some of the "non-confirmed" cases may have been a first-time COPD attack, and the medics were spot on. Or, perhaps some of the cases were actually, say, CHF, or pulmonary emboli. We aren't given any data on what this sizeable subgroup was ultimately diagnosed with.

Remember, though, that most other causes of hypoxia are treated with oxygen. With that in mind, we are left to consider the effect on mortality for the patients who did not have COPD. It does not seem likely that their treatment was improved by leaving them hypoxic.

By the way, this is the same reason you don't treat "hyperventilation" with a paper bag. Seriously, you aren't doing that, are you?

"Med control, we have a problem."

4. There was no difference in rates of mechanical ventilation.
In general, it's hard to show a difference in mortality for any given therapy, because deaths are far less frequent than other bad events. For instance, you need to treat 13 patients in CHF with non-invasive positive pressure ventilation (NIPPV) to prevent 1 death, but you only have to treat 8 patients to prevent an intubation (figures from The NNT).

In fact, we also know that NIPPV cuts the rate of mortality of COPD exacerbations by about 42%, but drops the intubation rate more, by 52%.

So it's kind of odd to see this profound difference in mortality, but no difference in the rates of mechanical ventilation. Similarly, there's no difference in the average length of hospital stay here, another sensitive measure of the effectiveness of a therapy.

5. Oxygen is not the issue.
Ultimately, the study is not asking a relevant question. We know that COPD is primarily an issue of impaired ventilation, and that NIPPV is the treatment of choice for severe exacerbations, along with steroids, bronchodilators, and antibiotics.

In a way, designing a study that only looks at levels of oxygen delivery in COPD exacerbation is sort of like designing a CHF study that only focused on fluid restriction, but didn't use nitroglycerin or NIPPV.

Yes, it would probably show a benefit of fluid restriction, but that's not the problem!

The Bottom line

1. Suppressing the "hypoxic drive" is a rare entity, and concern for it should not drive management.
2. Withholding oxygen could be very dangerous if you are wrong about the diagnosis.
3. Treat bad COPD with bronchodilators, steroids, antibiotics, NIPPV, and, if hypoxic below their baseline, oxygen. Intubate PRN.
4. We're looking forward to more high-quality studies from Tasmania!

COPD: Is EMS Killing Patients with Oxygen? (1)

So this was one of the first bits of medical "lore" I learned as a spanking-new EMT-B. ("Lore" meaning things that are not found in textbooks, but that everyone knows are true.) You don't give oxygen by NRB to a COPD patient.

And you always leave a note. (Hurry up Netflix!)

Well, it turns out a lot of things I learned at that time have been discarded; MAST pants, the EOA, the long spine board (soon, soon...). How has high-flow oxygen fared?

Are we killing patients?

A recent study suggests that the old-time myth was true. In fact, if this study is corroborated, we may need to change our practice somewhat. The one-sentence summary of Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial is:

For high flow oxygen treatment in patients with confirmed chronic obstructive pulmonary disease in the prehospital setting, the number needed to harm was 14; that is, for every 14 patients who are given high flow oxygen, one will die.

That's a really high number.

By comparison, when we rush a STEMI patient to the cath lab, or give then thrombolytics, we have to treat 50 patients to save one life. This study suggests that we can save far more lives by using a nasal cannula instead of a face mask. Can this be true?

Let's first take a look at some older evidence, giving us some context. In the following post we'll go over the new article that has generated so much interest, and see if some practical conclusions can be drawn.

Two ICU studies
The authors of Influence of inspired oxygen concentration on deadspace, respiratory drive, and PaCO2 in intubated patients with chronic obstructive pulmonary disease wanted to study this (possible) myth of the hypoxic drive. They studied the effect of increasing oxygen delivery to a very sick bunch of COPD-ers, 12 patients who had already been intubated after a bad COPD episode. These patients were just starting to recover, being weaned from the vent, able to breathe or their own, and were likely to be extubated in the next day or so. 

The researchers bumped up the oxygen level to 70% for 20 minutes, and checked what happened with the vent and the blood gas. Although 70% doesn't seem high, it is actually right about what we are delivering with a standard non-rebreather mask at 15 lpm (See Weingart's article for explanation; PDF if you prefer).

