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Quality Assurance of Prehospital 12-Lead ECG Programs

10 comments

I’m going to share with you my thoughts on quality assurance of prehospital 12-lead ECG programs.

This is a excerpt from one of my posts in the current discussion called EMS Role in Reducing the Symptom to Reflow Interval for AMI at the National Association of EMS Physicians Dialog Group.


I strongly believe that we need to start with:

1.) Making sure that the patients who are supposed to be getting a 12-lead ECG are getting one.

2.) Making sure that the ECG is captured early on in the patient care encounter, preferably with the first set of vital signs and within 5 minutes of arriving at the patient’s side (unless there is a very good reason as opposed to an excuse).

3.) Making sure that the ECG is captured with *excellent* data quality! There is a lot of room for improvement here.

4.) Making sure that the appropriate actions are taken when the patient meets the stated criteria of the EMS system (whether that is a “STEMI Alert”, transmitting the ECG to a decision maker, or both).

5.) Making sure that serial ECGs are captured (one of which should be captured on arrival at the receiving hospital).

Sometimes asynchronous clocks can cause problems, but they are solvable problems. For example, we can mandate that the cardiac monitor be “powered on” when the EMS crew arrives at the patient’s side so we can calculate the ”time to ECG”.

All of the rest can generally be QA/QI’d through retrospective case reviews or abstracted from ePCR. For example, patients who are diagnosed with ACS at the hospital and were transported by EMS but did not receive a 12-lead ECG in the field. We should find out why and use it as a learning opportunity.

We should also have regular meetings with the stakeholders on STEMI care so the people on the receiving end understand management’s expectations of patients who receiving a 12-lead ECG in the field (in other words, that they should be gowned and our approach is very standardized in the field).

Any STEMI Alerts that were called based on incorrect interpretation of the 12-lead ECG are learning opportunities and should be fed back to the line personnel as case reviews, along with tips for identifying that particular mimic in the future.

Often (but not always) what you’ll see is that poor data quality was a major factor. Sometimes it’s poor lead placement (limb leads on the chest) and sometimes it’s a very good mimic like an atypical strain pattern from left ventricular hypertrophy.

If the paramedics in the field are doing their part and the E2B/D2B times ”fall out” then a problem on the hospital’s side of the fence. Sometimes there are legitimate reasons for this (marginal cases, an unstable patient, another STEMI patient already on the cath table) but our attention should be on system failures where EMS failed to act appropriately.

It doesn’t take long to figure out if the problems encountered are training-related versus compliance-related. If you have paramedics out there who just “don’t believe in 12-leads” or “don’t need a 12-lead to tell them who’s having a heart attack” you need to find that out and address it.

It also doesn’t take long to figure out who the problem physicians are. If you plot out all of your acute STEMI cases for a year on a time graph you might be surprised to see that the same ED physician was on duty for all of the “fall out” cases and a different ED physician was on duty for all of the D2B times < 60 minutes. That’s a problem that the hospital needs to address through peer review.

What are your thoughts?

Posted by on May 30, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,

Are all STEMI patients the same?

1 comment

When it comes to regionalized STEMI care, we treat all STEMI patients the same. But are they the same?

The answer is, "No!"

Most EMS protocols include a maximum ground transport time of 30-60 when bypassing non-PCI hospitals (AHA Mission: Lifeline calls them "STEMI Referral Hospitals").

The idea is that when the "first medical contact-to-balloon" interval exceeds 90 minutes, the patient would be better served by transport to a non-PCI hospital for fibrinolytics.

Is this true?

The answer is, "Maybe!"

Consider Hospital delays in reperfusion for ST-elevation myocardial infarction: implications when selecting a reperfusion strategy. Circulation. 2006 Nov 7;114(19):2019-25

According to this table, the three variables to consider are:

  • Symptom duration ( 120 min.)
  • Age of the patient ( 65 years)
  • Infarction location (anterior vs. non-anterior)

For early presenters (< 120 min. symptom onset) the point at which primary PCI loses its benefit over fibrinolytic therapy is an additional 94 minutes (that's door-to-balloon minus door-to-needle or D2B-D2N).

For late presenters (> 120 min. symptom onset) primary PCI loses its benefit at 190 min. (D2B-D2N).

For patients 65 years of age primary PCI loses its benefit at 155 min. (D2B-D2N).

