Thursday, September 12, 2019

Chest pain, pelvic and abdominal pain, hypotension, and severe ischemia on the ECG

An elderly male was lethargic at the nursing home and complained of some pelvic pain, but then also chest pain and abdominal pain.  He was hypotensive.  His medications include beta blockers.

BP on arrival was 66/31, pulse 80, saturations 90% room air.  The patient was lethargic and shocky.

An ECG was recorded:
There is severe diffuse ST depression of subendocardial ischemia, with the obligatory reciprocal ST Elevation in aVR.
One might also think there are hyperacute T-waves in inferior leads, with reciprocal STD and T inversion in aVL.  

A bedside echo showed good LV function, no pericardial effusion, and normal right ventricle.  There were no B lines and the inferior vena cava looked somewhat flat.

Is this Acute Coronary Syndrome?  What do you think?
















The cath lab had been activated by the time I walked into the critical care area and saw this.

However, I was skeptical that this was ACS.  Not all severe ischemia is due to ACS.  Shock/Hypotension can be the cause of ischemia or the result of ischemia.

How do we differentiate?

If ACS is the cause, then shock/hypotension is cardiogenic shock.  Cardiogenic shock has 3 etiologies:
1. pump failure
2. dysrhythmia (too fast or too slow)
3. valve dysfunction

The rhythm is sinus.  The bedside echo showed good pump function.  There was no evidence of valve dysfunction on our bedside echo.

Because of the above considerations, I thought ACS was very unlikely.  I suspected some other catastrophe as an etiology of hypotension which then caused a decrease in coronary flow and consequent ischemia.

The patient responded to fluids, but also developed pulmonary edema.  Although ACS with valve dysfunction must be considered, this was not the etiology.   (Among the investigations was an aortic CT which was negative.)

Without going into detail, sepsis was discovered as the etiology of hypotension, which in turn resulted in ischemia.  Beta blockers prevented any compensating tachycardia.

In spite of adequate BP, his ECG did not improve by the next AM, but peak troponin I was only 0.200 ng/mL, confirming that acute ACS was not the initiating factor.

Learning Points:

1. When the ECG shows ischemia, it does NOT show the initiating event of the ischemia.
2. If there is good LV function and no dysrhythmia, and no valve dysfunction, then shock is not cardiogenic, and ACS cannot be blamed as the instigating factor.
3.  Thus, you need to look elsewhere for the many etiologies of shock.  Do not fixate on ACS just because there is severe ischemia.
4. ST Elevation in aVR does NOT mean left main occlusion.  Usually it does not even represent ACS.(1)

(1) Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.

How does acute left main occlusion present on the ECG?



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Comment by KEN GRAUER, MD (9/12/2019):
===================================
Interesting case! — with the important clinical point “brought home” that not all ischemia on ECG is due to ACS. It is worth memorizing Dr. Smith’s deductive reasoning for why the cause of this elderly man’s marked hypotension — was unlikely to be ACS.
  • Apparently the cath lab was initially activated — but we are not told if cardiac catheterization was done … or if the order for cath activation was cancelled. While not needed for effective management of this patient (whose hypotension was found to result from septicemia) — I’d be curious to know what cath would have shown … (See below).