So what happened? Apnea? Bradypnea? Failure of the hypoxic drive????

They, uh, got more oxygen. That's it. In this population of sick-sick-sick patients, nothing happened.


Okay, you say, perhaps they were a delicate population, but they had been getting beta-agonists and steroids, and probably antibiotics for a few days. That's the whole reason, after all, that they were being weaned off the vent - they were now better. 

Maybe we should instead look at patients who are not yet intubated, but might be if just one more thing tips them over.

"Our study included one patient - this guy"

So, back to the ICU. The authors of Oxygen therapy for hypercapnic patients with chronic obstructive pulmonary disease and acute respiratory failure: a randomized, controlled pilot study. looked at patients right on the brink, with PaCO2 > 50 mmHg, and PaO2 < 50 mmHG - members of the 50/50 club! They were not yet intubated, but it could go either way.


The investigators titrated oxygen up with Venturi masks to two different levels, either a PaO2 of > 50 mm Hg in 17 patients, and > 70 mm Hg in another 17 patients. They got all all the usual meds, of course. As expected, some of these very sick patients had to be intubated, and some even died. The rates of intubation and death, however, were the same in each group. And no CO2 retention either!

So why all the fuss? As an editorial in Critical Care Medicine pointed out, the main evidence for the harm of oxygen in COPD exacerbations comes from the 70s, a time before noninvasive ventilation, routine steroid use for COPD, and even Atrovent was barely a year old! Another editorial from the same journal lays into the medical-education complex for perpetuating this lore:

"One sample of medical mythology is the commonly told story that the administration of oxygen to a patient with chronic obstructive lung disease will shut down the patient's hypoxic respiratory drive and lead to apnea, cardiorespiratory arrest, and the subsequent death of the patient. ... It is not clear where this fallacious information comes from, but it seems to enter the medical information database at an early age, at the medical student or resident level, almost like a computer virus corrupting the appropriate function of the equipment. In addition, this myth becomes very difficult to extinguish during the career of the physician, even with clear factual information of long standing. The danger here is that this medical mythology will inappropriately influence treatment decisions in patients."

The Bottom Line
This is hardly a comprehensive review of all the literature out there on the topic, but most of the other studies are observational, and it's really hard to draw firm conclusions from that sort of data. I haven't bothered to review them here, because why waste our tine if higher-quality studies have been done?

With this background, I'll discuss the important EMS study from 2010 in the next post.

STEMI with a twist... and then a second twist!

This would make a lousy case for a EMS 12-Lead-style presentation, because it's a little to difficult to predict the outcome. And I can't really find a new EMS study, or even an old one, to present with this. If there is any lesson to learn from this case, it would have to be: patients will keep you humble.

The Patient
The history was a little iffy, as the patient was elderly and had a history of both CVAs and dementia, and was variably describing either a week of chest pain or "Nothing! I'm fine!"

EMS had called with a STEMI, though, so I met the paramedics at the ED door, and they handed me the ECG:

You know, they say "treat the patient, not the monitor," but when this shows up on the monitor, you treat that.

We grabbed another ECG after cards had been called for the cath lab activation:

By the way,  I know some sharp readers out there are already asking for right-sided leads, but V4R didn't reveal too much. But even without that, one could make a stab at guessing the infarct-related artery - it seems sort of classic. The STE in III versus aVF, the depressions in aVL and I, not to mention V2, all pointed to an RCA lesion. Intern stuff.

And then the cards fellow asks me if I've seen the patients old ECG. Oh, give me a break...

Twist #1
Now, I almost always check the old ECGs before I call cards, but in this case I was wondering how the old ECG could possibly be relevant to this clearly acute ischemia...

Ah. I see.

This ECG was recorded a number of months prior. The patient, at that time, had been brought to the hospital for another medical emergency, and was incidentally found to have an apparent STEMI. The catheterization revealed a totally occluded RCA, likely chronic.

"What a twist!"

Sooo, no cath then?

