ECG Blog #251 (65) — HOW Does the Cycle End?

The ECG in Figure-1 was obtained from an 85-year old man who presented with "dizziness".

 

QUESTION:

• Can you explain what is happening with each beat on this tracing?

  

Figure-1: 12-lead ECG and long lead II rhythm strip from a 85-yo man with dizziness (See text).

 

 

My Sequential Approach to Today's Case: This is indeed a challenging tracing! I allowed myself a brief look at the 12-lead ECG before delving into details of the complex lead II rhythm strip — since I wanted to first ensure that the cause of the rhythm was not an acute event.

• All of the beats on this tracing are narrow — therefore supraventricular! This means that the "usual" criteria for chamber enlargement and ST-T wave assessment can be applied.
• Several criteria for LVH are clearly satisfied — based on very deep S waves in V3,V4 (Peguero Criteria) — and very tall (overlapping) R waves in V5,V6  (For more on LVH — See ECG Blog #245 — with attention to the Audio Pearl and Figures in the Addendum for specifics).
• There is modest T wave inversion in a number of lateral leads (ie, leads I, aVL and V6) that is consistent with LV "strain" and/or some ischemia — but nothing that looks like an acute cardiac event! 

 

My Sequential Approach to the Rhythm:

As always — I began my systematic approach to the rhythm with assessment of the Ps, Qs and 3Rs (as discussed in detail in ECG Blog #185).

• P waves — A fairly (but not completely) regular atrial rhythm is seen (RED arrows highlighting sinus P waves in Figure-2).
• As previously stated — the QRS is narrow — which confirms that the rhythm is supraventricular.
• The rhythm is obviously not completely Regular — so the Rate varies. Regarding the 3rd R (ie, the "Relation" between P waves and neighboring QRS complexes) — it looks as if most of the sinus P waves (RED arrows) may be related to neighboring QRS complexes — but we need to look closer!

 

 

Figure-2: I've added RED arrows for the sinus P waves that were seen in Figure-1.

 

Additional QUESTIONS:

• Take another look at Figure-2. In addition to the sinus P waves (RED arrows) — Are there other signs of atrial activity in this tracing?
• Of all of the P waves that are seen in Figure-2 — WHICH ones do you suspect are (and are not) being conducted?

 

 

The Case Continues:

In additon to the sinus P waves (RED arrows) — I've labeled the signs of other atrial activity with a YELLOW and a BLUE arrow (Figure-3). The challenge is to figure out the relationship (if any) to neighboring QRS complexes for each of the P waves in Figure-3.

• PEARL #1: When faced with a complex rhythm that manifests a number of different features (such as the rhythm strip shown in Figure-3) — it is sometimes easiest to begin by looking to see IF there are any features that I can definitely explain. I then look to see if there is an "underlying rhythm" — and, I save for last the interpretation of those features that I am not yet certain about.
• In Figure-3 — Although a sinus P wave does precede beat #1 — this PR interval is clearly too short to conduct. Since QRS morphology of beat #1 is narrow and virtually identical to the QRS morphology of all other beats on this tracing — beat #1 is not sinus-conducted. Note the long pause that precedes beat #1. This suggests that beat #1 is probably a junctional escape beat.
• No QRS complex follows the negative P wave highlighted by the YELLOW arrow in Figure-3. This suggests that there is no "forward conduction" of this negative P wave (that looks very different in shape than the sinus P waves).
• The P wave highlighted by BLUE arrow also looks very different than the sinus P waves (RED arrows) in this tracing. As a result — beat #6 is not sinus-conducted. Note the pause (ie, of 7.5 large boxes = 1.5 second) between beat #6 and the preceding QRS complex. Given that QRS morphology of beat #6 is narrow and virtually identical to the QRS morphology of all other beats on this tracing — this suggests that beat #6 is most probably either an ectopic atrial or junctional escape beat. 

PEARL #2: The most common form of 2nd-degree AV block is Mobitz Type I ( = AV Wenckebach) — which is diagnosed by the finding of a progressively increasing PR interval until a beat is dropped. There follows a brief pause — after which the next Wenckebach cycle begins with a PR interval that is shorter than the longest PR interval that was seen right before the pause.

