No Dr. Topf, no EKG changes

On Monday night I was called by one of our fellows regarding a patient in the ED with a potassium of 8.5. They had already given insulin, glucose and kayexalate and the follow-up potassium was 8.1. This is not much improvemnt and less than you typically see. The patient was in acute renal failure with a creatinine of 3 and was anuric.

I asked if the patient had any EKG changes and according to the ER doc the patient had just a touch o’QRS widening. What do you think?

Peaked symmetric T’s

Link for more on EKG changes in hyperkalemia

That night his CPK was 5,000. The next day it rose to 341,680.

Now dat’s a spicy meatball!

– Initially posted using BlogPress from my iPhone

EKGs that will soil your shorts

A long time dialysis patient of ours came to the ED yesterday with the chief complaint of “weakness.”

She had not missed any dialysis in the last week. She had gone to the farmer’s market on Saturday (2 days prior to admission) and had purchased some melon. She ate two melons on Saturday and a third on Monday morning. Additionally, she had potatoes on Saturday night and Sunday morning.
On arrival to the ED this was her initial EKG (click on the image for a larger picture):

The potassium was still pending at this time and no action was taken on those peaked Ts and widened QRS.
Fourteen minutes later the EKG deteriorates to a terrifying sinusoidal pattern:

Potassium was still pending but based on the EKG and history of end-stage renal disease she was given two grams of calcium chloride. The CaCl2 was given via a peripheral line. Calcium chloride should be given only via a central line due to the devastating consequences of extravasation of calcium chloride. However, calcium chloride provides three times the calcium as calcium gluconate and is more effective at squashing hyperkalemic arrhythmias. I aplaud this boldness, as it looks like this patient is about to arrest.
The calcium worked great. A minute later things cool down:
Around this time the potassium came back at 9.4 mmol/L. The patient was then given 4 units of insulin. The low dose is typical of our ED as they tend to be skittish about giving 10 units of insulin to ESRD patients due to concern over symptomatic hypoglycemia. They chased the insulin with an amp of D50 and sixty grams of Kayexalate. The glucose was 84 mg/dL prior to the insulin and D50.
Eighteen minutes later the QRS is down to 128 msec from 168 on the initial EKG:

The patient then went for dialysis for 3.5 hours. Two hours with a zero potassium bath and 90 minutes on a one potassium bath. The potassium the next day was 5.5 mmol/L.

What’s new with hyperkalemia: EKG changes

Today I did a lecture for the fellows on hyperkalemia. It is interesting that nearly none of the content I use to teach the residents and students is used in a lecture for the fellows. Same subject complete rewrite.

I plan on doing four posts on hyperkalemia from this lecture:

  1. EKG changes
  2. Dialysis patients and hyperkalema
  3. Digoxen toxicity and hyperkalemia
  4. Renal adaptation to ACEi and aldo antagonists in CKD

The lecture started off with the case I blogged about last week with the scary EKG and the potassium of 9.9.


I focused on a well done study (Full Text) by Drs Montague, Ouellette and Buller from Yale. They looked at 90 patients with a potassium grreater than 6 and an EKG done within an hour of the potassium. They excluded hemolyzed specimens and patients with cardiac pacing or other conditions which would mask EKG changes.

They graded all the EKGs according to a prospective criteria and recorded the cardiologists assessment.
The average patient was 73 years old (20-93) and half had acute kidney injury (55%) and half had chronic kidney disease (47%). They did not comment on the degree of overlap between those groups. Half the patients had diabetes (55%). Only 31% were on ACEi and 30% on loop diuretics.

The reading cardiologist documented peaked T waves in only 3 of 90 patients with hyperkalemia. The investigators were able to find peaked T waves in only 29. QRS widening was found in only 6 patients. Of the 52 patients who could have been classified as having “Strict Criteria” (you needed a second EKG after resolution of the hyperkalemia and not everyone in the cohort had a second EKG) only 16 actually met strict criteria.
The authors found EKG criteria to be insensitive predictors of hyperkalemia:

  • Sensitivity of strict criteria: 18%
  • Sensitivity of any EKG change 52%

Interestingly, they found that acidosis decreased the likelihood of finding peaked T-waves.

When they looked at arrhythmias as an outcome, EKG changes continued to be a poor clinical guide. They were not sensitive: only one of the patients who subsequently developed an arrhythmia or cardiac arrest had previously met the strict criteria for EKG changes and only 7 had any T-wave findings at all. This is important because it emphasizes the fact that you can not be reassured by a normal EKG in a patient with hyperkalemia.

The study was unable to look at specificity because all of the patients had hyperkalemia. An earlier study by Wrenn, Slovis and Slovis was able to look at sensitivity and specificity because they did have patients without hyperkalemia in their cohort. They retrospectively reviewed the EKGs of 220 patients with either renal failure (n=133) or hyperkalemia (n=87):

  • Sensitivity: 39%
  • Specificity: 85%

When they restricted the cohort to patients with a potassium over 6.5 the sensitivity rose to 58%.

Take home message: a normal EKG should not rule out hyperkalemia and should not decerase your concearn for impending arrhythmia.

Here is the lecture this post is based on:

EKG Changes with hyperkalemia

Last week one of our second-year fellows was called into the ER for a potassium of 9.9 mEq/L. The EKG you see above was waiting for him. He arranged for emergent dialysis. In the morning the patients EKG looked like this:

Here is the time line of events:

  • 17:24 Na 128, HCO3 9, Cl 103, BUN 100, Cr 5.6 (no potassium was reported out on the initial labs)
  • 18:06 First EKG done
  • 18:28: K=9.9
  • 18:28: U/A Sp Grav 1.012, pH 5, random drug screen positive for opioids
  • 18:45: ABG 7.05/37/408/10
  • 18:45: urine Na 89, urine Cr 50.5, FENa 4.7%
  • 23:00 initiate dialysis: 2 hours on 1 K bath
  • 01:00 complete dialysis
  • 03:30 Na 140, K 5, Cl 107, HCO3 16, BUN 67, Cr 3.8, Ca 9.1, Phos 6.4, Mg 1.4, CPK 941
  • 03:30 ABG 7.22/40/117
  • 09:20 Na 142, K 4.8, Cl 111, HCO3 15, BUN 63, Cr 3.2
  • 10:00 ABG 7.20/42/96

This patient had AKI due to prolonged decreased po intake along with a loop diuretic and ACEi. The patient initially was anuric but rapidly began to recover and by the next morning was making over 100 mL of urine an hour.

His initial EKG is the best example of a sine wave from hyperkalemia I have ever seen. Below is a cardiac cycle from V4. With a quick glance it may look like a very wide QRS complex with the t wave somewhere to the right of the picture. In reality, the QRS duration is only 176 msec and the large upward thrust is the peaked T wave.


EKG Changes with hyperkalemia

  • Peaked T waves
  • Shortened QT interval
  • Widened QRS
  • Sine wave