Despite the vague history the patient provided, it seemed consistent enough with AMI. There was also some concern that the collaterals that were serving her right ventricle might have acutely occluded.On top of all that, the deep drop in her blood pressure (thankfully transient) after I gave her nitroglycerin seemed to confirm the ECG. Off to the cath lab she went, leaving me feeling only somewhat less sheepish.

Twist #2
And the infarct related artery was...

"Ta-da!"

The LAD.

A "hazy appearing" lesion was visualized fairly proximally in the LAD, just before the first diagonal. Just to be sure, they used the intravascular ultrasound to confirm the freshly-ulcerated plaque, and put in a few stents. All better!

Follow-up
Well, not really. Our patient suffers from "multiple comorbidities," and did not tolerate the procedure so well. A ballon-pump was placed to support her hypotension during the procedure, and during her subsequent hospital stay any number of issues have popped up; bleeding, sepsis, renal stuff.

And her current ECG, a month later?

Huh.

Bottom line
Stay humble. I like to think that I've gotten pretty good at guessing the culprit artery in STEMI, but I was out of my depth on this one!

Not yer usual STEMI.

The facts: a 35 year old male, with no medical history, presented with 1 week of chest pain that became acutely worse 1 hour prior. It was a "squeezing" feeling that radiated down his left arm. He had some mild dyspnea, and 1 nitro made it somewhat better. Some smoking, no cocaine.

The ECG:

The computer interpretation used caps lock,  had a lot of "***."

Cardiology was skeptical, but had him in the cath lab 30 minutes later. My resident put 50 cents down on a LAD occlusion, while I bet him a cup of (free) coffee that this was a classic first diagonal , or high lateral, STEMI. The two cardiology fellows agreed that we were both mistaken, and that they were certain to find a blocked circumflex. While the patient was in the lab the troponin came back as significantly elevated.

A few hours later, the cards fellow calls me back with the cath results.

Survey says!

No offense to Steve Harvey, but I'm a Dawson kinda guy.

Nada. Clean cath. "No significant fixed obstructive disease."

Interestingly, however, both ventriculography and an echo revealed hypokinesis of the high anterolateral wall, corresponding to the anatomy suggested by the ECG. He was given a diagnosis of focal myocarditis.

Focal Myocarditis

This isn't very common, but we can't say how uncommon. It is still uncommon enough to be worthy of case reports, at least in Texas. We know that about 3% of MIs have clean coronary arteries by angiography, but a number of those people have spasm or spontaneous reperfusion. The percentage may even be smaller with STEMI patterns, but we don't know.

The only way in the past to definitively diagnose myocarditis was through endomyocardial biopsy, which has a good number of shortcomings, in terms both of sensitivity, and of complications.

What could go wrong with this?

Advances in MRI techniques have enabled researchers to noninvasively study myocarditis. In a recent study it was found that 78% of patients who presented with an MI (64% with ST elevation), but a clean cath, had evidence of myocarditis on MRI.

Uh, yeah, I see it too...

Reciprocal changes

Now, I understand that the myocarditis can generate ST elevation, likely in the same manner that pericarditis does. I am really surprised, however, that our patient had such distinctive and appropriate reciprocal changes. Nonetheless, an ECG from a case report of myocarditis also shows reciprocal changes:

Turning to Stephan Smith's ECG Blog for some wisdom, I found this observation in "Is it MI or pericarditis?" (There's a lot of overlap between pericarditis and myocarditis, and many people link them on a spectrum; e.g myopericarditis.):

Pericarditis should never be assumed when there is even a hint of reciprocal ST depression.  Only localized pericarditis (most pericarditis is "diffuse" inflammation of the entire pericardium) ever has reciprocal ST depression, and localized pericarditis is very rare.  I suspect that many cases of "localized pericarditis" are really STEMI that went undiagnosed.

A great review article by Punja 2010 gives a few examples of ST elevation in myocarditis, but neither example shows reciprocal changes.

Nasty STE in myocarditis, but no ST depression

Sooo... Rare ECG finding? Not enough research? Incomplete diagnosis?

The Bottom Line

So, the next time you bring in that "for sure" STEMI, keep in mind there's a (3%*78%=) 2% chance it's myocarditis. Or higher. Or lower.

