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.

Saturday, March 31, 2012

When should you get an ECG?

The glucose-insulin-potassium study is grabbing all sorts of attention, out of all proportion to the underwhelming results (see here and here for analysis). There is nothing in that paper that a paramedic can use in the foreseeable future, let alone on the next shift. Folks in EMS tend to be very practical, and the use of that drug combo is still very theoretical.

When I looked through the issue of American Heart Journal that has that much-hyped study, though, I found another paper, one that appears more more useful. What's more, you can start using the results today, and could plausibly save a whole lot more lives (or at least myocardium) than with the "cardiac cocktail."

Ironically, the evidence is better for this cocktail in cardiac disease.
"A Prioritization Rule for Obtaining a 12-Lead ECG"

So, when do you decide to get an ECG on a patient in the field? If they have chest pain, sure, but probably not in all chest pain. And you're probably sharp enough to grab an ECG in the old guy with new nausea or dypsnea. But are you missing some STEMIs? Are you getting too many ECGs, and wasting your time? Someone outta do a study.

Well, Glickman et al. did, and I'll boil down the results that you can use on your next shift.

The study is called "Development and validation of a prioritization rule for obtaining an immediate 12-lead electrocardiogram in the emergency department to identify ST-elevation myocardial infarction." You really don't need to download the whole article, unless you have a deep interest in binary recursive partitioning.

A very, very deep interest in binary recursive partitioning...

The problem in emergency departments, just like in the field, is that a lot of STEMI patients do not show up with the classic chest pain symptoms. However, we want to identify all these STEMIs, but we also don't think we should get an ECG on everyone - it would just slow everything down. You also want a rule that is straightforward enough for a range of "non-physicians;" RNs, techs, and medics. (That being said, the results were very instructive for this physician.)

The researchers used a database of patients who came to a ED in North Carolina in 2007 and 2008, and looked at two things: who was diagnosed with a STEMI, and what the triage note listed as the chief complaint.

Funny: they used a computer program to search the triage notes for chief complaints, and called it the Emergency Medicine Text Processor (EMT-P).

A computerized EMT-P. ICWUDT.
Anyway they categorized the chief complaints of the 6464 patients who were diagnosed with a STEMI, then grabbed the records of about 3.5 million other patients who were matched to those same chief complaints, as well as age, gender, and other stuff. They found out a few important things.

1. Chest pain is less common in older folks with STEMI.

This is already well-known, but they have a good pair of graphs that make the point clear. Age has a huge impact on the predominant symptom that people feel with a STEMI.

There is a small difference between men and women, but it's the age-effect that is so evident here. For example, women under 50 years of age have chest pain as their chief symptom about 85% of the time, while men over the age of 70 only note chest pain around 70% of the time. In other words, chest pain can be more common in women if you look at different age groups.

2. Think:  ≥ 30, ≥ 50, and ≥ 80 years old.

When they fed all the data through C3P/EMT-P, they came up with a rule for deciding if you should get an ECG, based just on the age and chief complaint. They broke it down by 3 age groups, as noted above:

I want to emphasize the last bit there - this is a rule designed to assist non-physicians in screening a large number of patients rapidly, but it is constructed to supplement clinical judgment, not replace it.

Another way I might phrase the rule is:
  • Anybody over 30 y.o. with chest pain gets an ECG,
  • Anybody over 50 y.o with chest, head, and upper extremity complaints,
  • Anybody over 80 y.o. with any torso complaints (except maybe isolated diarrhea...)
This seems pretty inclusive - it's hard to see how an 81 y.o. in the ED would not get an ECG! Regardless, some people will get missed. The sensitivity of the rule is only 92% sensitive.

So, who were these 8% of STEMIs whom the rule would miss?

Who gets missed by this rule?

Again, a helpful diagram:

  • It misses younger patients, even the ones with chest pain.
  • It misses the young-ish patients with dyspnea.
  • It misses the 50-79 year-olds with GI presentations.
  • It misses the > 70 crowd that presents with... fever?!
Fever? Seriously, you can't win.

The Bottom Line

One way that EMS can save lives is to identify STEMI patients in the field, followed by proper triage and notification. But you can only identify a STEMI if you get an ECG. This paper shows us how wide a net we have to cast in order to catch most of them.

Use the decision rule to prompt you or your partner to do more ECGs. And even when the rule doesn't necessarily call for a 12-lead, listen to your gut and follow your clinical suspicion.

Wednesday, March 28, 2012

The IMMEDIATE trial: Should EMS give Glucose-Insulin-Potassium?

