A 12 lead ECG is performed.
What is your plan of treatment?
"Time to reperfusion is a major determinant of outcome in patients presenting with an ST-segment elevation myocardial infarction (STEMI). The American College of Cardiology/American Heart Association STEMI guidelines recommend that the emergency department physician make the decision regarding reperfusion therapy within 10 minutes of interpreting the initial diagnostic ECG, which may be challenging because clinical decisions are often made without a previous ECG result for comparison or time to observe evolutionary ST-segment changes or cardiac biomarker results..."Here's the bombshell:
Of the 1335 patients who underwent angiography, 187 (14%) did not have a clear culprit coronary artery, 10 patients (0.7%) had multiple potential culprit arteries (severe 3-vessel disease and positive cardiac biomarker results), and 1138 (85.3%) had a clear culprit artery. Patients with a culprit artery were treated with percutaneous coronary intervention (94%), coronary artery bypass surgery (4%), or medical management (2%). Retrospective review of the index ECG indicated that 24 atients (1.8%) did not have diagnostic ST-segment elevation but instead had ST-segment depression, T-wave inversion, or nonspecific ST-T changes, including 3 patients with positive biomarker results (2 with non-STEMI and 1 with a drug overdose) and 21 with negative cardiac biomarker results. These patients were included in the no-culprit artery group. The prevalence of false-positive catheterization laboratory activation with the no-culprit coronary artery criteria was 14%..."The authors then pose a difficult question:
"Achieving door-to-balloon times in less than 90 minutes is an important quality metric that is tied to pay for performance and has been the focus of recent quality improvement initiatives such as the American College of Cardiology’s D2B Alliance and the American Heart Association’s Mission: Lifeline. Upstream activation of the cardiac catheterization laboratory by the emergency department physician is one of the key strategies to reducing door-to balloon times. A major challenge for the emergency department physician is the patient who presents with nonspecific symptoms or subtle ST-segment elevation or QRS repolarization abnormalities that obscure or mimic ST segment elevation. In these cases, is it best to immediately activate the catheterization laboratory, considering the consequences of a false alarm, or take the time to obtain additional data, such as from serial ECGs, biomarkers, or an echocardiogram?"One final note that I found interesting:
"Patients with new or presumably new left bundle-branch block had an inordinately high prevalence of false positive catheterization laboratory activation (almost half did not have a culprit artery). Patients with a previous myocardial infarction or previous coronary bypass surgery had a significantly higher prevalence of no culprit artery, likely because of abnormal baseline ECG results."It would be interesting to know whether or not the false positive LBBB patients met Sgarbossa's criteria. The authors don't say it, but I can't help but wonder if the patients with previous MI "and abnormal baseline ECG results" had persistent ST segment elevation similar to (what we think of as) left ventricular aneurysm.
"[P]aramedics are now in a novel role, where they are able to diagnose STEMI faster and earlier than ever before using a prehospital EKG machine. This is important for two reasons: One is that hospital ED overcrowding has become a big issue and it's sometimes challenging for a walk-in STEMI patient to have an EKG in a timely manner in an ED where staff and beds are pushed to the limit. In contrast, paramedics provide one-on-one care, so they can do a prehospital EKG very quickly. The second thing is that it's increasingly recognized that a prehospital EKG done in isolation means nothing unless it's acted upon by the receiving hospital, which can get its ED, cardiac cath lab and ICU ready to receive the patient when he arrives..."Are you up for the E2B Challenge? Join the E2B listserv here.
"It's very exciting in 2008 that paramedics are in a unique position to trigger a whole cascade of events that can make a big difference in a STEMI patient's life," says Rokos. "Basically, the clock has always started at the hospital door. The current cardiology guidelines recommend that the blocked artery should be open within 90 minutes from the hospital door to balloon inflation, but we want to push it up another notch, raise the bar on perfusion speed and set the clock not at the hospital door, but in the patient's living room or office, or wherever the prehospital EKG shows a STEMI. That is the idea of the E2B Challenge."
