Thursday, February 22, 2024

How will you save this critically ill patient? A fundamental and lifesaving ECG interpretation that everyone must recognize instantly.

Written by Pendell Meyers


A woman in her 30s called EMS for acute symptoms including near-syncope, nausea, diaphoresis, and abdominal pain. EMS arrived and found her to appear altered, critically ill, and hypotensive. 

An ECG was performed:

What do you think?










Extremely wide complex monomorphic rhythm just over 100 bpm. The QRS is so wide and sinusoidal that the only real possibilities left are hyperkalemia or Na channel blockade. Hyperkalemia is by far more common.

Indeed, further history revealed two missed dialysis sessions. And of course on exam she has a dialysis fistula.

EMS reportedly gave 4 grams of calcium (unknown whether CaCl or gluconate) and 50 mEq of sodium bicarbonate. There was concern that the rhythm might represent ventricular tachycardia, so lidocaine was given and one attempt at cardioversion was performed. It is unclear what changes happened to the rhythm based on the EMS interventions, but the patient arrived to the ED remaining critically ill and with a very wide complex reported (no ECGs from ED available sadly).

Hyperkalemia was diagnosed and more treatment was given including more calcium, bicarb, insulin/dextrose, and albuterol.

The potassium level returned at 9.7 mEq/L.

Emergent dialysis was prioritized after stabilization. 

She did well and stabilized after dialysis. 

Here is her ECG the next day with normal potassium level:




She did well.



See our other countless hyperkalemia cases below:


General hyperkalemia cases:

A 50s year old man with lightheadedness and bradycardia


Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer. (Physician also reads it as normal)







Is this just right bundle branch block?



A 60-something who has non-specific generalized malaise and is ill appearing.


HyperKalemia with Cardiac Arrest. 


Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia


What will you do for this altered and bradycardic patient?


I saw this computer "normal" ECG in a stack of ECGs I was reading


What is the diagnosis?


Found comatose with prehospital ECG showing "bigeminal PVCs" and "Tachycardia at a rate of 156"


An elderly woman found down with bradycardia and hypotension





A Very Wide Complex Tachycardia. What is the Rhythm? Use Lewis Leads!!






Cases of hyperkalemia mimicking OMI:

Acute respiratory distress: Correct interpretation of the initial and serial ECG findings, with aggressive management, might have saved his life.














Another deadly and confusing ECG. Are you still one of the many people who will be fooled by this ECG, or do you recognize it instantly?








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Tuesday, February 20, 2024

Tachycardia and hyperkalemia. What will happen after therapy with 1 gram of Ca gluconate and some bicarbonate?

A 20-something type, 1 diabetic presented by EMS with altered mental status.  Blood pressure was 117/80, pulse 161, Resp 45, SpO2 100 on oxygen.

Here is the 12-lead ECG:

Wide complex tachycardia
What do you think?









The providers thought that this wide QRS was purely due to (severe) hyperkalemia.   They treated with 4 ampules (200 mL) of bicarb and 1 gram of calcium gluconate. 

Note: 1 g of calcium gluconate is insufficient. 1 g of calcium chloride has 3x as much calcium and is indeed a good start.

His pulse on the monitor suddenly went down to 140 and another 12-lead ECG was recorded:

Sinus tachycardia at a rate of 143
There are peaked T-waves typical of hyperkalemia


The K returned at 6.9 mEq/L.

What do YOU think happened here?  What is the diagnosis on the top ECG?  Do you think that this was simply hyperkalemia with a wide complex that resolved with bicarb and calcium?







That top ECG with a wide complex tachycardia has all the features of ventricular tachycardia (VT): slow onset of the QRS, absence of P-waves, very wide, absence of any LBBB or RBBB morphology.  It is VT until proven otherwise and electrical cardioversion is indicated.  

When I was told that this was hyperkalemia that resolved with bicarb and calcium, I told them that, no, this is VT induced by hyperkalemia and that it just happened to coincidentally spontaneously convert at the same time as the administration of (inadequate) hyperkalemia  medicines.

How do I know that it is VT?

