Monday, January 24, 2022

ECG Blog #278 — Most Likely Cause of this WCT?


The patient whose ECG is shown in Figure-1 — is a previously healthy 40-year old woman who presented to the ED (Emergency Department) with chest pain. BP = 170/85 mm Hg at the time this tracing was done.

QUESTIONS:
  • How would YOU interpret this ECG?
  • What treatment(s) would you consider?

Figure-1: This ECG is from a 40-year old woman with chest pain. What is the most likely cause of this WCT rhythm?


MY Approach to Today's Tracing:

The patient is symptomatic (ie, with chest pain) — albeit with a BP = 170/85 mm Hg. On seeing the ECG in Figure-1 — it's obvious that we are dealing with an extremely fast rhythm — so the initial priority is to determine whether or not immediate synchronized cardioversion is needed.

  • At this point — it matters less what the rhythm in Figure-1 is, since IF this patient is "hemodynamically unstable" — then regardless of whether the rhythm is VT (Ventricular Tachycardia) — or — an SVT (SupraVentricular Tachycardia) with either preexisting BBB (Bundle Branch Block) or aberrant conduction — the immediate treatment of choice is electricity (ie, synchronized cardioversion).
  • On the other hand — IF despite the tachycardia, the patient is stable and tolerating the arrhythmia — then by definition, we have at least a moment in time to better assess the rhythm and contemplate therapeutic options.
  • In today's case — a close "look" at the patient would be our 1st Priority — since we need to determine IF symptoms (ie, the patient's chest pain) in association with the fast heart rate on this ECG — are enough to mandate immediate cardioversion. (For more on determining Hemodynamic StabilitySee ECG Blog #220 — including the Audio Pearl in this post).


After ensuring that the patient is hemodynamically stable — I favor the systematic PsQs and 3Rs Approach for rhythm assessment (as discussed in detail in ECG Blog #185).

  • To emphasize — You do not have to go in sequence when applying the Ps, Qs, 3Rs approach. The point of this memory aid is simply to recall the 5 parameters that need to be assessed in whatever sequence seems best to you for the case at hand. 
  • In today's case — I looked first at QRS width. That the QRS is wide — is immediately evident from the appearance of the complexes in leads V1, V2 and V3.
  • The rhythm in Figure-1 is fast and Regular. As shown in the blow-up of leads I and II from today's tracing (Figure-2) — I estimate the Rate of the rhythm to be just under 250/minute

Figure-2: Application of the "Every-Other-Beat" Method for rapid estimation of heart rate in today's case. Looking at every-fifth-beat is easiest in this tracing — because I found a 5-beat period in the rhythm in which a part of the QRS at the beginning and at the end falls either on (or almost on) a heavy grid line (as per the 2 vertical RED lines in this Figure). The amount of time that it takes to record 5 beats (RED numbers in lead I) is just over 6 large boxes (BLUE numbers in this Figure). Therefore — ONE FIFTH the rate is a little less than 300/6 ~49/minute — which means that the actual rate for the rhythm in Figure-1 is ~49 X 5 or ~245/minute. (For more on the Every-Other-Beat Method — See ECG Blog #210).



Continuing with the last 2 parameters in the Ps, Qs, 3Rs Approach:
  • No P waves are seen in Figure-1. This of course means that there is no Relation between P waves and the QRS.

Putting It All Together:
The rhythm in Figure-1 is a regular WCT ( = Wide-Complex Tachycardia) at a rate just under 250/minute, without clear sign of atrial activity. For practical purposes — the Differential Diagnosis is either: i) VT (Ventricular Tachycardia); or, ii) SVT with either preexisting BBB or aberrant conduction

  • Statistically — the odds that a regular WCT rhythm without clear sign of atrial activity will turn out to be VT are at least 80%. As a result — we need to prove that a rhythm is not VT, rather than the other way around.
  • Assessment of QRS morphology can help to increase or decrease the statistical likelihood of our diagnosis. As discussed in ECG Blog #211 — the finding of QRS morphology typical for RBBB conduction favors a supraventricular etiology. This entails: i) An rSR' complex in lead V1, in which the S wave descends below the baseline — and in which there is a thin and taller "right rabbit ear" (ie, the R' is taller than the initial r wave); and, ii) The finding of wide, terminal S waves in lateral leads I and V6.
  • Completely typical QRS morphology for other forms of known conduction defects (ie, LAHB, LPHB, LBBB) will also favor a supraventricular etiology (See ECG Blog #203 and Blog #204 — for review of expected morphology for the hemiblocks and BBBs).
  • No set of morphologic criteria is perfect for distinguishing between VT vs SVT with preexisting BBB or aberrant conduction. There are always exceptions (ie, patients with severe underlying heart disease who have extremely unusual QRS morphology on their baseline tracing when in sinus rhythm). Nevertheless, as a general rule — QRS morphology consistent with a typical appearance of some known form of conduction defect favors a supraventricular etiology. In contrast — an "uglier" QRS morphology that does not resemble any known form of conduction defect will favor VT. 
  • Finding a baseline ECG on the patient can help — by showing you what QRS morphology normally looks like in sinus rhythm. IF this QRS morphology during sinus rhythm is identical in virtually all leads to the QRS morphology during the WCT rhythm — this strongly supports a supraventricular etiology.
  • To emphasize — Whereas a completely typical QRS morphology for a known form of conduction defect supports a supraventricular etiology — the opposite is not necessarily true. This is because QRS morphology will sometimes be atypical with BBB or aberrant conduction. Attention to other features will then be needed.
  • Among the most helpful features in my experience for predicting VT — is the presence of extreme axis deviation. By this I mean that the QRS is entirely negative in either lead I or in lead aVF. However, if there is any positivity (ie, such as the small-but-definitely-present initial r wave in lead I of Figure-1) — then this criterion does not apply (See ECG Blog #220 for additional criteria to distinguish between VT vs SVT).
  • Finally — IF at all in doubt about the etiology of a regular WCT rhythm without atrial activity — Assume VT. RememberWe need to prove that a rhythm is not VT, rather than the other way around.