"All that wheezes" - CHF and albuterol

Medics aren't happy unless they're arguing about something.

Since most paramedics are 1) intelligent, 2) clever,  and 3) convinced they are more clever than the other medic they're arguing with, they need an appropriate subject to engage in. The ideal topic should provide the opportunity for them to put their knowledge of physiology, gas laws, and hydrodynamics on display, but also allow them to parry with a quick "In my experience..." Ideally, there should be no clear empirical studies on the subject.

The "danger" of giving albuterol to a dyspneic patient who may have CHF is just such a topic.

Fortunately, a complete literature review on the topic easily will fit in one blog post, with plenty of room left over for a relevant case, complete with ECGs!

The Wheezer

"Hey Doc, you gotta see this guy next."

Generally I listen when an experienced nurse tells me that, so I went to see Mr Wheezer right then.

Not our patient.

He did not look good - sweaty, pale, working to breathe, with his second albuterol/ipratropium neb going. "I think it's my allergies," he says. So much for the patient telling me the diagnosis...

So I asked him to tell me about his "allergies." He'd been having some dyspnea on exertion over the past 2 weeks, with a nagging cough. But an hour ago, while at rest, he felt like his chest was being pressed in, right up into his jaw, and he had started sweating buckets. His breathing had worsened, and his wife called 911. He had a history of diabetes, hypertension, and stents in all 3 of the major coronary arteries.

The paramedics had started the series of neb treatments he was receiving, and a quick exam revealed why - he had the loudest, clearest, most unambiguous wheezes I have ever heard. No crackles, no rhonchi, no upper airway crud fouling it up. Textbook wheezes. Even the greenest of EMT-B's, using a Fisher-Price stethescope, could confidently diagnose these wheezes.

"And an S3. He's definitely got an S3."

On the other hand, the first ECG looked like this:

That's pretty bad case of allergies. I looked at his old ECG:

No slam-dunk STEMI here. I grabbed the ultrasound, and took a look at the heart and lungs. No pericardial effusion, no signs of a PE, but when I looked at his lungs, I saw the shimmering artifact that suggests wet lungs. For an example (not my patient):

I took off the neb, and popped in a tab of nitroglycerin. Within 2 minutes he had his color back, he didn't't look so drenched, and he was breathing easier. Like a lightswitch - click! -  he was improving.

I got cardiology involved pronto, before any labs, or even the chest x-ray came back. After they evaluated the patient and the ECG, they shared my concern, and were planning to take him for an urgent cardiac catheterization. Almost as an afterthought, we checked out the labs together.

Troponin - negative.
BNP - negative.

Huh.

We checked out the chest film - clear.

But the ball was rolling, and he went to the lab. Good thing, too, since he ended up having severe stenosis in his mid and distal LAD, as well as the circumflex, which all got new stents. The RCA, which previously been patent, was now totally and permanently occluded.

Soooo, that proves it was CHF, right?!? Well, he still had dyspnea after the procedure, though nowhere near as bad as before, so he got more tests and consults. I won't go through the details, but after being evaluated by 3 cardiologist, 2 pulmonologists, and one lowly ER doc, he had a diagnosis of "likely CHF."

This encounter made me consider a few questions:

How good are paramedics at diagnosing CHF?

The medic in my case only gave albuterol, no nitro or Lasix, and had not obtained an ECG, and so was clearly not considering CHF. But the diagnosis can be tough for physicians, even with all the clinical gizmos at our disposal.

With that in mind, how does the paramedic diagnosis of CHF stack up against the emergency physician's? Turns out, it's pretty good, within limits.

One study from 1995 looked prospectively at the paramedic's diagnosis compared with the ED physician diagnosis. Considering that the doctor had access to medical records, x-rays, labs, etc, the paramedics did fairly well, showing "good concurrence" with physician diagnosis. Another study looked at how well paramedics determined a cardiac cause of dyspnea. This could include angina or MI, as well as CHF, so it wasn't a perfect comparison, but the agreement between medic and doctor had a kappa of 0.71, or "good, approaching excellent."