• What is not commonly appreciated — is that there can be other ways that a Wenckebach cycle ends (See the Audio Pearl below).

  

Figure-3: I've labeled the additional signs of atrial activity with a YELLOW and a BLUE arrow.

 

  — The Case Continues BELOW today's Audio Pearl ... —

 

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NOTE: Some readers may prefer at this point to listen to the 6:20-minute ECG Audio PEARL before reading My Thoughts regarding the Laddergram that I derive below.

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Today's ECG Media PEARL #65 (6:20 minutes Audio) — Reviews the different ways that an AV Wenckebach cycle may end (as well as reviewing the "Footprints" of Wenckebach).

 

 

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Deriving the LADDERGRAM:

The complex mechanism of today's case is best explained by step-by-step derivation of a Laddergram (See ECG Blog #188 for review on how to read and/or draw Laddergrams).

• NOTE: Today's case provides an example in which I needed to construct a valid laddergram explanation in order to "solve" the arrhythmia.
• Sequential legends over the next 7 Figures illustrate my thought process as I derived this laddergram.

 

 

Figure-4: It is usually easiest to begin a laddergram by marking the path of sinus P waves through the Atrial Tier (RED lines drawn directly below the onset of each of the sinus P waves — as shown by the large GREEN arrows). Note that these RED lines in the Atrial Tier are nearly vertical — since conduction of sinus P waves through the atria is rapid. Note also that the P-P interval between successive sinus P waves (vertical RED lines) is equal!

 

Figure-5: The most challenging part of most laddergrams is construction of the AV Nodal Tier — so I generally save that for last. Therefore, after drawing sinus P waves into the Atrial Tier — I prefer to next add indication of all narrow QRS complexes into the Ventricular Tier. The large GREEN arrows show that my landmark for QRS complexes in the laddergram is the onset of the QRS. Note that the RED lines in the Ventricular Tier are also nearly vertical — since conduction of these narrow QRS complexes through the ventricles is rapid.

 

Figure-6: It's time to begin "solving" what we can in the laddergram. I do this by connecting those P waves in the Atrial Tier that might logically be conducting to narrow QRS complexes in the Ventricular Tier (slanted BLUE lines within the AV Nodal Tier). Doesn't it appear as if the angle of slant for these BLUE lines in the AV Nodal Tier is increasing?

 

Figure-7: Caliper measurement of the PR intervals for beats #2-thru-5 confirms progressive increase in the PR interval (from 340 to 440 msec.). The PR interval shortens before beat #7 (to 340 msec.) — and then lengthens again, to 410 msec. before beat #8. This is Wenckebach conduction! But unlike a typical Mobitz I block — the Wenckebach cycle from beats #2-thru-5 does not end with an on-time non-conducted sinus P wave. 

 

Figure-8: It's time to assess the "missing parts" of our laddergram. As we previously suggested — the PR interval of the sinus P wave preceding beat #1 is clearly too short to conduct. This strongly suggests that beat #1 is a junctional escape beat. We schematically represent this with a BLUE circle within the AV Nodal Tier that conducts retrograde (dotted BLUE line), thereby preventing forward conduction of this first sinus P wave. Since beat #6 is preceded by a dfferent-looking (negative) P wave with a short PR interval — this suggests beat #6 is a low atrial escape beat (BLUE circle within the Atrial Tier).

 

Figure-9: The remaining "missing part" of our laddergram relates to the small-amplitude negative P wave deflection highlighted by the YELLOW arrow. I introduced the concept of Echo beats in ECG Blog #239. The dotted BLUE lines propose retrograde conduction originating from the path of the sinus P wave that precedes beat #5 (as it passes through the AV Nodal Tier) as the source of this negative P wave. This is a logical proposal — because Echo beats are most likely to originate following PR interval prolongation (as discussed in detail in ECG Blog #239).