 

What about QRS Morphology in Figure-1?

Remember — Since the rhythm in Figure-1 is a regular WCT without clear sign of atrial activity — statistical odds that this rhythm is VT are ~80% even before we begin to look at QRS morphology.

  • In Figure-1 — QRS morphology superficially resembles RBBB with a hemiblock. That said — there are several atypical morphologic features that I believe strongly favor the diagnosis of Fascicular VT.
  • Although the QRS is all upright in lead V1, and manifests wide terminal S waves in lateral leads I and V6 — the QRS in lead V1 is unformed, in that it lacks a clear triphasic (rSR') pattern with an S wave that descends below the baseline — and it lacks a clean, tall and thin terminal "right rabbit ear".
  • Although the deep descent of the S wave in lead I is typical for LPHB — the QRS should be predominantly positive in both leads II and III with this conduction defect (and not predominantly negative in lead II as seen in Figure-1).
  • Although the predominantly negative QRS in lead II of Figure-1 is typical for LAHB — a similar predominantly negative QRS should also be seen in lead III with this conduction defect. In addition — the QRS should be predominantly positive in lead I when there is LAHB.
  • BOTTOM LINE: QRS morphology in Figure-1 is distinctly atypical for any known form of conduction defect. This increases the odds from ~80%, to over 90% that this rhythm is VT.


Do Previously Healthy Young Adults get VT?

Approximately 10% of patients who present with VT do not have ischemic or underlying structural heart disease. The importance of recognizing these patients with Idiopathic VT who have a structurally normal heart — is that the presentation, clinical course, and both short- and long-term management differ greatly compared to the ~90% of patients with the "usual" ischemic or structural forms of VT (See Figure-3 below in the Addendum for a Summary on the Idiopathic VTs).

  • The "good news" regarding patients who present with idiopathic VT — is that long-term prognosis of these patients tends to be surprisingly good (and much better than the usual prognosis of patients who present with frequent runs of ischemic VT).
  • The fact that the patient in today's case was a previously healthy 40-year old woman is consistent with the most common patient profile of idiopathic VT — in that younger adults without prior heart disease are most often affected.
  • In today's case — it is the partial resemblance to RBBB with hemiblock in this previously healthy 40-year old woman, that strongly suggested the diagnosis of Fascicular VT to me — so much so that I would have tried IV Verapamil as an initial therapy (See ECG Blog #197for more on the Idiopathic VTs).


P.S. (Beyond the Core) — There is a final possibility for the etiology of the rhythm in Figure-1. In addition to VT or SVT with either preexisting BBB or aberrant conduction — the etiology of this regular WCT rhythm could be the reentry SVT rhythm known as AVRT (AtrioVentricular Reciprocating Tachycardia) — in which an AP (Accessory Pathway) participates in the reentry circuit.

  • Depending on the initial direction of the impulse during the reentry tachycardia — AVRT will either be orthodromic or antidromic (ie, going initially down the AV node — or going initially down the AP).
  • Over 95% of AVRT rhythms are orthodromic (ie, traveling first down the normal AV nodal pathway — and then back to the atria by retrograde conduction over the AP). As a result — over 95% of AVRT rhythms will manifest a narrow QRS complex.
  • In those rare (~5%) instances in which AVRT is antidromic — the QRS complex will be wide (because the impulse bypasses the AV node — and travels first down the AP). In such cases — the AVRT rhythm may be indistinguishable from VT. It may only be after conversion to sinus rhythm that "telltale" delta waves of WPW can be identified.
  • Since AVRT is a supraventricular rhythm that utilizes the AV node as part of its reentry circuit — both orthodromic and antidromic forms of AVRT may respond to Adenosine, Verapamil/Diltiazem and/or Beta-Blockers (See ECG Blog #18for more on the types of arrhythmias seen in patients with WPW).
  • Because antidromic AVRT is so uncommon — we often don't think of it when formulating our differential diagnosis of the regular WCT rhythm. That said — it's good to be aware that this uncommon rhythm is a possibility (as it may explain some of the instances in which Adenosine or other AV nodal blocking agents are successful in converting an occasional WCT rhythm).
  • Finally, in Figure-1 — the exceedingly rapid rate of this WCT rhythm (ie, ~245/minute) does raise the possibility that rather than Fascicular VT — the etiology of this rhythm could be antidromic AVRT in a patient with WPW. Unfortunately — I do not have follow-up for this case. That said, regardless of whether the etiology of this rhythm was VT or AVRT — the fact that this patient was symptomatic with this WCT rhythm at such a fast rate of itself is indication for EP referral.



