One more word on needling the chest.

Of course, no sooner had I posted 4 things to know before you needle the chest, when I found a new article from Australia, just published, describing how new EMS guidelines and education improved their approach to tension pneumothorax. It describes a "new" approach to tension PTX, but also has some of the limitations of the older studies. 

"Improvement in the prehospital recognition of tension pneumothorax: The effect of a change to paramedic guidelines and education."

The authors of this study out of Melbourne had been concerned by the number of patients with a unrecognized tension PTX being brought into their hospital by EMS. Their guidelines for needle decompression evidently placed a certain amount of emphasis on certain physical signs for the diagnosis of progression to tension; e.g. tracheal tugging, subcutaneous emphysema, and JVD, amongst others. 

Realizing that these indications for decompression were vague and difficult to use in the field, they re-wrote the guidelines with an emphasis on the clinical situation most likely to present with a tension - an intubated patient with chest trauma.

On top of this, they made 7.5 cm IV needles available, as well as a 10 cm-long commercial device:

This Cook device comes with a crossguard, for effective parrying.

Fewer unrecognized tension PTXs
So the new guidelines and education worked. The rate of tension PTX that was treated by EMS went from about 66% to 90%. Put another way, the number of unrecognized tension pneumos went from 10 in one year, to 4. 

Since the EMS service had also started doing RSI intubations for trauma, the absolute number of tension PTXs also went up - this one EMS agency needled 81 patients in one year! (BTW, what the heck is going on in Melbourne?! That's a lot of serious trauma.)

Imagine what they could do if they had guns!

The limitations
So, how do we know that the paramedics were sticking needles into true tension pneumothoraces? 

Short answer: we don't, not for sure.

Longer answer: This has been the problem with older studies that merely reported, for example, a rate of needle decompression by medics, with no attempt at verification.  One prior study, however, used the subsequent presence of an air leak from a chest tube as a surrogate for tension PTX, and found a very low rate of "true" tension PTX - just 14% of the patients that were "needled" by EMS. An ultrasound-based study also casts doubt on the prehospital diagnosis of tension PTX.

The authors of the current paper used a "case definition" to identify tension PTX. That is, they went over all the clinical records and imaging studies, and made a best guess about what the patient had in the field. As you might imagine, this is an imperfect method, and we can only guess at the accuracy of the paramedics' diagnoses.

The bottom line
Despite these concerns about accuracy, there were fewer patients brought into the ED with a tension PTX, even as the rate of RSI, and thus positive-pressure ventilation, increased over the study period. That's a good thing, and it seems as though there was no large increase in complications. 

In the meantime, if anyone is planning a large prehospital study to look at PTXs, it sounds like Melbourne is the place for you!

4 things to know before you needle the chest.

Looking for a tension pneumothorax (PTX), and especially deciding to perform a needle decompression, can trip up even the most smartest EMS provider. There's a balance between the need for aggressiveness, and the wisdom of careful monitoring.

Ok, that was too aggressive - dial it back next time.

A few recent cases brought into Bridgeport Hospital, as well as some recent research, help us refine the approach to evaluation and treatment. 4 fun facts about tension PTX!

1. It's rare!
While some authors have described a 6% rate of tension PTX in prehospital trauma patients, the rate is probably far lower in most U.S. EMS systems, with some estimating it happens in fewer than 0.3% of blunt trauma patients.

Another study, published in 2013, found that about 1% of the trauma patients coming into a Level 1 center had received a needle by EMS for a suspected PTX, and that most of them ended up getting a chest tube in the ED or OR. 

Problem is, they weren't able to tell if the patients had had a tension PTX when EMS needled them, or just a plain ol' pneumo. So, at worst, 1% of severe trauma patients have a tension PTX.

2. Paramedics have trouble identifying it.
That last study showed that  paramedics are pretty good at diagnosing a pneumothorax. How good are they at diagnosing the tension part?


