In this episode of the EMS 12-Lead podcast we're joined by Kelly Arashin, ACNP, CCNS and Mike McEvoy, PhD, RN, CCRN, REMT-P at EMS Today 2013 in Washington D.C. We discuss the benefits and dangers of oxygen administration.
Kelly is a dual boarded advanced practice nurse and Chair of the Hypothermia Steering Committee at Hilton Head Hospital in Hilton Head Island, SC.
Mike describes himself as a nurse, paramedic, firefighter, and medical college professor. He is also Chair of the Resuscitation Committee for University Teaching Hospital in Albany, NY.
Mike is the author of the article Can Oxygen Hurt? and taught an educational session at Physio-Control University entitled To Give Oxygen or Not: That is the Question.
*** Update ***
Thanks to Brooks Walsh, M.D. for bringing this article to our attention:
In this episode of the EMS 12-Lead podcast we're joined by Brooks Walsh, M.D., Emergency Physician and Editor of Mill Hill Ave Command and Doc Cottle's Desk. We discuss paramedic education, ECGs, blogging, science fiction doctors, "treating the patient and not the monitor", reperfusion therapy for acute STEMI, and preactivation of the cardiac cath lab.
In this episode of the EMS 12-Lead podcast we're joined by Richard Price of the PulsePoint Foundation. If you're not familiar with PulsePoint it used to be referred to as the San Ramon Valley Fire Department app.
Here's a case submitted by a faithful reader who wishes to remain anonymous. He has submitted several cases before and they are always excellent so thank you, Mr. Anonymous!
EMS is called to the residence of a 69 year old female who is complaining of sudden onset of shortness of breath and weakness.
Past medical history: Healthy
Medications: None
The patient is seen in the emergency department of a local community hospital where she is found to have slight J-point elevation in the anterior leads.
(The vital signs and results of the physical exam are not available.)
Approximately 2 hours later there is a slight change in ST-segment morphology and new T-wave inversion in lead aVL. A cardiologist is consulted via telemedicine at the tertiary care center and the decision is made to transfer the patient.
Concurrently with this decision the patient is given 3 doses of SL NTG with complete resolution of her symptoms.
The transport ambulance arrives and records the following 12-lead ECG.
Several more are recorded en route. Here's the ECG captured on arrival at the PCI-hospital.
Do you think this patient is having a STEMI? Why or why not?
In this episode Tom Bouthillet sits down with Christopher Granger, M.D., Mayme Lou Roettig, R.N and James Jollis, M.D. from the RACE Program in North Carolina. In the course of our "unplugged" session some incredible insights are developed from one of the highest functioning STEMI systems in the United States!
On behalf of Team EMS 12-Lead (Tom Bouthillet, David Baumrind and Christopher Watford) I am pleased to officially acknowledge that the EMS 12-Lead blog won Judges' Choice for 2012 EMS Blog of the Year.
"Our judges will choose ten finalists from the first round of nominations. The finalists will then be eligible for a ‘Judge’s Choice’ prize as well as a ‘Reader’s Choice’ prize.
Judges will choose these finalists based on the following criteria:
Calibre of posts relating to the Fire and/or EMS fields
Frequency of posting Professionalism towards our service(s)
Quality of content
Longevity as a blogger
For the second part of the contest, readers will then be able to vote in our poll for their favorite blog, which will provide us with a ‘Reader’s Choice’ winner. The ‘Judge’s Choice’ winner will be ascertained by judges then considering the following criteria:
Use of other online channels to promote their content
I'd say we didn't bribe them but I haven't checked with David and Christopher yet.
It's been a good year for the EMS 12-Lead blog and we'd like to thank all of our friends, colleagues, followers, fellow bloggers and podcasters, and everyone else who helps to make the EMS blogosphere (EMS 2.0) a dynamic environment where learning can be interesting and "cool" again.
We'll do our best to continue innovating, sharing awesome cases, hosting interesting guests, expanding into new media and challenging you in engaging and participatory ways!
This is the conclusion to 88 year old male CC: Chest pain. You may wish to go back and review the history and clinical presentation.
First, let's look at the rhythm strip.
This shows an undetermined regular rhythm at a rate of about 60 with demand ventricular pacing.
This is an oversimplification but as long as the intrinsic rhythm has an R-R interval of 1000 ms or less (blue arrows for reference) the pacemaker will inhibit itself because it's not needed.