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Acknowledgment: My appreciation to Rasha M. Khalid (from Babil, Iraqfor the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.

  • ECG Blog #210 — Reviews the Every-Other-Beat Method for estimation of fast heart rates — and discusses another case of a reguar WCT Rhythm.

  • ECG Blog #203 — Reviews the expected QRS morphology for the Hemiblocks and Bifascicular Blocks (ie, LAHB, LPHB; RBBB/LAHB; RBBB/LPHB).

  • ECG Blog #204 — Reviews the expected QRS morphology for the Bundle Branch Blocks (ie, RBBB, LBBB, IVCD).

  • ECG Blog #211 — Reviews why Aberrant Conduction occurs (with illustration of those QRS morphologic features that predict aberrant conduction).

  • ECG Blog #196 — Reviews another Case of a Regular WCT Rhythm.

  • ECG Blog #197 — What is Idiopathic VT?WHY do we care? Special attention to the 2 most common forms = RVOT VT and Fascicular VT.

  • ECG Blog #220 — Case Study that reviews criteria for Distinction beween VT vs SVT with preexisting BBB or aberrant conduction (including Audio Pearl MP-37 Is the Patient Hemodynamically Stable?).

  • ECG Blog #38 and Blog #85 — Review of Fascicular VT.

  • ECG Blog #35 — Review of RVOT VT.
  • ECG Blog #42 — Comprehensive review of criteria for distinguishing VT vs Aberration.


 

==============================

ADDENDUM (1/24/2022):

I summarize KEY features regarding Idiopathic VT in Figure-3.


Figure-3: Review of KEY features regarding Idiopathic VT (See text).



Thursday, January 20, 2022

ECG Blog #277 — WHY those T Waves?


The ECG in Figure-1 was obtained from an older man with abdominal pain. He was alert, but hypotensive at the time this tracing was done. No chest pain.

 

QUESTIONS:

  • How would YOU interpret this tracing?
  • What about those T Waves?

 

HINT:

 

Figure-1: This ECG was obtained from an older adult with abdominal pain. How would YOU interpret this tracing?


 

MY Sequential Thoughts on the ECG in Figure-1:

Although artifact and curvature of this tracing make assessment more challenging — I believe that accurate interpretation still is possible.

  • The rhythm is sinus tachycardia at a rate of ~110/minute. Regarding intervals — the PR interval is normal and the QRS complex is narrow. Assessment of the QT interval is clearly more difficult with tachycardia. That said — despite the fast heart rate, the QTc appears to be markedly prolonged!
  • The frontal plane axis is normal (about +80-85 degrees). No chamber enlargement.

 

Regarding Q-R-S-T Changes:

  • Q Waves — Small but-definitely-present q waves are seen in each of the inferior leads (II,III,aVF). There is loss of r wave between lead V2-to-V3 — with development of a narrow but deep Q wave in lead V3, with persistence of small q waves through to lead V6.
  • R Wave Progression — Transition is normal (ie, the R wave becomes taller than the S wave is deep between leads V2-to-V3).

 

Regarding ST-T Wave Changes:

  • The most remarkable finding on this tracing is the deep, symmetric T wave inversion that is seen in no less than 9/12 leads in Figure-1 (ie, leads I, II,III,aVF; V2-V6). The depth of the T-wave inversion in lead V3 attains nearly 15 mm, which is huge! T wave depth measures 10 mm in lead V4 — and 9 mm in lead V2.
  • Additional important findings include 1 mm of ST elevation in each of the inferior leads, with suggestion of slight reciprocal ST depression in lead aVL — and — meaningful ST elevation in each of the chest leads showing T wave inversion.

 

COMMENT: The most remarkable finding in today's case is the presence of Giant T-Waves. As was discussed in detail in ECG Blog #276 — the designation of "Giant" T waves is reserved for a limited number of clinical entities that are likely to produce truly deep (>5-10 mm amplitude) T wave inversion.

  • PEARL #1: The clinical importance of recognizing the presence of Giant T Waves in today's tracing — is that this should immediately suggest the diagnostic considerations listed in Figure-2.
  • Despite the fact that the patient in today's case did not have chest pain — the 2 entities among those listed in Figure-2 that seem most likely to account for the Giant T waves in today's tracing are: i) Acute MIand iiTakotsubo CMP (CardioMyoPathy).
  • Unfortunately — a definitive diagnosis was never obtained in this case, because the decision was made to treat this severely ill patient conservatively. Details of management are lacking. It is known however, that among the complications that developed — Hyperkalemia (ie, K+ = 6.4 mEq/L) was present near the time that the ECG in Figure-1 was obtained.