MTHOUGHTS on this ECG: I found the ECG in this case especially interesting — since in my opinion a few of the findings did not “fit”. None of these alter the astute decision-making deductions by Dr. Smith — but in the interest of ECG discussion, I feel the following points worthy of mention:
  • There is generalized low voltage. That is, QRS amplitude in none of the limb leads exceeds 5mm — and relative QRS amplitude is small in all 6 chest leads. This is a nonspecific finding — which in this case appears not to be due to pericardial or pulmonary effusion, nor to acute infarction. No mention is made of the patient’s body habitus (obesity is a common cause of low voltage) — and, we know nothing about whether the patient has hypothyroidism or emphysema. Perhaps voltage increased after treatment of septicemia, and after an increase in this patient’s blood pressure … ? (MY POINT is to recognize low voltage — and to at least contemplate potential causes.)
  • There could be lead misplacement in the chest leads — since lead V2 looks “out of place”. Wouldn’t the sequence of both R wave and ST-T wave progression look more natural IF lead V2 was lead V3; and lead V3 was lead V2? (Repeat ECG after verifying electrode lead placement might help explain some of the questions I raise below.)
For all of the reasons mentioned by Dr. Smith (especially good pump function with lack of wall motion abnormality on Echo — no evidence of valvular dysfunction — no more than minimally elevated peak troponin) — this ECG should be interpreted not as ACS — but rather as consistent with subendocardial ischemia. However — the typical ECG presentation of diffuse subendocardial ischemia should show significant ST depression (sometimes with T wave inversion) in virtually all leads, with the exception of leads aVR (and sometimes lead V1) that show ST elevation. The ECG in this case does not quite fit with this picture:
  • As already noted — there is no more than modest ST depression in lead V3 (Lead V3 looks “out of place”…).
  • The waves in each of the inferior leads look hyperacute! This is most marked in leads III and aVF — in which compared to the QRS complex in these leads, T waves are HUGE, being disproportionately “fat” at their peak and wide at their base. In addition, the ST segment in lead aVF is flat before the onset of the T wave — and, the ST segment “takeoff” in lead III looks like it is about to be elevated.

WHY Might This Be? To answer this question — I’d love to see this patient’s baseline ECG — and if cath was done, I’d love to learn the results ...
  • I initially considered that the ST-T wave appearance in the inferior leads (with the mirror-image opposite ST-T wave picture of lead III being seen in lead aVL) — was the harbinger of acute coronary occlusion. But, as per Dr. Smith — results of bedside Echo, troponin and serial ECGs (which apparently did not evolve) — along with clinical confirmation of acute septicemia as the etiology for this patient’s hypotension all negated a theory of acute infarction.
  • My GUESS — is that this elderly patient may have had underlying multi-vessel coronary disease — in which hyperacute inferior lead changes might reflect a “cancelling out effect” with what otherwise might have been frank inferior lead ST depression. Could there have been spontaneous reperfusion ...?



Sunday, September 8, 2019

Do you recognize this ECG yet?

Case contributed by Dr. David Gordon

See if you can recognize this ECG without the clinical context:

















Sinus tachycardia
Wide QRS
Terminal R-wave in aVR, V1, and V2 with STE and coved downsloping ST segments
Slightly peaked T-waves, most evident in V5-6

Together, these features make this ECG consistent only with hyperkalemia or another toxic/metabolic abnormality such as Na channel blockade. Sometimes a patient with profound metabolic acidosis may have this pattern as well, generally in the context of profound metabolic intoxication, usually critically ill, with down time, peri-arrest, post-ROSC, etc. V1-V2 morphology would be consistent with Brudaga pattern, but this should generally be more isolated to V1-V3 and would not generally have findings in all leads as we see here.

The differential of the ECG is short, and the most common, most rapidly deadly, and most treatable etiology is hyperkalemia.


Now for some context:

The patient was a male in his 30s with type 1 diabetes presenting with chest pain and RUQ abdominal pain. His fingerstick read "Hi" and he stated he couldn't remember if he took his insulin the night before. Vitals were within normal limits with tachycardia.

The team recognized the ECG as possibly due to hyperkalemia, especially in the clinical context. Labs were not yet back.

They gave 2 gm calcium gluconate, then recorded this ECG:



The QRS is more narrow, however the peaked T-waves and Brugada morphology in V1-V2 persist.

The team administered another 2 gm calcium gluconate.

The initial K returned at 7.3 mEq/L.

After 4 gm calcium gluconate was adminstered, this repeat ECG was obtained:




Resolution of the peaked T-waves, as well as the STE and Brugada pattern in V1-V2.

Three serial troponins were negative. Hyperkalemia and DKA were effectively treated, and the patient did well.