A more recent, although retrospective, study looked only at the diagnosis of CHF. Interestingly, they studied all the patients whom the paramedic had given furosemide to, using this as a surrogate for a diagnosis. They then looked at the final diagnosis of the the emergency physician. Generally the medics did well, and the doctors agreed in 60 out of 94 cases.

The disagreements are thought-provoking though. Between pneumonia and COPD, a lot of furosemide was given to people to who didn't need it. Furthermore, there is evidence that suggests that treating pneumonia with diuretics is harmful.

Looking towards the future, however, if we can combine capnography and portable BNP analysis in the prehospital realm, EMS could end up being the gold standard for the ED to live up to!


How often does CHF present with wheezing?

Often enough!

In one study of older patients, it was found that about one third of  patients had wheezing with their acute episode. Perhaps not surprisingly, these patients usually were smokers, had a prior diagnosis of COPD, and were using bronchodilators at home. Unfortunately, they did worse with their CHF events, going to the ICU at a higher rate, for instance.

There aren't too many other studies that study the rate of wheezing, but we can also look at the rate of albuterol/beta-agonist administration as a rough equivalent. In one study 20% of patients got albuterol (in addition to other drugs), while in another study only 2% of CHF patients got albuterol (as the sole therapy). 

I think this evidence suggests that there can often be a component of wheezing with acute episodes of CHF, but that "pure" wheezing, without other indications of of CHF, is pretty rare.

Is there a danger in giving albuterol to a patient with CHF?

My patient ended up getting stented for cardiac ischemia. It seems reasonable to wonder if the 2 neb treatments, in addition to being ineffective, might have  exacerbated the ischemia, causing harm. However, looking at the clinical evidence is difficult, as much of it doesn't apply to emergency medicine, let alone paramedicine.

For example, there are a number of studies that analyze the harm associated with use of bronchodilators in patients who have diagnoses of both COPD and CHF. These studies, however, follow patients over months to years, and aren't very relevant.

One ICU study looked at the degree of tachycardia or number of tachyarrhythmias after albuterol neb treatment. They actually did not find much negative effect on the vital signs.

Well, what about studies in the ED or prehospital that look at truly relevant outcomes? Surprisingly, there only appear to be 2 relatively useful clinical studies available to guide us.

The first was a case-control study done in 1992, by Wuerz. They looked at about 500 dyspneic patients who had received prehospital treatments. They found that it was pretty bad to treat asthma or COPD, for example, with Lasix. However, when they looked at the 9 CHF patients who were mistakenly treated with beta-agonists, they found, reassuringly, that "none died."

The second study (Singer 2008) was bigger, using registry data on about 11,000 CHF patients treated in the ED. The nice thing about using such a data source is that you can get a lot of patients, and find associations. The bad news is that you often can't explain what you do find.

Such is the case with this study. About 20% of the patients received beta-agonists, either by EMS or in the ED, but had no pre-existing history of COPD or asthma. They used some statistical rejiggering to try and make fair comparisons, since CHF patients with a history of COPD are not exactly like CHF patients who don't have COPD. I won't bore you with the details, but that's what they mean by "adjusted with propensity analysis" on the following table.

Now, there wasn't any apparent difference in mortality, discharged alive form the ED, or ICU admission - that's what all those big red Xs mean. There was, however, an increased rate of intubation in those CHF patients who were treated with bronchodilators, but who had no history of COPD.Same for BiPAP and inpatient mechanical ventilation.

So what does this all mean? Now, this study wasn't randomized, and it really only shows an association, not cause and effect. The authors state (emphasis is mine):

Inhaled bronchodilator use in these heart failure patients without chronic obstructive pulmonary disease appeared to be associated with worse outcome. Because of the observational nature of these data, we cannot determine whether these patients’ outcomes were worse because they were more severely ill or because of a directly harmful effect of the inhaled bronchodilator.

However, this association persisted after adjustment for propensity score and standard risk factors for mortality. This finding suggests that inhaled bronchodilators may have contributed to the poorer outcomes observed in heart failure patients without chronic obstructive pulmonary disease who were treated with bronchodilators.