 

Figure-2: This graphic reviews the definition of Giant T-Wave Syndrome and — the Differential Diagnosis of this ECG finding (For more on Giant T Waves — See ECG Blog #276).

 

My thoughts on this case are the following:

 

ECG Findings in Favor of Acute MI:

The Q waves, ST elevation and T wave inversion in each of the 3 inferior leads in Figure-1 certainly suggests acute MI. Similarly — chest lead Q waves and diffuse ST elevation with deep T wave inversion could clearly be the result of a large infarction from acute LAD (Left Anterior Descending) coronary artery occlusion.

  • Acute LAD occlusion with a "wraparound" distribution to supply the inferior wall — could account for the presence of Q waves and ST-T wave changes in both inferior and antero-lateral leads in Figure-1.
  • The deep, diffuse T wave inversion could represent reperfusion T-waves occurring at a point in the process in which residual ST elevation was still present.

 


My HUNCH: Takotsubo Cardiomyopathy:

Realizing that I do not have access to definitive information in this case — I still think it interesting to speculate about what the final diagnosis might have been.

  • Although certainly possible that the ECG in Figure-1 could reflect the result of acute "wraparound" LAD occlusion, now in the stage showing deep reperfusion T waves — certain ECG findings go against this theory. These include: i) The markedly prolonged QTc interval in an alert patient; ii) The lack of chest pain in the history; andiii) The lack of localization of ECG findings (ie, deep T wave inversion is seen in no less than 9/12 leads).
  • Instead — I feel the ECG in Figure-1 and the clinical picture in today's case is more suggestive of Takotsubo Cardiomyopathy (See Figure-3which I've reproduced from ECG Blog #46). Findings in this case suggestive of Takotsubo CMP include: i) The markedly prolonged QTc interval; ii) The lack of chest pain in the history; iii) Sinus tachycardia (which is nonspecific, but common with Takotsubo CMP — related to increased sympathetic tone/catecholamine surge associated with this disorder)iv) A lack of reciprocal ST depression (because the area of myocardial dysfunction with typical Takotsubo CMP is mainly in the apex)andv) Diffuse ST elevation with deep T wave inversion without localization to a specific anatomic area (as would be expected with acute MI). Also relevant, is the fact that these ST-T wave changes are most marked in the chest leads of Figure-1 (as would be expected with Takotsubo CMP — because the area of myocardial dysfunction is mainly in the apex).
  • PEARL #2: Takotsubo CMP is easy to overlook — because there are no specific ECG findings to confirm the diagnosis. Instead, a variety of non-localized Q waves and ST-T wave changes may be seen (as suggested in Figure-3). Because these ECG abnormalities may be marked, there is a tendency to diagnose acute MI instead of Takotsubo.
  • Think of the possibility of Takotsubo CMP when confronted with a patient who presents with a markedly abnormal ECG that doesn't quite "fit" the clinical picture — as in today's case.

 

PEARL #3: As noted earlier — the patient in today's case developed renal failure, and was found to have a serum K+ = 6.4 mEq/L around the time that the ECG in Figure-1 was obtained.

  • While we expect to see tall, peaked T waves with hyperkalemia — negative T waves may sometimes be seen! The fact that many of the inverted T waves in the chest leads of Figure-1 are pointed at their deepest descent makes me wonder if hyperkalemia may have been contributing to this T wave appearance.


Figure-3: ECG Findings in Takotsubo Cardiomyopathy (For more on Takotsubo Cardiomyopathy — See ECG Blog #46).


 

==================================

Acknowledgment: My appreciation to Anil Kumar Kolli (from Indiafor the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  •  
  • ECG Blog #276 — Reviews the syndrome of Giant T-Waves (and the most common causes of this disorder).

  • ECG Blog #46 — Reviews ECG findings with Takotsubo Cardiomyopathy.



Sunday, January 16, 2022

ECG Blog #276 (81) — What About those T Waves?


You are given the ECG shown in Figure-1 — but without the benefit of any history. 

 

QUESTIONS:

  • How would YOU interpret this tracing?
  • What about those T Waves?

 

Figure-1: You are given this ECG without the benefit of any history. How would YOU interpret this tracing?


=======================================

NOTE: Some readers may prefer at this point to listen to the 9:50-minute ECG Video PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-81).

=======================================



Today's ECG Media PEARL #81 (9:50 minutes Video) — Summarizes my Systematic Approach to 12-lead ECG interpretation (during the first 2:50 minutes of this video) — after which I apply this Systematic Approach to the tracing shown below in Figure-2. I then work through the list of potential Causes of Giant T-Waves shown below in Figure-3.

 

Figure-2: Hard copy of the 12-lead ECG that is discussed in detail in the above ECG Video. The patient was a 50-year old man with chest pain. Which cause(s) of those listed in Figure-3 are most likely to account for the Giant T Waves in leads V4-V6?



