- To see video of this podcast — CLICK HERE —
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- PART 1: — "Common Errors in ECG Interpretation — that can Easily Be Corrected".
- PART 2: — "ECG Errors that Lead To Missing Acute Coronary Occlusion".
- Dr. Ken Grauer is with us today. He is Professor Emeritus in Family Medicine. Following his Residency in Family Medicine — he worked for 2 years in a busy Florida ED in south Florida — before moving to Gainesville, where he was full-time Faculty in the University of Florida, Family Medicine Residency Program for his 30-year career, until he retired from his academic practice in 2010. Dr. Grauer has written over 10 books on ECG and Arrhythmia interpretation — presented literally hundreds of talks and workshops locally and nationally on ECG Interpretation and other cardiology topics over his career — and has been as active-as-ever since “retiring” in 2010 — with over 3 million views on his own ECG Blog — as an Associate Editor and active contributor to Dr. Stephen Smith’s ECG Blog (that many of you probably follow) — as well as answering numerous daily queries addressed to him on any of the many international ECG internet forums that he regularly contributes to. — Dr. Ken Grauer …
- Ken — Let me start by asking HOW does a family physician get so good in ECG interpretation?
- What is your experience in teaching ECG interpretation?
- Why did you choose the topic, “Common Errors in ECG Interpretation — that Can Easily be Corrected!” for this podcast?
- Ken, we’ll be making this into a 2-Part Podcast. What do you intend to cover in each Part?
- Why did you put among the most important errors to correct — interpreting ECGs without including a brief, relevant History in your assessment — and failure to routinely use a Systematic Approach in your interpretation?
- I emphasize that I am not a cardiologist. Instead — I am a family physician by training — and taught this specialty as full-time faculty for 30 years at UF.
- But I became fascinated in ECGs in my 1st year of medical school — which hard to believe — was in 1970 — so I've been studying, interpreting and teaching ECG interpretation for over a half century.
- The BEST way to really learn a topic — is to TEACH it — so the way I got to where I am today is LOTS and LOTS of practice — interpreting in all clinical settings — reading a lot — learning from many wonderful cardiologists — and following up every case I could clinically, so as to get follow-up on as many ECGs as I could that I interpret.
- I taught our residents for 30 years — gave the ECG course to med students at UF for over 20 years — and taught numerous state-wide and national workshops for all different types of providers.
- I remain active teaching on numerous ECG internet forums. Doing so — I've noticed common oversights and errors that even experienced interpreters make — MOST of which could be fixed by a few SIMPLE steps ( = ergo the topic of this podcast!)
- Need for a short relevant History AND a systematic approach are the 2 most common oversights I've seen — and these are VERY easy to fix!
- But the breadth of my ECG exposure took off after I retired from academics in 2010 — and developed my ECG Blog and began participating in numerous international ECG forums.
- The internet has changed everything! There are literally hundreds of thousands of clinicians participating in numerous international ECG blogs and internet forums. People save their most challenging cases — so I get tagged and sent tracings to interpret all the time
- As I mentioned — I've been teaching ECG and Arrhythmia Interpretation for over 40 years. Writing over 10 books on this topic and literally giving several hundred local and national workshops on ECG interpretation to providers in all types of medical fields taught me how to effectively teach.
- And I'm always learning — and I'm continually teaching what I just learned.
- Ken — In Part 1, we covered the importance of incorporating the History and routine use of a Systematic Approach to both Rhythm and 12-Lead ECG interpretation. What do you plan to cover today in Part 2?
- What is an “OMI”?
- How then can you recognize acute coronary occlusion from the ECG if millimeter-based criteria for a STEMI are not present?
- Can AI help clinicians to improve their ability to recognize acute coronary occlusion?
- Along with Arrhythmia Interpretation — assessment of the ECG for ischemia/infarction is perhaps the most important function of the ECG in clinical medicine. WHO needs to go to the cath lab NOW?
- An "OMI" is an "occlusion"-based MI.
- WHAT to look for to Dx an OMI? — See Below!
- Up until very recently — computerized ECG interpretation programs would be good for measurements (ie, of intervals, axis, heart rates). You interviewed Dr. Robert Herman not that long ago from Powerful Medical — and his company continues to develop a superb AI Application (with assisstance from Drs. Smith and Meyers) — that already exceeds the abilities of many practicing clinicians (including cardiologists) — for recognizing OMI
- QOH continues to get better as this AI App "learns" from an expanding data set of ECGs with clinical follow-up.
- THAT SAID — My belief is that no matter how good QOH becomes — that oversight by a knowledgeable clinician remains important to ensure optimal decision-making.
- Paying closer attention to specific aspects of the History that are often ignored.
- Interpreting both Arrhythmias and 12-lead ECGs with a Systematic Approach.
- Correlating relevant history with the tracing in front of you.