Then we see the first 12-lead ECG.
Lead V1 is often a good place to see atrial activity. Now we can see flutter waves which explains why there is no atrial pacing (assuming this is a dual chambered pacemaker). You will note that the "wide" QRS complexes in the 12-lead ECG are exactly 1000 ms apart and are functioning in an apparent demand capacity which means these complexes are almost certainly paced.
As at least one person mentioned in the comments a typical paced rhythm with the pacing lead in the apex of the right ventricle will show LBBB morphology (this ECG shows RBBB morphology) so this is a bit unusual. However, in this modern day and age of mutlisite pacing none of these rules are set in stone.
I will say, however, that when I first saw this 12-lead ECG the T-waves in the right precordial leads (V1-V3) looked unusually large to me even though they are appropriately discordant with the QRS complex.
Now let's look at the next 12-lead ECG.
Interestingly, the intrinsic rhythm does not look particularly concerning in the right precordial leads (V1-V3). However, I do see a problem! To demonstrate I'm going to place leads V5 and V6 from 12-Lead 1 and 12-Lead 2 side-by-side.
This is a subtle finding but note the loss of upward concavity in the ST-segments between 12-Lead 1 and 12-Lead 2. In other words, there is a "straightening" of the ST-segment (it's not curved upward anymore) and that's bad!
Now let's look at the final 12-lead ECG.
This ECG appears to show acute lateral STEMI. Would it be better to have seen a previous 12-lead ECG with paced rhythm in the left precordial leads (V4-V6)? Absolutely! But clearly there is excessive discordance in leads V5 and V6 and the T-waves look hyperacute.
Here is the ECG that was taken in the emergency department.
These changes were not appreciated by the paramedics, the ED physician or the cardiologist.
Labs:
@ 2245
CKMB 2.14
CPK 58
Trop < 0.01
K+ 2.8 (low)
Na 142
Calcium 5.8 mg/dL (critical) – non-ionized
Renal profile WNL
@ 0535
CPK 254
CKMB 30.03
Trop 0.341
CT was negative for PE or aneurysm.
It was also noted in the chart that the patient had a history of AF and MVP S/P repair (could this explain the RBBB morphology with the paced rhythm?).
This was ultimately diagnosed as an acute coronary syndrome but not a STEMI. The case was handled medically (did not go to the lab) and the patient was discharged home.
Was it a missed STEMI? I can't say conclusively due to the abnormal lab values but I'm curious to hear what Stephen Smith, M.D. has to say!
EMS is called to a 88 year old male with a chief complaint of chest discomfort.
On arrival the patient meets EMS at the front door. His skin is slightly pale and moist. He appears anxious.
Past medical history: "Cardiac", pacemaker, hypertension, dyslipidemia
Medications: Numerous, unavailable at the time of EMS evaluation
Paramedics lead the man to a chair and the assessment begins.
Onset: 30 minutes prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: Poorly localized pressure
Radiate: Does not radiate
Severity: 7/10
Time: Admits to previous episodes but unable to give details
Vital signs are assessed.
RR: 18
Pulse: 70
NIBP: 140/92
SpO2: 90 on RA
Breath sounds: Clear in the apexes, diminished in the bases.
No JVD or pitting edema.
The patient is placed on the cardiac monitor.
A 12-lead ECG is obtained.
The patient is placed on oxygen via NC @ 4 LPM and is removed to the back of the ambulance. An IV is initiated and the patient is given 0.4 mg NTG spray SL.
As most of you know by now, "Team EMS-12 Lead" had a lot to celebrate at the EMS Today conference in Baltimore. Tom Bouthillet received his well deserved EMS 10 award, and his Code STEMI Web Series premiered as well. Lots of great stuff going on!
The premier of Code STEMI happening the same time as the EMS 10 award was very apropos. The web series–incredibly informative and well done–is a great example of Tom's ability to innovate. He is always pushing for new ways to raise the bar of cardiovascular education and care in this country and abroad.
Most of all, though, we want to celebrate you: our readers, listeners, and followers. We all have busy lives, with lots of ways to spend our free time. We've had over 2,000,000 page views and 5,500 comments on the website alone in the last 4 years! We want to thank you for choosing to spend some of your time with us.
As you improve your skills, you inspire us to keep getting better ourselves, always trying to provide worthwhile and interesting content. Not to mention, we learn something new from you guys and gals every day!