Learning Points:

Hyperkalemia can mimic almost anything on the ECG, including Occlusion MI, Brugada, etc. However, this pattern of STE in V1-V2 is an especially common and notable variant which we have reported many times on this blog:

You MUST recognize this pattern, even if it is not common







Calcium in hyperkalemia should be titrated to ECG normalization, and no there is no upper limit when the patient is critically ill or when the ECG shows severe effects of hyperkalemia.

See this article for more information on hyperkalemia


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Comment by KEN GRAUER, MD (9/9/2019):
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Our THANKS to Dr. David Gordon — for his contribution of this case! The title of this blog post = “Do You Recognize this ECG Yet?”, is indeed an appropriate one — since recognition of the pattern shown here is clinically essential for emergency providers.
  • That said — I’ll offer a different perspective on how one might describe the ECG findings in this case, along with differential diagnostic possibilities that this type of ECG pattern should prompt.
  • For clarity — I’ve lightened the 3 tracings in this case, and show them together in Figure-1.
Figure-1: The 3 sequential ECGs shown in this case (See text).



MTHOUGHTS: Dr. Ed Burns of Life-In-The-Fast-Lane has an excellent review on the ECG features of Sodium-Channel Blockade (CLICK HERE). These ECG features include:
  • Sinus tachycardia.
  • QRS prolongation to ≥0.10 second. (I would add that it is especially the terminal portion of the QRS complex that is prolonged with sodium channel blockade.)
  • RAD (Right Axis Deviation).
  • Addition of a significant terminal R wave component to the QRS complex in lead aVR (that is usually ≥3 mm in amplitude).

NOTE: The initial ECG in this case ( = ECG #1) illustrates each of these features of Sodium-Channel Blockade:
  • Sinus tachycardia (seen in ECG #1 at a rate of ~130/minute).
  • The QRS complex is clearly prolonged. Most of this QRS widening is a result of widening of the last part of the QRS complex.
  • The frontal plane axis is rightward — as demonstrated by predominant negative component to the QRS complex in lead I.
  • There is a tall, terminal R wave component in lead aVR.
THEREFORE: As per Drs. Gordon and Meyers — ECG #1 is completely consistent with any toxicity producing Sodium-Channel Blockade (ie, tricyclic antidepressant overdose; proarrhythmia from antiarrhythmics such as flecainide or procainamide — or other agents, as listed by Dr. Burns at the above LITFL link).

Beyond-the-Core: Returning for a moment to ECG #1 — I was not at all certain in my initial assessment of this tracing that there were P waves deforming the terminal portion of the T wave in the inferior leads (BLUE arrows in ECG #1). These deflections were not distinct, and they were not seen everywhere (PURPLE arrow) — so, given QRS widening in ECG #1 without indisputable sign of atrial activity — VT was among my diagnostic considerations for ECG #1.
  • That said — other features strongly supported the empiric treatment approach taken — andwithout much slowing of the rate at all, clear evidence of sinus P waves emerged in the next 2 tracings ( = ECGs #2 and #3) following treatment with Calcium Gluconate (as shown by RED arrows in ECGs #2 and 3).
As per the title of this blog post by Drs. Gordon and Meyers ("Do You Recognize this ECG Yet?" ) — we need to consider (anddepending on the History — we need to assume!) HyperKalemia as the cause of the findings in ECG #1 until we prove otherwise because:
  • The QRS complex is wide — and this widened QRS does not manifest a typical bundle branch block morphology.
  • Atrial activity was not clearly seen in ECG #1.
  • There is T wave peaking in some of the leads!
PEARL #1: By the time hyperkalemia has significantly widened QRS complexes — there will not always be diffuse, “Eiffel-tower-like” T wave peaking. Instead, you might only see slightly-more-pointed-than-expected T wave peaks in no more than a handful of leads (as suggested by the pointed T wave peaks in leads I, V4, V5 and V6 of ECG #1).
  • PEARL #2: As per Drs. Gordon and Meyers — Sometimes with severe hyperkalemia, more than 1 dose of Calcium Gluconate may need to be given!