 

Figure-10: For clarity — I've labeled the unusual elements in this tracing. The rhythm strip begins with a junctional escape beat (JE), which is beat #1. There follows a Wenckebach cycle for beats #2-thru-5, with progressively increasing PR intervals. Instead of ending with a non-conducted on-time P wave — this short run of Mobitz I, 2nd-Degree AV Block is terminated by an Echo beat (YELLOW arrow). Presumably — this Echo beat resets the SA Node — so that instead of a sinus P wave, the 1.5 second pause between beats #5-and-6 ends with a low atrial escape beat (AE). This finally allows enough time for the SA Node to recover (RED arrow preceding beat #7) — as the next Wenckebach cycle begins (ie, with beats #7 and 8).

 

Conclusion of Today's Case:

In addition to Mobitz I 2nd-Degree AV Block — this 85-year old man with dizziness had significant bradycardia with pauses on additional monitoring. A permanent pacemaker was placed.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3R Approach to Systematic Rhythm Interpretation.
•  
• ECG Blog #164 — Reviews a case of Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
• ECG Blog #236 — Reviews in our 15-minute Video Pearl #52 how to recognize the 2nd-Degree AV Blocks (including "high-grade" AV block). 
• ECG Blog #186 — Reviews when to suspect 2nd-Degree, Mobitz Type I.
•  
• ECG Blog #239 — Reviews the concept of Echo Beats, and its clinical applications (showing another case of Wenckebach terminated by Echo beats).
•  
• ECG Blog #188 — Reviews how to understand (and how to draw) Laddergrams!

ECG Blog #250 (64) — ST Depression and a Regular SVT

The ECG in Figure-1 was obtained from a previously healthy 60-year old man who presented to the ED (Emergency Department) with palpitations and new chest pain.

 

QUESTIONS:

• Should you activate the cath lab?
• What would you do first?

 

Figure-1: ECG from a 60-yo man with palpitations and chest pain.

 

My Approach to Today's Case: We are told that the patient in today's case is a 60-year old man who presents to the ED with palpitations and new chest pain. And, there is an "eye-catching" amount of ST depression seen in multiple leads in Figure-1. There is also a tachycardia ...

• KEY Point: The 1st thing to do in the assessment of any patient in a tachycardia — is to determine IF the patient is hemodynamically stable. We have not yet been told anything about this patient's hemodynamic status.
• As impressive as the amount of ST depression in ECG #1 is — interpretation of this tracing should follow the same Systematic Approach used for assessment of any ECG (as discussed in detail in ECG Blog #185 and Blog #205).

 

The Case Continues: Although this patient was having symptoms (ie, chest pain, palpitations) — it was felt that he was "stable enough" for initial assessment. Immediate cardioversion was not felt to be needed at this time. By the Ps, Qs & 3R Approach:

• P waves are not seen in any lead.
• The QRS is narrow (ie, clearly not more than half a large box in duration) — which means the rhythm in Figure-1 is supraventricular.
• The rhythm is fast and Regular. I estimate the Rate of the rhythm to be ~175-180/minute (See Figure-2). Since there is no sign of atrial activity — there is no "Relation" between P waves and neighboring QRS complexes.

 

Figure-2: I've labeled the long lead II rhythm strip from Figure-1 to illustrate use of the Every-Third-Beat Method for estimation of the ventricular rate (as explained in Video Pearl #27 in ECG Blog #210). Starting with a QRS complex that begins on a heavy line (1st vertical RED line in the long lead II rhythm strip) — it can be seen that the time that it takes to record 3 beats (RED numbers) is just over 5 large boxes on ECG grid paper (BLUE numbers). If it would have taken exactly 5 large boxes to record 3 beats — then 1/3 of the rate would have been 300 ÷ 5 = 60/minute. This means that 1/3 of the rate is a little bit slower than 60/minute — which means that the ventricular rate in Figure-2 is between 170-180/minute.

 

My Thoughts Thus Far: By the Ps, Qs & 3R Approach — we've determined that the rhythm is a regular SVT ( = SupraVentricular Tachycardia) at ~175/minute, without sign of atrial activity.

• Should you activate the cath lab?
• What is the rhythm in Figure-2 most likely to be?

 

  — The Case Continues BELOW, under today's Audio Pearl ...

 

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NOTE: Some readers may prefer at this point to listen to the 10:50-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-64).

