Saturday, September 4, 2021

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!



  • 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 #1How might you explain these events?



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).


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/minutethough 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); andv) 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 mmas 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.



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



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. 

  • 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.
  • 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).


  1. How might you explain the spontaneous change in rhythm?

    1. I suspect hyperkalemia was the cause of VT — and that the VT spontaneously resolved — and then subsequent treatments for the hyperkalemia prevented recurrence. That said — Wish I knew the precise sequence of when various treatments were given — and what the precise ECG response to such treatment were in "real time", without which I'm unfortunately reduced to speculating. But one of my main points in presenting this case was to emphasize that Hyperkalemia CAN be a cause of VT — and that in such cases, the treatment is IV Calcium rather than antiarrhythmic drugs. THANKS for your question!