A study done in Nashiville looked at 19 patients who got a needle decompression by EMS for suspected tension. About 1/4 of those patients were proven to have any sort PTX (tension or not), and only 2/14 of the living patients were considered to have had a tension PTX (based on finding an air leak after placing a chest tube).

So, only 14% of patients who got a needle actually had a tension PTX

3. Diminished lung sounds & crepitus ≠ tension
A patient can have complete collapse of a lung, and still not need a needle!

A few months ago one of the medics was concerned that they hadn't treated a trauma patient as aggressively as he should have. The patient had fallen a few days prior, and was complaing of shortness of breath. The medic noted bruising over the chest, paradoxical chest wall motion, and absent lung sounds. Nevertheless, the patient was breathing better on 2 lpm of oxygen, and the vitals were fine.

In the ED, the patient was promptly sent to the CT scan...

Pneumthorax, as well as subcutaneous air

... and got a chest tube right away! So the medic was concerned - should they have placed a needle in the field?

It doesn't sound like it. It's important to remember why a tension pneumo is bad. Progressive collapse of the lung leads to hypoxia, and the rise in intrapleural pressures compress the IVC, leading to hypotension. In other words, patients don't die from a pneumothorax - they die from hypoxia and shock. Rogue Medic wrote about this at some length, and you might enjoy his take on the subject.

So if subcutaneous emphysema and absent lung sounds don't require you to decompress, what signs should? A very thorough (and free!) review article from 2005 provided a list of the signs that trauma experts agree could warrant EMS attempting to decompress.

Just remember - hypoxia and hypotension!

Source

(Keep in mind that you should be suspecting tension pneumothorax - don't needle the patient with bradypnea, pinpoint pupils, and track marks just because she's hypoxic with a decrease LOC.)

It's only helped in one case report.

4. Your needle may be too short (or your patient too big...)
So, another medic brought in a trauma patient, thrown from a motorcycle, with pain over the left chest, and absent lung sounds as well. The medic had already needled the chest with the standard 14g IV catheter, but reported that lung sounds were still absent.

Sounded like a no-brainer to me; if the patient hadn't already needed a chest tube before, now they most likely did (since a needle decompression can also cause a pneumothorax). But when the patient was rolled into the trauma bay, we found no pneumo on chest x-ray, ultrasound, or even CT. Heck, looking at the CT, we realized there was no way the stubby 14 g ever made it near the lung!

This is a very common experience - unless you have a special long catheter, you may not be able to reach the pleural space, especially in the standard "midclavicular, 2nd intercostal space" that we've been taught. Why? Because we're all getting bigger, and the catheters are not!

A standard 14g iv catheter; 2" or 5 cm,

Seems big at first, but take a look at where we're trying to put this needle:

People can be thick, both in the 2nd ICS anteriorly (left),
as well as the 5th ICS laterally (right)
(Adapted from Schroeder et al)

That can be a lot of skin, fat and muscle to get through! A standard 5 cm catheter may reach the pleura in most Japanese patients, and some Turkish patients, but only in a minority of Americans.

One option is to place the needle at the 5th ICS, along the anterior axillary line, since there is generally less muscle and fat there than at the traditional 2nd ICS. One study, done in Los Angeles, found that a standard 5 cm (2 inch) needle placed at the 2nd ICS would be too short in 42% of patients, but only in 15% at the 5th ICS.

So, a lateral placement might help, but so might more needle. They make a longer 14 g iv catheter just for decompressing, extra long at 3.25 inches, or 8 cm. Of course, what's the downside of having an extra-long needle shoved into the left side of the chest?

"With a PTX, is the blood supposed to shoot out?"

The Bottom Line
A pneumothorax happens relatively often in severe trauma, but these do not require any specific prehospital treatment. A tension PTX, on the other hand, is rare, difficult to diagnose in the field, and there are some obstacles to treating it appropriately.