For anterior infarction primary PCI loses its benefit at 115 minutes (D2B-D2N)

For non-anterior infarction primary PCI loses it benefit at 112 minutes (D2B-D2N).

The following graph illustrates how these variables interact.

 

This suggets that young patients who present early with anterior STEMI should probably receive fibronolytics prior to transfer.

On the other hand, late presenters and/or patients > 65 years of age should probably be transferred for primary PCI even when transport times are prolonged.

An elderly patient who presents early with acute anterior STEMI is right on the edge (assuming other "high risk" criteria are not met) at 107 minutes (D2B-D2N).

Posted by on May 29, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , ,

66 year old male CC: Chest pain

21 comments

Here’s another great case submitted by Nick Ciaravella of Grady EMS in Atlanta, GA.

66 year old male presents to EMS with chest pain.

S – Chest Pain
A – None
M – Atenolol, HCTZ
P – HTN
L – meal, 7 hours prior to event
E – Mowing his lawn

O – Started while mowing his lawn
P – Provoked while exerting himself, Palliated initially when he sat down to rest
Q – Sharp
R – Substernal, initially radiating to his jaw, when he rested the pain was only in his chest
S – Initially 10/10, upon ems arrival 4/10, en route 8/10, 9/10, and 10/10 upon arrival at ED
T – No previous episodes

The patient initially presented to EMS with 4/10 pain and vitals as follows, 148/84, pulse 72, 18 respirations, SPO2 96%, Lung sounds clear and equal, BGL 103.

The patient was placed on 3 LPM O2 via NC, given 324 mg Aspirin PO, given 0.4 mg Nitro Tablet Sublingual and then 1 inch of Nitro Paste Transdermal. The Patients pain increased en route to the ED and began to radiate down his left arm en route.

12-lead ECG #1

12-lead ECG #2 (about 15 minutes later)

What do you think?

See also:

82 year old male CC: Chest pain

41 year old male CC: Chest pain

Found on the Lifenet Receiving Station

43 year old female CC: “Indigestion-like” chest discomfort

54 year old male CC: Chest pain

57 year old male CC: Chest pain

54 year old male CC: Chest pain

54 year old male CC: Chest pain – Discussion

58 year old male CC: Chest discomfort

Posted by on May 28, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,

41 year old male CC: Chest pain – Answer

17 comments

Thank you for all of the excellent comments on this case! I was delighted to see such a high level dialog when I checked my blog this morning.

Normally I would to answer each of you individually, but since there are 22 comments (so far) I thought I would try a different strategy and post the answer, along with tips for the correct interpretation of this ECG (at least in the context of “STEMI / not a STEMI” while you are out in the field).

This was not a STEMI.

It was most likely left ventricular hypertrophy with a strain pattern and mild hyperkalemia.

First, let’s look at the 12-lead ECG and make the case for LVH.

You’ll recall from my previous posts on the topic that I’ve said it’s more important to recognize the so-called “strain pattern” than the voltage criteria.

The reason is simple.

If the “strain pattern” isn’t causing a problem (mimicking an acute anterior STEMI) then you’re waisting your time calculating the QRS voltage.

This ECG has the general appearance of “T-wave discordance”. In other words, the T-waves are deflected opposite the main deflection of the QRS complex, which is highly suggestive of a secondary ST-T wave abnormality.

In this case, the most likey cause is left ventricular hypertrophy.

I say “generally appearance of T-wave discordance” because it’s not true in every lead. That’s why I mentioned in a previous post that there are “some caveats”.

When I’m looking for appropriate T-wave discordance, I mentally remove isoelectric or equiphasic leads, particularly in the transition zone (the point at which a QRS goes from mostly negative to mostly positive in the precordial leads).

Let’s circle the leads I would mentally remove from this 12-lead ECG to decide whether or not “T-wave discordance” is present.



With those leads removed, are the T-wave deflected opposite the QRS complexes?

Absolutely!

Could that be a coincidence?

Highly unlikely!

The high lateral leads in particular are showing a very typical looking strain pattern.

This can be a problem because it could easily be mistaken for “lateral ischemia” or reciprocal changes secondary to acute STEMI!

Does this ECG meet the voltage criteria for LVH?

Not exactly, but I believe we can make the case using the Romhilt-Estes point scoring system. This ECG would get at least a 4 (probable LVH), and it’s right on the borderline for left atrial enlargement and delayed intrinsicoid deflection in leads V5 and V6 which would give it a score of 5 or 6.

But I don’t think that’s important.