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Today's ECG Media PEARL #64 (10:50 minutes Audio) — Reviews my LIST #2: Common Causes of a Regular SVT Rhythm.

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NOTE: I allude to a number of important concepts in arrhythmia interpretation in today's Audio Pearl. For easy reference — I list below LINKS with more on these concepts.

• ECG Blog #185 — reviews the Ps, Qs & 3R Approach (Listen to Audio Pearl #3 in this post).
• ECG Blog #210 — reviews the Every-Other-Beat Method for rapid estimation of heart rate (See Video Pearl #27 in this post).
• ECG Blog #220 — reviews my LIST #1: Causes of a Regular WCT and — HOW to assess Hemodynamic Stability (Listen to Audio Pearl #37 in this post).
• ECG Blog #229 — reviews distinction between AFlutter vs ATach (and WHY AFlutter is so commonly overlooked — Listen to Audio Pearl #45).
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.

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The Case Continues:

Although there is marked, diffuse ST depression in ECG #1 — the highest priority at this time is to determine the rhythm because:

• The rhythm does not appear to be sinus (since upright P waves are not seen in lead II).
• If sinus rhythm and rate control could be established — it’s possible that much (most) of the ST depression might resolve. It may be that the ST depression we see in today's tracing is not the result of an acute coronary syndrome.
• Even if this patient did have an acute coronary syndrome — it would not be advisable to activate the cath lab until after the arrhythmia was diagnosed and rate control was reestablished.

 

LIST #2: Common Causes of a Regular SVT Rhythm:

We have described the rhythm in today’s case as a regular SVT (SupraVentricular Tachycardia) at ~170-180/minute, without clear sign of atrial activity. As discussed in the above Audio Pearl (ECG-MP-64) — the LIST that I favor for the differential diagnosis consists of 4 Causes:

• Sinus Tachycardia (Sinus Tach).
• Atrial Flutter (AFlutter).
• A Reentry SVT (ie, AVNRT or AVRT).
• Atrial Tachycardia (ATach).

PEARL #1: Of the 4 Causes that I’ve listed for a regular SVT rhythm without sign of atrial activity — the least common in my experience is Atrial Tachycardia (ATach). ATach may result in a regular SVT rhythm with either 1:1 or 2:1 AV conduction. The atrial rate may vary from anything over 100/minute — to 240 per minute (or rarely, even faster than this).

• ATach with Block used to be a common manifestation of Digitalis toxicity. With dramatic reduction in the use of Digitalis in recent years (and with lower doses being used in most of those patients who still are receiving this medication) — ATach with Block is seen much less often than in the past.
• When ATach is seen — it will often present with group beating from Wenckebach conduction. As a result — there will commonly be changing conduction ratios, with periodic short pauses — and IF the rhythm is ATach, then P waves that conduct will usually be seen before the first beat at the end of such pauses. Although for completeness, I list ATach as one of the 4 Causes in my SVT LIST — ATach will not commonly present as a strictly regular SVT rhythm without any P waves.

PEARL #2: Determining the heart rate may provide an important clue to the etiology of a regular SVT without clear sign of atrial activity.

• In a supine adult (ie, an adult who has not just exercised) — it is not common for sinus tachycardia to exceed ~170/minute. This is not to say that you will never see sinus tachycardia this fast in a non-exercising adult — but rather to suggest that the very rapid heart rate in today’s case (ie, ~175/minute) makes sinus tachycardia less likely.
• Untreated AFlutter most commonly presents with 2:1 AV conduction, in which the atrial rate of flutter is close to 300/minute (ie, ~250-to-350/minute range) — and the ventricular rate close to half that, or ~150/minute (ie, ~130-to-160/minute range). The ventricular rate of ~175/minute in today's case would imply an atrial rate of 175 X 2 = 350/minute, which is faster than the usual atrial rate for AFlutter.
• From these points — it can be seen that when the rate of a regular SVT rhythm is not more than 150-160/minute — any of the entities on the SVT LIST could be operative. However, when the ventricular rate is greater than ~170/minute — a reentry SVT rhythm becomes much more likely!