The results of the IMMEDIATE trial have been popping up repeatedly today on Facebook, partly because I "like" a few EMS FB pages, and also because one of the authors (Hi Carin!) is a FB friend (IRL too!).

Here's an example of the way the trial is being described:

"Cut the risk of death in half." Sounds great!

The result they are describing, to be specific, is that 8.7% of the people getting the placebo had a cardiac arrest, or died while they were hospitalized, while only 4.4% of the patients getting the study drug did. That's either an (absolute) difference of 4.3%, or about a (relative) 50% decline.

Such an effect would be stunning.  In the years after thrombolytics and aspirin were introduced, the incremental benefits of new therapies for AMI have been getting smaller and smaller. This result here would blow the others out of the water.

For instance, back in 1988, it was shown that either the use of aspirin or of thrombolytics reduced the risk of death in MI by about 2-3% over placebo. The combination was better of course.

After that, it's been harder to show that the more complicated and expensive therapies save that many more lives. When we send a patient to the cath lab for an AMI (instead of giving a thrombolytic in the ED), for example, there isn't that huge a benefit. One recent analysis suggested that, overall, you could only find a 0.7% difference in mortality (6.6% vs 5.9%) between lysed patients, and those that went for PCI. A lot of money for not much gain.

So, if this combination of glucose, insulin, and potassium (GIK) could cut mortality in AMI from 6.6% to, say, 3.3%, it would be freakin' amazing.

"I bet there's a catch. There's always a catch."
Well, I don't mean to be an Eeyore, but the perhaps we should wait for, yes, "further study." I offer three reasons why:

1. They weren't studying mortality.

The principle outcome they were studying was whether the initial presentation of ACS would progress to an MI, or it would be an "aborted" MI. This is the outcome that they believed had the most biochemical and clinical justification, and they clearly thought that it had a reasonable chance of being demonstrated.

It turns out there was no difference in the percent of people who progressed to completed MI - the GIK infusion did not help, at least not here. So the trial is negative for the real primary outcome.

2. There were 12 secondary outcomes.

Look at the table of the results:

Remember: the outcome they staked the success of the trial on was the one at the top: "Progression to MI," for all participants.  The rest are a bunch of secondary outcomes, and they don't count to the same degree as the primary outcome.

Analogy: A friend is flipping a coin, and you call heads. That's your primary outcome of interest. But if you also say to your friend "Okay, I call heads, but I also call it if you drop the coin, if it flips over 5 times in the air, if your phone rings in the next 30 seconds, or if your nose starts to itch in the next 10 seconds.

Now, you may be wrong about heads, but say your friend's nose does indeed start to itch in the next 10 seconds? Will he concede defeat? What will he say?

"No pick! NO PICK!" 
Most likely your friend will point out that the most relevant and important prediction you made was heads vs tails. Furthermore, you called out such a long list of other items that you were almost certain to come up with a positive result. He will insistent on another coin toss, where the primary outcome is now nose-itching, not heads or tails.

The same holds in statistics and study design, and is also why the authors state in their conclusion (my emphasis):
"The primary end point was not significantly different between groups, and the observed favorable results of GIK were based on prespecified but secondary end points, although biologically plausible and consistent with preclinical studies. The study tested one primary hypothesis, 3 major secondary, and 6 other secondary hypotheses. All were prespecified and no adjustment for multiple comparisons among the secondary end points was made; thus, reported significance levels should be considered approximate. Accordingly, given the lack of complete consistency of the findings, and the modest P values for most of the statistically significant findings, it would be appropriate to describe the observed favorable effects on the secondary outcomes as generating clinically testable hypotheses for evaluation in larger cohorts."

3. 30 day mortality seems pretty important too...

Ok, say you can take the "cardiac arrest or in-hospital mortality" results at face value. What, then, shall we make of the 30-day mortality? It was shown to be basically the same in both groups.

We just saw this discussion take place last month. A study from Japan showed that giving epinephrine in cardiac arrest got people to the hospital with ROSC more often, but the 30-day mortality was no different (We'll leave the neuro results alone for now.).

It would be nice if epi put all the dots on the right side of the graph. But it doesn't.
So, say the results are right - people don't die or arrest in the hospital as often, but they still die in the first 30 days just as often. Now, maybe everyone's hospital stay was over 30 days, but I doubt it.

Still feel excited?

Bottom line:

I believe that EMS has an essential role in managing ACS, of course. But, as it stands, giving this mixture to your ACS patients is not yet ready to be added to your drug box.

