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

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?
• What are your first clinical considerations?

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:

Our 1st clinical consideration given the ECG shown in Figure-1 — is to ensure that this patient is hemodynamically stable.

• Determination of hemodynamic stability is not readily apparent from the brief history we are given (ie, Today’s patient is short of breath — but not in pain; The heart rate is ~130/minute, but we do not know the patient’s blood pressure).
• Sometimes, “Ya just gotta be there” — in order to determine if the patient is sufficiently stable to allow a moment to more closely assess the rhythm.

Let’s assume that this patient is hemodynamically stable! 

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 itself is Regular.
• The QRS is obviously wide (at least 4 large boxes in duration ==> ≥0.16 second — which is very wide).
• The Rate of the ventricular rhythm is ~130/minute.
• P waves are absent (which means that the 5th Parameter = Are P waves Related to neighboring QRS complexes? — is to be answered with a “No” —). 

As is 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.

• This leads us to our next STEPs in assessing a regular WCT without P waves: i) LOOK at QRS morphology. We want to determine if QRS morphology during the WCT rhythm provides further clue to the etiology of the rhythm (ie, A QRS morphology not consistent with any known form of conduction defect would strengthen our assumption of VT).
• At the same time: ii) We want to look at ST-T waves during the WCT rhythm to see if this suggests acute ischemia or other abnormality.

Take another LOOK at QRS and ST-T wave morphology in Figure-1.

• Consider that this patient has recently felt ill (malaise) — 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 for the ECG in Figure-1 is consistent with LBBB conduction (ie, Monophasic R wave in leads I and V6 — with 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 for pointed positive and negative T wave below in Figure-2).
• 
  
• And WHY is the QRS so wide (can be seen to be at least 4 small boxes in duration in leads like V3,V4 ==> 0.16 second).

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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CASE Follow-Up:

The above observations were appreciated by emergency providers:

• Based on this acutely ill patient's description of "difficulty urinating" — a foley catheter was inserted, and resulted in ~1,500 cc of urine within minutes.
• Based on a presumptive diagnosis of acute renal insufficiency — several empiric IV Calcium doses were given (before serum K+ levels returned). Within minutes — the QRS complex narrowed as the rhythm slowed and the patient stabilized (Unfortunately — I was unable to obtain those follow-up tracings).
• Lab results returned: Serum K+ = 8.7 mEq/L.
• The patient went for emergency dialysis.

COMMENT:

• I'll refer the reader to my ECG Blog #516 — in which I detail empiric use of IV Calcium (formulations and dosing — with emphasis on the minimal downside from giving empiric IV Ca++ when the clinical situation is suggestive and the ECG shows a worrisome "too fast or too slow" arrhythmia).
• Also in ECG Blog #516 — I reviewed the challenges of assessing the rhythm when serum K+ is markedly elevated.
• More on hyperkalemia in ECG Blog #275 (including the textbook sequence of ECG changes with hyperK+ — with emphasis on why not all patients "read" the textbook).
• With yet one more hyperK case of another regular WCT in ECG Blog #244 — in which the cath lab was activated (reviewing how common Brugada-1 patterns may be seen with hyperK).
• And — More on "decreased urine output and acute kidney injury" in this review article by Chenitz and Lane-Fall (Anesthesiol Clin 30(3):513-526, 2012).

 

 

 

 

 

 

 

 

 

 

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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