1. It just looks like VT

2. First part of QRS has slow onset: look at lead II.  

From onset of QRS to nadir of S-wave is a very long 140 ms.  This is possible with HyperK only, but unlikely.  

In V6, from onset of QRS to nadir of S-wave is 160 ms

3. It does not look like simple hyperkalemia, especially at a level of 6.9 mEq/L.  It might possibly have that appearance with such a wide complex if the K was at a much higher level.

4. It would not resolve with only bicarb and 1 g of calcium gluconate (= 1/3 of a gram of calcium chloride). That is minimal therapy for hyperK.

5. The heart rate changed instantly from 168 to 143.  That is typical of conversion from a re-entrant rhythm. 

6. P-waves appear on the followup ECG and they would not go from absent to present with such minimal therapy

Months later, when I was writing this up, I found the prehospital ECG:

This is typical hyperkalemia without VT.  Classic.  Notice the heart rate is approximately 130


This EMS ECG proves that the rhythm of the top ECG is VT.  It is not sinus tachycardia with hyperkalemia, or even sinoventricular rhythm.

What is sinoventricular rhythm?

Here are 4 cases of sinoventricular rhythm.


2 hours later









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Sunday, February 18, 2024

Acute dyspnea in an older woman, is it OMI?

 Written by Willy Frick

A woman in her 90s with a history of end stage renal disease and complete heart block status post dual chamber pacemaker presented from home with acute onset dyspnea. ECG is shown below.

What do you think?







The ST and T wave abnormalities jump off the page, but let's set that aside just for a moment to review the tracing systematically. 

The rate is 60 (and remember, slower heart rates are often seen in OMI). 

Close inspection reveals ventricular pacing spikes, best seen in aVL. Many ECG readers will not comment any further on rhythm once ventricular pacing has been identified, but it is still critical to determine the atrial rhythm. In this case, it is atrial fibrillation. This could be easily overlooked since there is complete heart block, but recognizing the atrial arrhythmia may mean prescribing anticoagulation to prevent stroke.

See this case: 

Computer often fails to diagnose atrial fibrillation in ventricular paced rhythm, and that can be catastrophic


Given that this is a ventricular paced rhythm, we judge the presence or absence of OMI using Smith Modified Sgarbossa Criteria. It is hard to identify exactly how deep the S waves in I and aVL are, but there could be disproportionate ST elevation and hyperacute T waves with reciprocal changes in III and aVF, altogether concerning for high lateral OMI.

The ER immediately contacted cardiology for consideration of emergent catheterization. Cardiology felt that there was baseline artifact and recommended immediate repeat ECG which is shown below.


This ECG actually has even more baseline wander than the first. In addition to having a particularly bizarre T wave morphology, it is curious that among the limb leads, lead II seems to look relatively normal, just as it did in the first ECG. What could explain this very bizarre looking ST-T morphology which completely spares lead II?

Answer: Arterial pulse tapping artifact!

The vector mathematics are explained in detail in the above post, but the important point for localization is recognition that lead II is spared. Lead II connects the R arm and L leg, therefore by process of elimination, the problem is with the L arm electrode. (Remember that the R leg is the ground electrode.) On exam, the L arm electrode was overlying the patient's AV fistula. After repositioning the electrode, repeat ECG was obtained showing resolution of the artifact.


Learning points:
  • Arterial pulse tapping artifact causes bizarre ST-T morphology
  • It also characteristically spares exactly one of the limb leads, and the spared lead tells you which electrode is causing the artifact
  • Repeat ECG will reproduce the artifact if the electrodes are not repositioned
  • Ventricular paced rhythm is an incomplete rhythm analysis, you must also determine the atrial rhythm




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MY Comment, by KEN GRAUER, MD (2/18/2024): 