QUESTION: How do you know when you need to repeat Calcium Gluconate?


ANSWER: You don’t always know! That said:
  • If the cause is severe hyperkalemia — the patient may die without more Calcium. So if you suspect this diagnosis — then repeat the Calcium.
  • The HISTORY often provides an essential clue. (The patient in this case presented with DKA, without any hint in the history of drug overdose or toxicity — and severe acidosis may result in marked increase in extracellular K+.)
  • And — after giving the 1st dose of Calcium Gluconate in this case — the next ECG done shortly thereafter (ECG #2clearly shows improvement, in the form of: iLess RAD (the S wave in lead I of ECG #2 is not as negative as it was in ECG #1); andiiThe QRS is less wide (most noticeable in seeing that the S waves in leads I, V4, V5 and V6 of ECG #2 are not as wide as they were in ECG #1).

MPERSPECTIVE: There is a Brugada-ECG pattern in ECG #1, which if anything — is even more pronounced in leads V1 and V2 of ECG #2.
  • In my opinion — the ECG appearance of ECG #1 is not hyperkalemia that “looks like a Brugada pattern” — but rather a manifestation of Brugada Phenocopy — in which a Brugada-1 ECG pattern is seen as a result of some other factor. I discuss this distinction in detail in My Comment to the January 30, 2019 Dr. Smith post — and, beginning at 9:17 in my ECG Video on Brugada Syndrome.
  • If you want more on Brugada — Check out Josep Brugada’s 2018 State-of-the-Art Review on Brugada Syndrome.
  • For another very similar ECG case + related discussion — Please see My Comment on the 8/20/2019 ECG Guru (Scroll to the TOP of that page for the initial ECG).

NOTE: I fully acknowledge that you might call it “semantics” as to whether ECG manifestations that we see in ECG #1 reflect hyperkalemia vs Brugada Phenocopy caused by hyperkalemia — because in either case, these ECG manifestations resolve once hyperkalemia is treated (Note resolution of QRS widening, RAD, T wave peaking, and Brugada-1 ECG changes in ECG #3!). That said — I feel it important that:
  • Clinicians appreciate that there is an entity known as Brugada Phenocopy — in which a Brugada-1 ECG pattern identical to that seen in true Brugada Syndrome may be seen as a result of some other cause.
  • That among the LIST of potential other causes” of a Brugada-1 ECG pattern are certain DRUGS (calcium channel blockers; ß-blockers; antianginals; psychotropics; ETOH; cocaine; others …) — acute febrile illness — variations in autonomic tone — hypothermia — electrolyte imbalance (hyperkalemia; hypokalemia) — ischemia/infarction — bradycardia — post-cardioversion/defibrillation. There may be others ...
  • That the entities I just listed should be considered in your differential diagnosis whenever you see a Brugada-1 ECG pattern.
  • The GOOD NEWS — is that if instead of true Brugada “Syndrome”, the reason for the Brugada-1 ECG pattern in your patient turns out to be Brugada Phenocopy precipitated by one or more of the above causes — and, that IF you find and “fix” the precipitating cause (as was done in this case of hyperkalemia due to DKA) — then longterm prognosis of the patient may not be adversely affected (and an ICD may not be needed, as it would be if true Brugada Syndrome was present)!



Monday, September 2, 2019

What is the differential of this very unusual ECG?


Take a look at this ECG first without clinical context:
What do you think?








There is sinus bradycardia with very unusual shortened QT interval (approximately 400 ms), for a QTc (Bazett) 358 ms. The T-waves have high amplitude and narrow bases, reminiscent of hyperkalemia, maybe also with hypercalcemia. The T-waves are not bulky or fat, and are therefore not hyperacute regardless of their amplitude.

Short QTc is rare, but has been described as less than 360 ms for males and less than 370 ms for females. Furthermore, less than 330 ms (males) or less than 340 ms (females) can be termed "very short QTc" and, in the absence of reversible causes, is considered by some to be diagnostic of Short QT Syndrome (SQTS) in an appropriate setting.