You're looking for a patient with not just absent lung sounds, but persistent hypoxia, and worsening hypotension. And when you place the catheter, you have to make sure it's actually reaching the pleura - but not too far in!

Medics for cath lab activation of STEMI? Non merci!

Although we often talk about "prehospital activation" of the cath lab for STEMI, it isn't always clear what we're talking about. For example, in some EMS systems, the medics give a "heads-up" to the ED, so that a physician can meet them on arrival to confirm a STEMI. Other systems rely on the paramedics to interpret the ECGs themselves, and make a judgement about activation on their own initiative.

A group of Québécois cardiologists, however, decided that they wanted to try a new system, where neither the paramedic, nor the ED physician, would make the decision. Heck, it wouldn't even be a cardiologist. Instead, the turned the decision over to...

"Beep boop click tweet" (Translate: "I could go for some poutine.")

The Study
The prehospital providers in Laval, Quebec, were trained to obtain a 12-lead ECG on patients with chest pain or dyspnea, but did not receive any instruction on interpretation. If the machine (a Zoll, not actually an R2 unit!) gave an interpretation of *** AMI ***, the EMTs put in a call to the hospital paging system to activate the cath team. The ECG was not immediately analyzed or transmitted, although it was saved.

Over the course of 2 years the EMTs activated the cath lab 157 times, and most of those went to angiography and were found to have coronary occlusion (a "true STEMI"). A few patients (5%) had a very suggestive ECG, but had nothing on cath ("false positive activation"). It happens.

Unfortunately, 12% of the group were found to be "inappropriate activations," meaning that the ECG shouldn't have led to activation. The authors divide these up into human factors (poor quality tracings, lots of artifact), and machine factors (the machine tried to interpret STEMI during a SVT).

What's helpful about this study
It's good that they have distinguished between "false-positive" and "inappropriate" activations, since these concepts often are mixed up in these kinds of studies. They also highlight the importance of obtaining a quality ECG, free of artifact, as well as the perils of diagnosing a STEMI during tachycardia.

What's not so helpful
The authors focus quite a bit on decreasing the rate of non-STEMI cath lab activations, which is of course a worthy goal. But there is little discussion of the STEMIs that EMS did not catch with the automated system. I.e., this study demonstrated the specificity of the system, but said nothing about the sensitivity.

Look at it this way. Laval is a big town, with about 400,000 residents in the city. Based on estimates of the incidence rate of STEMIs (about 100 STEMIs/year per 100,000 people), there should have been about 800 STEMI patients in Laval during the study period.

In other words, where were the other 800 - 128 = 672 STEMIs? 

How many of those 672 patients were transported by EMS? How many were "missed," either because of a bad-quality tracing, a misinterpretation by the algorithm, or because they presented with atypical symptoms, and so never even  received an ECG by EMS? We have no idea.

So, while decreasing false or inappropriate cath lab activations is a worthy goal, so is making sure that we're not missing anyone who should be sent there!

On the other hand, in Denmark...
A recent article out of Denmark described the experience with a "modern" approach to cath lab activation (e.g., activation based on smaller degrees of ST segment elevation, inclusion of old LBBB patients, use of EMS activation). The Danish cardiologists found a whooping 20% rate of negative coronary caths - and were totally fine with it. In their discussion, they express more concern with missing the opportunity for an early intervention, than with the "false negative"rate. They conclude that

a triage program with acute angiogram for all suspected STEMI patients should anticipate that 1 of 5 patients will not need primary PCI.

Now, I'm not endorsing this rate of negative caths as a goal, and some of their comments suggest that they may have swung the pendulum a bit too vigorously (E.g. "liberal access to acute coronary angiography means some of the patients had a “rule-out” angiogram, for example younger patients with chest pain and an ECG compatible with pericarditis.").
Nonetheless, it's clear that the authors are concerned with catching everyone they can in their cardiology "net."