In this excellent article from the March 2007 Journal of the Emergency Medical Services, Tim Phalen discusses the importance of performing serial 12 lead ECGs."Acute myocardial infarctions (AMIs) aren't like broken bones and, therefore, ECGs aren't static like X-rays. If an EMS crew were treating a hip fracture and could somehow perform the X-ray on scene, what would it show? A broken hip, of course. And if the X-ray wasn't performed until the patient arrived at the
emergency department (ED), would the broken hip still be visible?
Absolutely.
When dealing with a fracture, whether the X-ray is obtained immediately, in 10 minutes or in 10 hours, the interpretation and diagnosis usually won't change. But what's true for X-rays isn't necessarily true for ECGs. In fact, an ECG can significantly change in a very sort period of time -- as can the corresponding interpretation."
"[I]t can be difficult to determine if the presence of LBBB on the ECG of a suspected AMI patient is preexisting or is a new onset. If the LBBB is infarct-induced, it has a high mortality rate -- up to 60%. Therefore, the patients who may need reperfusion the most are the least likely to receive it. However, dynamic changes on serial ECGs shed light on the situation. A hallmark of infarct is change over time. If a patient has had an LBBB for the past 15 years, it's not likely to change much during the next 15 minutes. But when changes occur in a short period of time, suspect AMI."
In the absence of contraindications, reperfusion therapy should be administered to patients with symptom onset within the prior 12 hours and ST elevation greater than 0.1 mV (1 mm) in at least 2 contiguous precordial leads or at least 2 adjacent limb leads, or new or presumably new LBBB on the presenting ECG.
This criterion is problematic [...] acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients. Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.
"ST segment elevation is perhaps the "most demanding" of the electrocardiographic features seen in the chest pain patient; it is "demanding" in that its presence must be explained and, if the etiology involves AMI, urgent therapeutic decisions must be made. Unfortunately, STE is a not uncommon finding on the ECG of the chest pain patient; its cause infrequently involves AMI."
"AMI is not the most common cause of ST elevation in ED chest pain patients. LVH is most often responsible for electrocardiographic STE followed by AMI and LBBB which occur at equal frequencies."
"Paramedics diagnosed over half of patients as having ST elevation AMI, when in fact they did not. One reason for this may be that the paramedics were concerned about missing patients with this condition. The number of false-positive diagnoses may also have been increased due to the problem of differentiating ST elevation AMI from other electrocardiographic abnormalities that result in ST-segment elevation..."
"The paramedics’ diagnosis of ST elevation AMI was confirmed in 55 patients (45.5%) by acute angiography. In an additional 4 patients (3.5%) who did not undergo angiography due to high-risk assessment or other causes, the diagnosis was confirmed clinically by typical electrocardiographic changes in evolving ST elevation AMI accompanied by transient elevation of creatine kinase-MB. Thus, the paramedics’ true positive rate was 49% (n = 59). The paramedics’ decision was not confirmed in the 23 patients (19%) with no thrombus at angiography, and in the 38 (31%) who did not undergo coronary angiography because the attending cardiologist judged them not to have an evolving ST elevation AMI [...] The false-positive rate by paramedics was 51% (n = 62)..."
"The incidence of poor quality ECGs recorded by the paramedics was calculated to determine the paramedics’ performance in electrocardiographic acquisition. In 13 of 124 patients (10.5%), the ECGs were characterized as poor quality..."
"This study concludes that paramedics’ true-positive rate of ST elevation AMI diagnosis is high in patients presenting without confounding factors, but decreases when the ECG has confounding factors. This is in contrast to an experienced cardiologist whose true-positive rate was high and not affected by confounding factors. The results demonstrate that before implementation of electrocardiographic transmission directly to a cardiologist’s handheld device, there is a need to provide education and training to paramedics responsible for acquiring and interpreting prehospital ECGs, with special emphasis on confounders..."
"Fifty-one percent of patients whose prehospital 12-lead ECG met 1 mm or more ST segment elevation criteria had non-myocardial infarction diagnoses. ST segment elevation alone lacks the positive predictive value necessary for reliable prehospital myocardial infarction diagnosis. Inclusion of reciprocal changes in prehospital ECG myocardial infarction criteria improved the positive predictive value to more than 90% and included a significant majority (62% to 86%) of acute myocardial infarction patients with ST segment elevation who received thrombolytic therapy within five hours after hospital arrival. ST segment elevation criteria that include reciprocal changes identify patients who stand to benefit most from early interventional strategies."
