Posted by: medicblog999 | June 6, 2010

ECG Geek 10

This time I want to discuss a little more than the ECG itself, as this case got my mind going a little bit and I thought I would share.

I am going to give you a brief history of the incident,  then show you the 12 lead ECG. I want to know your interpretation of the ECG then in the next post I will give you my interpretation and then have the discussion that I really want to have.

But first, the ECG…..

This gentleman was a 32 yr old male who had called for an ambulance after feeling a ‘little unwell’ and having a fall (? Collapse) and injuring his right knee.

On arrival, he was fully conscious, alert and orientated. His colour was good, skin was normal, and he did not complain of any other pain or concerning symptoms other than pain to the medial part of his right knee. There was no chest pain, no dizzyness or headache, and no palpitiations or other possible cardiac symptoms. He had slight swelling and tenderness to the medial side of his right knee but was able to weight bare and hobble about his house.

His observations were all within normal acceptable limits

Pulse 93, regular and strong

BP 138/75

SaO2 98% on room air

Due to the fact that he had fallen and cant really remember why, he got a ECG for a rhythm strip and a 12 lead. His rhythm was sinus and his 12 lead is as shown :

click to enlarge

So, what is going on with this chaps ECG and what is your next course of action?

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Responses

  1. Okay, here goes!! I bet this is horrifically wrong!! As he's young, and there is what looks like a saddlebag sign in V1 as well as the ST elevation in other leads, I reckon this is an atypical presentation of pericarditis.

  2. Hi A bit rusty as it has been a while since i did This, but it looks like a high take off and enlarged T wave in V1 V2 V3, no actual ST elevation, no physical symptoms that would suggest MI, would hazard a guess that there maybe raised potassium? Elevation is in V1-3 so no reciprocal leads.Tall peaked T waves ofter are a sign of Hyperkalemia

  3. Okay, here goes!! I bet this is horrifically wrong!! As he's young, and there is what looks like a saddlebag sign in V1 as well as the ST elevation in other leads, I reckon this is an atypical presentation of pericarditis.

  4. Hi A bit rusty as it has been a while since i did This, but it looks like a high take off and enlarged T wave in V1 V2 V3, no actual ST elevation, no physical symptoms that would suggest MI, would hazard a guess that there maybe raised potassium? Elevation is in V1-3 so no reciprocal leads.Tall peaked T waves ofter are a sign of Hyperkalemia

  5. Wouldn't Pericarditis present with ST elevation in a lot of leads and chest discomfort/pain?

  6. I would say LVH with atypical strain pattern vs. benign early repolarization.Tom

  7. Left sided cardio myopathy… Stab in the dark!

  8. I concur with Tom's interpretation. LVH, possible BER. Atrial enlargement to boot.ST-elevation on thie 12-lead ECG is most likely benign.

  9. meets criteria for LVH and/or BER. notching in V3-V5. concave st segment likely benign.saw on FB someone mentioned there are no reciprocal changes, but only posterior leads are reciprocal to anteroseptal leads in question here.

  10. I agree with most of above – definitely LVH, most probably high-takeoff. T-waves are a bit tall but I would expect it to be more widespread if it was a HyperK+Any PMH or recent illness?

  11. I think I'm going w/ LVH based on size of QRS complexes. Is there something up w/ the T Waves in V1 with the notching. My other question is regarding the shape of the ST segment in V1. It appears a bit different than V2 & V3…is there something there? It says 0130 on the ECG…alcohol involved? I was under the impression that you might get reciprocal depression w/ a high anterior MI in the inferior leads…?

  12. I think I'm going w/ LVH based on size of QRS complexes. Is there something up w/ the T Waves in V1 with the notching. My other question is regarding the shape of the ST segment in V1. It appears a bit different than V2 & V3…is there something there? It says 0130 on the ECG…alcohol involved? I was under the impression that you might get reciprocal depression w/ a high anterior MI in the inferior leads…?

  13. Tough call between LVH or early-repolarization (dropping the word “benign” from my use of the term these days), with both of those a good deal more likely than AMI. It probably wouldn't hurt to slip him some ASA anyway, mostly since I'd imagine it's hard to argue against a computer printout of “extensive myocardial infarction” in court, and the possible benefits usually far outweigh the risks depending on the patient's medical history. Possible syncope with LVH findings raises the possibility of cardiomyopathy, even without some of the more classical indications (there's no true diagnostic findings on ECG). Also, recent literature shows a correlation between sudden cardiac arrest and a higher rate of early repolarization on the baseline ECG, so that's always something to keep in the back of your mind, although more study into this phenomenon is definitely indicated. Serial 12-leads on the off chance those actually are hyperacute T's that may change, and be prepared for to possibility of v-fib/tach associated with either cardiomyopathy or early-repole. In the end, probably a normal ECG and patient, but our job is to worry about the abnormal in the patient's short term care.

  14. I'd blame the notching in V1 on artifact

  15. very strictly speaking, reciprocal leads are only within the same plane. so, only limb leads can be reciprocal to limb leads (for instance, the common pairing of II, III, aVF and I, aVL), and only V leads can be reciprocal to other V leads. limb leads and V leads are in planes that are 90 degrees from each other, and can therefore not be reciprocal to each other.

