Friday, January 31, 2020

H/o MI and stents with brief angina has this ED ECG. And what is Fractional Flow Reserve?

A middle-aged man complained of 15 minutes of classic angina that resolved upon arrival to the ED.

Here is his initial ECG:
What do you think?











There is sinus rhythm with RBBB and possible LPFB (see Dr. Grauer's detail below).  There is ST elevation in II, III, and aVF, and reciprocal ST depression in aVL.  And there are Q-waves in both inferior and lateral leads.   So this is indeed diagnostic of myocardial infarction.

Should we activate the cath lab?

No! Not immediately, at least, because this is NOT diagnostic of ACUTE (occlusion) myocardial infarction (Acute OMI).  We need to do some more investigation.

Although diagnostic of MI, it is highly suspicious for "Old inferior MI with persistent ST Elevation" or "inferior aneurysm morphology" because of the well-formed Q-waves and the flat T-waves.

Inferior aneurysm can look a lot like ACUTE inferior MI because it does not usually have QS-waves (as anterior LV aneurysm usually does); instead, inferior aneurysm usually has QR-waves, which in inferior MI are often seen in BOTH acute and old MI.   QS-waves imply no remaining deplorizing forces toward the overlying lead.  To repeat: in contrast, anterior aneurysm is much more easily distinguished from acute MI due to the QS-waves.

I immediately looked for old charts, which were only available from another hospital, and an old echo confirmed inferior "akinesis" (which may also have persistent ST elevation).  A true anatomic aneurysm has "dyskinesis" (systolic outpouching of the ventricular wall) or "diastolic distortion" (diastolic outpouching of the ventricular wall).

See any of these posts for more on anterior LV aneurysm.

Here are other cases of inferior LV aneurysm.

How did I strongly suspect that this was NOT acute?

1.  The patient's chest pain had resolved by the time of the ECG
2.  There are well-formed Q-waves
3.  The T-waves are flat.  Acute T-waves are large, even if not necessarily hyperacute.


Although this ECG does not demand immediate cath lab activation, it is very worrisome.  It could be acute, though probably is not.  But it does prove that the patient has coronary disease and makes the probability that his chest pain is due to ACS very very high.

In fact, his first troponin I returned at 0.128 ng/mL, with a subsequent falling value, diagnostic of MI.

So I made an ED diagnosis of Non-Occlusion Myocardial Infarction (NOMI), and his next day angiogram confirmed NOMI.  He was treated with aspirin and heparin.

Angiogram:
Widely patent RCA and LAD stents.

Culprit Lesion: Angiographically indeterminate 50% stenosis in the proximal OM2 was assessed further with instantaneous wave free ratio (iFR) of 0.96, which is normal (see below for description of iFR*).

"After normalization in the left main, the pressure wire was advanced to the distal OM2, and iFR was 0.96, suggesting no hemodynamic significance, and no significant drift on pull back."

Therefore, no stent was placed.  (No culprit could be identified, and FFR was negative)

Impression and Recommendations:
Widely patient RCA and LAD stents
No evidence for hemodynamic significance of 50% proximal OM2 stenosis
Diffuse mild to moderate CAD without evidence for severe epicardial stenosis
_______________

A bit about fractional flow reserve (FFR) (with my limited understanding of this, and I put a link in to an excellent article on this below): This is an angiographic technique to assess the pressure gradient across coronary lesions.  It is proven better than angiography alone in stable angina, and also has been shown to improve decisions on stenting non-culprit lesions in ACS.  However, if a culprit lesion is identified in ACS, and has low pressure gradient ("negative" FFR assessment), this does NOT mean it should not be stented -- FFR is not a good assessment for culprit lesions.

*Instantaneous wave-free ratio is performed using high fidelity pressure wires that are passed distal to the coronary stenosis. iFR isolates a specific period in diastole, called the wave-free period, and uses the ratio of distal coronary pressure (Pd) to the pressure observed in the aorta (Pa) over this period. During this wave-free period, the competing forces (waves) that affect coronary flow are quiescent meaning pressure and flow are linearly related as compared to the rest of the cardiac cycle.