- Highlighting KEY aspects of 12-lead ECG interpretation, as this relates to the diagnosis of acute ischemia, and especially to acute coronary occlusion.
- To convey the concept of "OMI", emphasizing appreciation of how the older (and outdated) STEMI paradigm misses at least 30% of acute coronary occlusions that can be picked up by using the newer OMI paradigm.
- Citing the ECG findings that facilitate early identification of an acute OMI — which include recognition of hyperacute T waves — looking for “mirror-image” ST-T wave changes (ie, between leads III and aVL with inferior OMI — and in leads V1-thru-V4 for posterior OMI) — and optimizing use of serial ECGs, with time-related correlation of each ECG to the presence and relative severity of chest pain.
- Applying a time-efficient technique for how to compare one ECG to another.
- "Hindsight is 100% in the Retrospectoscope" ...
- So I don't mean to be critical ...
- My GOAL in today's Podcast — is based on some 40+ years of teaching ECG and Arrhythmia interpretation — which has provided me the insight of recognizing some SIMPLE things that we all can do (if we are not already doing them) — that can greatly improve both the time-efficiency and accuracy of our interpretations. I want to share some of these with you.
SO — I am sent a Tracing:
- Sometimes I'm sent tracings without even being given the AGE of the patient ...
- OR — the opposite — in that I'm told a LIST of things that have little to do with the information I need to optimally interpret the tracing.
- I usually get a quick idea of the ECG interpretation ability of the person sending me the tracing by what they include (or leave out) — of the Hx they tell me.
- Most clinicians do not have a lot of "extra time" (be they Paramedics called to the scene of a sick patient — Physicians in the office or in the ED — Nurses on a hospital floor).
- No more — than 2-to-3 lines ... !!!
- I need the AGE of the patient (I'd like to know if male or female)
- WHY was the ECG done?
- Patient SYMPTOMS?
- — When did Sx begin?
- — How long did they last? — Constant? / Increasing? / Decreasing?
- And some thought to anything else that might be relevant.
- The identical tracing may be interpreted VERY differently — depending on what the Hx is!
- Previously healthy middle-aged MAN calls EMS for new CP — that awoke him from sleep. CP has been constant for the past 2 hours. This is all that I need to know.
- We instantly know that this patient is in a "higher" prevalency group for having an acute event — which means that we are starting with the realization that we need to rule out an acute event (rather than the other way around ... ).
- We need to be aware of the "Pseudo-Normalization" Period (in between the time that ST segments go up — and then T waves invert — the ST segments may pass thru a period in which they look fairly normal ...).
- Young adult male (say in 20s or 30s) — with shorter episodes of non-cardiac-sounding CP?
- IF you see peaked T waves, taller than you are used to seeing — Could this be a repolarization variant?
- vs those same taller-than-expected T waves in a patient with cardiac-sounding CP — in whom these may be hyperacute T waves?
- IF this younger adult had a recent viral infection — Could this be myocarditis?
- An older adult with fainting and bradycardia — Any rate-slowing Meds?
- IF you see a Brugada pattern in V1,V2 – rest of tracing looks OK (Is this Phenocopy? — ie, Does the patient have Fever? HyperK+ ? )
- OR — You see an irregular rhythm with lots of different looking P waves — and you are thinking could this be MAT?
- The mistake is failure to inquire in the Hx about 1 of the 2 Clinical Settings in which MAT almost always occurs ( = Pulm. disease & “Sick Pt” )
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An associated ERROR — is not forcing oneself to commit to a Dx or an Impression.
- I get sent lots of tracings from people who say, "I don't know what this ECG shows. Tell me what you see?"
- That's a person who is not going to learn much if I just tell them the answer – because they never forced themselves to think about what is relevant in the Hx — and they never forced themselves to TRY to interpret the ECG.
- The BEST way to present a talk on a topic — OR — to make a medical presentation to a colleage — is to: i) Tell them in a sentence what you are going to say; ii) Then briefly tell them WHY you think so; and, iii) Then close by telling them what you said. In order to be able to do this — you really have to think about what you're going to say — and critically evaluate the info you have.
- EXAMPLE:
- — I'm worried about an acute MI. This 60yo man has known coronary disease — and he has had recent CP. I don't have a prior ECG for comparison — but I see some ST changes of concern ...
- All-too-many Providers in my experience (even those who are very experienced … ) — do not use a system.
- I could talk for an hour just on this — but in order to cover more material — I’ll be BRIEF …
- Having a SYSTEM for Rhythm and 12-Lead ECG Interpretation does not slow you down!
- Instead — It speeds you up — because you have a few simple parameters to assess (and do not have to keep coming back, wondering if you missed anything)
- Having a system prevents you from missing anything — It’s your “Checklist” — so that even when you do not know the answer, you narrow down the diagnostic possibilities.