  16. having said that, if there is a big enough area of affected tissue, you are likely going to see reciprocal changes in pairings like you mentioned. it just depends on the location and size.

  17. Oh, and left atrial enlargement (notched p-waves in V1-V4), which may or may not add anything to the likelihood of the LVH/cardiomyopathy scenarios. Younger guys always have tough ECG's for these diagnoses.

  18. Usually yes, hence the word “atypical”

  19. BER or LVH, STE consistent w/ QRS complex size, fishhooks at the J-points lead me to BER.

  20. I would call immediately for ALS. I have no idea what that is, but it looks bad, and I'm only BLS

  21. we have to think about the Brugada diagnosis !!

  22. we have to think about the Brugada diagnosis !!

  23. Around here he'd be far more likely to get a pointless board and collar than a 12-lead.

  24. Not an MI, not Brugarda, not Pericarditis. The Dx of MI is not based soley long ECG changes. Look at the clinical picture, other than possible syncope, there is nothing suggestive of MI. Syncope in young people itself is not suggestive of MI, that's mostly a finding in elderly patients. I've never heard that reciprocal changes for anterio-septal MIs are restricted to posterior leads, I'd expect to see some evidence of that in the inferior leads as well. When you hear hoof beats, think horses, not Zebras. At least outside of Africa.

  25. Not an MI, not Brugarda, not Pericarditis. The Dx of MI is not based soley long ECG changes. Look at the clinical picture, other than possible syncope, there is nothing suggestive of MI. Syncope in young people itself is not suggestive of MI, that's mostly a finding in elderly patients. I've never heard that reciprocal changes for anterio-septal MIs are restricted to posterior leads, I'd expect to see some evidence of that in the inferior leads as well. When you hear hoof beats, think horses, not Zebras. At least outside of Africa.

  26. […] you need to see the patient presentation, then¬†click here to read part one of this […]

  27. Based on this 12 lead and the fact that this otherwise healthy 32 year old male had collapsed for no apparent reason and does not remember the event i would call it an MI until proven otherwise by lab thest or a cardiac catheterization. This has stemi all over it. this guy meets MONA and is a priority transport to the appropriate cardiac capable hospital. If you ignore the electrical activity of the heart and he is having an MI then you are screwed, if you rn emergent and it turns out to be nothing then you were overcautious and hopefuly the cardiologist will understand and explain his findings to you.

  28. Based on this 12 lead and the fact that this otherwise healthy 32 year old male had collapsed for no apparent reason and does not remember the event i would call it an MI until proven otherwise by lab thest or a cardiac catheterization. This has stemi all over it. this guy meets MONA and is a priority transport to the appropriate cardiac capable hospital. If you ignore the electrical activity of the heart and he is having an MI then you are screwed, if you rn emergent and it turns out to be nothing then you were overcautious and hopefuly the cardiologist will understand and explain his findings to you.

  29. Looks like early repolarization. In the presence of chest pain one would have to consider acute MI until the doc can pull up the patients previous 12-lead and compare.

  30. Chris, if you're going with MI and you say greet the pt w/ MONA, my question is in the absence of pain how would you titrate your nitro and morphine administration?

  31. Hmm… well you cant do MONA if this patient is asymptomatic and he has absolutely no clinical indications of MI. as far as ST elevation it could be something else like pericarditis. I would monitor pt initiate rapid transport and notify the recieving facility

  32. I've had time to research some of the conditions mentioned because I haven't heard of some of them in a long time. LVH in my understanding is usually global. As for early repolarization it only appears early in V1, 2, 3 and maybe in V4, but none of the rest of the leads. Knowing that I've had time to look these things up doesn't help during the actual call where you would not be able to research. As you know, you have to may quick decisions on the spot. I would lead toward a septal wall MI. While it is not common, it is also not impossible to have an MI at 32 years old. In the description given for this ECG we were not given the patient's PMH or family hx. As is always my rule of thumb, Syncope is always cardiac until proven otherwise.

  33. As far as protocols are concerned, most should have a statement that read “These are not a substitue for good clinical judgement”. While the patient may not have “Chest Pain” does not mean that he/she is not having a cardiac event that would benefit from treatment. If you don't dare go against your protocols for the good of the patient, then do what I always tell my students, “When in doubt, call medical control”. Plead your case to the doctor and let them make the decision. CYA!

  34. Titrate to ECG. Repeat ECG to monitor changes in the ST segment. Just a thought.

  35. While there certainly is ST elevation, the fact that there seem to be no reciprical changes is cause for suspicion. Oxygen is a given, and so is an IV. Aspirin would certainly not hurt either considering it doesn't take effect immediately, namely because of the route of absorption as well as final distribution to the platelets. I think most people forget that nitro and morphine do more than act as pain management tools. They act as vasodilators as well as reduce myocardial oxygen demand for starters. Cardiomyopathies can very likely produce no pain at all (i.e. silent heart attack). Cardiac tissue itself does not have well defined pain receptors and we are often clued in by the radiating or referred pain. But, even this pain sometimes does not manifest itself. The differental diagnonsis of pericarditis and early repolaration are good ones, but one cannot forget that the longer one doubts tissue infarction, the worse off the patient is in the end. Time is tissue. I would certainly confer with Med Control before trying anything else if not to simply give them a good picture of this puzzling patient they are about to receive. I might go ahead and switch my leads to the right side of the chest for another picture of the heart and also for good measure. I reason that the ST elevation may also be do to coronary spasm.