So as we celebrate Tom and his terrific accomplishments, we want to also celebrate you as well.
Thanks for your support, what you do makes a difference!
"Team EMS-12 Lead" (Christopher Watford, Tom Bouthillet and David Baumrind) at the EMS 10 Awards
It's been an amazing week at EMS Today 2012! As you probably already know (if you've been following our Facebook page) I won an EMS 10 Award on Wednesday night.
I was nominated by our good friend David Hiltz from the American Heart Association (a previous EMS 10 Award honoree and well known for his work with HeartSafe Communites) and co-nominated by Associate Editors Christopher Watford and David Baumrind.
This is a tremendous honor but I'm very congizant that I couldn't do it without such awesome friends and mentors! The EMS 12-Lead blog and podcast would not be what it is without Christopher and David.
Photo credit: Chris Montera
"Podmedic" Jamie Davis, Tom Bouthillet and Ted Setla discuss the Code STEMI Web Series on the MedicCast
This week was also marked by the release of Episode 1 of the Code STEMI Web Series at First Responders Network! I've seen the first episode a couple of times but being there at the premier was really amazing!
Special thanks to Ted Setla and Chris Eldridge from First Responders Network and Erik Denny from Physio-Control (our indispensable partner on the road) for making this possible! I'm delighted to have been a part of it!
Episode 1 was very well received! In fact, a couple of top-notch EMS systems are very interested in having us come out to feature their STEMI systems and the locations sound amazing! So keep your fingers crossed. We'd love to continue this series!
If you haven't watched the first episode yet, what are you waiting for? CLICK HERE!
Photo credit: Dave Konig
Premier of the Code STEMI Web Series at the Physio-Control Learning Center
Kelly and I are having a wonderful time. We're seeing lots of old friends and making some new ones, too! EMS 2.0 has been called an idea and it's been called a movement. More than anything else we've come to realize it's about friendship and it's about relationships.
It may have started online but it's accomplishing some amazing things in the real world!
Heading to EMS Today 2012? Then we have an announcement for you!
Episode 1 of the Code STEMI Web Series will released at EMS Today 2012 in Baltimore! This is the rural episode that features the emerging system of care in South Dakota and the work of AHA Mission: Lifeline. It includes EMTs, paramedics, nurses, physicians, administrators and STEMI survivor Forrest "Mick" Stanton.
Jodi Doering, RN – Director of Mission: Lifeline South Dakota
The screenings will take place at the Physio-Control booth (#2907).
Thursday, March 1 @ 7:00 p.m. – Premier (Invite only)
Complete a product tour at the Physio-Control booth and you will receive as a special gift web-access to an exclusive version of the 12-Lead ECG Challenge app by Tom Bouthillet and Limmer Creative including 10 new cases and a 12-lead ECG quiz!
I went to the emergency department with a kidney stone yesterday.
Here's the estimate I was provided at discharge.
ER Level 4: $4,631.94
Insurance contractual discount: -$4,154.03
Adjusted estimated charges: $477.91
Estimated insurance responsibility: -$257.33
Patient co-pay: $125.00
Patient applied co-insurance: $95.58
Estimated patient responsibility: $220.58
So, I paid $220.58 on my way out the door (on a credit card). I imagine I'll also be receiving bills from the ED physician and radiologist.
What really amazes me about this estimate is the fact that $4,154.03 (almost 90% of the bill) was written off because of the contract between the hospital and Blue Cross.
Keep in mind that doesn't mean Blue Cross paid this amount. It just goes into oblivion. But it was a made-up number in the first place. No reasonable person believes that $4,631.94 is an appropriate amount of money for a visit to the emergency department.
Now imagine that I didn't have insurance. What would my bill have been? $4,631.94.
So, all you folks out there that buy into the propaganda that we don't need health care reform, be glad you have insurance. The system is stacked against the most vulnerable.
For years now many have complained about the AHA's official recommendation that primary PCI for acute STEMI be accomplished within 90 minutes of first medical contact (which can be a Critical Access Hospital 1 or 2 hours away from a PCI hospital or a volunteer BLS EMS system in the rural setting).
There are two main reasons the 90-minute standard for rural patients is problematic.
We hold PCI hospitals to a 90-minute standard for walk-in patients
You could argue that it's time to change the recommendation from 90-minutes to 60-minutes for walk-in patients at PCI hopsitals (which I agree with). But even so, for many patients the mortality benefit of primary PCI over fibrinolytic therapy persists well past 90-minutes.
