Tuesday, February 18, 2025

After seeing this ECG, are there any medications you would consider giving?

Written by Willy Frick

A man in his 50s with COPD presented with dizziness and hypotension. He had worked overnight the night before and presented to the hospital after his shift. His first recorded blood pressure was 88/53 mm Hg.

Here is his presenting ECG:

What do you think?




The ECG shows sinus rhythm. The T waves are suspiciously symmetric, but not hyperacute looking. In contrast to hyperacute T waves which are characteristically broad (Dr. Smith describes them as "puffed full of air"), these T waves have a very narrow base. The concavity is especially pronounced. Altogether, this ECG is suspicious (but probably not diagnostic) for hyperkalemia.

I sent this ECG to Dr. Meyers with no context, and he replied "mild hyperkalemia effect possible." This is an extremely subtle ECG. However, we can make our job a little easier using comparison to a prior ECG.


Here are the leads side by side:


This serial comparison significantly increases our suspicion for hyperkalemia, highlighting how sharply peaked the T waves are relative to prior.

The patient was treated with methylprednisolone, ipratropium-albuterol, and 1 L NS. Forty five minutes later, his blood pressure increased to 157/125 mm Hg, but his heart rate was now in the 30s. Repeat ECG was performed.


This is a very poor quality ECG which limits interpretation. It should have been repeated immediately. However, we can at least make the following observations:
  • The QRS has widened
  • There are no longer any identifiable P waves
  • The ventricular rate is much slower, in the 30s
These are all features of hyperkalemia. If we were suspicious before, it is now certain. The patient needs calcium immediately. Although labs were drawn on arrival to the ED, this hospital apparently has a very slow lab and the results were not back yet (and would not result for another half hour). This ECG was not recognized as showing hyperkalemia.

Instead, the patient received atropine and his heart rate rose to the 80s. The next recorded blood pressure was 211/175 mm Hg, and in response the patient was started on continuous nitroglycerin infusion. His heart rate dropped back into the 30s, and he arrested. He received CPR and was intubated. Repeat ECG is shown:


It looks similar to prior, but with less artifact. At this point, lab called with critical potassium 6.8 mEq/L and the patient finally received 2 g IV. Repeat ECG is shown below.


Much better! Although the QRS has narrowed and the sinus node has gone back to work, there is still subtle upsloping STD in the lateral precordial leads and subtle T wave peaking. The patient's long term outcome is unknown.

Discussion:

This is a case of an initial ECG showing very subtle signs of hyperkalemia. In just 90 minutes from presentation, the patient progressed from that very subtle ECG to cardiac arrest. Dr. McLaren recently wrote an excellent blog post on a similar case. Some advocate that calcium should not be given for "just" peaked T waves, but I disagree. If a patient comes in sick with this ECG, and the cause for illness is not immediately apparent, it is most appropriate to give empiric IV calcium while awaiting the results of further workup. Earlier recognition and administration of treatment may have saved this patient an arrest.

Learning points:
  • Identify subtle ECG evidence of hyperkalemia
  • When in doubt, give calcium

Here are a couple other cases of hyperkalemia with small, but peaked, T-waves:

A Tragic Case, related to the last post (this one is especially interesting and terrible)






Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer. (Physician also reads it as normal)


This is on a previous visit with K = 6.6:



After treatment: 



ST Elevation in I and aVL, with reciprocal ST depression in lead III






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MY Comment, by KEN GRAUER, MD (2/18/2025):

===================================
There are always "lessons to be learned" from the multiple clinical presentations of hyperkalemia. Today's case by Dr. Frick highlights this clinical reality in a patient whose initial ECG could easily pass for "normal". Among the "lessons" from today's case are the following:
  • Although many patients follow the "textbook sequence" of ECG changes with their hyperkalemia — a significant percentage of patients do not. 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.
  • The above said — today's initial ECG does show T wave peaking in 8/12 leads! As per Drs. Frick and Meyers — it is the composite picture (ie, that 8/12 leads show subtle-but-real T wave peakingthat will prompt the astute clinician to wonder if that isn't 5 or 6 leads too many to show upright, symmetric T waves that are all peaked at their highest point (with another lesson being that peaked hyperkalemic T waves are not necessarily tall).
  • Finding a prior ECG on today's patient simplified our diagnostic task — as the comparison of prior with current ECGs provided by Dr. Frick left no doubt that there has been new, diffuse T wave peaking (with the inescapable conclusion of knowing that the serum K+ level needs to be immediately checked).
  • The other distinct ECG finding that the astute clinician will appreciate from today's initial ECG — is a uniquely flat ST segment. As I've emphasized in the February 10, 2025 and March 19, 2019 posts — hyperkalemia and hypocalcemia often occur together, and often produce a readily identifiable pattern of flat ST segments ending in peaked T waves that we see in today's case.
  • Finally — Today's case shows the consequences of not heeding the ECG signs that are diagnostic of significant hyperkalemia (rapid progression to marked bradycardia — loss of P waves — QRS widening— demonstrating once more the need to treat with IV Calcium without waiting for the lab to confirm what you already know from arrhythmia progression over the course of 2 ECGs (with the need for IV Calcium being that much more urgent in today's patient whose initial ECG suggests serum Ca++ is already low).
  •  =  =  =  =  =  =  =  =  =  =
  • P.S.: We are not provided with information in this case as to WHY this patient developed hyperkalemia! So part of the ED evaluation should also consist of evaluating for: i) Renal function (esp. for any potential recent worsening of renal function that might predispose to hyperkalemia); ii) Volume status (ie, hypovolemia may precipitate an increase in serum K+ levels); iii) Any potential K+-retaining medications that the patient might be taking? (ie, K+ supplements? K+-retaining diuretic or ACE-Inhibitor or ARB); — and, iv) Anything else that might potentially predispose to subtle development of unsuspected hyperkalemia.



 


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