Figure-3: Reviews KEY content of the above ECG Video — including the definition of Giant T-Wave Syndrome and, the Differential Diagnosis of this ECG finding.


  

MY Sequential Thoughts on the ECG in Figure-1:

For clarity — I've colored QRST complexes in leads V1, V2 and V3 of today's tracing (Figure-4). As always for interpretation — I favor use of a Systematic Approach (which I review in ECG Blog #205 — as well as during the first 2:50 minutes in today's ECG Video):

  • The rhythm is sinus bradycardia at a rate of ~45-50/minute. The PR, QRS and QTc intervals are all normal (ie, Given the slow heart rate — the QTc is at most no more than minimally prolonged). The frontal plane axis is normal (about +40 degrees).
  • Even though we don't know the age of this patient — QRS amplitudes are increased to such an extent that voltage criteria for LVH are likely to be satisfied regardless of the patient's age (See ECG Blog #245 regarding criteria I favor for ECG diagnosis of LVH).

 

Regarding Q-R-S-T Changes:

  • Q Waves — None.
  • R Wave Progression — Transition occurs early — as a sizeable R wave is already present in lead V1 — and — by lead V2, R wave amplitude equals S wave depth. There follows predominant R wave positivity beginning with lead V3.

 

Regarding ST-T Wave Changes:

  • The most remarkable finding on this tracing is the deep, symmetric T wave inversion that is seen in no less than 9/12 leads in Figure-4. The depth of the T-wave inversion in lead V3 attains nearly 15 mm, which is huge!
  • Additional less obvious findings include slight ST elevation (in leads III and V1) — and — 1-to-1.5 mm of J-point ST depression in virtually all leads that manifest T wave inversion.

 

Figure-4: I've colored QRST complexes in the anterior leads from Figure-1 — so as to highlight the zone of transition in the chest leads (RED, GREEN and BLUE complexes in leads V1, V2 and V3).

 

Clinical Impression: The ECG in Figure-4 shows fairly marked sinus bradycardia — LVH — and — 1-to-1.5 mm of J-point ST depression, followed by deep, symmetric T wave inversion in multiple leads that could be consistent wth LV "strain" and/or ischemia.

  • Clearly — some History is needed for clinical interpretation of this tracing (ie, Is this ECG from a young, relatively asymptomatic athletic adult? — or — from an older patient with recent or new-onset chest pain?). Without any history — we can merely suggest likely possibilities.
  • That said — the following 2 PEARLS can go a long way toward suggesting the most likely possibilities.

  

PEARL #1: More than simply "deep, symmetric T wave inversion" in Figure-4 — there are Giant T-Waves. As defined in today's ECG Video (and above in Figure-3) — the designation of "Giant" T waves is reserved for a limited number of clinical entities that are likely to produce truly deep (>5-10 mm amplitude) T wave inversion.

  • The definition of "Giant" T waves is satisfied for the tracing in Figure-4 by the nearly 15 mm of T wave inversion in lead V3. The T wave in lead V4 is at least 8 mm — and the T wave exceeds 5 mm in leads V2 and V5. 
  • Truly "giant" T waves are not overly common. The advantage of identifying this entity — is that doing so should immediately suggest the diagnostic considerations listed in Figure-3.
  • While impossible to determine WHICH of the entities in Figure-3 is (are) most likely — the lack of significant QTc prolongation would seem to make a severe CNS disorder and Takotsubo Cardiomyopathy less likely. The presence of marked voltage for LVH is in favor of Apical Cardiomyopathy. The 1-to-1.5 mm of J-point ST depression in multiple leads is in favor of ischemia.

  

PEARL #2 — It is tempting on seeing the biphasic T wave with steep downsloping terminal component in lead V2 of Figure-4 (drawn in GREEN) — to think of Wellens’ Syndrome. That said — Wellens’ Syndrome is unlikely to be present in this case

  • While acute coronary disease is a diagnostic possibility when there are Giant T waves (ie, acute ischemia is included among the entities listed in Figure-3) — it is well to remember that there are other causes of the ST-T wave picture seen in lead V2 of Figure-4. These include (among others) — LVH, cardiomyopathy, coronary reperfusion. 
  • In Figure-4 — I suspect the reason for the biphasic T wave in lead V2 (drawn in GREEN) — is simply a reflection of the increased QRS and ST-T wave amplitude that we see, with lead V2 representing a “transition lead” placed between the fairly tall positive T wave in lead V1 (drawn in RED) — and the very deep negative T wave in lead V3 (drawn in BLUE).
  • Remember that the diagnosis of Wellens' Syndrome is far less reliable in the presence of LVH — especially in the presence of ST-T wave changes of LV "strain" and/or ischemia (as is seen in Figure-4).
  • With true Wellens' Syndrome — one would not expect such prominent R wave amplitude in the anterior leads as is seen in Figure-4.
  • T wave inversion is generally not this widespread with Wellens' Syndrome — as it is in Figure-4
  • NOTE: For more on what Wellens' Syndrome is and is notSee ECG Blog #254

 

==============================

I conclude today's ECG Blog post with a final example of Giant T Waves.