It's also important to remember that many patients have contraindications to fibrinolytic therapy, meet high-risk criteria (pulmonary edema, hypotension, tachycardia) that make primary PCI necessary, and that up to 30% of patients who receive fibrinolytic therapy will have "failed fibrinolysis" (their symptoms and ST-elevation will not resolve after being given clot-busing drugs indicating that they have not been reperfused).
In other words, all hospitals need (in the words of Jodi Doering, R.N.) "a Plan A, a Plan B and a Plan C." This is far too important to leave to chance. There is mounting evidence that transfer PCI takes too long and that rural hospitals are not achieving door-in to door-out (DIDO) times of less than 30-minutes so there is plenty of room for improvement and my intent here is not to blame the guidelines for preventable delays.
Having said that it's simply not possible for some patients who would benefit from primary PCI to have their infarct-related artery opened up on the cath table within 90-minutes of first medical contact (which, let's face it, is not even being measured in the vast majority of STEMI "systems" — the word "systems" in scare quotes because if it's not measured it's not a system.)
5.2.2.2. Primary PCI of the Infarct Artery: Recommendations
Class I
Primary PCI should be performed in patients within 12 hours of onset of STEMI. (Level of Evidence: A)
Primary PCI should be performed in patients with STEMI presenting to a hospital with PCI capability within 90 minutes of first medical contact as a systems goal.(Level of Evidence: B)
Primary PCI should be performed in patients with STEMI presenting to a hospital without PCI capability within 120 minutes of first medical contact as a systems goal.(Level of Evidence: B)
Primary PCI should be performed in patients with STEMI who develop severe heart failure or cardiogenic shock and are suitable candidates for revascularization as soon as possible, irrespective of time delay. (Level of Evidence: B)
Primary PCI should be performed as soon as possible in patients with STEMI and contraindications to fibrinolytic therapy with ischemic symptoms for less than 12 hours. (Level of Evidence: B)
Class IIa
Primary PCI is reasonable in patients with STEMI if there is clinical and/or electrocardiographic evidence of ongoing ischemia between 12 and 24 hours after symptom onset. (Level of Evidence: B)
Class IIb
Primary PCI might be considered in asymptomatic patients with STEMI and higher risk presenting between 12 and 24 hours after symptom onset. (Level of Evidence: C)
Class III: HARM
PCI should not be performed in a noninfarct artery at the time of primary PCI in patients with STEMI without hemodynamic compromise. (Level of Evidence: B)
The following statement accompanies the change in guidelines:
"Several reports have shown excellent outcomes for patients with STEMI undergoing interhospital transfer where first medical contact–to-door balloon time modestly exceeded the systematic goal of <90 minutes. In these reports, the referring hospital and the receiving hospital established a transfer protocol that minimized transfer delays, and outcomes were similar to those of direct-admission patients. On the basis of these results, the PCI and STEMI guideline writing committees have modified the first medical contact–to-device time goal from 90 minutes to 120 minutes for interhospital transfer patients, while emphasizing that systems should continue to strive for times ≤90 minutes. Hospitals that cannot meet these criteria should use fibrinolytic therapy as their primary reperfusion strategy."
This is an important change that every state, Critical Access Hopsital and rural EMS system should make note of and take steps to act upon.
The lives of our rural STEMI patients may depend upon it!
This is the conclusion to 90 year old male CC: "Possible stroke". You might want to go back and familiarize yourself with the details of the case. Let's take another look at the 12-lead ECG.
Now with the computerized interpretive algorithm.
On Facebook I had asked whether or not this ECG showed signs of ischemia.
This ECG shows ST-depression in the lateral leads (I, aVL, V5 and V6) and modest ST-elevation in the right precordial leads (V1-V3). That's because it shows a strain pattern or secondary repolarization abormality due to left ventricular hypertrophy.
According to at least one study this is the most common cause of ST-elevation in chest pain patients. Hence, it is a very important pattern for paramedics to recognize in the field (although it's rare for LVH with strain to fool the GE-Marquette 12SL interpretive algorithm).
How would we know it's a strain pattern?
When we look at any 12-lead ECG we should consider the Six Step Method (or some other standardized approach).
Here we see that the patient is in sinus rhythm with a normal frontal plane axis. The QRS duration is < 120 ms so it's not a bundle branch block or paced rhythm.
