Editor’s note: We asked columnist Tom Bouthillet to pick a winner to this month’s challenge and he wrote: “My pick as winner for the May 2011 EMS 12-lead column is Nick Adams, whose answer can be seen in the comment block.
I thought his comments combined the best understanding of the ECG findings and pathophysiology of hyperkalemia along with the most appropriate treatment plan. Congratulations and enjoy the T-shirt and bottle opener.”
Haven’t read the initial case presentation? Read: ECG Challenge: What in the wide, wide world of sports?
Let’s take another look at the patient’s ECG.
This ECG shows an undetermined rhythm with wide QRS complexes at a rate of about 60 beats per minute.
When QRS complexes are wide we have to consider the possibility that we are dealing with a ventricular rhythm.
However, this is a special case because the QRS complexes are so incredibly wide! In fact, they are greater than 200 ms.
When QRS complexes get that wide, hyperkalemia should be top on your list!
While there is no single way that life-threatening hyperkalemia presents on an electrocardiogram, many features of this case are “classic”.
- Absence of P-waves
- Extremely wide QRS complexes (> 180 ms)
- Nonspecific intraventricular conduction defect
- Peaked T-waves (with a late take-off)
What do we mean by “nonspecific intraventricular conduction defect”?
It just means that the QRS complex is wide and shows a pattern that is not consistent with left or right bundle branch block.
That’s not unusual for a ventricular rhythm, but with hyperkalemia it’s impossible to tell whether or not we’re dealing with sinus rhythm with invisible P-waves, a junctional rhythm or a ventricular rhythm.
In this case we have left bundle branch morphology in lead V1 (QS complex) but right bundle branch morphology in lead I (Rs complex).
When an ECG shows left bundle branch block in the precordial leads and right bundle branch block in the limb leads, we call it a nonspecific intraventricular conduction defect.
That’s one of the reasons I don’t like the “turn signal” method for identifying right and left bundle branch block. You need to check the precordial leads against the limb leads!
Now let’s talk about the T-waves.
We’ve all heard that “peaked T-waves” are a sign of hyperkalemia and that’s true, but we should also consider how the QRS complex merges into the T-wave.
Take a good look at this 12-lead ECG, especially the left precordial leads (V4-V6) and commit the pattern to memory.
This ECG is almost to the point of being a “sine-wave” ECG, also sometimes referred to as a “Z-fold” pattern which suggests that cardiac arrest could be imminent.
Here’s how the 2010 AHA ECC Guidelines explain it:
“Although severe hyperkalemia may cause flaccid paralysis, paresthesia, depressed deep tendon reflexes, or respiratory difficulties, the first indicator of hyperkalemia may be the presence of peaked T waves (tenting) on the electrocardiogram (ECG). As serum potassium rises, the ECG may progressively develop flattened or absent P waves, a prolonged PR interval, widened QRS complex, deepened S waves, and merging of S and T waves. If hyperkalemia is left untreated, a sine-wave pattern, idioventricular rhythms, and asystolic cardiac arrest may develop.”
So how should we treat a patient with suspected life-threatening hyperkalemia?
The most important treatment, by far, is calcium! This will stabilize the myocardial cell membrane.
The guidelines recommend:
Calcium chloride (10%): 5 to 10 mL (500 to 1000 mg) IV over 2 to 5 minutes or calcium gluconate (10%): 15 to 30 mL IV over 2 to 5 minutes.
The good news is that the calcium is cheap, benign, and will start to take effect within minutes!
Other treatments applicable to the prehospital environment include sodium bicarbonate and nebulized albuterol (10-20 mg nebulized over 15 minutes).