In the first place, it's an incomplete 12 lead ECG. Lead V1 is missing. This is probably the reason the GE/Marquette 12SL interpretive algorithm is giving the "Data quality prohobits interpretation" statement.
That's that tag line of a tremendous article that appeared in the March 2007 issue of Emergency Medical Services entitled Out-of-Hospital STEMI Alert by David Jaslow, MD, MPH, EMT-P, FAAEM. I think the tag line sums up the frustration many of us "STEMI activists" feel when our prehospital 12 lead ECG programs flounder."One of my favorite citations to point out how ridiculous it is that we still don't have widespread capability to diagnose patients with STEMIs, institute aggressive EMS care and move them toward cath labs is from the premiere episode of Emergency! This show depicted what was actually happening in the early 1970s as Los Angeles County implemented one of the first ALS systems in the country. If you listen carefully to the discussion between Gage and DeSoto during their tour of the new Squad 51 (paramedic responder/light rescue vehicle), there's distinct mention that the Datascope cardiac monitor is capable of acquiring and transmitting full 12-lead ECGs..."Sound familiar? Mine used to get thrown on the little silver table next to the patient's bed (a process Ivan Rokos, MD now refers to as the "silver table treatment").
"EMS personnel must be appropriately trained in the acquisition, interpretation and/or transmission of the 12-lead ECGs (which should take place in initial paramedic education courses) and must have the technology to do it all. As well, there must be a robust CQI system in place to identify and correct deficiencies in the system [...] Options for ECG interpretation include training paramedics to read the study on their own and make a diagnosis without physician backup (no transmission), diagnosing suspected acute MIs and transmitting only those to a base station for physician overread (selected transmission), or mandating transmission of every 12-lead ECG acquired without any paramedic interpretation. Intense education must also be focused on the concept of transport to the closest appropriate facility, not just the closest facility..."
"[T]he net needs to be cast wide when deciding who needs a 12-lead ECG other than the standard patient who actually complains of chest pain. Patients who are also candidates include those with shortness of breath, abdominal pain, weakness and general ill feeling for which there is no obvious noncardiac explanation..."
"Many urban EDs are in crisis due to overworked staff members, staffing deficiencies, overcrowding, lack of emergency medicine-trained physicians and nurses credentialed as CENs, poor throughput and a host of other factors. Poor staff morale can create a culture of apathy and indifference that's counterproductive to attempts to improve patient care-something that requires effort on the part of every individual. I have witnessed paramedic-acquired ECGs thrown in the trash, detailed EMS reports of critically ill patients with potential STEMIs ignored and other hostile EMS/hospital interface issues..."
Since we're in monitor mode, we're not in the standard 12 lead ECG format. In other words, lead II is on top, lead III is in the middle, and lead I is on the bottom. By the way, this wasn't my choice. This is just how my fire department chose to configure the default settings of the Lifepak 12 (either that or it's how it came from the factory).
Where is the artifact on this tracing? Leads III and I. How about lead II? That looks fine. So which electrode is responsible for the poor data quality?
Let's think about it. For lead II, the negative is the white electrode on the right shoulder. The positive is the red electrode on the left leg. Since lead II looks fine, we can deduce that the white and red electrodes are not responsible for this poor data quality. Which electrode do leads III and I have in common? The negative for lead III is the black electrode on the left shoulder. It also happens to be the positive electrode for lead I.
Ding, ding, ding! We have a winner! Or should I say, we have found our culprit. Check the black electrode. If necessary, peel it off, wipe the skin, and replace it with a new one.
Here's another example.
I have a confession to make. I induced this abnormality on an emergency call the other day by partially peeling back one of the electrodes. But which one?
Lead III looks fine. The negative for lead III is the black electrode on the left shoulder. The positive for lead III is the red electrode on the left leg. We can speculate that the black and red leads are not responsible for this poor data quality. What's left? The white electrode on the right shoulder. Do leads II and I share this electrode? You bet.
Make sense?
Here's the coup de grâce.
This is from an actual emergency call.
The paramedics were called to the scene of an elderly male who wasn't answering the phone at his apartment. The son went to check on him, and found him unresponsive and not breathing. When paramedics arrived at the scene, it appeared to be an obvious 10-7 (although there was no rigor mortis in the fingers and no dependent lividity was noted).