At this point we might pick up on ST-depression in the lateral leads but it's too early to call it ischemia. We need to consider other possible causes. Since left ventricular hypertrophy often presents with ST-depression in the lateral leads that is a likely culprit.
Let's add the depth of the S-wave in lead V2 with the height of the R-wave in lead V5 (or V6 — they're both about the same). Is the result equal or greater than 35 mm?
Yes!
You don't need calipers for this because it doesn't have to be perfect. 35 mm is 7 large blocks so eye-ball it. The S-wave in lead V2 is at least 4 large blocks deep (it's actually more than 5 but this is the "fast and dirty" method) and the R-wave in lead V6 is at least 3 large blocks in amplitude. That's greater than 35 mm so you've met the criteria.
There are other criteria for LVH but this is the most important for ruling out STEMI mimics because LVH is usually an anterior STEMI mimic so the most important issue here is the depth of the S-waves in the right precordial leads (V1-V3). With a "strain pattern" the deeper the S-waves the more pronounced the secondary ST-T abnormality in the opposite direction.
Conversely, the taller the R-waves, the more pronounced the ST-depression and T-wave inversion. A lot of people talk about the shape of the ST-segments and T-waves in the presence of LVH, how it should be asymmetrical and upwardly or downwardly concave. That's ususally true but it's not always the case.
In this case the "strain pattern" is fairly modest. The ST-elevation in V1-V3 is not particularly impressive. Other times the result can be quite profound.
If you're still not clear on what a "strain pattern" is with LVH, take a look at the precordial leads. The QRS complex starts out negative in lead V1 and ends up positive in lead V6. The transition lead is lead V4 (which is equiphastic). As the QRS complex transitions from negative to positive, the T-wave transitions from positive to negative.
That's what we call a "widened QRS/T angle" which means that there is more than 100 degrees difference between the QRS axis and the T-wave axis. Let's take a look at the computerized measurements. The QRS axis is 16 degrees and the T-wave axis is 148 degrees.
To be much simpler about it, with a strain pattern positive QRS complexes have negative T-waves and negative QRS complexes have upright T-waves. (You should not include isoelectric or equiphasic QRS complexes in this analysis).
The general appearance of this 12-lead ECG is one of T-wave discordance. That's a finding that should almost always make you pause and consider that you're dealing with a secondary ST-T abnormality — in other words a STEMI mimic.
This patient received a fairly extensive workup for his near-syncope including a CT scan and nothing was found. He was discharged from the emergency department.
You can find previous posts about left ventricular hypertrophy here.
EMS responds to a 90 year old male with a "possible stroke".
On arrival the patient is found sitting on the toilet (lid down). His spouse states that he had walked outside to retrieve the newpaper when he lost his balance and skinned his knee. She helped him inside and sat him down on the toilet in the bathroom when his eyes rolled back in his head and he started "shaking all over".
At the time of evaluation he is conscious, alert and oriented to person, place and time. He remembers falling while retrieving the newspaper but denies losing consciousness in the bathroom.
His skin is pale and diaphoretic.
He denies chest pain or shortness of breath.
Past medical history: Mild cognitive impairment, HTN, dyslipidemia
As you probably already know if you've been following EMS 12-Lead or First Responders Network on Twitter or Facebook, we're working on a new web series called Code STEMI.
We just got back from AHA Scientific Sessions 2011 in Orlando which was our first location. We met some incredibly passionate people and had some amazing experiences!
Ted Setla, Jamie Davis and I discussed it on a special episode of the EMS 12-Lead podcast.
In this episode Tom Bouthillet, David Baumrind, Executive Producer Jamie Davis (MedicCast and ProMed Network) and Rob Theriault (Paramedic Tutor and EMS EduCast) discuss 12-lead ECG interpretation, regional systems of care for acute STEMI, and quality and process improvement for cardiac arrest.
Specifically we discuss Physio-Control's CODE STAT Suite software and ZOLL Medical Corp's CPR Dashboard and See Thru CPR.
We discuss the ReadyLink 12-Lead ECG by Physio-Control , the RescueNet 12-Lead by ZOLL Medical Corp., 12-lead ECG interpretation, regional STEMI care, and ECG transmission in general.
This ECG shows a regular narrow complex tachycardia at a rate of 170.
Could it be sinus tachycardia? One of the "rules of thumb" for the maximum sinus rate is 220 minus age. This patient is 83 years old. 220 – 83 = 137. Granted, this is just a rule of thumb so I'm sure expections exist but 170 is a good distance from 137.