- There are 6 Things to think about:
- #1 = Is the patient hemodynamically stable? If not — then it does not matter what the rhythm is! = Cardiovert
- IF the patient is STABLE — then you can easily remember the 5 Parameters = Watch Your Ps, Qs & 3Rs !!!
- — P waves? — QRS width? — 3 Rs = Rate — Regularity of Rhythm — If P waves, are they Related?
- It does not matter in what sequence you ask yourself these 5 parameters — and I often change (Whichever parameter is easiest to see).
- Even after interpreting a few million tracings over the past 50 or so years — I find myself still saying, Watch Ps, Qs, 3Rs !!!
- Using this system speeds you up — Makes you sound intelligent — and even if you do not know the rhythm diagnosis — You will narrow your differential diagnosis.
- A picture is worth 1,000 words! — So it is difficult to talk about arrhythmias without seeing the ECG ... — but I'll describe a few common situations ...
- — I get LOTS of tracings sent to me with the clinician saying, “I think this is VT” — or — “I think this is SVT”.
- The ERROR that all-too-many clinicians make = "Premature Closure" = ie, They think there are only 2 Answers to this question (ie, Either VT or SVT) —
- BUT — there are actually 3 possible Answers = i) Definitely VT; ii) Definitely SVT; — or — iii) It’s a probability statement … and — And, many times even the BEST of clinicians often do not know for certain at the time they need to begin treating the patient — what the rhythm is ... (which is FINE!).
- The ERROR when you are not 100% certain if VT or SVT — is not to know what the BEST Answer is — which is simply what you get from applying the Ps,Qs,3Rs = This is a regular WCT ( = Wide Complex Tachycardia) at 150 = the RATE — without clear sign of atrial activity.
- NOT appreciating for HOW Long a patient can remain hemodynamically stable despite being in VT !!! — — for Minutes — Hours? — Days?
- NOT appreciating Statistical Odds — I see so many clinicians when they are not sure about what a regular WCT rhythm is — call it “aberrancy” — especially if it looks a little like VT ...
- #1) = Ventricular Tachycardia
- #2) = VT
- #3 — 4,5,6, 7 and 8 = VT,VT,VT until proven otherwise !!!
- #9) — The QRS could be wide because of BBB - or - Preexisting BBB ...
- #10) — Something else! (ie, WPW-related rhythm - Hyper-K+ - other Toxicity)
- There is a literature suggesting that in an unselected population of adults — that ~80% of these rhythms will turn out to be VT — even before you look at the ECG !!!
- IF the patient is "older" and has heart disease — you increase the likelihood of that a regular WCT will turn out to be VT to >90% !!!
- The overall approach is the same! = Watch Ps, Qs, 3Rs !!!
- And, if the QRS is narrow — then you have a supraventricular rhythm!
- The common situation is — by the Ps,Qs,3Rs — that we have a regular SVT.
- Sinus Tach
- Reentry SVT (ie, AVNRT, AVRT)
- Atrial Tach
- Atrial Flutter
- Not appreciating that the most commonly overlooked rhythm = AFlutter.
- Untreated AFlutter = = > Vent. Rate usually close to 150/minute.
- IF a reg. SVT at ~150/minute (140-160/minute) — Think AFlutter until proven otherwise ....
- IF a reg. SVT at ~180/minute:
- — Too fast for 2:1 AFlutter (and too slow for 1:1)
- — Faster than Sinus Tach in a horizontal patient (different if pt just ran 100-yard dash)
- — ATach (possible — relatively uncommon ... )
- — Most like some form of re-entry SVT (ie, AVRT, AVNRT)
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- There is tendency to “jump” at the obvious finding — Let’s say ST elevation, without seeing the long QTc — and sometimes even without realizing that the rhythm is not sinus! — The 1st thing I do with any 12-lead I am given is to spend 3 seconds looking at long lead rhythm for P waves !!!!
- Rate and Rhythm = sames as the Ps,Qs,3Rs …
- Intervals (PR - QRS - QTc)
- Axis
- Chamber Enlargement (there are 4 chambers …)
- Q-R-S-T Changes (Looking for changes of Ischemia/Infarction)
- With students — I have them write this down. — I realize many clinicians in practice don’t have time to write this all down — but still important to go thru with every patient.
- Even after a few million tracings — I miss things if I don’t do this …
- The process of ECG interpretation has 2 STEPS:
- — #1) = Descriptive Analysis — this is EASY (and mindless) — just go thru the System (Rate-Rhythm-Intervals — Axis-Hypertrophy- QRST Changes)
- — #2) = The Clinical Impression — Only after you've gone thru your system do you then correlate to the Hx (the clinical situation).
- Because IF the QRS is wide — You need to find out WHY before proceeding !!! (All criteria for hypertrophy AND infarction change if you have BBB or other cause for widening …).
