Potassium 6.2 with narrow QRS: any indication for calcium?

Written by Jesse McLaren

 

An 80 year old patient with diabetes/hypertension/cirrhosis had a recent increase in candesartan for their hypertension, and was also on spirolactone and nadolol. They presented to a hospital clinic for routine paracentesis, after which they developed nausea and syncope attributed to a vasovagal episode from the procedure. Labs showed a non-hemolyzed potassium of 6.2, normal glucose, and mild acute on chronic renal failure (Creatinine from 140 to 170 umol/L), and the following ECG, and they were sent to the ED. What do you think and how would you treat?

There’s sinus bradycardia, borderline PR interval, narrow QRS; normal axis/R wave progression; low precordial voltages, and subtle peaked T waves (most obvious in V2, but all T waves are symmetric with a narrow base). There’s no prior ECG to compare - but the bradycardia, prolonged PR and peaked T waves could all be from hyperkalemia. But does this patient with narrow complex ECG require calcium if the potassium is only 6.2?

 

The patient was seen three hours later in the ED, with triage vitals showing BP 50 and BP 106/60. There was no abdominal tenderness after paracentesis but the patient had ongoing nausea, and the following repeat ECG:

Slightly worse bradycardia but no other changes. Because of the narrow complex QRS and potassium of only 6.2 from the clinic, the patient was treated with fluids, insulin and dextrose but not calcium. ED labs showed a repeat K of 6.6 just as the patient was receiving their treatment, so no additional steps were taken.

Two hours later the patient became somnolent and the monitor showed the following rapid changes:

ECG after ROSC

Repeat K was 6.4 and the patient was given more insulin/dextrose/calcium and admitted to ICU. Follow up ECG showed resolution of sinus brady with ongoing PR prolongation:

Hyperkalemic ECGs and BRASH syndrome

This was my rude awakening years ago to the importance of ECG interpretation in hyperkalemia, and the dangers of the BRASH syndrome.

In med school and residency I’d been taught (and there are still multiple online examples of similar infographics) that the ECG in hyperkalemia goes through a gradual, progressive and predictable series of changes that correlate with serum potassium level – from peaked T waves at mild elevation, to loss of P wave and widening of the QRS at moderate elevation, then sine wave at severe elevation, and only then cardiac arrest. But this patient developed a deteriorating but persistent narrow complex brady-asystole preceded by only subtle ECG changes and with initial potassium of only 6.2. A good reminder of recommendations for calcium for either K>6 with any ECG changes (when the patient was first seen) or K>6.5 regardless of the ECG (when the repeat level came back).[1]

In a review of hyperkalemia in the ED, all adverse events occurred prior to calcium and usually with multiple signs of hyperkalemia (like the first ECG) – with the biggest predictors not only wide QRS, but also bradycardia and/or junctional rhythm.[2] Curiously, ACLS does not include consideration of calcium in its bradycardia algorithm, which could have prevented the arrest and which along with the epi produced ROSC.

Another learning point for me was the clinical deterioration out of proportion to the initial ECG and potassium level, which characterizes the vicious cycle of BRASH syndrome [3]. This patient had:

-    Bradycardia from the nadolol (and maybe worsened by vagal tone from the nausea 

         post-paracentesis), worsened by hyperkalemia, and contributing to shock  

-    Renal failure from the increase candesartan, worsening the hyperkalemia

-    AV nodal blockade from the nadolol, worsened by the hyperkalemia

-    Shock, from the bradycardia and hyperkalemia, worsening the renal failure

-    Hyperkalemia, from spirolactone/candesartan and new AKI, worsening all the above

In hindsight – and for future reference - a patient on AV nodal blocker and potassium sparing medication, presenting with bradycardia and a soft BP, and subtle hyperkalemic ECG changes is a classic candidate for BRASH syndrome – requiring immediate treatment of all the elements including calcium - even if only subtle ECG changes and moderate potassium level. And even without the subtle peaked T waves, bradycardia secondary to hyperkalemia is a high risk feature.

 

Take away

1.  Hyperkalemia can produce multiple abnormalities in rate/rhythm (including brady, junctional or wide complex rhythms), conduction (prolonged PR and QRS), axis, and repolarization abnormalities (including peaked T waves, or Brugada phenocopy) - and multiple abnormalities indicate high risk.

2. Hyperkalemia requires calcium if >6.5 regardless of the ECG, or >6 with any ECG  changes – with special attention to bradycardia, junctional rhythm, or wide QRS.

3. Consider BRASH syndrome which can produce clinical instability out of proportion to the ECG or potassium levels.

4. See below

See other cases of BRASH

 

Smith comments:

See Case 3 of this post, which demonstrates:

1) how easy it is to confuse the T-waves of Early repol from hyperkalemia and

2) how even with only peaked T-waves, HyperK can lead to ventricular fibrillation.

HyperKalemia with Cardiac Arrest. Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia

Recognize subtle findings of hyperK and, if present, treat with Calcium immediately!

