As in Incident command...

IC established!
We'll have several different sections reporting in - recent research, local topics, or highlighting areas of the Sponsor Hospital Council of Greater Bridgeport protocols.

*** Keep in mind - this website does not replace your protocols, and these posts do not reflect SHCGB or Bridgeport Hospital policies. This is a place to discuss research, controversies, or discuss possible future protocols. When in doubt, check your current protocols through the official source.

Tuesday, June 26, 2012

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.

Monday, June 18, 2012

"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.


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.