- Another EXAMPLE:
- — Takotsubo Cardiomyopathy — easy to overlook because it often presents with markedly abnormal ST-T wave changes that don't have the usual distribution for a given "culprit" artery — or maybe very deep T wave inversion.
- — So knowing the QTc is markedly long early in your assessment starts you to consider Takotsubo ...
BOTTOM LINE:
- It's comforting to have a system ... (I know that even if I am not certain about what the Dx is — I won't be missing any findings).
- I'll be faster (because I'm following a system).
- I'll look like I know what I'm doing.
- And even when I don't know the answer — I'll narrow my Diff. Dx
- AI is a powerful tool! But there are PROs and CONs to its use …
- Up until recently — computerized programs offered the advantage of providing an additional opinion — in that they make you STOP and think about your interpretation if it differs from the computer interpretation.
- But such computer ECG reports were not optimally accurate. They were good for number, intervals, axis — but in my experience — routinely missed complex rhythms and subtle MIs
- A while back — you did a podcast with Robert Herman of Powerful Medical. Robert’s company is in process of changing the “playing field” — with assistance from Drs. Stephen Smith and Pendell Meyers, who are helping to program the AI Bot known as “Queen of Hearts” to pick up subtle signs of acute coronary occlusion that even cardiologists miss.
- The potential of this new AI app is tremendous!
- That said — I still believe that there always needs to be clinician oversight to ensure that AI readings make sense.
- Like any computer — AI only can do what it is programmed to do — and we’ve not yet figured out all of the data that needs to be programmed. So VERY PROMISING — and ALREADY very good at picking up OMIs — but not yet perfect.
- My Opinion — there will never be an AI program able to pick up all complex arrhythmias. I feel there are simply too many rhythm possibilities — and as one who loves interpreting complex arrhythmias — You often have to think “out of the box” (with there not being enough data to provide adequate experience in this to AI programs).
- QUESTION: What is the main thing we care about when assessing the patient with new CP?
- ANSWER: We want to know IF the patient has acute coronary occlusion …
- — because these are the patients for whom we can do the most good by prompt cath with PCI to reperfuse the acutely occluded coronary vessel.
- The “STEMI” Paradigm is wrong and outdated. Smith & Meyers have shown that at least 30% (if not more) of patients with acute coronary occlusion will be missed if you insist on looking for millimeter-defined STEMI criteria!
- How many of YOU have encountered this? — Your interventionist turns to you and says, “We won’t do a cath — because the ECG does not yet show a STEMI?
- Some of these patients eventually develop STEMI criteria — but you often have to wait many HOURS until finally “enough” ST elevation is seen (and by that time — you have lost valuable myocardium!).
- Others — NEVER develop STEMI criteria — despite having acute coronary occlusion that may produce extensive damage with troponin values in the thousands.
- ERROR #2 — Many of these patient (with troponins in the thousands but never with an ECG that meets millimeter-based STEMI criteria — are diagnosed as having a NSTEMI …
- — So ERROR #2 — is not appreciating that “NSTEMI” is a useless Term (that probably ought to be abandoned …) — because it simply says that at the time that the ECG was done, it did not show enough ST elevation to satisfy a millimeter-based definition — but it tells you nothing about whether or not there is an OMI — because at least 25-30% (or more) of all OMIs will not satisfy STEMI criteria.
This leads us to — ERROR #3 — Not appreciating the ECG Findings to LOOK For! So the new Paradigm — should be to look for ECG findings of OMI = acute Occlusion-based Myocardial Infarction!
- In a pt with new CP — ECG findings of acute OMI include:
- There is no universally accepted definition … It’s like “recognizing a face” ( = hard to describe with words … ) — but you know it when you see it!
- Here is a PEARL — As you look at the ECG of a pt with CP — IF you see 1 or 2 leads that are definitely abnormal (ie, with hyperacute T waves) — I become highly suspicious of an OMI until proven otherwise.
- And — IF you then look closer at remaining 10 leads — You’ll usually see more subtle abns. in many of these leads.
- I look for neighboring leads (ie, IF you see a hyperacute T wave in lead V3 — then look extra carefully at leads V2 and V4 …).
- IF you have a prior ECG — You can often recognize hyperacute T waves by how different they now look compared to old ECG
- If there is inferior lead ST elev. ==> Look for the “magical Reciprocal relationship” in Lead aVL
- Amazing how consistent this is !!!! (Rare to have acute Inf. MI without mirror-image opposite picture for the ST-T wave between leads III and aVL).
- Post MI = one of the most commonly overlooked Dx …
- The REASON? = dependence on Posterior Leads … (V7,8,9)
- — Placement of posterior leads requires the electrical activity to travel thru the thick BACK musculature — so amplitudes are reduced. Many post. MIs do not produce visible ST elevation …
- You don’t need posterior leads!