I agree with some commenters that atrial fibrillation can appear regular at very fast heart rates. However, a trained eye can still pick up on some irregularity with rates < 200. You can also use calipers or fold the ECG paper in half and line up the R-waves to verify that the rhythm is regular.
In this case the rhythm is clearly regular which rules out atrial fibrillation but not 2:1 atrial flutter.
In lead V1 we can see atrial complexes (inverted or "retrograde" P-waves) after the QRS complex. We're narrowing in on the mechanism of this tachycardia. If we play the odds there's a good chance this is AV nodal reentrant tachycardia (AVNRT). However, it could still be 2:1 atrial flutter or the less common (but not uncommon) orthodromic AVRT.
You will recall that the paramedics documented "cannon waves" that corresponded to the heart rhythm. Some of you asked, "What are cannon waves?" Cannon waves are pulsations that are visible in the external jugular veins when the right atrium contracts against a closed AV valve.
Normally atrial systole is an end-diastolic event (the so-called "atrial kick"). When the P-waves follow the QRS complexes the pressure generated by ventricular systole have already forced the AV valves shut. Hence, the atria contract against closed AV valves and back pressure creates a visible "wave" or pulsation that is transmitted back up the superior vena-cava and to the external jugular veins.
Here's an example to give you an idea although this patient's external jugular veins are severely distended and the heart rate is much slower. For the current case study the patient's cannon waves were fast, regular and visible just above the clavicle on the right side.
Does determining the exact mechanism of the tachycardia matter in the field? No, because that's not possible. We don't have an EP lab. However, we can carefully document the arrhythmia before and after treatment on those occasions where the patient is not critically unstable!
The first thing the treating paramedics did was put this patient in a supine position and place him on oxygen which perked him up a little bit. Remember, BLS before ALS. I am aware of the controversy associated with placing a patient in Trendelenberg. However, I think we can all agree that lying flat is better than sitting or standing when you're hypotensive!
Vagal maneuvers were attempted (the patient was asked to "bear down" and blow into an empty syringe) with no effect to the tachycardia. An IV was started but unfortunately the only good peripheral access was a 20 G IV in the back of the left hand.
Many (perhaps most) lf you recommended synchronized cardioversion for this patient. I have no quarrel with that. However, I do know that it's easier to say than do when you have a conscious, talking patient in the back of the ambulance. It also helps if you carry the right drugs and don't have to play "mother may I" with online medical control.
In this case paramedics pushed the PRINT button and gave 6 mg of adenosine followed by a 5 ml "flush" of 0.9% NS. It took more than 30 seconds to have an effect (Clinical tip: always follow adenosine with a minimum of a 20 ml flush) but here's what happened. The next four strips are continuous.
With the conversion to sinus rhythm the patient felt much better.
Vital signs were re-assessed.
RR: 18
Pulse: 100
NIBP: 138/81
SpO2: 100
A post-conversion 12-lead ECG was captured.
The patient was transported to the hospital in a position of comfort.
EMS is dispatched to a "cardiac patient in distress".
On arrival paramedics are led to the bathroom where the patient is found sitting on a foot stool. He is conscious but appears acutely ill. Skin is pale and he is slumped over. He states that he feels weak.
Past medical history: High blood pressure, high cholesterol, valve surgery.
Medications: Numerous but his spouse can't locate them. When the patient is asked for his medication list he states, "Ask my wife."
Vital signs:
RR: 18
Pulse: Rapid and weak
NIBP: 85/53
SpO2: 99 on RA
Breath sounds: Clear bilaterally.
Cannon waves are noted at the patient's neck.
The cardiac monitor is attached.
A 12-lead ECG is captured (retrieved here from the LIFENET).
In a previous review of the ACLS Review app by Limmer Creative I announced that I was working together with Limmer Creative to create a 12-Lead ECG Challenge app.
I'm pleased to announce that the app is now available for Android and Apple iOS! The product made its debut at EMS World Expo 2011 in Las Vegas.
The app has 150 12-lead ECGs that were taken from actual patient encounters.
The user of the app is given a brief scenario. For example, a 95 year old female with a chief complaint of altered level of consciousness.
You can tap on the little magnifying glass to enlarge and expand the 12-lead ECG.
Once you think you know the answer you tap the ANSWER button, the card flips, and the answer text comes up along with (in most cases) an ANSWER graphic.