References

1. Lindner et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med 2020.

2. Durfey et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events. West J Emerg Med 2017.

3. Farkas et al. BRASH syndrome: Bradycardia, Renal Failure, AV blockade, Shock, and Hyperkalemia. J Emerg Med 2020.

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MY Comment, by KEN GRAUER, MD (2/10/2025):  

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Today's case by Dr. McLaren serves as an important reminder of critical pitfalls in the treatment of hyperkalemia. 

• In the interest of stimulating discussion — I focus my comments on some additional clinical implications of the initial ECG to those reviewed in the above discussion by Dr. McLaren.  

The diagnosis of hyperkalemia was never in question in today's case because: 

• i) The initial ECG (reproduced in Figure-1) — strongly suggests significant hyperkalemia.
• ii) The initial serum K+ = 6.2 mEq/L in a non-hemolyzed specimen. 
• iii) The patient has multiple "predisposing conditions" for hyperkalemia. These include 3 medications known to potentially exacerbate hyperkalemia (ie, Aldactone — an ARB — and a non-selective ß-blocker) — with recent increase in the dose of the ARB Candasartan.
• iv) This 80-year old patient with known diabetes, hypertension and renal insufficiency — has worsening renal function on this admission.

Today's Initial ECG in Figure-1:

The reason I interpreted the initial ECG as suggestive of significant hyperkalemia is because:

• No less than 8/12 leads show characteristic T wave peaking (ie, with symmetric T wave ascent and descent, and a relatively narrow T wave base — in a "picture" resembling the tall, slender Eiffel Tower). That is, despite relatively reduced amplitude of these T waves (ie, the only really tall T wave is in lead V2) — overall QRS voltage is so low, that 6 of these 8 leads with peaked T waves manifest T wave amplitude equal to or greater than R wave amplitude in the corresponding lead.
• In addition — there is bradycardia with a borderline PR interval prolongation.

Two additional ECG findings in Figure-1 "caught my eye":

• The ST segment is surprisingly flat in all 12 leads! (Blue arrows highlight this ST segment flattening in leads V4,5,6 — but this finding is seen virtually everywhere! ).
• As I emphasized in the March 19, 2019 post — the characteristic ECG picture of hypocalcemia is that of a flat and prolonged ST segment, at the end of which occurs a surprisingly normal-looking T wave. But this "normal" T wave appearance of hypocalcemia may be altered if the patient also has hyperkalemia (and both hyperkalemia and hypocalcemia are often seen together in renal failure). 
• So while the QTc interval is not actually prolonged in Figure-1 — it "looks" prolonged because of how flat the ST segments are (such that this ECG picture of long, flat ST segments followed by T wave peaking should suggest possible associated hypocalcemia). The reason this is clinically important — is that if hypocalcemia is present, this may further exacerbate the adverse cardiac effects of hyperkalemia (Barboza de Oliveira et al — Rev Bras Cir Cardiovasc 29(3):432-436, 2014).
• This is relevant to today's case — because the ECG in Figure-1 manifests low voltage (No limb lead QRS greater than 5 mm — and except for lead V2, surprisingly low QRS amplitudes in the other 5 chest leads). As I noted in the November 12, 2020 post — among the causes of low ECG voltage is depressed LV function, which could further potentiate the above list of factors predisposing to cardiac decompensation.

Figure-1: The initial ECG in today's case.

WHY Isn't the QRS Wide?

As per Dr. McClaren — the "textbook" sequence of ECG findings seen with progressive degrees of hyperkalemia is not seen in all patients. As I emphasized in My Comment in the February 27, 2023 post in Dr. Smith's ECG Blog — some patients may develop everything except QRS widening. Others may not show T wave peaking — or may only show this finding as a later change. And despite marked hyperkalemia — some patients may not show any ECG changes at all. 

• So while I still feel it helpful to be familiar with the sequence of "textbook ECG changes" of hyperkalemia (that I review in that Feb. 27, 2023 post) — it's essential to appreciate that a significant percentage of hyperkalemic patients do not read the textbook!

But the Serum K+ is "only" 6.2 mEq/L ...

As emphasized by Dr. McLaren — this level of hyperkalemia is sufficiently high to predispose to clinical decompensation unless treated with IV Calcium because:

• Bradycardia is a major predictor of adverse events in patients with hyperkalemia.
• This 6.2 mEq/L level is associated with ECG abnormalities.
• The vicious cycle of "BRASH" Syndrome is operative.

To this — I'd add the following: 

• Some patients with significant hyperkalemia potentially causing severe rhythm disturbances do not develop any ECG abnormalities at all.
• Rather than the numerical value of serum K+ — it is the rate of change in serum K+ levels that is more important as a predisposing factor for hemodynamic deterioration (Simon et al — StatPearls, 2023). Today's case features many factors predisposing to potentially rapid K+ ion shifts between intra- and extracellular compartments.
• Did the patient also have hypocalcemia?
• Was LV function already depressed before onset of the vicious cycle of BRASH Syndrome changes?