- IF your pt has CP — and ST depression maximal in leads V2, V3 or V4 = posterior OMI (differs from DSI - Diffuse Subendocardial Ischemia — in which ST dep is diffuse and not maximal in V2,V3 or V4 …).
- I use the Mirror Test to help recognize acute Post. MI.
- (The anterior leads — provide a mirror-image opposite picture of what posterior leads would show — except with larger amplitude — because electrical activity does not have to pass thru the thick BACK musculature.
- Since I began writing about the Mirror Test in my books and blogs in 1983 — I don’t think I have ever seen a Post. MI with a negative Mirror Test — that was only diagnosed by posterior leads.
- IF your patient has CP — and the 1st ECG does not show acute changes — BUT when you repeat the ECG you see definite ST-T wave changes — this IS DATA = it’s called “dynamic” ECG changes — and in a pt with new CP, it is indication for prompt cath even if neither ECG by itself was diagnostic!
- The process of evolving an acute MI is dynamic.
- There is acute coronary occlusion (accompanied by onset of CP — and ST elevation).
- Myocardial damage can be limited if there can be acute reperfusion of the acutely occluded ( = the “culprit” artery).
- Reperfusion is accomplished medically by acute cardiac cath with angioplasty (PCI) — or in centers without prompt cath capability — by thrombolytic agents.
- IF the “culprit” artery is reperfused in a timely manner — the pt’s CP is reduced (or relieved) — and ST elevation decreases (or resolves).
- This is usually followed by reperfusion ST-T wave changes ( = T wave inversion in those leads that showed ST elevation).
- NOT commonly appreciated — is that reperfusion of the “culprit” artery will often be spontaneous — even before medical personnel arrive on the scene.
- The History can give us clues that spontaneous reperfusion may have occurred (ie, severe CP is suddenly relieved)
- The problem — is that what spontaneously opened — may just as easily spontaneously reocclude !!!!! This is why if you can diagnose that there was coronary occlusion, that then spontaneously opened — the patient needs prompt cath with PCI to prevent spontaneous reocclusion.
- Get serial ECGs (in acutely evolving OMI — Repeat the ECG no later than 15 minutes after 1st ECG — and continue repeating at some frequency until you are comfortable with the Dx ).
- Write down ON the actual ECG the presence & severity of CP !!! In my experience — this is rarely done — but you lose soooo much KEY information. For example — Say the initial ECG looks relatively normal (with no more than some ST flattening). IF the pt had severe CP 20 minutes earlier but now CP is relieved — then this relatively normal ECG may reflect an intermediate stage ….
- IF CP now recurs — and you begin to see some slight ST elevation — this is a dynamic ST-T wave change (and it is diagnostic of OMI).
- HOW to COMPARE serial ECGs? — LOOK side-by-side going lead-by-lead !!!!
- — Otherwise it is toooo easy to miss subtle changes !!!!
- Being "stuck" on only 2 possibilities = acute MI or no acute MI ...
ERROR #7 — Not Learning from Our Cases ...
- Get follow-up! — not always easy but essential for learning.
- — "Experience is Errors" (not necessarily only from the "errors" ).
ERROR #5 — XXXX
- mmmm
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Failure to Recognize ARTIFACT!
- The reason we often fail to recognize these — is that they are not real common — but they definitely DO occur!
- Lead Reversal DOES Occur
- The most common = LA-RA Reversal (Global negativity in lead I — I looks like R — P neg in II )
- But the 2nd-most common that I’ve seen which is very easy to overlook = LA-LL Reversal (P in I > II )
- Pulse Tap Artifact (often bizarre QRS or ST-T wave — artifact related to the QRST, because it is from electrode contact with a pulsating artery)
- How to tell WHICH Extremity? — Based on Einthoven’s Triangle — Max artifact in 2 limb leads but nothing in the 3rd limb lead — and Max in 1 Augmented lead ( ~ 1/2 max in the other 2 Aug leads!)
- THINK Artifact — IF the funny-looking deflections look geometric (too straight) and esp. IF underneath the artifact you can see a normal rhythm.
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Next Error — The Provider Does NOT Force Him-HerSelf to Decide!
- I find the BEST way to explain this — is to think of the process when the patient is examined — and you hear a MURMUR.
- HOW do you describe the murmur? — Murmurs are tough to recognize, esp. if you don’t hear them that often.
- How many of you are “tempted” to write, “loud murmur heard in the patient’s chest!”
- The only way to get better at recognizing heart murmurs — is to FORCE Yourself to objectively describe what you hear — and then based on that — to TRY to come up with the diagnosis (ie, to WRITE on the chart that “I hear a diamond-shaped, harsh 3/6 murmur at the left base that radiates into the neck — so I think this is Aortic Stenosis).
- mmm
- HOW Does this Relate to ECG Interpretation?
- — I’ll be asked — “Is this VT?” — or — “Is this SVT?” – or “Is it an MI?”
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From My AUDIO-PEARLS!