The next question we want to ask is, is the degree of the secondary ST-T wave abnormality proportional to the amplitude of the QRS complex in the opposite direction?

The answer is yes.

Remember, we’re looking at the ST-segments and the T-waves together.

At first glance it looks like there might be more ST-elevation in lead V1 than lead V2. However, I believe this is an optical illusion created by the biphasic P-waves in lead V1, as well as the more defined (less diffuse) J-points in lead V1.

Let’s blow this up a little bit.



When we use the TP-segments as a baseline, we can see that it’s debatable as to whether or not lead V1 shows more ST-elevation, but it’s obvious that lead V2 shows a more pronounced ST-T wave abnormality.

The T-waves seem a little bit narrower than we might have expected with LVH, perhaps with a slightly later take-off. Also, the QTc is well within “normal” at 419 ms.

I don’t have the exact lab value, but the feedback I received on this case was that the patient had a potassium level that was “on the high end of mild hyperkalemia” (so I’m guessing between a 6 and 7).

Consider the following graphic that compares the T-waves of hyperkalemia to the T-waves of acute anterior STEMI.



There isn’t much documentation out there as to what hyperkalemia is supposed to look like in the presence of a secondary ST-T wave abnormality, but you’ll notice that with hyperkalemia, the T-waves are narrow and have a late take-off, while with acute anterior STEMI, the T-waves are more “broad-based”.

This was a very difficult case. So what can we learn from it?

In my mind, it’s very simple (and it needs to be simple for field use — complicated equations involving calipers are not simple).

T-wave discordance strongly suggests the possibility of a secondary ST-T wave abnormality. That being the case, I would wait for changes on serially obtained ECGs before calling a STEMI Alert.

Remember, in some studies LVH is the most common cause of ST-elevation in chest pain patients, so we need a solid strategy to deal with this STE-mimic!

I hope we can continue our useful discussion about this ECG! I look forward to reading more of your comments.

See also:

41 year old male: CC: Chest pain

Posted by on May 26, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

41 year old male CC: Chest pain

27 comments

A 41 year old male is pulled over during morning rush-hour by sheriff’s deputies.

He states that he is on his way to the hospital because he is having chest pain. EMS is called to the scene.

The patient is awake, alert, and oriented to person, place, time, and event.

His skin is pink, warm, and moist.

He appears acutely ill and anxious.

He states that he has a history of high blood pressure and renal insufficiency. He takes several medications, but he can only recall that one of them is a beta blocker.

Onset: 1 hour ago while sleeping.
Provoke: Nothing makes the pain better or worse.
Quality: Patient describes the pain as a poorly localized “fullness” or “pressure”.
Radiate: The patient cannot tell whether or not the pain radiates.
Severity: The patient reluctantly gives the pain a 7/10.
Time: The patient states he has had the pain on several occasions over the past few months but did not seek medical treatment.

Vital signs are assessed.

Resp: 20
Pulse: 76
BP: 138/78
SpO2: 99 on RA

The cardiac monitor is attached.



A 12-lead ECG is captured.



What is your analysis of this ECG?

Does anything about it concern you?

Is this a STEMI?

Why or why not?

Note: This 12-lead ECG was captured in the back of an ambulance with the motor and generator running, but it shows excellent data quality.

See also:

41 year old male: CC: Chest pain – ANSWER

Posted by on May 24, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

PowerPoint Presentation on Strain Patterns!

5 comments

This is an awesome PowerPoint presentation from one of my favorite ECG textbooks, 12-Lead ECG – The Art of Interpretation.

You owe it to yourself to purchase this book (and no, they don’t pay me to say that).

Make sure you use “full screen” so you can see all of the features of this important presentation. Pay special attention to slides 33-47!

Slide 45 shows a strain pattern from left ventricular hypertrophy (LVH).

Slide 47 shows a split screen with a strain pattern from right ventricular hypertrophy (RVH) on the left and acute infero-posterior STEMI on the right.

This is the book that taught me how to recognize strain patterns! So pay attention because this is one of the most important STEMI mimics!

Chapter14

http://www.authorstream.com/player/player.swf?p=368628_634066207134918456

See also:

Left ventricular hypertrophy – Part I

Left ventricular hypertrophy – Part II

Right ventricular hypertrophy vs. isolated posterior STEMI

Posted by on May 22, 2010 • Filed under: Uncategorized • Tagged: , ,

Left ventricular hypertrophy – Part II

10 comments

I know I promised to go over the voltage criteria for left ventricular hypertrophy (LVH) but I lied!