In this case we are dealing with a bifascicular block (right bundle branch block and left anterior fascicular block) as evidenced by the supraventricular rhythm with a QRS duration > 120 ms, the RBBB morphology in lead V1 and a left axis deviation (QRS complexes positive in lead I and negative in leads II and aVF).
The 12-Lead ECG Challenge app strongly emphasizes acute STEMI and the STEMI mimics (including benign early repolarization, left ventricular hypertrophy, paced rhythm, left bundle branch block, pericarditis, left ventricular aneurysm, hyperkalemia, hypothermia, WPW and Brugada) so it's a great study tool to help paramedics minimize false positive cardiac cath lab activations.
For example, here's an answer graphic that demonstrates the relevant findings for a patient whose 12-lead ECG was consistent with pericarditis.
The app is priced at $4.99, a bargain when you consider that online 12-lead ECG tutorials start at around $45.00. Our goal was to appeal to a world-wide market and make it affordable for everyone.
This is the conclusion to 88 year old male CC: Chest pain. You may wish to review the previous post for the history and clinical presentation.
Let's take another look at the 12-lead ECG.
Now with the computerized interpretation.
This 12-lead ECG shows bifascicular block and is very suspicious for acute STEMI.
The first thing that jumps out at me when I look at this 12-lead ECG is the concordant T-wave in lead V2.
With right bundle branch block (RBBB) the T-wave should be deflected opposite the terminal (last) wave of the QRS complex. Because the QRS complex ends in an R-wave the T-wave should be negative. However, in this case it is positive. This is sometimes referred to as "pseudo-normalization" of the T-wave with RBBB. You will also note that the ST-segment is slightly elevated.
Now let's take a closer look at the high lateral leads I and aVL.
Do not let your eye be fooled! I have noticed that in the setting of RBBB the S-wave is often "lifted" when ST-elevation is present. That can create the illusion that the ST-segment is isoelectric. In this case, if you look carefully you will see that the J-point is clearly elevated.
It's debatable as to whether or not 1 mm of ST-elevation is present in the high lateral leads but some ST-elevation is present. Remember, the conventional criterion of 1 mm of ST-elevation in 2 or more contiguous leads is a gross oversimplification. However, computerized interpretive algorithms obey the rules and this ECG has not triggered the ***ACUTE MI SUSPECTED*** message (yet).
When ST-elevation is present in the high lateral leads (I and aVL) we should inspect the inferior leads (II, III and aVF) for reciprocal changes. The converse is also true.
ST-depression is present in leads II, III and aVF. If you're not sure of the exact location of the J-point in leads II and III you can find the J-point in lead I and draw an imaginary line straight down to help you find your landmarks. This finding is subtle (most obvious in lead aVF) but to me this is the strongest evidence that the concordant T-wave in lead V2 and slight J-point elevation in leads I and aVL are pathological.
It can't be repeated often enough. When looking at any ECG abnormality "consider the company it keeps." We might blow off a single lead showing a concordant T-wave. We might blow off a single lead showing a slight amount of J-point elevation. We might blow off a single lead showing an inverted T-wave or ST-depression, but put them all together and a picture starts to emerge.
In this case the picture that emerges is a high-risk patient who is almost certainly experiencing an acute coronary syndrome!
Unfortunately, this crew obtained only one 12-lead ECG and did not recognize these abnormalities. One of the best quotes I've heard about serial 12-lead ECGs came from Tim Phalen. He said, "Taking a single 12-lead ECG is like taking a single photograph of Old Faithful. Is it a geyser, or is it a hole in the ground?"
One imagines that if this ECG were to have been repeated it would have shown changes to suggest the dynamic oxygen supply vs. demand characteristics of ACS.
On the plus side, this ECG was transmitted to the hospital and the ED physician found it to be suspicious. The 12-lead ECG was repeated in the emergency department (we do not have a copy of this ECG) and a "Code STEMI" was called. The patient was taken to the cardiac cath lab. We do not have a copy of the cath report. However, we do know that for some reason the cath was unsuccessful and the patient was sent to the OR for a 3-vessel CABG.
In this episode Tom Bouthillet and David Baumrind are joined by Trudie Lobban of STARS (Syncope Trust And Reflex anoxic Seizures) — a not-for-profit organization that works together with individuals, families and medical professionals to offer support and information about unexplained loss of consciousness (syncope).
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