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Having taught ECG and Arrhythmia Interpetation over the past 40-plus years — it dawned on me that there are a number of things clinicians do that are counterproductive to time-efficient ECG interpretation — while at the same time also being counterproductive to achieving optimal accuracy. For the purpose of this Audio Pearl — I'll take the liberty of calling these actions by clinicians "errors" — to ensure that I capture your attention. I’ll emphasize that my comments purely reflect my personal opinion, based on my observations from teaching medical professionals from all medicals fields, and of all levels of competency — ranging from complete beginners to seasoned clinicians with years of on-the-job experience.
The 1st Error that I’ll comment on — is the Failure to use a systematic approach. Regardless of user experience — the failure to use some kind of system (both for rhythm, as well as 12-lead interpretation) — is alarmingly common in my experience. WHY do I call the failure to routinely use some sort of system an “error”? — My answer to is simply that without regular use of some kind of system — it not only takes the clinician longer to interpret the tracing — but without a system, even experienced clinicians miss important findings. This is because their attention jumps to the obvious finding — say, the acute infarction — without ever realizing that the rhythm is not sinus. So interpreters who don’t follow a specific system are less accurate (whether they admit it or not) — because they do not consider all diagnostic possibilities. So, — WHY do I say these interpreters are also slower? After all, they come up with the most obvious diagnosis within seconds of seeing the tracing … The reason these interpreters (who do not have a system that they use with every tracing) … the reason these interpreters are slower — is their tendency to go around in circles as they assess a tracing. For example, they immediately see the obvious infarct — they then look at a few other parameters — and then because they don’t have a system, it’s all-tooEASY to forget what they has or has not covered.
Let me comment on a number of errors specifically related to this failure to routinely use a system — beginning with the 1st thing to do when interpreting any 12-lead ECG — which is, to find a long lead rhythm strip on the patient. Ideally this will be found under the 12-lead, and simultaneously recorded with the 12-lead to enable comparison of morphology in all 12 leads for each beat in the entire rhythm strip. But I realize that many pre-hospital systems do not routinely have the capability of recording a simultaneous long lead 2 rhythm strip. So, — Use whatever you have! The KEY is to find a long lead rhythm strip — spend the 3-to-4 seconds it takes to look in front of each QRS complex — to see IF each QRS is preceded by a P wave. The advantage of using a lead II to accomplish this — is that IF an upright P wave with constant PR interval is not found in front of each QRS in a lead 2 recording — then, assuming you don’t have lead misplacement or dextrocardia — IF there is no upright P wave in front of each QRS — then the rhythm is something other than sinus. The reason this initial step is important — is that because the rhythm will be sinus in the overwhelming majority of cases … — we become immune and almost routinely assume that the rhythm will be sinus, almost withoutlooking (or looking but not really seeing …. ). IF it is part of your system, that with each and every ECG that you ever see — that you look in a long lead II to verify that there are upright P waves in front of each QRS — then you won’t overlook non-sinus rhythms. IF you don’t do this — I guarantee (whether you admit it or not) — that you are overlooking some non-sinus rhythms — which at times may be very important to optimal clinical management.
Which system to use? There are many systems — and each has its merits. I really do not care which system you choose (mine or someone else’s) — as long as you’re aware of those system features that must be included in whatever systematic approach you choose to use. For rhythm interpretation — after you’ve ensured that the patient is hemodynamically stable — the 5 parameters that need to be included in your interpretation are Looking for P waves (or for other signs of atrial activity — such as flutter waves) — seeing if the QRS is wide — determining IF the rhythm is Regular — figuring out the Rate (looking at both atrial and ventricular rates, if these are different) — and if P waves are present, determining if P waves are Related to neighboring QRS complexes. I remember these 5 parameters by “Watching my Ps, Qs — and the 3 R’s”. — Looking for P waves — QRS width —Rate and Regularity of the Rhythm — and if P waves are Related to neighboring QRS complexes… Using this type of a system allows you to accurately describe the rhythm within seconds! An example of such a description might be to say that — the rhythm is a regular wide tachycardia at 150 per minute (or at whatever the rate might be) — with or without clear sign of atrial activity. And once you’ve described the rhythm in this manner — with assessment of the Ps, Qs and 3Rs — it becomes much easier to determine the precise rhythm diagnosis (as I’ll discuss next).