If you’re really interested you can check out the Wikipedia article HERE, the ECG Learning Center HERE, or Tom Evans’ crib sheet HERE.

Personally? I think it’s a distraction. As far as STEMI recognition goes, it misses the point entirely!

The ECG will either show a so-called “strain pattern” (or repolarization abnormality) or it will not! If it does, there’s a chance it will mimic an acute anterior STEMI.

Just because the voltage criteria for LVH is satisfied on a particular ECG does not mean that a secondary ST-T wave abnormality will be present! Even if it is, it will not necessarily mimic acute anterior STEMI.

What I’m trying to say (again) is this:

It’s far more important to recognize a strain pattern than it is to calculate the voltage criteria for left ventricular hypertrophy on a 12-lead ECG!

Having said that, I do know most of the voltage criteria for left ventricular hypertrophy, so I’m not trying to discourage you from learning. I just want to put it in context!

Let’s look at a couple of examples courtesy of my friend Tom Bernesser who is a paramedic in North Carolina. Both of these ECGs are actual “false positives” from North Carolina’s RACE program.

That means they presented with signs and symptoms consistent with ACS, acute STEMI was identified on the prehospital 12-lead ECG (including the computerized interpretive statement), the paramedic and the ED physician agreed the patient satisfied the reperfusion criteria, the patient was fast-tracked to the cardiac cath lab, and no culprit artery was found.

Example #1.



This is an atypical “strain pattern” with many typical features.

I suspect the possibility that leads V1 and V2 might have been accidentally transposed but that doesn’t really matter. For the purposes of STEMI recognition, the typical features outweigh the atypical features.

In the first place, you should immediately notice the “widened QRS-T angle” that is the hallmark of a secondary repolarization abnormality. You will notice the same finding for LBBB and paced rhythm!

Importantly, the degree of the secondary ST-T abnormality is, generally speaking (there are some caveats), proportional to the size (or amplitude) of the QRS complex in the opposite direction!

If you take nothing else away from this post, please learn this “trick”.

It’s really no different from the concept I demonstrated in the post called Wolff-Parkinson-White (WPW) – STEMI Mimic.

Herein lies a problem with prehospital 12-lead ECGs!

With left ventricular hypertrophy (LVH) the QRS complexes are often “cut off” at the top or bottom or they run together with other QRS complexes which can create the illusion that the QRS complexes are smaller, so you have to train your eye!

Take a look at this ECG and find the most severe ST-T wave abnormality.

That’s easy! Lead I clearly shows the most pronounced ST-T wave abnormality. The ST-segment is depressed, downwardly concave, and shows a deep inverted T-wave.

Does the amplitude of the R-wave in the opposite direction explain it? No way! It’s even smaller than the QRS complex in lead II, and the ST-T wave abnormality in lead II isn’t nearly as severe!

What is the second-worse ST-T wave abnormality? Lead V3! Does the depth of the S-wave in the opposite direction explain it? Not really.

But wait! Are we certain we’re getting an accurate “read” on the amplitude of the R-wave in lead I and the depth of the S-wave in lead V3?

I’m not so sure!



I suspect the possibility that the computer is “cropping” the QRS complexes to fit them on the ECG paper. See the little horizontal line that marks the “top” and “bottom” of these QRS complexes?

I’ve seen it many times before!

So ask yourself this question:

Generally speaking, does there seem to be a relationship between the QRS-complex and the degree of ST-elevation or depression in the opposite direction?

If the answer is “Yes!” then don’t call the STEMI Alert. Instead, perform serial ECGs and look for changing ST-segments and T-waves! ST-segments and T-waves shouldn’t “evolve” or change over time if it’s a simple secondary ST-T wave abnormality!

Example #2



Using the new “trick” you have learned, what do you think of this ECG?

More discussion to follow.

See also:

Left ventricular hypertrophy – Part I

Left Ventricular Hypertrophy May Result In Profound ST Elevation – Dr. Smith’s ECG Blog

Posted by on May 21, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,

62 year old male CC: Chest pain

10 comments

62 year old male presents to the emergency department complaining of chest discomfort.

Past medical history is significant for dyslipidemia and ulcerative colitis. Also prior history of significant tobacco use.

Maternal history of CAD. Maternal and paternal history of CVA.

