But perhaps not the computer…
The underlying rhythm is unclear, due to artifact, but there are very wide QRS complexes. The computer measures the QRS as 158 ms, which is clearly wrong. A conservative measurement in V1-V3 suggests a width of at least 200 ms.
Such a wide QRS would be unusual for a bundle-branch block, as Dr Stephen Smith has pointed out. Of course, this could be a ventricular rhythm, but the classic sine-wave pattern (best seen in V1, and V5, V6) instead suggests severe hyperkalemia.
On the other hand, there is no bradycardia, there are no â€œtentedâ€ T-waves, and the absence of atrial activity is likely just due to pre-existing atrial fibrillation. But the wide QRS and characteristic QRST morphology overwhelmingly points to hyperkalemia.
Other examples of ECGs of severe hyperkalemia show much the same pattern:
The paramedic proceeded to a PCI center that was also â€œright around the corner,â€ so she fortunately did not have to make that decision! But she decided against requesting a prehospital activation of the cath lab, despite the computerized interpretation, feeling that hyperkalemia was far more likely. In the ED they repeated the ECG which demonstrated an unchanged pattern.
A stat chemistry showed the potassium to be 9.
Treatments were started, and a subsequent ECG showed improvement in the QRS width.
Note, however, that tented T waves are now prominent, and that the more severe signs of hyperkalemia have begun to resolve.The patient was found to be in renal failure, likely due to sepsis from a pulmonary infection, and eventually recovered.
What about the *** MEETS ST ELEVATION MI CRITERIA *** message?
A number of readers suggested that proceeding to the more distant PCI center would be preferable.
However, not a single person described the ECG changes that they felt could represent a STEMI on this ECG!
While hyperkalemia is infamous for causing STE and STD that mimics ACS (occasionally with tragic results), there were no any such ST changes on this patient ECG. In a few leads (e.g. aVL and I) there is “pseudo-STD,” which is actually just the terminal part of the wide QRS. If you disagree, let me know.
In one example from my own experience, a patient in DKA presented with a K of 7.5. The ECG demonstrated a concerning pattern of ST segment changes:
However, these ST segments normalized after empiric calcium administration, before the K level was obtained, and a subsequent angiogram was negative for significant occlusion.
This patient didnâ€™t need a PCI center. They needed calcium first, hopefully from EMS, and likely many grams of it, not just â€œone box and done.â€ Albuterol also likely could have helped, as well as IV fluids
But they then needed insulin, dextrose and emergent hemodialysis. (Iâ€™m going to leave the sodium bicarbonate and Kayexalate/sodium polystyrene debate for another time). Almost any hospital can provide these services. However, these therapies need to be started immediately, as the ECG strongly suggests that the rhythm could degenerate to to VF at any point.
My advice – Do not bypass a hospital when your patient has this ECG!
Dave Baumrind and I previously wrote about hyperkalemia, and it deserve re-reading, even if the title seems a bit… dated. In HyperK and Shades of Grey we discussed 4 myths regarding EMS evaluation and treatment of hyperkalemia.
TL;WR? Here’s a summary!
- MYTH: Dialysis patients tolerate hyperkalemia better than other people.
- MYTH: If the ECG doesn’t show QRS widening, then the patient is at low risk.
- MYTH: The ECG shows a predictable sequence of changes as the potassium level increases.
- MYTH: Calcium is a dangerous medication.