Very good summary of the data on Fractional Flow Reserve and Instantaneous Wave Free Ratio:  https://www.acc.org/latest-in-cardiology/articles/2017/05/25/08/34/ffr-in-2017-current-status-in-pci-management







===================================
MY Comment by KEN GRAUER, MD (1/31/2020):
===================================
Interesting case to review! We are told that this middle-aged male patient has a history of prior MI with stents. He presents with an episode of brief, new-onset chest pain that had resolved by the time ECG #1 was obtained.
  • For clarity — I’ve reproduced and labeled the ECG shown in this case (Figure-1).

Figure-1: The initial ECG that was done in the ED (See text).



I’d add the following thoughts to the comments by Dr. Smith.
  • Although there is resemblance to an rsR’ pattern in lead V1 — this ECG does not represent a typicalRBBB. YES, there is a RBBB — because there is a predominant positive triphasic complex in lead V1 that occurs in association with wide terminal S waves in lateral leads I and V6. But a closer look at lead V1 reveals marked fragmentation of the QRS complex in both the small S wave downward deflection, as well as in the bifid terminal R’ (Be sure to look at the magnified view of ECG #1, by clicking on the Figure!).
  • Fragmentation of the QRS complex is marked, and present in numerous leads in ECG #1 (ie, in each of the inferior leads — and, dramatically so in the upslope of the S wave in lead V2, and to a lesser extent in the S wave of lead V3). The phenomenon of fragmentation has been discussed and illustrated numerous times on Dr. Smith’s ECG Blog (I’ll add reference to THIS CASE of mine). The importance of recognizing fragmentation (especially when it is as marked as it is in ECG #1) — is that it tells us there has been scarring, which may be the result of prior infarction, cardiomyopathy, or some other form of structural heart disease. Such fragmentation does not tell us whether heart disease is acute or has been present long-term — but even IF we had not been told that the patient in this case had prior MI with stents — it would be very clear from the fragmentation we see in ECG #1, that this patient has severe underlying structural heart disease!
  • There are 2 clues that scarring in ECG #1 is the result of prior MI: i) There is even fragmentation within 2 of the 3 inferior Q waves (RED arrows); andii) Q waves are not only present in the chest leads, but these Q waves begin as early as lead V3 (BLUE arrows— and extend through to lead V6 (with the Q in V6 being deeper-than-is-likely-to-be-seen with a normal septal q wave). It is uncommon that you will see septal q waves as far over as lead V4. Septal q waves should simply not occur as early as lead V3. And — the presence of RBBB does not account for Q waves in these 4 chest leads. BOTTOM Line: The presence of inferior and antero-lateral Q waves in ECG #1 is diagnostic of inferior and anterolateral MI that must have occurred at some point in time.

Otherwise — I would not diagnose LPHB (Left Posterior HemiBlock) on this tracing ( = my opinion). Instead — I would describe the conduction defection as RBBB alone.
  • It is well to keep in mind that among the bifascicular blocks (ie, RBBB/LAHB and RBBB/LPHB) — RBBB/LAHB is far more common (ie, more than 90-95% of the bifascicular blocks in my experience manifest Left Anterior HemiBlock instead of LPHB). The reasons for this are simple: i) The left posterior hemifascicle is much thicker anatomically than the left anterior hemifascicle; andii) The posterior hemifascicle has a dual blood supply. As a result of these 2 factors — much more extensive damage is needed to produce true RBBB/LPHB.
  • NOTE — It is rare to see a true isolated LPHB. Instead, when LPHB does occur — it is almost always seen in association with RBBB, as a form of bifascicular block. In contrast — isolated LAHB is extremely common, especially in older individuals. And as just mentioned — RBBB/LAHB is by far the most common form of bifascicular block.
  • Terminology  While I have seen significant variation among cardiologists regarding the criteria they use for diagnosing LPHB — the criteria I have always used require clear predominant negativity for the QRS complex in lead I. When assessing a tracing for possible LPHB in a patient who also has RBBB — it is the straight downward portion of R wave descent into the S wave in lead I that should be assessed (ie, the portion of the QRS before the terminal delay produced by the RBBB). Predominant negativity of the QRS complex in lead I is not present in ECG #1. Note the positive portion of this straight-line descent (ie, the vertical RED line in lead Iequals the negative portion (ie, the vertical GREEN line in lead I) — so predominant negativity is lacking.