So, the next error that I want to describe — is the feeling that you have to come up with a definitive answer. For example — providers often feel that they have to say on the spot — whether a wide tachycardia is VT or SVT — that they have to give an either-or answer — “This rhythm is VT” — or — “the rhythm is an SVT”. I think that’s the wrong answer! Every ECG diagnosis is a relative probability statement — and what that relative probability is, makes up an important part of your answer. But your systematic approach has made this easy — because in a matter of seconds, you’ve been able to determine if you are dealing with a wide or narrow tachycardia — at what rate? — and with or without what type of atrial activitty? So, a much BETTER answer in my opinion, than premature closure that reaches a 1-word conclusion (such as, “VT” — or “SVT”) — is simply describe what you see (For example — “I see a regular wide tachycardia at 180 per minute, without clear sign of atrial activity — and with QRS morphology that does not resemble any known conduction defect — therefore, most probably VT, with need to treat accordingly until proven otherwise). Beyond the scope of this brief Auido Pearl — are all the intricacies that favor VT versus some sort of supraventricular tachycardia (I’ll leave LINKS to material that assists in this differentiation in today’s Blog post) — but awareness that before you even begin to look at the ECG of a regular wide tachycardia without clear sign of atrial activity — that at least 80 per cent of such rhythms are VT — allows you to predict relative odds of VT from your Ps, Qs, 3R description. The Related Error? — Since the odds for a regular wide tachycardia so strongly favor VT — the provider needs to assume VT until proven otherwise — and not the other way around. Many providers, when they see a wide tachycardia with an upright QRS in lead V1 with slight resemblance to a Right Bundle Branch Block pattern — assume Aberrant conduction — which is an error. Even when the R wave is upright in lead V1 — Assume VT until proven otherwise.
A related error to what we’ve just discussed — is failure to appreciate that there are a limited number of possibilities. For example — IF you’ve determined the rhythm is a regular SVT (that is, narrow-complex tachycardia) — at say, 150 per minute, without clear sign of P waves — then by overwhelming odds, you are dealing with 1 of 4 possible rhythms — which are sinus tachycardia (in which sinus P waves are hidden within preceding T waves) — atrial flutter — atrial tachycardia — or a reentry SVT rhythm such as AVNRT or AVRT. And that’s about it. And it helps to know this. Related errors — are the failure to appreciate that you may not be able to know with certainty what the rhythm is at the time that you need to begin treatment — and that this is not only OK, but it is VERY common in practice that have to you begin treatment measures before you have such certainty.
Finally — there’s a failure to appreciate the need for a multifaceted approach for arriving at a final diagnosis. Does the patient have previous tracings that you can compare the current tracing with? (which can be especially helpful when the QRS is wide — and you want to see if on prior tracings the patient had the same wide QRS morphology during sinus rhythm). Also — Repeating the ECG may be insightful. Especially IF the patient converts to sinus rhythm (either spontaneously — or following your intervention) — Repeat the ECG — as comparison post-conversion with the tracing during tachycardia may reveal a definitive answer.
In Part 2 of my observation of Common Errors — I'd like to address a few thoughts about 12-lead Interpretation. As was the case for arrhythmia interpretation — some organized system for interpreting 12-lead ECGs is needed — in which you look at the same parameters in the identical sequence each time you interpret an ECG. Too many clinicians commit the error of failing to appreciate that there are 2 (Not 1! ) — BUT 2 Steps in optimal time-efficient 12-lead ECG interpretation. I call these 2 Steps — Descriptive Analysis and the Clinical Impression. The 1st step (which is Descriptive Analysis) — is EASY — because it is routine. You simply go through your system without (and I’ll emphasize without) — without yet contemplating what your findings might mean. The 6 parameters I use for my systematic approach to descriptive analysis are — Rate and Rhythm (as we've already discussed) — Intervals(looking at the 3 12-lead intervals, which are the PR — QRS and QTc intervals) — Axis — Chamber Enlargement — and then assessment of QRST Changes (with attention to ischemia and infarction). Rate—Rhythm—Intervals— Axis—Chamber Enlargement— and QRST Changes, in which I look in all 12 leads for Q waves — R wave progression — and ST segment-and-T wave changes. Even after interpreting a few million tracings — I find that when I skip any of these sequential steps in my system — that I overlook findings because I wasn't systematic.
The “fun part” of interpretation comes NOW. After you have assessed the ECG for Rate, Rhythm, Intervals — then Axis, Hypertrophy and QRST Changes — now is the time to clinically APPLY what you have observed to the clinical case at hand. If the patient in question is an otherwise healthy young adult, who needed an ECG as part of his or her pre-participation physical exam — then some type of repolarization variant will be a far more likely explanation for tall, peaked T waves — than if you saw the identical ECG in the Emergency Department, obtained from an older adult with new chest pain — in which case we'd be concerned about hyperacute T waves signaling a possible early infarction.. So the error — is the failure to appreciate that the identical ECG (with the identical Descriptive Analysis) may lend itself a dramatically different clinical interpretation depending on the history. You can not optimally interpret an ECG in the absence of a brief, relevant clinical history — and the error that I so commonly see, is the failure to give adequate attention to the clinical history.
