EXTRA COPY - ECG Blog #518 — WCT with Low Urine Output — EXTRA COPY

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The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who presented to the ED (Emergency Department) with acute shortness of breath. The patient complained of malaise — but no chest pain or other bodily pain. He has had difficulty urinating.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• How would you treat this rhythm?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Rhythm in Figure-1:

By the P's, Q's, 3R Approach (See ECG Blog #185) — the rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia):

• The rhythm is Regular.
• The QRS is obviously wide (at least 4 large boxes in duration ==> 0.16 second).
• The Rate of the rhythm is ~130/minute.
• P waves are absent.

As often emphasized in this ECG Blog — We need to assume VT until proven otherwise whenever we see a regular WCT rhythm without clear sign of P waves.

• BUT — Take another LOOK at QRST morphology in Figure-1.
• Consider that this patient has recently been ill — and has had trouble urinating ...

Figure-1: Take another LOOK at the ECG in Figure-1 ...

Taking Another LOOK: 

As noted above — the rhythm in Figure-1 is a regular WCT at ~130/minute, without clear sign of P waves.

• QRS morphology  in Figure-1 is consistent with LBBB conduction (Monophasic R wave in leads I and V6 — and predominantly negative QRS in the anterior leads).
• BUT — Aren't T waves in many of the leads tall and peaked (if not pointed)?
• Not only are positive T waves peaked (and quite pointed in leads II,III,aVF; and V3,V4,V5) — but the negative T waves in leads I and aVL are also pointed at their deepest part! (See this Eiffel Tower effect below in Figure-2).

Figure-2: Note the Eiffel Tower effect of both positive and negative T waves in many of the leads in today's ECG.

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I'll refer the reader to my recent ECG Blog #516 — in which I highlighted XXX — as well as indications for empiric treatment of suspected hyperkalemia with IV Calcium even before the serum K+ level returns from the laboratory.

https://ecg-interpretation.blogspot.com/2026/01/ecg-blog-516-patient-is-post-op.html

Hyperkalemia

ECG Blog #275

https://ecg-interpretation.blogspot.com/2022/01/ecg-blog-275-58-what-chart-audit.html

Review when to give empiric IV Calcium !!!! — and the sequence of ECG changes with hyperK

Also — Audio Pearl on HyperK

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ECG Blog #244

https://ecg-interpretation.blogspot.com/2021/07/ecg-blog-244-58-cath-lab-was-activated.html

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

 

 

 

 

 

The 2nd ECG Diagnosis = Severe HyperKalemia:

For clarity — I've added Figure-2, 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-2 to be extremely helpful.

• The usual earliest sign of hyperkalemia ( = T wave peaking) 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.
• I love the image of the Eiffel Tower. With progressive degrees of hyperkalemia — the T wave 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.
• P.S. — As helpful as I find Figure-2 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-2: The "textbook" sequence of ECG findings with hyperkalemia.

 

 

ECG Changes of Hyperkalemia in Today's Case:

The reasons I instantly suspected severe hyperkalemia in today's case were:

• Significant QRS widening (to at least 0.11 second in leads I, II, aVL and others).
• T wave morphology that is typical for hyperkalemia. As shown in Figure-3 — the T waves in multiple leads resemble the Eiffel Tower (ie, not only are the T waves in leads I, II, aVL; V4, V5 and V6 tall, peaked and pointed — but these T waves are symmetric with an equally steep angle of rise and fall — with a narrow T wave base).
• There is a Brugada-1 ECG pattern in leads V1, V2 and V3. As emphasized above — it is common to see Brugada Phenocopy in association with severe hyperkalemia.

 

 

 

PEARL #3: 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-2); ii) As serum K+ goes up — the QRS widens; and, iii) In addition to bradycardia — any form of AV block may develop, and 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 rhythm, or like the rhythm is VT if the heart rate is faster.
• NOTE: We do not see P waves in most of the leads in Figure-3 — and it's difficult to be certain if the deflection in lead II is a sinus P wave (RED arrow). Fortunately — a definite P wave is seen in lead aVF, which confirms that the rhythm is still sinus (ie, sinus tachycardia at ~135/minute). But without lead aVF — I would not have been at all certain what the rhythm was.