  • What differences do you see between the 2 ECGs in Figure-5?

 

Figure-5: Compare this final example of Giant T Waves (TOP Panel) — with the initial ECG in today's post ( = Figure-1shown in the LOWER Panel). Both tracings exhibit Giant T waves. What differences exist between these 2 tracings? (NOTE: I've adapted the ECG in the TOP Panel from the June 22, 2020 post in Dr. Smith's ECG Blog).


ANSWER:

Although both tracings in Figure-5 show Giant T Waves — there are a number of differences between these 2 ECGs.

  • The heart rate is significantly faster in the TOP tracing.
  • QRS amplitude is less in the TOP tracing. That said — voltage for LVH is still satisfied in this TOP tracing by Peguero Criteria (ie, sum of deepest S in any chest lead + S in V4 ≥23 [female] or ≥28 [male]). In this TOP ECG — the S wave in lead V3 (18+ the S in V4 (13) = 31 (See ECG Blog #245 for my review of LVH criteria).
  • The QTc is greatly prolonged in the TOP tracing (it makes up almost 3/4 of the R-R interval) — whereas considering the slow heart rate, the QTc in the LOWER tracing is no more than minimally prolonged.

 

PEARL #3 — While each of the diagnostic considerations for Giant T Waves that are listed in Figure-3 can potentially lengthen the QT interval — the degree of QTc prolongation seen in the TOP tracing of Figure-5 is more likely to result from Takotsubo Cardiomyopathy or from a severe CNS disorder (ie, CNS bleed, stroke, tumor, trauma, seizure, coma).

  • Wellens' Syndrome seems less likely to cause the ST-T wave appearance seen in the TOP tracing — because the excessively prolonged QTc and diffuseness of T wave inversion are not regular features of Wellens' Syndrome. 
  • As was the case in Figure-4 — I suspect the reason for the ST-T wave appearance in lead V2 of the TOP tracing, is that this lead serves as a "transition lead" between notable T wave positivity in lead V1 — and profound T wave inversion in lead V3.
  • Follow-Up: It turns out that the patient whose ECG is shown in the TOP panel of Figure-5 was having alcohol withdrawal seizures, which I suspect was the principal cause of the Giant T Waves and marked QTc prolongation (ie, severe CNS disorder). Additional details with discussion of this case represented by the TOP tracing in Figure-5 can be found in My Comment at the bottom of the page in the June 22, 2020 post of Dr. Smith's ECG Blog. 

 

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  •  
  • ECG Blog #245 — Reviews the ECG diagnosis on LVH (with a 9-minute Audio Pearl in this post on this topic).
  •  
  • ECG Blog #254 — Reviews what Wellens' Syndrome is — and what it is not (with a 7:40 minute Audio Pearl in this post on this topic).
  •  
  • ECG Blog #46 — Reviews ECG findings with Takotsubo Cardiomyopathy.
  •  
  • The June 22, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews the case of Giant T-Waves with prolonged QTc that is shown in the TOP panel of Figure-5 above.



Wednesday, January 12, 2022

ECG Blog #275 (58) — What Chart Audit Suggests?


This ECG is taken from chart audit of an older patient seen in the field. Unfortunately — many details of this case are lacking.

  • How would YOU interpret this tracing?
  • What diagnoses do you suspect?

 

Figure-1: ECG taken from chart audit of an older patient seen in the field (See text).

 

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NOTE: Some readers may prefer at this point to listen to the 8:30-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-58).

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Today's ECG Media PEARL #58 (8:30 minutes Audio) — Reviews some lesser-known Pearls for ECG recognition of Hyperkalemia.

 

 

MSequential Thoughts on the ECG in Figure-1:

It's always challenging to try to interpret an ECG without benefit of the clinical history. Nevertheless — We are often asked to do so. Herewith follow my sequential thoughts on seeing this tracing, knowing only that this patient was found "in the field".

  • The rhythm is obviously slow (ie, the rate is in the low 40s/minute). Although there is no long lead rhythm strip — the rhythm is surprisingly regular. 
  • Sinus P waves are seen in multiple leads, albeit these P waves are of very low amplitude (RED arrows in Figure-2).
  • The PR interval is constant, albeit prolonged (ie, to at least 0.32 second) — therefore 1st-Degree AV Block.
  • The QRS complex is very wide (ie, vertical BLUE lines in lead aVF suggest that the QRS complex is prolonged to ~0.20 second).
  • QRS morphology is extremely unusual. It resembles LBBB in the limb leads (albeit with initial Q waves in leads I and aVL). In the chest leads — QRS morphology resembles RBBB (qR pattern in lead V1; wide terminal S wave in lead V6).
  • There is marked left axis deviation (about -60 degrees) in the frontal plane.
  • In addition to the Q waves in limb leads I and aVL — Q waves are also present in leads V1 and V2, with a tiny initial q wave in lead V3.
  • There are marked ST-T wave abnormalities. These include ST elevation with T wave inversion in limb leads I and aVL — ST coving with T wave inversion in leads V2, V3 — and — an unusual coved-shape of ST elevation in lateral chest leads V4,V5,V6.

