tag:blogger.com,1999:blog-549949223388475481.post2400256399921385341..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: A patient with cardiac arrest, ROSC, and right bundle branch block (RBBB). Unknownnoreply@blogger.comBlogger9125tag:blogger.com,1999:blog-549949223388475481.post-47231905834139327572019-03-06T21:16:39.502-06:002019-03-06T21:16:39.502-06:00@ Abdullah — When the QRS widens because of marked...@ Abdullah — When the QRS widens because of marked hyperkalemia — the ST-T wave may also widen, in which case the base of the T wave may not be so narrow. But T waves are still quite peaked (almost pointed) in many leads of ECG #1 here — which given the degree of QRS widening, IS a T wave change consistent with marked hyperkalemia. I find looking for a narrow T wave base in association with T wave peaking to be most helpful when the QRS complex is still narrow.ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-16947777188979476452019-03-06T20:45:45.552-06:002019-03-06T20:45:45.552-06:00Thanks Jerry! I've stopped trying to figure ou...Thanks Jerry! I've stopped trying to figure out "mechanisms" for some of these hyper-K+ arrhythmias, as they defy my interpretation ability (and they most often resolve once K+ returns to normal) — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-47235496056932985612019-03-02T13:17:45.257-06:002019-03-02T13:17:45.257-06:00the base of T wave looks too broad for hyper Kthe base of T wave looks too broad for hyper KAnonymoushttps://www.blogger.com/profile/03598220742341150917noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-43102041559831118172019-03-01T20:59:04.888-06:002019-03-01T20:59:04.888-06:00I saw your question and it is a question that I (a...I saw your question and it is a question that I (and I'm sure Steve and Ken) have been asked many, many times. Steve is absolutely right! You have to see a lot of them to develop a sense of which one you are dealing with. The best hint is the context within which you are seeing the patient. Is the patient having classic ACS-type chest pain or did they miss their last 4 dialysis appointments? The internet is filled with examples of both kinds of T waves. Find them, print them out and study them.<br /><br />Next, don't fixate on tall, narrow peaked T waves as hyperkalemic. They are only going to be present 22% of the time - that means that 78% of the time you won't see them - even with significant hyperkalemia. Focus more on the QRS complexes and get a good idea when something doesn't seem right for a bundle branch block or even a "slow" v-tach. Typical hyperkalemic T waves are tall, very narrow and sharply peaked. But they CAN be relatively short with bases that aren't at all narrow and peaked but not sharply peaked. They do tend to be symmetrical. The T waves in these two tracings are excellent examples of that.Jerry W. Jones, MD FACEP FAAEMhttps://www.blogger.com/profile/10333187745825224414noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-53830969840355736252019-03-01T20:42:30.344-06:002019-03-01T20:42:30.344-06:00Ken...
I think your sentence "Of course, ANY...Ken...<br /><br />I think your sentence "Of course, ANYTHING is possible given marked hyperkalemia — which affects conduction in so many sites and in so many ways" pretty much says all there is to say about dysrhythmias during hyperK+!Jerry W. Jones, MD FACEP FAAEMhttps://www.blogger.com/profile/10333187745825224414noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-63010419519821163102019-03-01T19:19:29.659-06:002019-03-01T19:19:29.659-06:00THANKS as always (!) for your comments Jerry — whi...THANKS as always (!) for your comments Jerry — which are always excellent for educational purposes. I’ll respond to a few of them. The R-R interval preceding beat #6 = 1.5 second. I called it a “pause” because it is the longest R-R interval we see (can’t be sure about what happens before beat #1 or after beat #9), and because this longer R-R interval occurs unexpectedly given the cadence of other beats. I called it “short”, because 1.5 second is relatively short for a pause. <br /><br />Your thought that beats #4, 5, 7, , 8 and 9 (each preceded by a small negative P wave with constant PR interval) are junctional in the lead II rhythm strip at the bottom of ECG #1 is interesting — and I had a similar thought. The reason I opted to call these atrial beats, is that I otherwise did not know what to call beats #3 and 6, which are not preceded by any P waves at all — and in addition these 5 beats (that are each preceded by a negative P wave) are more irregular than is usually seen with junctional escape rhythms — especially given how so soon afterward (in ECG #2) we have what looks like a regular junctional escape rhythm. Of course, ANYTHING is possible given marked hyperkalemia — which affects conduction in so many sites and in so many ways. <br /><br />I agree that the rhythm in ECG #2 is most likely accelerated junctional. The reasons I postulated as a possibility (not probability) that the rhythm in ECG #2 might be sinoventricular are: i) If the underlying rhythm in ECG #1 was ectopic atrial — then why after treatment would the site of impulse formation shift to a lower location (in the AV node); and ii) My suspicion that perhaps the actual degree of hyperkalemia was much more severe than is likely to occur at a serum K+ level of 7.1 mEq/L, which is high — but not so high as one might expect given the number and severity of conduction disturbances that we see in ECG #1. Unfortunately, details about when blood levels were drawn, how severe the acidosis of cardiac arrest & PEA really were, how long the patient went before treatment, etc are missing — but I theorized that given the situation we were told — that serum K+ might have been much higher than 7.1 mEq/L, and therefore that much more likely to produce a sinoventricular rhythm. Again, I agree with you & Steve that a junctional rhythm is still the most probable rhythm in ECG #2.<br /><br />I agree entirely with you that hyperkalemia may produce sometimes very impressive ST elevation. But given that hyperkalemia IS a cause of Brugada phenotype — don’t we then get into the difficulty of distinguishing between ST elevation from hyperkalemia itself vs hyperkalemia producing a secondary Brugada ECG pattern that then results in ST elevation? The “good news” (one of the points I tried to emphasize in my comments) — is that while ECG patterns and rhythms associated with hyperkalemia may be perplexing — they usually “go away” after hyperkalemia has been corrected.<br /><br />Finally — I’d add to your comment regarding 1st degree AV block — that as with most (almost all) conduction disturbances — clinical significance depends in LARGE part on the clinical situation in which it occurs.<br /><br />THANKS again Jerry for your intriguing comments. It is always fun and educational to debate these issues with you! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-4990212868905642162019-03-01T17:16:02.628-06:002019-03-01T17:16:02.628-06:00you really just have to see it over and over again...you really just have to see it over and over again. You can see dozens of examples here.Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-37278282790263161482019-03-01T16:27:46.501-06:002019-03-01T16:27:46.501-06:00Steve...