FOLLOW-UP in Today's Case:

By the process of elimination — the rhythm in today's case was diagnosed as a reentry SVT — and treated with Adenosine. This promptly converted the rhythm to sinus — with resolution of the patient's symptoms and resolution of much of the ST depression.

• Cardiac cath was performed given the patient’s age and the presenting symptom of chest pain, in association with such marked and diffuse ST depression. Cardiac cath showed no more than minimal coronary disease.

 

Final PEARL #3: An important ECG pattern to recognize — is diffuse ST depression (in ≥7 leads) that occurs in association with ST elevation in lead aVR. It should be emphasized that this ECG pattern is not a sign of acute coronary occlusion. Instead, it suggests diffuse Subendocardial Ischemia, which may be due to one of the following:

• Severe Coronary Disease (due to LMain, proximal LAD, or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
• Subendocardial ichemia from another Cause (ie, sustained tachyarrhythmia; shock/profound hypotension; GI bleeding; anemia; etc.).

 

KEY Learning Points from Today's Case: 

It is good that despite profound ST depression in the initial ECG — the cath lab was not activated. Instead, initial management appropriately focused on diagnosis and treatment of the cardiac rhythm. 

• The finding on cardiac cath of no more than minimal coronary disease provides insight how even profound and diffuse subendocardial ischemia may sometimes not be the result of severe coronary disease. 
• Finally — persistent tachycardia can be the cause of marked ST depression.

  

 

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ADDENDUM (September 8, 2021): The 2 LISTS that I favor for the diagnosis of cardiac arrhythmias assist in assessment of regular wide and narrow tachycardias. Discussion in today's blog post focused on LIST #2 = the Causes of a Regular SVT.

• I've added Figure-3 below, as review of the Causes in my LIST #1.

 

 

Figure-3: Shown here is my LIST #1: Causes of a Regular WCT ( = Wide-Complex Tachycardia) Rhythm of Uncertain Etiology (ie, without clear sign of sinus P waves). This list is discussed in detail in ECG Blog #220.

 

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3R Approach to Systematic Rhythm Interpretation. 
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #210 — Reviews a case of a Regular WCT Rhythm (Media Pearl #27 in this blog post is a Video that reviews the Every-Other-Beat Method for estimation of heart rate when the rhythm is fast).
• ECG Blog #220 — Reviews the differential diagnosis for List #1: Causes of a Regular WCT Rhythm without clear sign of atrial activity (Media Pearl #37 in this blog post is an Audio that reviews assessment to determine IF the patient is Hemodynamically Stable).
•  
• ECG Blog #229 — reviews distinction between AFlutter vs ATach (and WHY AFlutter is so commonly overlooked — Listen to Audio Pearl #45).
•  
• The November 12, 2019 post in Dr. Smith's ECG Blog — Reviews another case of a Regular SVT rhythm. 
• The October 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews my approach to another case of a Regular SVT rhythm. 
• 
  
• ECG Blog #196 — Reviews "My Take" on assessing the Regular WCT (Wide-Complex Tachycardia) — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.

ECG Blog #249 (63) — Can You Explain What Happened?

The 2 ECGs shown in Figure-1 were obtained from the same patient just 20 minutes apart. This 40-year old man had a long history of alcohol abuse — and was admitted for advanced cirrhosis with ascites. He was on a number of medications — and reportedly had reduced oral intake with decreased urine output in recent days.

• ECG #1 was obtained because of chest discomfort and palpitations — but the patient was alert and hemodynamically stable the entire time that he was in this rhythm.
• Without any specific therapy for the rhythm seen in ECG #1 — 20 minutes later, ECG #2 was obtained. The patient remained hemodynamically stable throughout this entire time!

 

QUESTIONS:

• HOW would you interpret the 2 tracings shown in Figure-1?
• How might you explain the spontaneous change in rhythm?

 

Figure-1: ECGs obtained 20 minutes apart from the same patient. No specific treatment was given for the rhythm in ECG #1. How might you explain these events?

 

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NOTE: Some readers may prefer at this point to listen to the 3:15-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-63).