  36. Was this man a healthy person or an athlete? When a healthy person has a syncopal episode (and not a knee locking fall), I always think of hypertrophic obstructive cardiomyopathy. I noticed that there is ST Elevation in Leads V1, V2 and V3. As for medical control, I would immediately email the 12-lead to the Doc on duty. I would also try to convince the pt that they needed an evaluation. Last time I transported a syncope pt with a 12-lead that looked weird (and had a lot of words at the top), the pt became angry at me because there was nothing wrong (and I was happy). I agree with the person that remarked that if that 12-lead was shown in court we would be extremely seriously screwed. Better to err on the side of caution, because a jury of peers will normal people (not medical, most likely) and will not understand that you make up your mind first before you read the 12-lead machine's opinion. High flow O2, IVx2, aspirin, ongoing 12-leads (depending on transport time) and perhaps a 2nd opinion and maybe switch machines if you feel like it.

  37. The deep S waves in V1 and V2 together with the large R waves in V3-V5 suggest left ventricular hypertrophy. The fact that the largest R wave is on the anteroseptal leads would suggest to be a mainly interventricular septal hypertrophy and together with the patients history I would go for the diagnosis of hypertrophic obstructive cardiomyopathy (HOCM).25% of individuals with HOCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction.The clinical course of HCM is variable. Many patients are asymptomatic or mildly symptomatic. The symptoms of HCM include dyspnea (shortness of breath), chest pain (sometimes known as angina), uncomfortable awareness of the heart beat (palpitations), lightheadedness, fatigue, fainting (called syncope) and sudden cardiac death.

  38. poss septal mi aquire 2nd ekg to confirm recheck leads

  39. you say no mona but rapid tx how much sense does that make ?sure treat the pt not the monitor, but why run emergent tx?

  40. poss septal mi aquire 2nd ekg to confirm recheck leads

  41. you say no mona but rapid tx how much sense does that make ?sure treat the pt not the monitor, but why run emergent tx?

  42. Based on the 12 lead, patient vitals and the story behind it I would certainly continue to monitor the patient, a blood glucose check wouldn't hurt either, O2, IV, ASA and NTG. While there is no chest pain there does appear to be ST elevation in V1, V2 and to a lesser extent V3. While patient couldn't report any relief in pain from the NTG (since there is none to begin with) I would reassess patient blood pressure after each (of course) and pass him onto the hospital.

  43. While there is technically some obviously *apparent* ST elevation in V-1 — V-3, it appears to be of the “pulled up” variety and preceeds tall, peaked t-waves, not the “tombstones” typical of STEMI infarction. Combined with the very deep S waves it looks far more like a case of HOC (as astutely noted by Shahram already). Another possible cause of this could be hyper K, which could also account for the fall of unknown cause. Too much potassium is every bit as troublesome as too little. This by no means would seem consistent with an MI to me, even after close scrutiny, and we have to always be mindful that we — and the doctors — must interpret what appears, despite the usually (but not always) helpful (and sometimes accurate) interpretations contained in the database of a portable EKG machine. One of the most common misreadings is variations on “anterior infarct”, though the fact the Lifepak in question actually suggests therapies as well is a concern. Of course when in doubt, we here (in Maryland, USA) are urged always to send the EKG as part of a consult with the base physician, who can easily read and make the call for us. With no correlating symptoms this really looks very innocent (insofar as an acute coronary event is concerned) and would likely result in echocardiographic exam tor rule out HOC, as well as labs to check electrolytes.

  44. While there is technically some obviously *apparent* ST elevation in V-1 — V-3, it appears to be of the “pulled up” variety and preceeds tall, peaked t-waves, not the “tombstones” typical of STEMI infarction. Combined with the very deep S waves it looks far more like a case of HOC (as astutely noted by Shahram already). Another possible cause of this could be hyper K, which could also account for the fall of unknown cause. Too much potassium is every bit as troublesome as too little. This by no means would seem consistent with an MI to me, even after close scrutiny, and we have to always be mindful that we — and the doctors — must interpret what appears, despite the usually (but not always) helpful (and sometimes accurate) interpretations contained in the database of a portable EKG machine. One of the most common misreadings is variations on “anterior infarct”, though the fact the Lifepak in question actually suggests therapies as well is a concern. Of course when in doubt, we here (in Maryland, USA) are urged always to send the EKG as part of a consult with the base physician, who can easily read and make the call for us. With no correlating symptoms this really looks very innocent (insofar as an acute coronary event is concerned) and would likely result in echocardiographic exam tor rule out HOC, as well as labs to check electrolytes.


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