Wednesday, March 14, 2012

Using Dextrose in Cardiac Arrest

You know that there's a lot of controversy about how to run a cardiac arrest - intubating or not, how often to ventilate, or doing a short trial of CPR before defibrillation. This is especially true regarding the "code drugs," like epinephrine. 
Well, okay. Epi works.
But at least when it comes to epinephrine and amiodarone, there are some studies out there, some base of evidence to start the discussion from. This is not true for D50
If you look in the 2000 ACLS guidelines, you'll see the list of the "reversible causes" of cardiac arrest. It doesn't include hypoglycemia.
If you don't believe me, look at the fine print at the bottom.
Now skip ahead 5 years, and we now see that hypoglycemia has been added (2005 ACLS):
Down in the green box, at the bottom.
Read through the guidelines, though, and you'll see that not a word is uttered about why this was added.

Now, fast-forward to 2010, and they've taken it out! And, just like they added it without comment, it's gone without a trace.
Since the AHA elected not to review any relevant evidence about the topic, I decided to answer some questions about hypoglycemia, cardiac arrest, and the relative benefit of trying to squeeze that huge syringe of syrup into an IO.

1. Does hypoglycemia cause cardiac arrest? 
You figure this would be easy enough to answer, but there is almost no direct data that says so. One case series in 1995 reviewed 3 arrests that the authors thought were associated with hypoglycemia. These patients all had significant other problems (active CAD, cerebral hemorrhage, and severe pancreatitis).

Another case series, looking at patients with severe heart failure, thought that one cardiac arrest was due to hypoglycemia (oddly enough, she didn't have diabetes). And in one last example, a patient in the ICU became asystolic at the same time her blood sugar was plummeting, although she also was developing a severe hyperkalemia at the same time.

The problem with this handful of case reports is that, given the uncontrolled nature of the situations, it's hard to point out cause and effect. Just because one thing occurred at the same time as something else, or even right after, doesn't mean they're related.

Well, look at this from a different point of view. Is there a proposed "mechanism," some physiological reason that hypoglycemia could cause an arrest?

 There is the phenomenon of the "dead in bed" syndrome, where a relatively healthy diabetic is found deceased in the morning. A number of researchers think they've found a link - the usual dip in blood sugar levels at night can cause a prolongation of the QT interval. And long QT intervals can sometimes cause problems! (See these examples at Dr. Smith's ECG Blog.)

A long QTc. (source)
They've been able to show this effect both in the lab (giving insulin to healthy people) and at home (people on continuous ECG and glucose monitoring).

But, just because you can show a longer QT, doesn't mean you have a smoking gun! Others have pointed out that there are probably a number of other factors involved. For instance, it may not be the hypoglycemia that triggers the QT changes, but in fact may be the body's own epinephrine that kicks off the arrythmias!
Now epinephrine is bad for the heart?!?

So, we just don't know!

2. Is the finger stick accurate in cardiac arrest?
Usually, the capillary blood glucose is pretty close to the venous level, close enough that we all trust it. However, in the critically ill patient, the capillary level becomes less accurate, as a number of studies have shown.

Only one study looked at patients getting CPR, though.  This was a pretty big study by cardiac arrest standards - they checked the venous and capillary glucose levels in 50 cardiac arrest patient. It wasn't encouraging. There were 4 patients with "true" hypoglycemia, found on the venous samples sent to the lab. The fingerstick missed 1 of those, and also managed to misdiagnose 5 patients as having hypoglycemia, when they really didn't. (The fingerstick was 75% sensitive, and 38% specific).

Not so accurate!

 3. Okay, we might over-diagnose hypoglycemia. What's the harm?
Glad you asked.

It's the same reason we're trying to cool people down after we get a pulse back  - neurologic outcomes. In some studies, they gave dextrose to some cats before they put 'em into cardiac arrest, while other cats they didn't. The cats who didn't get sugar beforehand had better brains afterwards.

You can't really do this same kind of study in humans (for example). One group in Helsinki, though, checked the blood sugar on VF cardiac arrests, and looked at how well they recovered. Patients who had increases in their glucose after resuscitation didn't survive to hospital discharge as often. This is just the latest evidence - see this review article (50% dextrose: antidote or toxin?) for plenty of other examples.

4. Any evidence giving sugar helps? 
Well, yes and no. There is no evidence that pumping liquid rock candy into someone's tibia helps in cardiac arrest.

Now, there are a lot of other sick people out there, people teetering on the edge, critically ill, septic, metabolically deranged - with a blood sugar headed south, and fast. You have to find those folks and treat them quick. Some of these are kids, with weird metabolic problems, or with sepsis.  But the key is to get to them before they crash.