Finally — As per Dr. Smith, the ST-wave changes we see in ECG #1 dnot look acute. Instead, T waves in multiple leads (ie, leads I, aVL, V2-thru-V6) look flat. In addition, ST segments in these leads lack the gentle upsloping that is usually seen in a normal tracing.
  • Typically, with simple RBBB — there is slight ST depression with more marked T wave inversion in lead V1 than we see in ECG #1.
  • There is ~1 mm of ST elevation in each of the inferior leads. That said — the shape of the ST segment in these inferior leads manifests gentle upsloping (ie, it just doesn’t look acute).
  • Although there is some scooping to the ST segment in lead aVL — the J-point in lead aVL is not depressed. Therefore, the magical” reciprocal relationship seen between leads III and aVL with acute inferior OMI is not seen in ECG #1 (See My Comment in the 1/29/2020 postamong many other references to this phenomenon in Dr. Smith’s blog).
  • THE ABOVE SAID — We can not overlook the fact that: i) This middle-aged man has documented severe underlying coronary disease — and, he presents with new (albeit short-lived) chest pain; ii) There is ST elevation in each of the inferior leads in ECG #1iii) We were not given a prior tracing for comparison (so we do not know for certain which ECG changes are old) — andiv) It is possible that the ST-T wave flattening we see so diffusely in ECG #1 could be, at least in part, a “net effect” of prior ST-T depression + new ST elevation, in which the "net" result is some cancelling out of opposing forces (ie, "pseudo-normalization"). 
  • BOTTOM LINE: I agree entirely with Dr. Smith. The ECG findings we see in ECG #1 do not look acute — BUT — it is impossible to be certain that these findings are not acute from this single ECG, which is why more investigation was indicated for final decision-making.

Our THANKS to Dr. Smith for presenting this case!




Wednesday, January 29, 2020

A 20-something woman with Chest Pain

A 20-something woman presented with 30 minutes of sudden onset chest pressure that started while in the bathroom. She had no relief from nitro x1. ASA 325 given by EMS.

Here is her prehospital ECG:

What do you think?



Here are limb leads magnified:


Precordial leads magnified:
Notice the hyperacute T-waves in V4





She arrived in the ED with her pain diminishing.

Here is her ED ECG:
What do you think?










The first ECG is diagnostic of inferior OMI, with probable lateral involvement as well (V4-V6).

In the 2nd (ED) ECG, the inferior findings are gone.  The lateral ST segments remain elevated.  The T-waves appear hyperacute.   If there had been no prehospital ECG, one may not have noticed these subtle findings. 

The ED physicians immediately recognized inferior OMI and activated the cath lab.


Angiogram

Culprit is 100% occlusion of the Distal LAD due to athorosclerotic thrombosis (not spontaneous coronary dissection), affecting the inferoapical LAD hence an inferior (II, III, aVF) and apical (V4-V6) MI.

Peak troponin I was 4.7 ng/mL (99th %-ile URL = 0.030 ng/mL).

Echo

Normal left ventricular size, thickness, and systolic function with an estimated EF of 61%.
Very small regional wall motion abnormality--hypokinesis of the apical inferior and apical lateral segments.

Here is the next day ECG:
All ST segments are isoelectric, proving that BOTH the inferior and lateral ST elevation was indeed ischemic ST elevation.

She had extremely rapid reperfusion of this 100% obstructed distal LAD and thus had a lot of myocardium salvaged.

These docs and medics did a great job!