Now for the clinical context:

This was a young man with a gunshot wound to the head, who arrived comatose and critically ill. CT scan showed severe brain injury and cerebral edema.

As we have shown on this blog, intracranial hemorrhage can cause various ECG findings, sometimes imitating ischemia, often with bizarre long QT syndromes reminiscent of takotsubo / stress cardiomyopathy. However this is the first time I have seen dramatically shortened QT in this setting. There was no prior for comparison, but this finding would be extremely unlikely to be present on baseline, in the absence of congenital short QT syndrome.

The potassium and calcium levels were within normal limits.



Learning Points:
This ECG in another clinical context should make you consider hyperkalemia and/or hypercalcemia, but would not be consistent with hyperacute T-waves.

ICH / Brain injury can manifest in many bizarre ways on the ECG, usually with long QT with bizarre morphology, but many other findings may be possible. These ECG findings typically correlate with worse outcomes, however most practitioners would say that ECG findings rarely, if ever, add prognostic information beyond standard clinical evaluation in this setting.


Reference:

Viskin S. The QT interval: too long, too short or just right. Heart Rhythm 2009 May;6(5):711-5.


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Comment by KEN GRAUER, MD (9/2/2019):
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Great case by Dr. Meyers about an important ECG entity that is not commonly seen. As I suspect many of those reading this column did — I initially put hyperkalemia at the top of my differential diagnosis list.
  • That said — these T waves would be among the tallest and “skinniest” I’ve ever seen, if the etiology of this T wave appearance turned out to be hyperkalemia ...
Dr. Meyers highlights that an equally impressive finding as T wave appearance in this tracing is the shortened QTc interval. And, there’s another finding ...
  • For clarity — I’ve numbered the beats in the long lead V1 rhythm in Figure-1.

QUESTION #1: What is the rhythm in Figure-1?

Figure-1: The ECG shown in this case. What is the rhythm?


ANSWER: The QRS complex is narrow. Although easy to overlook if not carefully measured — the R-R interval in the long lead V1 rhythm strip is not regular. Figure-2 shows the variation in R-R intervals (BLUE numbers indicating R-R interval duration in milliseconds).
  • Upright P waves with a fixed PR interval precede beats #3,4,5 and 6 (RED arrows in the long lead V1 rhythm strip). Presumably, these are sinus P waves — albeit the P wave is extremely small in amplitude, and the PR interval looks to be relatively short.
  • We only see 1 QRS complex for lead II. This is beat #1 — which is not preceded by any P wave at all.
  • I believe the small-amplitude negative “dip” preceding beat #2 in the long lead V1 is artifact. I don’t believe any P wave precedes beat #2.
  • Beat #7 is cut off — and, the RED question mark, followed by a drop in the PR interval indicates there is artifact. I don’t believe any conclusion can be made about atrial activity for beat #7.
  • BOTTOM LINE: The longest R-R interval in the long lead V1 is between beats #1 and 2 (Figure-2) — and neither of these 2 beats is preceded by any P wave. Therefore, beats #1 and 2 are junctional escape beats. The underlying rhythm in Figure-1 is marked sinus bradycardia with sinus arrhythmia — and when the sinus rate slows enough, junctional escape beats arise.
Figure-2: I’ve numbered and labeled key parts of Figure-1 (See text).


QUESTION #2: How short is the QTc?