The cardiac monitor was attached and showed this tracing. The paramedics were surprised to see VF on the monitor. It seemed strange that lead II showed asystole, but CPR was initiated, the patient was defibrillated (many times), and the patient was ultimately transported lights and sirens to the emergency department.
Afterward, the paramedic in charge of the call faxed this ECG to me and asked my opinion as to why lead II showed flat line, when leads III and I showed VF.
My answer was simple. Did you check the black electrode?
What is the more likely scenario? That the VF was isoelectric in lead II (a theory a physician rendered at an ACLS class where this strip was shown) or something was wrong with the black electrode?
Let's look at the history. This was an unwitnessed cardiac arrest! My money is on asystole and a bad black electrode!
Background: Most out-of-hospital ventricular fibrillation (VF) is prolonged (>5 minutes), and defibrillation from prolonged VF typically results in asystole or pulseless electrical activity. Recent visual epicardial observations in an open-chest, open-pericardium model of swine VF indicate that blood flows from the high-pressure arterial system to the lower-pressure venous system during untreated VF, thereby overdistending the right ventricle and apparently decreasing left ventricular size. Therefore, inadequate left ventricular stroke volume after defibrillation from prolonged VF has been postulated as a major contributor to the development of pulseless rhythms.
Conclusion: In this closed-chest swine model of VF, substantial right ventricular volume changes occurred early and did not result in smaller left ventricular volumes. The changes in ventricular volumes before the late development of stone heart do not explain why defibrillation from brief duration VF (<5 minutes) typically results in a pulsatile rhythm with return of spontaneous circulation, whereas defibrillation from prolonged VF (5 to 15 minutes) does not.
The AHA Scientific Statement Implementation and Integration of Prehospital ECGs Into Systems of Care for Acute Coronary Syndrome was published online ahead of print on August 13, 2008.
The ACC's Cardiosource posted a good summary of the document on August 21, 2008 that included these 10 talking points:
TheHeart.org's heartwire interviewed the study's lead author, Dr. Henry Ting of the Mayo Clinic, in an article published on August 13, 2008. Some of his comments were interesting.
"We've coordinated the emergency department, the cath lab, and the cardiology group and have done well with reducing door-to-balloon times, but we've not truly engaged the prehospital phase of care. This is critically important."Where is the value in that?
"For the past 10 years, this equipment has been available to many paramedics, but what is happening is that when they acquire the ECG it's not really utilized [...] the patient is placed in a critical-care room and receives another ECG. Where's the value in that?"
I'm an EMT-B that just found your blog. My agency allows EMT-Bs to perform 12-leads prehospital, so that doctors and paramedics at the hospital have a printout to look at. Also, if our monitor sees an Acute MI or something critical going on with the heart, we know to hurry it up.
Do you have a 12-lead placement diagram? I've been taught where and so on and so forth, but after reading your blog, I'm betting you'd have a nifty diagram. I'm going to print it out and tuck it in my protocol book for reference.
You can also download a quick reference card from Physio-Control here.
Update 12/06/08: This is one of the most frequently visited pages on the Prehospital 12 Lead ECG blog. Since many of you are looking for right sided and posterior lead placement, here are some additional diagrams.
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Right sided precordial leads
Posterior leads V7 (posterior axillary line), V8 (midscapular), and V9 (paraspinal)
Determining the success of a 12-lead ECG program is easy. Does it lead to advance notification of the receiving facility, speed diagnosis and shorten the time to reperfusion? The bottom line: Does it reduce damage to the heart muscle and save lives?She goes on to say:
Early identification of an ST-segment elevation myocardial infarction (STEMI) and the speedy activation of the hospital’s cath lab have been proven to dramatically reduce wait time for patients who need cardiac catheterization. However, despite compelling clinical studies, many 12-lead programs have floundered. The primary culprit is often a lack of cooperation between EMS and the medical community.
The problem is that many hospitals are reluctant to activate a catheterization team at a cost of thousands of dollars based on the recommendation of paramedics, even when a 12-lead ECG has been transmitted from the field.What she doesn't say is that many ED physicians still don't have the authority to activate the cardiac cath lab! That's been one of the major priorities of the D2B Alliance. Activating the cath lab based on the prehospital 12 lead ECG is necessarily a stepwise process.