Or may not have contributed - we just don't know. The authors allow that treatment with bronchodilators may just a marker for bad CHF, but not a cause of bad CHF. I'm sympathetic to that point of view.

The Bottom Line

 If you're pretty sure the patient has CHF, they need nitro and CPAP. Lasix is old school, and might hurt people when you're wrong about the diagnosis, and there is no evidence that albuterol will help with edema.

On the other hand, if you get fooled by wheezes, don't feel too bad. It might not have helped, but it probably didn't do much of anything at all.

The most difficult step in obtaining an ECG.

Quick post today, concerning a very common error I see both in EMS and ED patients - misplaced ECG leads. I would call this a pet peeve (as the techs and nurses I work with are well aware!), except that a peeve does not usually carry significant clinical implications.

An article in the curent issue of EMS World argues for the acquisition and transmission of prehospital ECGs by BLS crews. No argument there - that is exactly what happens in the ED. A tech acquires the ECG and runs it to me. If your system allows for easy transmission of ECGs, and if paramedics are scarce, this would be a common-sense approach to take.

Unfortunately, an accompanying illustration distracts from the main message.

Source

In an unfortunate twist, there are two errors of lead placement here. These errors are both common and possibly clinically significant.

The problems.

First, I believe V1 and V2 are located too high on the chest.

These leads should be located in the forth intercostal space (ICS), which in males is often within a fingerbreadth of the horizontal nipple line.

Reference

Another clue to V1 & V2 misplacement is their location relative to lead V4. Given that V4 should be located in the fifth ICS, the large vertical distance between V2 and V4 in the illustration suggests misplacement of V1 and V2 as well.

A second apparent error is that V3 is shown slightly medial to V2.

 It should properly be placed halfway in between leads V2 and V4.

Why is this important?

Misplacement of ECG leads, and especially V1 and V2, are common. One study compared the accuracy of cardiac techs, compared with nurse, physicians, and even cardiologists. No one, except the techs, came out looking too good.

The ovals represent the range of misplacement for each lead, broken down by training level. Ref.

These errors are not trivial. "Pseudo-infarction" patterns can be generated from incorrect lead placement, leading to erroneous cardiac catheterization lab activation, cost, and diversion of resources. In the example below, simply moving the V1 and V2 leads from the 4th ICS, then to the 3rd, and then the 2nd, produced ECG changes which the computer interpreted as suggestive of ACS.

Reference

Another example - you can see how an rSR' pattern is falsely generated as V1 and V2 are moved from the 4th ICS (in B-1) to the 3rd ICS, and then 2nd ICS (in B-3).

Reference

(Interesting aside - placing the leads in a higher ICS is used to assess for an occult Brugada pattern, But this is sort of a specialized technique, and I leave it to the electrophysiologists.)

Source

The Bottom Line

A recent post from Captain Chair Confessions highlighted the importance of proper lead placement, not only with regard to accuracy, but also in assuring that EMS appears professional and competent. I second that, but I have to acknowledge that many paramedics likely learned the incorrect position from preceptors within the hospital. Heck, in one of the studies mentioned above, the cardiologists were the people least likely to properly position V1 and V2!

So, kudos to David Howerton and the other authors on making a good argument for ECG acquisition as a BLS skill! But strive to demonstrate proper lead placement - it makes a difference

Cath lab cancelation after EMS activation

In the last 2 posts, I reviewed recent studies that looked at the decision to obtain a prehospital ECG, and a novel method to teach STEMI identification to novice ECG readers. This leads to the last installment in this trilogy: How often does EMS mistakenly activate the cath lab? For that matter, how good are emergency physicians?

Reference

(Side note: This is the second paper I have reviewed that has Jon Studnek as an author. He's a paramedic who also has a PhD, and is faculty at Carolinas Medical Center. He writes a lot, and I probably could fill all of my posts with reviews of his publications.)

AKA "Dr. Medic"

This study uses data from the Reperfusion of Acute Myocardial Infarction in Carolina Emergency Departments (RACE) program in North Carolina. This program has already been shown to improve time to PCI or lytics for patients with a STEMI,  as well as other process measures. While recent data on actual patient outcomes is mixed, there is no doubt that this ambitious collaboration has brought some order to the notoriously fragmented emergency health care system in the U.S.!