So, should we take medics out of the loop on STEMI?
Well, as usual, "it depends." There are so many local factors that go into the design of every EMS system, and this may be the most appropriate response, say, in an area that will likely never be able to support the training and QA/QI that ALS systems require. And, frankly, if all you want your EMS system to do is identify the obvious STEMI cases, this is probably the way to go.

Except, you probably want your EMS system to do more. 

You want to identify and treat the NSTEMI patients who need early intervention, as well as STEMI patients. You want medics to identify the potential, "hyperacute," STEMIs. You want them to find and treat CHF, distinguishing "cardiac asthma" from plain ol' asthma, and even discriminate between primary and compensatory tachycardias.

But the "automated" STEMI activation doesn't provide any benefit beyond getting one small slice of the EMS patient population earlier care. That's fine, great even, but it's still a limited benefit. Why not aim just a bit higher?

"Cardiac anaphylaxis" after IM epinephrine?

Can IM epinephrine, at the proper dose, cause an MI? A lot of paramedics worry about this, and, as a result, under-treat anaphylaxis. This is a problem, since this is one of the small group of problems where paramedics can truly save a life.

Another example: whatever this guy is doing (source)

Of course, some of the previous descriptions of complications after epinephrine therapy involve mistakes in dosing or route. For example, this case report states that a young woman developed an AMI after getting "low-dose" epinephrine. Well, she actually received 100 µg IV, or 0.1 mg, which is about ten times what these allergy experts used in their study. 

"Start at 5-15 µg/min"
NOT 100µg/min.

Or even worse - how about giving 2mg epi IV instead of Narcan! Can you imagine the paperwork you would have to fill out after doing that?

A recent case report might cause some EMS providers to worry about administering the appropriate IM dose of 0.3 mg. I don't think that it should - let me explain more.

"Cardiac anaphylaxis: A case of acute ST-segment elevation myocardial infarction after IM epinephrine for anaphylactic shock."

This case report describes the clinical course of a middle-aged gentleman:

A 62-year-old male smoker with no other comorbidities presented to emergency department at 6 am with complaints of generalized pruritus and shortness of breath after taking diclofenac for toothache 1 hour back. On examination, pulse was 97/min; blood pressure, 84/60 mm Hg; jvp, normal; cardiovascular system, unremarkable; respiratory system, rhonchi bilaterally.

Sounds like anaphylaxis! The  ECG, before epinephrine, showed:

"Nonspecific [ECG] changes on arrival"

He then received 1 mg epinephrine IM, which is 3 times the recommended dose. Interestingly, they describe the IM administration as having been given over 5 minutes.

A second ECG was obtained after the patient developed chest pain:

He underwent PCI, and a thrombus was sucked out of his LAD. He ended up doing well.

Was the STEMI really due to the epinephrine?
I'm not so sure - take a closer look at the initial, "non-specific," ECG:

Close up of V1-V3

That looks like quite a bit of ST elevation, especially relative to the QRS, in V2 and V3. But why would someone have a STEMI before getting epinephrine?

Well, sometimes anaphylaxis itself can cause an MI. It's called Kounis Syndrome, and there a number of case reports out there:

Acute coronary syndrome triggered by honeybee sting: a case report.

ST-segment elevation myocardial infarction following a hymenoptera (bee) sting.

Acute anterior myocardial infarction after multiple bee stings.

The Bottom Line
The authors acknowledge this possibility, and also acknowledge that epinephrine-related MI is not typical.

Acute myocardial infarction (MI) following anaphylaxis ("cardiac anaphylaxis") is rare. Epinephrine causing ST elevation in these anaphylactic patients is even more rare.

 In this case, I wonder about the initial "nonspecific" ECG, and the role of epinephrine in causing his STEMI.  Despite the authors' certainty that "high-dose epinephrine 1 mg (1:1000) IM has triggered the formation of a thrombus in the left anterior descending artery," I wonder if the STEMI was underway before they gave the epinephrine. 

What do you think?

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.