Learning Point:

1. Don't forget that young women have myocardial infarction too!
2. Prehospital ECGs are critical
3. Always look for hyperacute T-waves and for reciprocal ST depression in lead aVL.

See this case:

24 yo woman with chest pain: Is this STEMI? Pericarditis? Beware a negative Bedside ultrasound.







===================================
MY Comment by KEN GRAUER, MD (1/29/2020):
===================================
Illustrative case with the important Learning Points put forth by Dr. Smith. These include:
  • Young women can (and do) have acute MIs.
  • Prehospital ECGs can be invaluable to our interpretation about what is going on.
  • KEY findings on ECG to look for include hyperacute T waves — and, that magical” reciprocal relationship with inferior OMI between leads III and lead aVL (For more on this “magical” relationship — Please see My Comment in these Dr. Smith posts — from 8/9/2018 — andfrom 10/6/2018).

I focus my comments on some additional subtle changes seen in ECG #1, and confirmed by comparison with ECG #2 (Figure-1).

Figure-1: The first 2 ECGs in this case (See text).



MThoughts oECG #1:
Although resolution of this tracing is clearly suboptimal — this Pre-Hospital ECG ( = ECG #1) in a patient with new-onset chest discomfort is clearly of concern.
  • The rhythm is sinus at 60-65/minute. All intervals are normal. The frontal plane QRS axis is normal at about +30 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Small and narrow Q waves are seen in leads I and aVL.
  • R wave progression is appropriate, with Transition (where R wave height exceeds S wave depth) occurring at a normal position, here between leads V3-to-V4.
  • As per Dr. Smith — ST segments are elevated in each of the inferior leads — and in lateral chest leads (V4, V5, V6) — and, possibly also in high lateral lead I.


QUESTION: What distinguishes ECG #1 — from a tracing that might simply reflect a repolarization variant in a 20-something woman?



ANSWER: What distinguishes ECG #1 from a repolarization variant is a number of subtle findings that just should not be there in a normal tracing:
  • Normal variants do not manifest the reciprocal ST depression that we see in lead aVL of ECG #1.
  • T waves that are fatter-than-they-should-be at their peak in the inferior leads, and in leads V3 and V4. In addition — T waves are disproportionately taller-than-they-should-be (considering R wave amplitude) in leads V3 and V4. In the context of new-onset chest discomfort — all of these T waves qualify as hyperacute changes.
  • Lead V2 in ECG #1 is clearly abnormal. Missing is the slightly elevated, upward sloping ST segment — that is replaced in ECG #1 with a relatively flat ST segment in lead V2, with disproportionately taller-than-it-should-be T wave in this lead.
  • Lead V6 shows significantly more ST elevation than-should-be-seen in this most lateral chest lead.
  • BOTTOM Line: Taken together — this makes for 10 out of the 12 leads in ECG #1 that show suspicious changes in this patient with new chest discomfort.

NOTE: Technically — ECG #1 is a challenging tracing to interpret. This is especially true for leads III and aVL— for which we are trying to establish that “magical” reciprocal relationship.
  • For example — there is significant variation in QRST morphology for the 3 complexes that we see in these 2 leads (RED numbers 1, 2, 3). Which of these 3 beats in these 2 leads should we use to assess for ST-T wave morphology? Clearly the 2nd beat in lead III, and the 2nd beat in lead aVL look the most worrisome.
  • PEARL  Many tracings manifest far less than perfect quality. It’s important to “take this in” as you assess any ECG — and then render an overall Gestalt impression on the theme of the ECG findings you see. In ECG #1 — that theme includes inferior lead ST elevation with reciprocal ST depression in aVL.