The investigators used data from the 14 hospitals in North Carolina that acted as the receiving centers for STEMI patients transferred for emergent percutaneous coronary intervention (PCI).They looked at  sub-groups of patients, broken down in three different ways:

• Patients who first presented to a PCI center, or to a non-PCI center;
• Patients who had the cath lab activated by EMS, or in the ED; and
• Patients who used EMS, or those who "walked in" to the ED.

Because of the size of the program, they were able to look at a total of almost 4000 catheterization lab activations. That's one of the main strengths of this study - they have a lot of data.

Another aspect of the study that gives it some "real-world" applicability is how they defined an "inappropriate" activation of the cath lab. While other authors have described a "clean cath" as an inappropriate activation, the authors acknowledge that there are many scenarios where PCI for presumed STEMI is appropriate, despite the 20/20 hindsight of a negative cath. Takotsubo cardiomyopathy, for example, often requires an emergent angiogram to clarify the diagnosis.

So, instead they defined an inappropriate cath lab activation "If catheterization was canceled because of ECG reinterpretation or if the patient was deemed not to be a candidate" for PCI. Clinical factors, such as age or DNR status, were used to determine candidacy.

The overall results, comparing paramedics and ED physicians were that 15% of activations were inappropriate:

They analyze the results further, breaking down the data into the subgroups described above. The group of interest is all the patients who were transported by EMS, and had their initial activation by EMS. In other words, none of these patients were "walk-ins," but it included both patients who were brought to PCI and to non-PCI centers (initially).

They compare these activations against all the patients who had cath lab activation performed by the ED physicians (both at PCI centers and non-PCI centers), with patients who either came in by EMS or car.

There are a couple different ways to analyze these results, but overall the physicans performed better that the medics. Well, 7+ years of training ought to pay off somewhere, and and incremental accuracy in ECG interpretation is a reasonable expectation.

However, you can't even conclude this from the data presented, since an activation may have been deemed "inappropriate" because of a patient's DNR code status, say, or severe comorbidities (e.g. sepsis, or terminal disease). Specifically, we don't have the break-down for ECG accuracy versus judging cath lab candidacy for the 2 groups - it may well be the case that medics are just as good as emergency physicians at reading ECGs, but the physicians are better at judging which patients actually warrant an emergent catheterization.

The last table emphasizes the point that, while this sort of study is great at generating statistically-significant results, there is a lot of "granularity" that is not accessible to us.

Clearly, not all EMS agencies or EDs are equal - some systems are better than others. In this table, note the range of appropriate activations:

There are few EMS agencies and EDs who are evidently did not generate a single inappropriate activation! However, a 100% appropriate activation rate may also suggest a system that is too restrictive, and is missing too many STEMIs.

On the other hand, it is concerning that some EDs, even at the big hospitals with cath labs, have a "false-positive" rate of 25%. Similarly, some EMS agency inappropriately activates the cath lab 1/3 of the time!

The Bottom Line

This isn't a study that you can use to change your clinical practice in the next shift. It isn't even very useful at changing practice at your EMS agency or ED. However, it points the way to doing the more practical research, by highlighting important aspects.

For example, how do paramedics at different agencies decide to activate the cath lab, and how do these methods correlate with accuracy? Could a closer look at the 65% - 100% range in appropriate activations suggest a "best practice" for EMS? Should we rely more on intensive continuing education for paramedics? Alternatively, should there be more emphasis on computerized and/or human algorithms for ECG interpretation?

Furthermore, since the "Not Cath Lab Candidate"group accounted for such a large proportion of the inappropriate activations (4.3%), might their be a better way to anticipate this exclusion? To a large degree, the cardiologist is the individual who is deciding the patient's candidacy for the cath lab, and it is often difficult for the emergency physician, let alone the paramedic, to anticipate their decision. I'm not sure that the accuracy of prehospital STEMI activation should be judged using such "soft criteria."

So, more research is called for, as usual. But this paper serves as a very useful guide for the future.