===================================
Today's patient is a woman in her 90s with a dual-chamber pacemaker — who presents with acute dyspnea. I focus My Comment on a few additional thoughts to Dr. Frick's excellent discussion regarding ECG findings in today's initial ECG (that I have reproduced in Figure-1).
  • Being told that today's patient has a permanent pacemaker is extremely helpful in keying us in to the need to look especially close for pacemaker spikes (that had we not been told the patient had a pacemaker — might be extremely easy to overlook).
  • As I discussed in detail in My Comment at the bottom of the page in the January 13, 2024 post in Dr. Smith's ECG Blog — pacemaker spikes tend to be a high frequency signal. As a result — they are often effectively filtered out by a monitor mode setting of 0.5-to-40 Hz. If this is the filter setting used — then pacer spikes may simply not be visible on ECG. 
  • Instead — a broader passband (typically from 0.05 Hz to 150 Hz) is recommended for diagnostic mode, for which emphasis is on optimally accurate ST segment analysis (and for a much better chance of seeing pacemaker spikes on ECG). We were not told the frequencies used in today's ECGs.
  • As per Dr. Frick — pacemaker spikes are best seen in lead aVL of ECG #1. Knowing this relative location of pacemaker spikes in lead aVL with respect to the QRS complex in this lead facilitates recognizing the even smaller pacemaker spikes present in a number of other leads (within the GREEN circles in Figure-1).


Recognition of PTA (Pulse-Tap Artifact):
Dr. Frick highlights a number of essential points for recognizing PTA. These include:
  • Realization that artifact often produces bizarre ST-T wave morphology.
  • Awareness that one of the 3 standard limb leads is often "spared" from this bizarre ST-T wave morphology (which is lead II in Figure-1).
  • Remembering to look at the patient for a potential cause of artifact (which was the presence of the patient's dialysis AV fistula in her left arm in today's case).
  • Repeating the ECG after repositioning and verifying correct electrode lead placement.

Figure-1: I've labeled the artifact in today's initial ECG.


Finding the "Culprit" Extremity: 
As per Dr. Frick — the "culprit" extremity in today's case is the LA electrode. As I review in the August 26, 2022 post of Dr. Smith's ECG Blog — when the cause of artifact is attributable to a single extremity, it is EASY to quickly determine the "culprit" extremity:
  • A single extremity is suggested as the cause of artifact when the amount of artifactual ST segment deviation is approximately equal in 2 of the 3 standard limb leads (ie, outlined in RED in leads I and III of ECG #1) — and essentially not seen in the 3rd standard limb lead (ie, there is minimal ST segment deviation in lead II of ECG #1).

  • By Einthoven's Triangle (See Figure-2) — the finding of equal ST segment amplitude artifact in Lead I and Lead III, localizes the "culprit" extremity to the LA ( = Left Arm) electrode.
  • The absence of ST elevation or depression in lead II is consistent with this — because, derivation of the standard bipolar limb lead II is determined by the electrical difference between the RA and LL electrodes, which will not be affected if the source of the artifact is the left arm (as in Figure-2).

  • By Einthoven's Triangle — the finding of maximal amplitude artifact in unipolar lead aVL confirms that the left arm is the "culprit" extremity (highlighted in RED in lead aVL of ECG #1).
  • By the electrophysiologic principles of Rowlands & Moore (J Electrocardiology 40:475, 2007) — the amplitude of the artifact in the other 2 augmented leads (ie, leads aVR and aVF) — is about 1/2 the amplitude of the artifact in lead aVL (BLUE outline of the depressed ST segments in leads aVR and aVF of ECG #1).
= = = = = = = = = = = = = = = = = = = = =  
  • KEY Take-Home POINT: When the cause of artifact originates from a single extremity — the relative amount of artifact will be maximal in 2 of the 3 standard limb leads — absent in the 3rd standard limb lead — and maximal in the unipolar augmented electrode of the "culprit" extremity (which as per the RED outline in Figure-1 — is lead aVL). Appreciation of these electrophysiologic principles allowed me to instantly identify lead aVL as the "culprit" extremity in today's case — because this is the augmented lead with maximal artifact!
= = = = = = = = = = = = = = = = = = = = = 
Figure-2: Use of Einthoven's Triangle to determine the electrical voltages in the 3 standard limb leads.



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Links to Examples of ARTIFACT 
More technical "misadventures" are referenced here — some from Dr. Smith's ECG Blog — some from other sources (NOTE: As I did not previously keep track of these — there are additional examples of artifact sprinkled through Dr. Smith's ECG Blog that I have not yet included here ... ).



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