A related error (similar to the situation I described earlier when applying the systematic approach to rhythm analysis) — is the tendency to gravitate to an "all-or-none" diagnosis, especially with the diagnosis of an acute STEMI (ST-Elevation Myocardial Infarction). At least 25-to-30 per cent of all acute coronary occlusions will be missed if providers get "stuck" on a millimeter-dependent diagnosis for a STEMI — and if these providers fail to activate the cath lab until strict STEMI criteria are reached. Additional related errors to this situation are several: ONE — The failure to appreciate that in a patient with new-onset chest pain — T waves that are taller-than-expected (given the size of the R wave or S wave in that lead) — but taller-than-expected, "fatter"-at-their peak — and wider-at-their-base than expected — these T waves should be assumed hyperacute until proven otherwise. TWO — Once you find one or 2 leads with definitely abnormal ST-dash-T wave changes — less obvious-but-still-abnormal changes in neighboring leads are also probably abnormal. THREE — The more leads on a 12-lead tracing in a patient with chest pain that are abnormal — the more concern we need to have for an acutely evolving cardiac event regardless of whether millimeter criteria for a STEMI are satisfied. Remember — At least 25-to-30 per cent of all OMIs (that is, Occlusion-based Myocardial Infarctions) — can be diagnosed on ECG despite not satisfying the number of millimeters of ST elevation required to qualify as a STEMI. The cath lab should be activated for such patients — and in fact, current Guidelines state that persistent chest pain with ECG changes suspicious for acute ischemia (even in the absence of a definite STEMI) — is indication for prompt cardiac cath to define the anatomy for potential reperfusion. Failure to appreciate the concept of an OMI, with resultant delay in the wait for STEMI criteria to be fulfilled is a potentially lethal error.
The final error I’ll mention regarding the interpretation of 12-lead ECGs — relates to the ONE time in which I do abort my systematic approach in the middle of my assessment. This is when, in the process of assessing a supraventricular rhythm — you discover that the QRS complex is wide. So, the rhythm is not VT — and, you’ve completed your assessment of Rate and Rhythm — and while assessing Intervals, you note that the QRS complex is wide. STOP your systematic approach at this point! Before proceeding — Determine WHY the QRS is wide. IF you’ve determined that the rhythm is supraventricular, and the QRS is wide — assuming you are not dealing with WPW — there are only 3 possible reasons for QRS widening — which are Right Bundle Branch Block — Left Bundle Branch Block — or IVCD (which stands for an intra-ventricular conduction defect not due to either Right or Left Bundle Branch Block). The reason I stress not worrying about Axis, Hypertrophy or QRST Changes of Infarction-Ischemia until you determine WHY the QRS is wide — is because the criteria to use for determining Axis, Hypertrophiy and Ischemia-Infarction-related changes are different when you have Bundle Branch Block or IVCD. So — After you determine the type of conduction defect (be it Right Bundle Branch Block — Left Bundle Branch Block — or IVCD) — THEN continue with your systematic approach, armed with the knowledge that criteria for Axis, Hypertrophy and Ischemia-Infarction will need to be modified accordingly.
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BE SURE TO COVER !!!
— AFlutter - reg SVT at ~150/minute
— Look for atrial activity (which leads - II,V1 — III,aVF,aVR)
— How to use calipers (not with a crashing patient - but afterward)
— How to compare tracings (1-to-the-other)
— Looking for dynamic changes
— Comparing "apples with apples" — and not with oranges
— Concept of OMI (which patient needs to go to the cath lab NOW?)
— Correlating the history to the ECG (often ignored) — looking for the presence and severity of CP
— How much I learned from my computer studies — inter- and intra-interpreter variation 20-30%
— AI is great — BUT — in my opinion you need a clinician to overview the tracing (I intentionally say “clinician” — because not all physicians are better interpreters than non-physician interpreters — be they nurse, paramedic, physician assistant or whatever)
— AI is great — BUT — I am not one to depend only on the computer
— Computer will never do arrhythmias …
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LINKS:
STEMI criteria … vs OMI
— Blog 193
— Blog 272 - Use this tracing !!!! - 9/12 leads - hyperacute T waves !!!
— Blog 218 - hyperacute T waves
— Blog- Acute MI with Subtle AV Block - 2:1 - Use this tracing !!!
Systematic Approach- for Rhythm
Systematic Approach- for 12-leads
Diagnosis of BBB
Diagnosis of Axis/Hemiblocks
What is SVT
Idiopathic VT
Blog 220 (Jennifer Carlquist Approach)
Why do beats conduct with Aberration
Blog 42 - VT vs SVT
dependence on fixed criteria (STEMI, LVH)
failure to appreciate the importance of history (same ecg has different interps depending on history)
misuse of the computer
failure to use a system - both for rhythm and 12-lead
they look for a "single answer"
rhythms - must begin to treat before you known definite answer
failure to see when there is BAD data that you just can't interpret (if you can't see P waves- you can't comment on relationships (artifact, baseline wander - the wrong leads)
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