 

MClinical Impression: The ECG findings in Figure-2 suggest 2 Diagnoses to me: i) Hyperkalemia until proven otherwise; andii) An associated acute evolving STEMI.

  • Although the tall, peaked T waves with narrow base that are characteristic of hyperkalemia are not seen in today's ECG — other findings strongly suggest Hyperkalemia until proven otherwise. These include: aMarked bradycardia; b) 1st-degree AV Block with a very prolonged PR interval; c) The tiny size of P waves; andd) The marked QRS widening (ie, to 0.20 second) — with an unusual QRS morphology not resembling any known conduction disturbance.
  • QRST Changes in different lead areas suggest recent (if not actively ongoingInfarction. High lateral leads I and aVL each show Q waves, ST elevation and T wave inversion (with subtle suggestion of reciprocal ST segment and T wave changes to lead aVL in lead III). Anterior leads V1,V2,V3 all show initial Q waves — with ST coving and T wave inversion in lead V2 — and ST coving with terminal T wave positivity in lead V3. Finally — each of the lateral chest leads (V4,5,6) show ≥2 mm of coved ST elevation.

 

Figure-2: I've labeled KEY findings from Figure-1 . The horizontal dotted RED lines in leads I, aVL; V4,V5,V6 show there is definite ST elevation with respect to the PR segment baseline (See text). 

 

CASE Follow-Up:

Chart audit revealed that this patient was unresponsive when found in the field. She died soon after emergency services (EMS) arrived. Because of her rapid demise — lab tests were not drawn. The terminal rhythm was PEA — with an extremely slow rhythm and a markedly widened QRS.

  • I don't know if IV Calcium was given.

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Important Points about HyperKalemia:

Rapid recognition of Hyperkalemia is among the most important of skills for emergency providers to master. The reasons for this are simple: 

  • i) Hyperkalemia is potentially life-threatening.
  • ii) There is an empiric treatment (ie, IV 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.
  • iii) Not-to-recognize hyperkalemia as the cause of QRS widening, unusual rhythm disturbances and/or ST-T wave abnormalities will lead you down the path of potentially serious misdiagnosis.

 

PEARL #1: Be aware that IF you suspect potentially life-threatening hyperkalemia — that IV Calcium should be immediately given without the need to wait for lab confirmation.

  • IV Calcium works fast (ie, within 2-3 minutes) by an action that stabilizes myocardial membrane potential, thereby reducing cardiac membrane excitability provoked by hyperkalemia (thereby protecting against cardiac arrhythmias). IV Calcium does not cause intracellular potassium shift, and it does not facilitate elimination of this cation.
  • Either Calcium Chloride or Calcium Gluconate can be used (10 mL given IV over 3-5 minutes with ECG monitoring)NOTE: The chloride form contains 3X the amount of calcium per 10 mL dose (10 ml 10% CaCl = 6.8 mmol Ca++ vs 10 ml 10% CaGlu = 2.3 mmol Ca++)
  • IV Calcium should be repeated IF there is no effect (ie, narrowing of the QRS on ECG) after 5-10 minutes. More of the gluconate form may need to be given (since it contains less calcium). The duration of IV Calcium is only ~30-60 minutes — but this should allow sufficient time for other treatments to be given.
  • CaGlu can be given through a peripheral IV line. Because CaCl is more likely to cause tissue necrosis if there is extravasation — a central line is recommended (except if your patient is in cardiac arrest). 
  • Other treatments will often be needed (ie, Glucose/Insulin; Albuterol inhalation; Sodium Bicarbonate — and in refractory cases, hemodialysis) — but IV Calcium is the treatment of immediate choice for potentially life-threatening hyperkalemia.
  • IV Calcium is not indicated for the treatment of peaked T waves with a narrow QRS and reasonable rhythm — as this is not a life-threatening situation.

 

The Textbook Sequence of ECG Changes:

For clarity — I've added Figure-3, which presents the "textbook" sequence of ECG findings seen with progressive degrees of hyperkalemia. While fully acknowledging that "not all patients read the textbook" — and that there will be variations in the various ECG findings from one patient-to-the-next — I have found awareness of the generalizations for these ECG signs in Figure-3 to be extremely helpful.

  • The most common earliest sign of Hyperkalemia is T wave peaking. This may begin with no more than minimal K+ elevation (ie, K+ between 5.5-6.0 mEq/L) — although in some patients, T wave peaking won't be seen until much later (and in some patients — T wave peaking is never seen).
  • PEARL #2: I love the image of the Eiffel Tower. With progressive degrees of hyperkalemia — the T wave (like the Eiffel Tower) 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.
  • PEARL #3: As helpful as I find Figure-3 is for providing insight to the ECG changes we look for when suspecting clinically significant hyperkalemia — progression from sinus rhythm to VFib as the 1st ECG sign of hyperkalemia has been documented. Not all patients read the textbook(emDocs, 2017 — Management of Hyperkalemia).