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Today's ECG Media PEARL #63 (3:15 minutes Audio) — Examines the question of whether Hyperkalemia can cause VT? (and whether this matters clinically?).

• NOTE: ECG signs of hyperkalemia are thoroughly reviewed in ECG Blog #244.

 

 

MY Sequential Approach to ECG #1:

We are told that the patient was alert and hemodynamically stable at the time ECG #1 was obtained. This is important — because regardless of what this initial rhythm turns out to be, the fact that the patient remains hemodynamically stable means that you have at least a "moment of time" to gather your thoughts and contemplate management.

• Other than a beat or two — we really don't see lead V5 in ECG #1. No matter — as the other 11 leads provide more than enough informaton to render a diagnosis.
• The overall rhythm in ECG #1 is fast (probably ~200/minute — though the ECG grid is not easy to make out) — regular — and very wide. There is no clear sign of atrial activity (ie, No P waves!). QRS morphology is amorphous — without resemblance to any known form of conduction block. Statistical odds that the rhythm in ECG #1 is VT (Ventricular Tachycardia) — are over 90% (See ECG Blog #196).
• PEARL #1: Specifics regarding QRS morphology in ECG #1 that greatly increase the likelihood that this rhythm is VT include: i) The almost all negative frontal plane axis (with no more than the tiniest r wave in lead I); ii) The all positive QRS in lead aVR; iii) The completely amorphous (shapeless) QRS morphology in lead V1; iv) The almost all negative QRS complex in lead V6 (Since lead V6 virtually always manifests more positive electrical activity than seen here when the rhythm is supraventricular); and, v) The overall "ugly" appearance of this very wide and formless QRS (an appearance that strongly suggests electrical activity is originating from outside of the conduction system).

The Case Continues with ECG #2:

Without any specific treatment — 20 minutes later, the patient spontaneously converted to the rhythm shown in ECG #2.

• The mechanism of the rhythm in ECG #2 is now sinus — as upright P waves with a constant PR interval are seen in lead II. Thus, the rhythm is now sinus tachycardia, at ~105/minute.
• Although the QRS complex "looks a bit wide" — it doesn't measure more than half a large box in duration (ie, 0.10 second) — therefore not qualifying as QRS widening.
• I measure the PR interval as 1 large box in duration (ie, ~0.20 second). Although this does not meet ECG criteria for 1st-degree AV block — given the increased rate (ie, 105/minute), the PR interval is longer than expected (ie, the PR interval usually shortens with tachycardia).
• Given this faster rate — the QTc is probably not prolonged.
• There is slight LAD (Left Axis Deviation) — in that the S wave in lead aVF is more negative than positive. But since the QRS is still predominantly positive in lead II — this does not qualify as a hemiblock.
• Regarding chamber enlargement — the S wave in lead V2 is extremely deep (ie, >25 mm — as this S wave overlaps with the R and S wave in lead V3). This satisfies voltage criteria for LVH (Left Ventricular Hypertrophy).
• Regarding Q-R-S-T Changes — there are small Q waves in leads I, aVL — R wave progression is poor (with delayed transition until leads V5-V6) — ST segments are straightened, if not slightly depressed in the inferior and lateral chest leads — and T waves look more peaked than-they-should-be in multiple leads (even though these T waves are not overly tall in the inferior and lateral chest leads).

IMPRESSION: Putting It All Together!

I like this case — because it provides an excellent example of clinical ECG interpretation when the answers are not clear cut.

• The "easy part" of this case lies with interpretation of ECG #1 — because the rhythm in this tracing is almost certain to be VT!

Not so simple is determining the likely etiology of this ventricular tachycardia — and deciding on optimal initial treatment. Fortunately — ECG #2 provides clues!