The patient’s only medication is Lipitor but he took an aspinin en route to the hospital.

Onset: Patient states the pain started that morning and became progressively worse since lunch time
Provoke: Nothing makes the pain better or worse
Quality: Sharp and nonpleuritic
Radiate: The pain radiates down the right arm to the bicep
Severity: 7/10
Time: Patient states he experienced a similar pain in his right upper chest several days prior while playing tennis. He stopped exercising and the pain resolved.

The pain makes the patient feel “a little clammy.” He denies shortness of breath. He states that he feels “a little dizzy” but denies palpitations. He had a negative stress test 3-4 years ago.

He has a known history of left bundle branch block.

The patient’s skin is warm and dry.

Breath sounds clear bilaterally. No JVD. Neuro exam normal.

Vital signs:

Resp: 18
Pulse: 60
BP: 140/72
SpO2: 98 on RA

A 12-lead ECG is captured and presented to the ED physician within 5 minutes of arrival.

An “old” ECG is pulled from the computer system for comparison.

What is your impression?

*** UPDATE ***

After oxygen and nitroglycerin the patient reports a significant decrease in pain.

An additional 12-lead ECG is captured.

There is now slightly less ST-elevation in leads V3 and V4.

Remember that a secondary ST-segment abnormality (as opposed to a primary ST-segment abnormality) should not “improve” with oxygen and nitroglycerin!

In other words, if this ST-elevation was caused just by the LBBB, it shouldn’t be “getting better”. Changing ST-segments suggest the dynamic supply vs. demand characteristics of ACS!

Now, let’s go back to the initial 12-lead ECG. Is the ST-elevation in the anterior leads cause for concern?

Go back and read Identifying AMI in the presence of left bundle branch block (or paced rhythm).

Remember, discordant ST-elevation = or > 5 mm is the least specific of Sgarbossa’s criteria! That’s why we use the modified rule that I learned from Dr. Stephen Smith of Dr. Smith’s ECG Blog.

That criterion states that discordant ST-elevation should not be more than 0.2 (or 20%) the depth of the S-wave in the setting of left bundle branch block (ST/QRS ratio).

Using that criterion, how does this ECG measure up? Let’s take a look.

The patient was ultimately cathed and angiography revealed 100% occlusion of the LAD.

Final thought:

Does it get any more difficult that that? If Dr. Smith’s decision rule works this great, shouldn’t we be shouting it from the rooftops?

See also:

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part I

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part II

Discordant ST-segment elevation in LBBB or paced rhythm

Found on the Lifenet Receiving Station (LBBB with concordant ST-depression in leads V3 and V4)

58 year old female CC: Chest pain

58 year old female CC: Chest pain – Conclusion (meets all 3 of Sgarbossa’s criteria)

Posted by on May 19, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , , ,

Right ventricular hypertrophy vs. isolated posterior STEMI

3 comments

A reader of the Prehospital 12-Lead ECG blog asks, “How can you tell the difference (based on ECG criteria alone) between right ventricular hypertrophy and acute isolated posterior STEMI?”

Well, the good news is you don’t have to tell “based on ECG criteria alone” and I’m sure all of my regular readers know that I don’t advocate interpreting an ECG “in a vacuum”.

Having said that, it’s not that difficult to tell these conditions apart. But before we talk about that, let’s talk about what makes them similar.

You might recall from my previous post “Differential diagnosis of tall R-waves in lead V1” that both right ventricular hypertrophy and posterior MI can cause tall R-waves in lead V1. Sometimes this is referred to as the R/S ratio, and it should be less than 1 (although I always take a second look when the R/S ratio is greater than 1 in lead V2 as well).

Keep in mind that acute isolated posterior STEMI need not show tall R-waves in lead V1! That tends to be a “late” finding (since the tall R-waves are really reciprocal Q-waves from the posterior wall). In fact, most if not all of the acute isolated posterior STEMIs I’ve shown on this blog have not shown tall R-waves in lead V1.

But let’s say you have a patient who presents with chest pain and tall R-waves in lead V1, and it’s not a right bundle branch block.

Let’s say this ECG looks like this:

How would you know it’s right ventricular hypertrophy (with a right ventricular strain pattern) and not acute posterior STEMI or anterior ischemia?

The short answer is, because it shows a right axis deviation* as well as a “typical” looking right ventricular strain pattern in the right precordial leads (V1-V3).

What makes it “typical”?