Thanks again for great learning/teaching...Steve...<br /><br />Thanks again for great learning/teaching experience with this ECG (and one of my favorite topics). And the points outlined by Ken were spot on! However... I do have a few things to add.<br /><br />Ken, in your comments under the section " What is the Rhythm in ECG #1?" you mention that beat #6 is a junctional escape beat "because it ends a short pause..." I think you meant it ends a LONG pause. Granted, we've all seen longer pauses, but this pause is long for this tracing.<br /><br />The rhythm perplexes me as much as it did both of you. Here's my take on it: I think it is junctional in both ECGs though ECG #1 may be manifesting some late sinoventricular conduction that is about to give way to a junctional ectopic rhythm. The inverted P' waves noted in the bottom rhythm strip I think are actually a manifestation of the junctional rhythm. When a junctional rhythm manifests inverted P' waves BEFORE the QRS under more normal circumstances, the P'-R interval is typically very, very short. But here we have a rather profound hyperkalemia that is adversely affecting conduction velocities throughout the heart. I think there appears to be more delay going toward the ventricles than back into the atria. That could also explain the constant P'-R intervals when they are visible (due to the fact that they are equally part of the junctional complex). Here's what really perplexes me: the fact that there are retrograde P' waves present at all! The mere presence of sinoatrial conduction means that the working atrial myocytes can no longer repolarize and are thus paralyzed by the hyperkalemia. Perhaps ECG #1 captured that moment just before all the atrial myocytes were left in a depolarized state but most of the conduction was sinoatrial. I have no confident answer for that.<br /><br />Regarding ECG #2, I agree completely that it is a junctional rhythm. Conduction is much faster now and the QRS intervals are much narrower; this allows the retrograde P' waves to be hidden in the QRS intervals as they usually are. It was suggested that it could still be sinoventricular but I doubt it. If the sinus node had recovered enough to produce a regular rhythm at a rate around 75/min, I would expect the atria to have recovered enough to produce a P wave or two. I still think it's junctional - AV dissociation by usurpation.<br /><br />I totally agree with Ken that QRS axis in the presence of hyperkalemia is "anyone's guess." Hyperkalemia affects the conduction velocity of different myocardial tissues in different ways. The mean QRS axis is likely going to be a perplexing surprise. I think that QRS complexes in Lead I in both tracings demonstrate a net negativity amd thus right axis deviation in both tracings.<br /><br />There are two other things I think that clinicians interpreting ECGs should be aware of: <br /><br />First, hyperkalemia can produce ST elevation that is very impressive. However, the STE typical of hyperK+ (to me) looks much more like the elevation one sees in Brugada syndrome. In retrospect, that seems somewhat appropriate because Brugada Syndrome is caused by a Na+ channel defect and hyperkalemia exerts its effect by depolarizing the myocytes and rendering their Na+ channels inactive.<br /><br />Second, if you have a fairly young patient (<45-50 years) with risk factors for hyperkalemia (hypertensive, diabetic, early renal disease, elevated serum myoglobin due to muscular injury) and you see a 1st degree AV block, perhaps in addition to some T waves of which you are only mildly suspicious - be aware that this may be an additional suggestion of hyperkalemia. Don't immediately write-off 1st degree AV block in a young person as benign; it is present in only about 1% of the population below age 50. If it's present in someone under the age of 50 yrs, it is probably there for a specific reason. Granted, above age 50 it becomes somewhat common but below age 50 - be careful!Jerry W. Jones, MD FACEP FAAEMhttps://www.blogger.com/profile/10333187745825224414noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-49695480659419175842019-03-01T09:38:39.943-06:002019-03-01T09:38:39.943-06:00What is the most basic difference between the Hype...What is the most basic difference between the Hyperacute T of Hyperkalemia and MI ? Is there a definite criteria ? or one just have to recognize the pattern ?Swagatahttps://www.blogger.com/profile/16417581885823267552noreply@blogger.com