In a small study from rural Wisconsin, Kellum et al. implemented an EMS protocol consisting of an initial series of uninterrupted chest compressions, passive oxygen administration with no active ventilation, rhythm analysis with a single shock, 200 immediate postshock chest compressions before pulse check or rhythm reanalysis, and delayed tracheal intubation. In comparison of data for 3 years before (n=92) and after (n=89) the protocol change, neurologically intact survival for patients with witnessed shockable rhythms improved from 15% to 39%, comparable with the best site in the ROC study [...] These data show that protocol and technique can be more important than location for survival of OCHA.The best site in the ROC study is, of course, Seattle.
Animal evidence and one large case series suggests that ventilation is unnecessary for the first few minutes after primary VF cardiac arrest. But ventilation is important in asphyxial arrest (e.g. most arrests in children and many noncardiac arrests, such as drowning and drug overdose). Some conference participants suggested that recommendations provide the option of omitting ventilation for the first few minutes unless the victim is a child or the possibility of asphyxial cardiac arrest exists (e.g. drowning). To simplify lay rescuer education, the consensus among conference participants was to strive for a universal sequence of resuscitation (emphasis added).And then in the next section:
The obvious challenge was how to translate the need to increase chest compressions into recommendations that would be simple and appropriate for both asphyxial and VF cardiac arrest. There was agreement that continuous chest compressions could be appropriate in the first minutes of VF arrest, but ventilations would be more important for asphyxial arrest and all forms of prolonged arrest. There was also agreement that it would be too complicated to teach lay rescuers different sequences of CPR for different circumstances (emphasis added). For simplicity, a universal compression-ventilation ratio of 30:2 for lone rescuers of victims from infancy (excluding neonates) through adulthood was agreed on by consensus based on integration of the best human, animal, maniken, and theoretical models available. For two-rescuer CPR in children, a compression-ventilation ratio of 15:2 was recommended.Are we in EMS lay rescuers or are we professionals? If the latter, then why should uninterrupted chest compressions be a novel therapy during the first 2 minutes of a resuscitation attempt for witnessed sudden cardiac death (down times > 4 minutes and no bystander CPR prior to EMS arrival)? More EMS systems are adopting this approach as a best practice, but why did we treat ourselves as laypersons in the first place?
In case you missed it, there's an outstanding webinar available at the D2B Alliance website that discusses Prehospital ECG Activation of the Cardiac Cath Lab. It's hosted by Dr. Ivan Rokos, Dr. Christopher Granger, Dr. Robert O'Connor, and Dr. William French. The webinar discusses Regional STEMI networks in Southern California, the RACE program in North Carolina, and the AHA's Mission: Lifeline (click on the Mission: Lifeline link and tell me whether or not the paramedic in the video looks like John Candy).
As you can see, in the last 4 days, I've had visitors from England, Germany, Turkey, Iraq, South Africa, India, Australia, Canada, and all over the United States!
This is an ECG of a 26 year old recruit firefighter. When it was taken, he's was lying down on the kitchen counter at the fire station. One thing you should know about Station 6 is that it's almost always cold. They don't call it the "Ice House" for nothing (t-shirts available). You will notice muscle tremor artifact in every lead.
For this ECG we placed a large towel over the recruit firefighter to keep him warm. That's quite an improvement, isn't it? Keep your patient warm, have him relax and breath normally, and make sure he's not propping himself up with his arms on the rail of the gurney (or any other type of furniture). Tension on skeletal muscles may be transmitted into the ECG.
This diagram represents the layout of the first 6 leads of the 12 lead ECG in the standard format. You will notice that when we draw a line between the perpendicular leads, they crisscross in the center.
If you commit this pattern to memory, there's only one reason you'll need the hexaxial reference system, and that's to read the answer! In fact, once you get used to the numerical values that correspond to the various leads, you won't even need that.
Let's look at an example.
Which lead in the frontal plane shows the most equiphasic QRS complexes? Lead II. Which lead is perpendicular to lead II in the hexaxial reference system? The lead across from lead II (according to the cheat sheet diagram we just went over) is lead aVL. If you check the hexaxial reference system it will confirm that leads II and aVL are perpendicular to each other (electrically speaking).