MThoughts oECG #2:
We are looking for dynamic ST-T wave changes. How is ECG #2 different from ECG #1?
  • As per Dr. Smith — the inferior lead ST elevation is essentially gone (albeit harder to assess this in lead II of ECG #2, due to so much baseline wander).
  • Did YOU notice the change in Axis between the 2 tracings? That is — the QRS in Lead III was all positive in ECG #1 — but in ECG #2, the QRS in lead III is predominantly negative. That said — the reduction in inferior ST elevation between the 2 tracings looks real despite this change in frontal plane axis.
  • Given that QRS morphology in lead aVL is very similar (a qR complex) in the 2 tracings — the change from a depressed ST segment to a flat ST segment is real.
  • Overall QRS morphology in the chest leads of both tracings looks similar (albeit with slight change in amplitudes). This strongly suggests that the change in lead V2 appearance (which now shows a coved ST segment in ECG #2) is a real change.
  • As per Dr. Smith — the hyperacute T waves and ST elevation in lateral chest leads persist.
  • BOTTOM Line: There are subtle-but-real ECG findings on these serial tracings. There has been dynamic change + persistent lateral chest lead abnormalities in the follow-up tracing ( = ECG #2) — which taken together, strongly support the premise of an acute ongoing event.



Sunday, January 26, 2020

A woman in her 50s with dyspnea and bradycardia

Written by Pendell Meyers

A patient in her 50s presented with shortness of breath and fatigue worsening over 1 week. Her vital signs were within normal limits except for bradycardia at 55 bpm.

Here is her ECG recorded at triage:

What do you think?









It is probably sinus bradycardia with very small/depressed P-waves and prolonged PR interval. The QRS is about 150 ms, and has morphology consistent with LAFB. The T-waves are peaked. All findings are concerning for hyperkalemia.


Here was the baseline ECG on file:





The hyperkalemia was not yet identified, and the chemistry was pending.

To us, this is clearly hyperkalemia, and we only present what should be an obvious diagnosis because people continue to miss this.  Repetition. Repetition. Repetition.

Another ECG was recorded when a "change in the monitor" was noted:



The first half of the ECG is the same as above, but the second half shows a suddenly wider QRS complex with RBBB morphology. This likely represents an escape rhythm (possibly originating in the LBB). The QRS width of the RBBB beats is just over 200 msec. This is far too wide for normal RBBB, and also implies hyperkalemia or other QRS widening disturbance. The T-waves are markedly hyperacute.

The potassium level came back at 7.8 mEq/L.

The patient was treated for hyperkalemia and this was the repeat ECG:


Much improved, narrower QRS.


The patient did well.




Learning Points:

Always consider hyperK with slow, wide QRS complexes, among other patterns.

It is extremely rare for RBBB to have a QRS width greater than 190ms outside the influence of hyperkalemia or other QRS widening abnormality.


See these other related cases:

A patient with cardiac arrest, ROSC, and right bundle branch block (RBBB).




Is this just right bundle branch block?







===================================
MY Comment by KEN GRAUER, MD (1/26/2020):
===================================
Dr. Smith’s ECG Blog has presented too-numerous-to-count cases of hyperkalemia (See My Comment in the 12/11/2018 post — there are many others!). Clearly, recognition of Hyperkalemia is among the most important challenges faced by emergency providers because: i) this electrolyte disorder is potentially life-threatening; ii) there is an empiric treatment (ie, calcium) that can be life-saving, and which should often be given prior to lab confirmation of hyperkalemia, because cautious administration is safe — and not-to-promptly treat the patient risks losing the patient; andiii) Not-to-recognize hyperkalemia as the cause of QRS widening and/or ST-T wave abnormalities will lead you down the path of potentially serious mis-diagnosis.
  • BOTTOM Line: Emergency providers must be expert in recognizing hyperkalemia (and in recognizing those cases in which a presumptive diagnosis of hyperkalemia must be made until proven otherwise — knowing that in the meantime while waiting for lab confirmation, they should treat accordingly for presumed hyperkalemia).

It was not always this way! I trained in the mid-1970s. At that time, far fewer patients lived long enough with kidney failure to receive dialysis. End-stage renal failure (to the point of predisposing to frequent episodes of hyperkalemia) — was simply not a common disorder. So, in earlier days of my career — I saw much less hyperkalemia. 
  • Nowadays, any provider who frequents any of the many international ECG internet forums will see numerous cases of hyperkalemia posted daily. We need to always keep this diagnosis in the forefront of our differential diagnosis!