ANSWER: The QTc is determined by taking the longest QT interval that you can confidently measure on the 12-lead ECG — and then correcting this QT interval for heart rate.
  • With heart rates over 60/minute (if using the Bazett formula) — the QTc will be more than the QT interval that you measure.
  • With slower heart rates (under 60/minute, if using the Bazett formula) — the QTc will be less than the QT interval that you measure.
Looking at the 12-lead tracing in Figure-2 — I thought the longest QT interval that I could clearly measure was in either lead V2 or V3. I measured 360 ms (thin vertical BLUE lines in V3 showing from where I measured). The R-R intervals both preceding and including this longest measured QT interval correspond to a heart rate of ~43/minute.
  • MD CALC is a handy link that provides near instant correction of the measured QT according to heart rate — allowing you to calculate the QTc by any of the 4 most commonly used corrective formulas ( = Bazett — Fridericia — Framingham — Hodges).
A measured QT interval of 360 ms = small boxes on ECG grid paper. Plugging in this number into MD CALC for a heart rate of 43/minute yields the following results for the QTc:
  • Bazett formula QTc = 305 ms.
  • Fridericia formula QTc = 322 ms.
  • Framingham formula QTc = 299 ms.
  • Hodges formula QTc = 330 ms.
Conclusions:
  • None of the formulas are perfect. Each has its advocates. There is some variation in QTc value determinations — but it’s clear in Figure-2 that the QTc is very short.
  • Because the heart rate is so slow — the QTc turns out to be significantly less than the longest measured QT interval (which was 360 ms).


QUESTION #3: What is the “Short QT Syndrome” ?



ANSWER: A nice review of Short QSyndrome (SQTSappears in Arrhythm Electrophysiol Rev (2014 — by Rudic et al) — CLICK HERE.
  • As emphasized in this article — SQTS is an inherited cardiac channelopathy determined by the presence of symptoms (syncope, cardiac arrest), positive family history, and the ECG finding of an abnormally short QTc interval.
  • SQTS is a relatively new diagnosis that has only been recognized as a distinct clinical entity since 2000. The disorder is rare — but its importance is as a potential cause of atrial and ventricular arrhythmias, including cardiac arrest. Treatment is by ICD (implantable cardioverter defibrillator).
  • Males with a QTc ≤330 ms — and females with a QTc ≤340 ms are defined as having SQTS, even if they are asymptomatic.
  • Males with a QTc ≤360 ms — and females with a QTc ≤370 ms are said to have a short” QTc. Such patients may have SQTS if, in addition to the "short" QTc there is a history of cardiac arrest, unexplained syncope or atrial fibrillation at an early age.


QUESTION #4: What are the ECG features of “Short QT Syndrome” ?



ANSWER: A series of gene mutations have been described in association with SQTS (See link to the Rudic article above). By definition — these gene mutations are all associated with a short QTc interval, as defined above in answer to Question #3.
  • Sometimes, the only ECG abnormality is an overly short QTc interval.
  • BUT — some patients with SQTS manifest specific ECG patterns. One of these patterns consists of T waves that are tall, peaked, symmetrical and narrow-based with a morphology that is completely consistent with the T waves in Figure-2 (especially the T waves in leads V2, V3 and V4).
  • U waves are often prominent with SQTS (This is best seen in lead V2 of Figure-2).
  • Sometimes the ST segment is absent (ie, the QRS complex may seem to immediately follow the T wave). This was not the case in Figure-2 — as a short ST segment is present here.
BOTTOM LINE: This tragic case of a young man critically ill with a gunshot wound to the head provides us with the fascinating ECG shown in Figure-1.
  • The principal findings of exceedingly tall, peaked and pointed T waves with narrow base an exceedingly short QTc were not explained by either hyperkalemia or hypercalcemia — as both electrolytes were within the normal range.
  • CNS catastrophes (as in the case of this comatose patient) — typically present with marked QTc prolongation — and morphologically, with broad T waves that fan out to a broad base. If anything — bradycardia should further prolong the QT. Other than this bradycardia, one would not expect the ECG findings seen here with coma from CNS trauma.
  • I learned from this case that the T wave morphology seen in Figure-1 is perfectly consistent with one of the ECG patterns of SQTS, in this patient with a markedly shortened QTc (See Figure-1 in the above referenced review by Rudic et al).
  • As per Dr. Meyers (and in the absence of a prior ECG for comparison) — we can strongly suspect that the ECG of this patient incidentally revealed a previously undetected congenital SQTS.
  • P.S.  It is easy to overlook a short QTc. Don't forget to look for this in patients with syncope, cardiac arrest and/or unexplained arrhythmias.


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