The authors of the only review I found on this topic concluded that (my emphasis):
"This is obviously a controversial issue and raises the point of whether we should still be teaching that hypoglycaemia is a reversible cause of cardiac arrest when there seems to be not enough evidence to support this. 
Current evidence would suggest that patients may suffer cardio-respiratory arrest with hypoglycaemia, but not because of it." 
The Bottom Line
It's in the protocols, you can certainly give dextrose if you think it's warrented. In he field, though, there's a lot to be done, and sometimes there's not enough hands to do the work. If there's enough crew around, maybe it's fine to dedicate one person to squeezing the D50 in. If space and time are limited, whoever, it's important to understand the effectiveness and and evidence for your therapies.

Sunday, March 4, 2012

Sodium bicarb in a code -Still no evidence

Not sure why, but an EMS Facebook page decided to highlight a JEMS article written over a year ago. It got me to thinking, however.

The JEMS article is titled "Sodium Bicarbonate: Should it be considered as a treatment?" The author is Jim Davis, a FF/RN/EMT-P, and he covers some of the physiologic rationale for the use of bicarb in cardiac arrest, as well as some of the animal and clinical evidence. In the end, he comes out fairly strongly in favor of using it. He concludes:
The routine use of NaHCO3 may warrant a greater role in the delivery of prehospital care for cardiac arrest patients in the prehospital setting.
Until other options exist for the prehospital assessment and treatment of acidosis, EMS providers need to pay more attention to the length of the patient’s down time and recognize the importance of considering acidosis early on, as well as recognizing that NaHCO3 may be a viable treatment option.
I earned my first ACLS card in 1996, long after bicarb had fallen out of fashion, so I had never reviewed the data personally that supported its use in cardiac arrest. Given the number of comments that followed the FB post, however, it appears that this old drug still has a number of "fans" (125 likes!), so I thought that I should acquaint myself with the studies.

Didn't take long - there are only 2 human clinical trials that the AHA cites in the 2010 ACLS guidelines. Let's look at the first.

The first was from 2005, "Improved resuscitation outcome in emergency medical systems with increased usage of sodium bicarbonate" It reviews data from a trial that took place from 1990 to 1992, and it has an interesting design.

First of all, the study (named BRCT III) was primarily designed to look at high-dose versus escalating-dose epinephrine. (High-dose turned out to be a bad idea.) So, basically, the whole paper is an exercise in "data-dredging," because the trial was never designed to look specifically at the use of sodium bicarbonate in cardiac arrest.

They had 16 EMS agencies involved in their study, and some used bicarb almost all the time, while others hardly ever busted out the big yellow box.

 So, they compared the EMS agencies that were "high users" against those that were "low users"

SB = sodium bicarb; ACLS = first defibrillation
 When they identified these agencies who gave bicarb more often and earlier in cardiac arrest (purple box), they found that their patients were more often alive, and neurologically intact, 6 months later (red box). On the other hand, these same "high SB users" were also much better at getting in the first defibrillation faster (blue box), as well as getting in a line, etc. These agencies, simply put, seemed to better at running cardiac arrests in general!

Given the study design, there's no way to piece apart how much, if anything, the bicarb helped.

Anyway, there were a lot of other interesting points in the paper (e.g. giving bicarb earlier doesn't have a physiologic rationale...), but let's move on to paper #2!

The design of this study is even shakier than the preceding study. Weaver et al., conducted a study that ran from 1983-1985 with Seattle EMS, looking at whether it was better to give lido or epi in refractory VF. To summarize the whole paper, I'll just show you this graph:

No difference! Hey, what about the bicarb!? Wasn't there supposed to be bicarb in the study?

Here's how they got bicarb in the study. They decided to look at the cardiac arrests that Seattle EMS had treated in the 2 years proceeding the study, i.e. in the years 1981-1982. Ancient history, indeed.

One of the medics in the study, preparing the bicarb.

During that time period, the common practice had been to start a slow sodium bicarb drip, and not give epi or lido. So they compared the patients from their "true" study with this historical cohort - that's a pretty messy study! And the results were:

Hey, wasn't this supposed to be one of the papers supporting bicarb in cardiac arrest? Instead, the authors conclude that:
In this study, there was no clinical evidence to support any form of drug therapy for initial treatment of persistent ventricular fibrillation.
The Bottom Line
The Bridgeport protocols (PDF download) suggest the use of sodium bicarb in only a few situations:
  • Hyperkalemia
  • Tricyclic OD
  • Metabolic Acidosis 
 Based on this review of the studies cited by the AHA, there does not appear to be any reason to add cardiac arrest to the list. If you hear of any better evidence, send it this way!