For clarity — I’ve added in Figure-1 the “textbook” sequence of ECG findings seen with progressive degrees of hyperkalemia. While fully acknowledging that not all patients read the textbook” — I have found awareness of the ECG generalizations in Figure-1 to be extremely helpful.
  • PEARL #1  Even if in an individual patient — these “general rules” are not strictly followed (ie, if QRS widening in your patient is seen before the serum K+ level = 8 mEq/L) — in any given patient, the sequence for development of the ECG findings suggested in Figure-1 tends to be surprisingly accurate (in my experience) over the patient’s early hospital course.

Figure-1: The “textbook” sequence of ECG findings with hyperkalemia (See text).



PEARL #2  I love the image of the Eiffel Tower — and I have taught this visual aid for decades. Like the Eiffel Tower — the T wave with progressive degrees of hyperkalemia becomes tall, peaked (pointed) with a narrow base. While patients with repolarization variants or acute ischemia (including the DeWinter T wave pattern) often manifest peaked T waves — the T waves with ischemia or repolarization variants tend not to be as pointed as is seen with hyperkalemia — and, the base of those T waves tends not to be as narrow as occurs with hyperkalemia.
  • Take a Look at Figure-2 — in which for clarity, I have reproduced the first 3 tracings shown in this case. Don’t YOU See the Eiffel Tower effect for the T waves in ECG #1 — and especially for the T waves in ECG #3?

Figure-2: The first 3 ECGs in this case (See text).



PEARL #3  In my experience, “All bets are OFF regarding QRS morphology” in the presence of significant hyperkalemia. For example, in ECG #1 — Despite the markedly leftward axis — this is not the typical picture of LAHB because: i) the inferior r waves are so tiny; andii) there are virtually no positive forces in lateral chest leads (ie, there is no more than a tiny r wave in leads V4-thru-V6). As a result — I immediately suspected something else was going on!
  • Also — Although there is a tall R wave in lead V1 of ECG #3 — there should be NO way this picture is confused with RBBB becausei) this QRS in lead V1 is both amorphous and very wide (nearly 0.20 second); ii) the QRS complex in ECG #3 is already all negative by lead V3, and stays virtually all negative through to lead V6 (and you virtually never see this with RBBB); andiii) the Eiffel Tower effect is especially obvious in ECG #3 — so we should KNOW that “All Bets are OFF” regarding QRS morphology with an ECG like this, in which the reason for QRS widening is almost certain to be hyperkalemia.

PEARL #4  In my opinion, it is not worth wasting time trying to figure out the specific rhythm diagnosis of a bradycardia when there is hyperkalemia. I used to spend hours trying to do this — but after years of doing so, I finally realized: i) That a specific rhythm diagnosis is rarely possible when there is significant hyperkalemia — and, even if you succeed in making a diagnosis such as Wenckebach — chances are as serum K+ intra/extracellular fluxes change, that the cardiac rhythm will also soon change; andii) Clinically — it does not matter what the specific rhythm diagnosis is once you recognize hyperkalemia that needs to be immediately treated — because usually within minutes after giving IV calcium, the “bad” rhythm will probably “go away” (often with surprisingly rapid reestablishment of sinus rhythm).

PEARL #5  Reasons why assessment of the rhythm with significant hyperkalemia is so difficult are: i) As serum K+ goes up, P wave amplitude decreases, and eventually P waves disappear (See Panels D and E in Figure-1); andii) As serum K+ goes up — the QRS widens.
  • Think for a moment what the ECG is going to look like IF you can’t clearly see P waves (or can’t see P waves at all) — and, the QRS is wide? ANSWER: The ECG will look like there is a ventricular escape rhythmor like the rhythm is VT if the heart rate is faster.
  • Ultimately, patients with progressively worsening degrees of hyperkalemia may die — and, VT/VFib is one of the likely mechanisms of death. (See THIS CASE  in which we never knew for certain IF the wide QRS was the result of hyperkalemia alone, or of hyperkalemic-induced VT — though this did not matter clinically, since in either case the immediate treatment of choice would be IV calcium that this patient was given).