Figure-3: The "textbook" sequence of ECG findings with hyperkalemia.

 

PEARL #4: Assessment of the rhythm with severe hyperkalemia is often extremely difficult because: i) As serum K+ goes up — P wave amplitude decreases, and eventually P waves disappear (See Panels D and E in Figure-3)ii) As serum K+ goes up — the QRS widensandiii) In addition to bradycardia — any form of AV block may develop (ie, AV conduction disturbances with severe hyperkalemia often do not "obey the rules" — See Figure-4).

  • THINK for a MOMENT what the ECG will 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.
  • NOTE: P waves are extremely small in Figure-2. It is likely that with further increase in the serum K+ level — that P waves would no longer be seen. This would leave us with a slow rhythm without P waves, and with a very wide QRS complex — which would then be indistinguishable from a slow IVR (IdioVentricular Rhythm).

 

PEARL #5: As we have just noted, 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 in such cases, even though no P wave may be seen on ECG. This is known as a sinoventricular rhythm.

 


PEARL #6: 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).

 

Figure-4: Why assessing the rhythm with hyperkalemia is difficult (See text).


 

PEARL #7: With marked hyperkalemia — it is impossible to know how much the elevated serum K+ is influencing QRS width and ST-T wave morphology until you normalize serum K+ and then REPEAT the ECG!

  • For example — IF there was significant ST depression on the baseline tracing — then the "net effect" of such ST depression might sufficiently attentuate the T wave peaking of hyperkalemia in a way that produces "pseudo-normalization" of ST segments and T waves.
  • Hyperkalemia may mask the ST-T wave changes of acute infarction. Alternatively — hyperkalemia may produce a "pseudo-STEMI" pattern that simulates acute infarction.
  • With severe hyperkalemia — You can get an idea of the extent that excess serum K+ is altering the ECG by the improvement seen within minutes of giving IV Calcium. However, because the duration of action of IV Calcium is limited (ie, to ~30-60 minutes) — improvement of hyperkalemia-induced ECG changes following a dose of IV Calcium will be transient (until other measures produce a longer-lasting effect).

 

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Final THOUGHTS regarding Today's Case:

I was asked to interpret the ECG in Figure-1 in the "retrospectoscope" (ie, from the comfort of my desk armchair, sipping a cool drink as I viewed the tracing on my large screen desktop computer). This is admittedly a very different situation than being on-the-scene with an acutely ill patient under suboptimal conditions.

 

That said — the reason I immediately suspected severe hyperkalemia (despite the lack of T wave peaking)— was the combination of these 4 ECG findings:

  • Marked bradycardia
  • 1st-degree AV block with marked PR interval prolongation.
  • The tiny size of P waves.
  • Marked QRS widening (up to 0.20 second) — with an unusual QRS morphology not resembling any known form of conduction defect. 

In addition — acute infarction was suggested by:

  • Q waves, ST elevation and T wave inversion in leads I and aVL.
  • Q waves in V1,V2 (tiny q in V3) — with ST-T wave changes in these leads that potentially were recent — plus — definite coved ST elevation in lateral chest leads.

 

My THOUGHTS in the Retrospectoscope:

  • Given that this patient was unresponsive when found on the scene — one or more doses of IV Calcium was indicated (even before any labs might be drawn to confirm suspected hyperkalemia). There is little to lose by such treatment in this critical patient — and it might work if there was severe hyperkalemia.
  • IF there was significant hyperkalemia — then improvement in the above ECG findings would be expected within minutes after giving IV Calcium — at which point decisions could be made on the likelihood of acute infarction.
  • I have no idea if the above treatment might have helped in this case ...

 

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Acknowledgment: My appreciation to David Didlake (USA) for allowing me to use this case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #185 — Reviews my Systematic Approach to Rhythm Interpretation (Assessment using the Ps,Qs & 3R Approach).

  • ECG Blog #244 — Reviews a case of Hyperkalemia + Brugada Phenocopy.
  •  
  • The January 26, 2020 post in Dr. Smith's ECG Blog — Reviews a number of examples of hyperkalemia (with My Comment at the bottom of the page).
  • The September 5, 2020 post in Dr. Smith's ECG Blog — Reviews another case of Brugada Phenocopy from Hyperkalemia (with My Comment at the bottom of the page). 
  • The October 21, 2020 post in Dr. Smith's ECG Blog — Reviews a case of Hyperkalemia which highlights the difficulty of determining the Rhythm (with My Comment at the bottom of the page).

  • NOTE: There are links to numerous cases of life-threatening Hyperkalemia with "other" ECG findings (beyond tall peaked T waves) — in the excellent January 16, 2022 post by Drs. Meyers & Smith, in Dr. Smith's ECG Blog. Please also check out MY COMMENT at the very bottom of this page!