The fact that the ST-depression and T-wave inversion is “pouty-lipped” (downwardly concave) and the degree of the secondary ST-T wave abnormality is proportional to the size of the R-wave!

In other words, the tallest R-waves are in lead V2 and lead V2 shows the most pronounced secondary ST-T wave abnormality in the opposite direction.

The bottom line is, when you see a right axis deviation (often with right atrial enlargement), and tall R-waves in the right precordial leads, take any ST-depression and T-wave inversion in the right precordial leads (V1-V3) with a grain of salt!

Perform serial ECGs and capture modified chest leads V7-V9 to help with the diagnosis of acute ischemia or acute isolated posterior STEMI!

* So yes, we can add this to the large list of reasons that axis determination is a critical skill for any serious student of electrocardiography to master.

Posted by on May 17, 2010 • Filed under: Uncategorized • Tagged: , ,

26 year old male CC: Chest pain

18 comments

Here’s a great case submitted by a faithful reader who wishes to remain anonymous.

EMS is called to a 26 year old male complaining of chest pain.

On arrival patient is found sitting on his living room couch. He appears anxious and acutely ill.

He states that he was riding his bike when he became anxious, had a “coughing spell” and started to experience chest discomfort.

The location of the chest discomfort is in the center of his chest and slightly to the left.

Onset: Sudden while riding a bike
Provoke: Nothing makes the pain better or worse
Quality: Difficult to describe but with prompting the patient calls it “pressure”
Radiate: Left jaw and left arm
Severity: 7/10
Time: No previous episodes

The patients skin is warm and moist. The color is normal.

The patient denies shortness of breath. Breath sounds are clear bilaterally.

He is nauseated but he has not vomited.

Past medical history: Healthy
Medications: None

Vital signs are assessed.

Resp: 22
Pulse: 98
BP: 140/84
SpO2: 100 with oxygen via NRB @ 15 LPM

The cardiac monitor is attached.

A 12-lead ECG is captured.

What is your impression?

*** UPDATE  ***

The importance of serial ECGs cannot be over-emphasized.

In this case, a second 12-lead ECG was captured just prior to arrival at the hospital.

Does this new information shed any light on the probably diagnosis?

What else could you have done?

ANSWER:  Apply posterior chest leads V7, V8, and V9

Just for fun, here’s what the follow-up ECG looks like “flipped” over and held up to a light.

Do you see the STEMI now?

See also:

48 year old male CC: Chest discomfort, shortness of breath

Anterior ischemia or posterior STEMI? (at Paramedicine 101)

50 year old male CC: Respiratory distress, chest pain

74 year old male CC: Chest pain

74 year old male CC: Chest pain – Update

74 year old male CC: Chest pain – Final update (angiograms)

Right ventricular hypertrophy vs. isolated posterior STEMI

66 year old male CC: Chest pain

Posted by on May 13, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , ,

Town of Hilton Head Island receives honorable mention for IAFC and Physio-Control’s Heart Safe Community Award

5 comments

I’m pleased to announce that the Town of Hilton Head Island, SC has received honorable mention for the International Association of Fire Chiefs and Physio-Control’s Heart Safe Community Award!

The ceremony took place this morning at The Orleans Hotel in Las Vegas, NV at Fire-Rescue Med 2010.

The winners were announced immediately following the general session “EMS and the Department of Homeland Security” delivered by the Assistant Secretary for Health Affairs and DHS Chief Medical Officer Alexander Garza, MD, FACP.

Norris W. Croom, III, Mike Metro, John Sinclair, Tom Bouthillet,
Alex Garza, Gary Ludwig, J. Robert Brown, Jr., David Becker
Photo credit: Mark Lockhart

2010 Heart Safe Community Award Winners

Winner – Small Community

Town of Colonie Emergency Medical Services System, NY

Honorable Mention – Small Community

Hilton Head Island Fire & Rescue, Hilton Head Island, SC
Rib Mountain Fire Department, Wausau, WI

Winner – Large Community

Anchorage Fire Department / Big Wild Heart of Alaska Initiative, AK

Honorable Mention – Large Community

Dane County Emergency Medical Service, WI
City of Arlington Fire Department, TX

It was a tremendous honor to accept this honorable mention on behalf of the Town of Hilton Head Island, Hilton Head Island Fire & Rescue, and Hilton Head Hospital.

Posted by on May 4, 2010 • Filed under: ems-topics • Tagged: , , , , , , , ,