PEARL #6  As noted above, with progressive hyperkalemia — P wave amplitude decreases until ultimately P waves disappear. Interestingly, the sinus node is often still able to transmit the electrical impulse to the ventricles, even though no P wave may be seen on ECG. This is known as a sinoventricular rhythm.
  • Take Another Look at the rhythm in ECG #1. It is extremely difficult to know IF there are (or are not) P waves in this tracing (ie, some small amplitude deflections that might be P waves seem to be present in the long lead V1 rhythm strip in front of beats #2 and 4, and perhaps elsewhere — or perhaps not ...). In addition — Note slight-but-real irregularity of the R-R interval in this tracing (ie, the initial R-R interval is 7.0 large boxes, but then decreases and remains slightly irregular). Rather than AFib — I suspect we are seeing a sinoventricular rhythm in ECG #1 — with some sinus arrhythmia.

PEARL #7  We can use CALIPERS to assist with rhythm interpretation. I used them to verify the slight-but-real irregularity present for the rhythm in ECG #1. This is relevant — because this underlying irregular sinoventricular rhythm intermittently slows enough to allow a slightly accelerated ventricular escape rhythm at a slightly faster rate to take over.
  • Note that beginning with beat #5 in ECG #3 — the QRS complex widens markedly! This does not reflect sudden development of RBBB (as we discussed in PEARL #3). Further support that beat #5 instead marks the beginning of a ventricular escape rhythm — is forthcoming from measurement of R-R intervals in the long lead V1 rhythm strip. Calipers make such measurement fastEASY and accurate. Note that the R-R interval for the sinoventricular rhythm ( = beats #2, 3 and 4 in ECG #3) is longer (ie, 6.6-to-6.8 large boxes) — than the R-R interval for the slightly accelerated ventricular escape focus (which measures 6.3 large boxes for the first 2 beats). Thus, there isreason why the ventricular escape focus takes over the rhythm — which is, that the ventricular escape focus is slightly faster than the underlying sinoventricular rhythm.
  • Beyond-the-Core — Did YOU Notice what happens before beat #2 in the long lead V1 rhythm strip of ECG #3? Unfortunately, the beginning of this rhythm strip was cut off — but we DO see a very wide and deep T wave (just above the #1) that tells us that beat #1 was from the ventricular escape focus! The reason the sinoventricular rhythm was able to prevail for beats #2, 3 and 4 — is that the R-R interval prior to beat #2 is shorter than the R-R interval of the ventricular escape focus. This confirms that change to a much wider QRS in the rhythm strip of ECG #3 is rate-related — with the ventricular escape focus taking over when the sinoventricular rate drops below the slightly accelerated ventricular focus.

PEARL #8  It is impossible to know how much the hyperkalemia is influencing QRS width and ST-T wave morphology until you normalize serum K+ and then REPEAT the ECG! Appreciation of this PEARL #8 is important for assessing ischemia — because hyperkalemia may either mimic or mask ischemic ECG changes!
  • In the case at hand — it turned out that the unusual QRS morphology in ECG #1 was in fact indicative of LAHB, despite how tiny the initial r waves in each of the inferior leads were. We know this because the baseline ECG ( = ECG #2) showed a nearly identical QRS morphology in the inferior leads (albeit the QRS was narrower in this baseline tracing).
  • That said — QRS morphology in virtually all chest leads is significantly different in the baseline tracing ( = ECG #2) — compared to the initial ED tracing ( = ECG #1). Note how the peaked, hyperkalemic T waves in ECG #1 masked the shallow, ischemic T wave inversion in the baseline tracing. Hyperkalemia shows the net effect of what underlying ST-T waves looked like + T wave peaking with narrow base from increased serum K+. Only after correcting hyperkalemia — will you be able to determine whether ischemic ST-T wave changes exist.

Our THANKS to Dr. Meyers for presenting this truly interesting case!


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