 

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

 

 

Follow-Up to the Case:

The cardiac cath was negative (Clean coronary arteries! ). That said — the patient's condition precipitously declined after catheterization — and he was emergently intubated. Pertinent lab findings on admission included a pH = 6.94 — glucose over 1,100 mg/dL — serum K+ = 7.5 mEq/L.

• Fortunately — the patient's DKA (Diabetic KetoAcidosis) responded to treatment, with normalization of lab values.
• I was unable to obtain follow-up ECGs that could have confirmed my suspicion of Brugada Phenocopy.

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Hello Dr. Grauer I am Hamid. Working as Emergency Medicine Doc in Slovakia. I would love to get your insight on an ECG. The patient 42 years old, past history only hyperlipidemia (No hypertension!), presenting to ER with difficulty breathing for the past two days. Malaise. No chest pain. No complaint of pain. Stool normal. Urine he says for the past few days he has increased urgency with low urine output. Obj: GCS 15, diaphoretic, pale, breathing: crackles bilaterally. Blue protocol: Sliding present, B-Lines diffusely bilat.

MY REPLY:

This is an interesting tracing. I see a regular WCT ( = Wide-Complex Tachycardia at ~135/minute. There are NO sinus P waves ( = NO upright P wave in lead II. I really do not see sign of 2:1 atrial activity. T waves are PEAKED in many leads — so I'd be concerned about HyperK+ (ie, the patient may need IV Calcium ... — which depending on the clinical situation, I might even give empirically here ...) If serum K+ is normal — then QRS morphology could potentially be consistent with LBBB conduction (finding a prior tracing would help) — so I could not rule out a supraventricular etiology based on this single tracing — but HyperK is my suspicion. What happened?

HAMID HIMAT REPLY:

Thank you. I will keep that in mind for the future. You are absolutely spot on. I administered calcium before the lab values were available, based on the fact that the patient urinated approximately 1.5 liters within minutes after the Foley catheter was inserted. The assumption was hyperkalemia due to post-ren AKI with pulmonary edema. Following repetitive doses of calcium IV, the QRS complexes started to shorten, and the patient was taken for urgent dialysis. The potassium level was 8.71 mmol/L. Unfortunately, I do not have access to the ICU ECGs, but the system indicates the patient is stable. My specific question is, how do you differentiate between a wide QRS tachycardia that is V-tach versus one that is metabolic or supraventricular tachycardia with aberrancy in such patients?

MY REPLY:

Great question you ask! And often it is VERY difficult !!!

#1) Does the clinical setting predispose? Your patient's history is subtle — but inability to urinate — a history of HTN (What MEDS was he taking ???) — and now pulmonary edema DO potentially predispose him to HyperK.

#2) The ECG shows a wide QRS — without really showing indication of what it is! Always USE calipers when you have a moment to reflect (obviously you can't use calipers if your patient is crashing in front of you) — and doing so, I do NOT see any indication of 2:1 atrial activity (so NOT AFlutter). 

QRS morphology does resemble LBBB conduction (all upright in leads I, V6 — and predominantly negative in V1-thru-V4 — so I can't rule out a supraventricular etiology (finding a prior ECG would be VERY helpful in assessing this!) — but looking carefully, I see peaked T waves in 7 leads! (RED rectangles).

I also see a "point" to the negative T waves in 2 leads (BLUE rectangles).

When suspicious and in doubt — there is minimal morbidity from prudent Ca++ administration — and you can cure the patient — so you diid the RIGHT THING by giving IV Ca++ BEFORE the serum K+ value came back.

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Acknowledgment: My appreciation to Hamid Himat (from Bratislava, Slovakia) — for allowing me to use this case and these tracings.

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