Now look at the ECG. Is lead aVL positive or negative? It's positive! Now look at the copy of the hexaxial reference system that you printed out in Part IV. Look for the aVL with the little "up" arrow in front of it. What is the numerical value? It's -30 degrees! We estimate the QRS axis at -30 degrees.
Let's check our work. Go to the top of this sample ECG and look for R-QRS-T Axes. The middle number will show you the QRS axis in the frontal plane. The computer measures it at -26 degrees. We're only off by 4 degrees!
Is this making sense? If you attempt this on every 12 lead ECG, you will be amazed how simple it is. Not only that, patterns will emerge that will deepen your understanding of the 12 lead ECG.
My girlfriend is an emergency nurse in grad school to be a Clinical Nurse Specialist, and it annoys her to no end that I can glance at an ECG and predict the QRS axis in the frontal plane within 15 degrees.
To the uninitiated it seems like magic! :)
To re-enforce this lesson, click here. It's one of the coolest ECG related things I've ever found on the Internet. Scroll down and click on Frontal Axis Demo. When it appears on your computer screen, click and drag the dial around the hexaxial reference system, and see what it does to the sample ECG on the screen. It's quite fascinating! This is an incredible teaching aid and I only wish I'd thought of it!
In Part VI, we'll go over the ranges for the QRS axis in the frontal plane.
In the meantime, I'm going to look for a statcounter so I can figure out if anyone is reading my blog!
If so, please attend "EMS and STEMI: The Evolution of a Major Paradigm Shift" on Thursday, October 16, at 3:00 p.m. It will be presented by Ivan Rokos, MD, FACEP.
Dr. Rokos had done a terrific job as the EM representative to the D2B Alliance. He has been a tireless advocate for EMS and a pioneer for integrating the prehospital 12 lead ECG into a systems-based approach to STEMI management. Please stop by, watch the presentation, and thank him for all he's done to advance STEMI care and the EMS profession!
Before we break down the finished diagram, let's look at the hexaxial reference system laying on top of the patient's anterior chest, with the arrows and leads in the position of the positive electrodes.
In Part II, we discussed the heart's mean electrical vector and how Einthoven's Triangle (leads I, II, and III) can be redrawn to form the first 3 spokes of the hexaxial reference system. Essentially, we ended up with a shape like the one on the right.
For example, the negative for lead aVR is the combination of the black (left arm) and red (left leg) electrodes. The positive electrode for lead aVR is the white electrode (right arm). This has the effect of making the vector for lead aVR point toward the right shoulder.
You will recall that in Part I we examined how Einthoven was able to refer to leads I, II, and III as Einthoven's Equilateral Triangle even though anatomically speaking, leads I, II, and III form a scalene triangle on the human body.
Clear as mud? Here's the fun part.
Now let's go back to Einthoven's (electrically) Equilateral Triangle. Imagine that the red arrow is the heart's mean electrical vector. To help explain what happens next, I'm going to quote 12 Lead ECG - Art of Interpretation, by Tomas Garcia, MD and Neil Holtz, BS, NREMT-P. In my opinion, this is one of the best 12 lead ECG books you can buy (and no they don't pay me to say that).
Since this is a critical point that is difficult to understand, I'm going to take this a step further. I interpret this to mean that lead I sees the mean electrical vector like the diagram to the left. In other words, it sees the heart's mean electrical vector relative to its own vector created by its negative and positive electrodes.
Because this is true, we can take the three vectors (or sides) of Einthoven's Triangle and make them intersect in the center.
You'll notice in the image to the right that Einthoven's arms and his left leg are immersed in buckets of salt water. At the time, this was the only way to obtain a signal for the electrocardiograph. Even after the invention of the electrode, they continued to be placed on the subject's arms and legs. From this configuration, leads I, II, and III were born, and they are called the "limb leads" to this day.
If you're like me, you're reading this and it sounds very confusing. After all, if you look at the image on the left, it's clear that anatomically, leads I, II, and III form a scalene triangle, not an equilateral triangle. So what in the world was Einthoven talking about?
Now let's plug these values into the equation for Einthoven's Law.