• PEARL #2: There are a limited number of clinical conditions that predispose to hyperkalemia. These incude: i) Acute or chronic renal failure; ii) Certain medications (ie, potassium-sparing diuretics; NSAIDS; ACE-inhibitors; ARBs); iii) Dehydration; iv) Acidosis; and, v) Trauma (ie, crush inuries leading to rhabdomyolysis; severe burns).
• The patient in today's case had several of the above predisposing factors (ie, recent reduced oral intake and decreased urine output — therefore probable dehydration and perhaps a component of renal failure; alcohol abuse with cirrhosis and ascites — therefore probably being treated with aldactone). As a result, even before seeing this patient's ECG — our index of suspicion for Hyperkalemia should be increased!
• Although ECG #2 shows definite voltage for LVH (as well as ST elevation in leads V1,V2 that is consistent with LV "strain" in these anterior leads) — and — ST segment flattening in the inferior and lateral chest leads that could be ischemic — I thought the most remarkable ECG finding in this patient with several potential predisposing factors for Hyperkalemia, was the peaked (almost pointed) T waves in multiple leads (ie, in leads II,III,aVF: and in V1-thru-V6).
• PEARL #3: Given the above predisposing factors for Hyperkalemia and T waves more peaked than-they-should-be in multiple leads — I interpreted the very subtle suggestion of a QRS complex that "looks a bit wide" (even though it does not actually measure as wide) — and a PR interval somewhat "longer-than-expected" (given the tachycardia) as 2 additional findings supportive of my suspicion of significant Hyperkalemia.
• PEARL #4: Remember: The ECG represents the "net" effect of all forces that are operative. By this I mean that it's possible the reason the peaked T waves in ECG #2 are not as tall as we usually expect with Hyperkalemia — is because the flattened ST segments that we see in multiple leads were significantly more depressed in this patient's "baseline" ECG before Hyperkalemia developed — and that the height of the peaked T waves that we now see may have been attenuated by this baseline ST depression. NOTE: We do not know this is true — but I think it insightful to consider that in the context of several conditions predisposing to Hyperkalemia + a PR interval and QRS duration that look longer-than-they-should-be + the diffuse ST segment flattening — that the small-amplitude peaked T waves that we see in ECG #2 are strongly suggestive of Hyperkalemia.

PEARL #5: The reasons I focus so closely on the possibility of significant Hyperkalemia as my interpretation for ECG #2 are: 

• Because significant Hyperkalemia may lead to VT (as per the above Audio Pearl #63) — and —
• Regardless of whether hyperkalemia directly "caused" the rhythm in ECG #1 or not — the immediate initial treatment of choice for a wide tachycardia without P waves that occurs in association with strongly suspected Hyperkalemia (even before the serum K+ level returns from the lab to confirm hyperkalemia) — is IV Calcium.

Follow-Up to this Case:

As noted — this 40-year old man had advanced cirrhosis with ascites as sequelae from a long history of alcohol abuse. Among his medications was a potassium-sparing diuretic — which together with dehydration and an element of renal failure, resulted in his elevated serum K+ = 6.7 mEq/L at the time ECG #2 was obtained.

• The patient's hyperkalemia was treated with calcium gluconate; glucose-insulin; and albuterol nebulization. Spironolactone was stopped. (NOTE: Details regarding the timing of these interventions with respect to when ECGs #1 and #2 were obtained is uncertain).
• PEARL #6: Given significant elevation of the serum K+ level (to 6.7 mEq/L) at the time ECG #2 was obtained — it would be impossible to assess the ECG for findings such as axis deviation, PR and QRS duration, LVH — and especially for possible ischemic changes until another ECG is obtained after correction of the serum K+ level.

 

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

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3R Approach to Systematic Rhythm Interpretation. 
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
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• ECG Blog #244 — Reviews a case of Brugada Phenocopy caused by Hyperkalemia. Additional information in this blog post includes Audio Pearl #58 (on Pearls for ECG Recognition of Hyperkalemia) — as well as Figure-2 on the "textbook sequence" of ECG signs of Hyperkalemia — and Figure-4 that reviews effects of hyperkalemia on the cardiac rhythm. 
• ECG Blog #196 — Reviews "My Take" on assessing the regular WCT (Wide-Complex Tachycardia) — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.
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• ECG Blog #52 — Reviews a another case in which it was difficult to distinguish between new VT vs a wide QRS rhythm from Hyperkalemia (or both).
• The January 26, 2020 post in Dr. Smith's ECG Blog — Reviews a number of examples of Hyperkalemia (with clinical PEARLS in My Comment at the bottom of the page).