Triage: Sent from PCP office for low K.  No symptoms

History of Present Illness: A woman in her mid 70’s with a history of HTN on unknown meds is sent to the ER for low potassium.  She denies any symptoms.

Vital Signs: Pulse 72, BP 145/83, Resps 18, temp 98.1

Physical Exam: She appears her stated age and is notably short and thin.  Physical exam is normal with clear lungs, no splinting and no murmur and no peripheral edema

An ECG is done:

Computer Read: NSR at 69 with short PR, low QRS voltage, 

What is the most likely cause of ECG findings in this patient?

  • A) ACS
  • B) Hypokalemia
  • C) PE
  • D) Drug effect
  • E) None of the above

SCROLL DOWN FOR ANSWERS & 1-MINUTE CONSULT

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ANSWER:

  • A) ACS
  • B) Hypokalemia
  • C) PE
  • D) Drug effect
  • E) None of the above – CORRECT – K was actually 6.3 and Cr 1.9 and bicarb 17

My Read: There is ST depression in the inferior and lateral leads with maybe a touch of ST elevation in V1-V2, thought that might be normal (would be nice to compare to a prior ECG).  I was handed this ECG from triage long before I saw the patient and was initially worried about ischemia due to the ST depression in multiple leads, but then I was told she had no symptoms and was there for low K.  Low K can also cause ST depression.

CASE CONCLUSION: After being handed the ECG I then read the triage not and it said patient had no symptoms but was sent in for low potassium from blood drawn yesterday at the PCP office.  I then went to see the patient.  I had a little confirmation bias and overconfidence, knowing hypokalemia could cause ST depression.  I asked if she was on HCTZ and she, replied “Yes I am pretty sure that is one of them”.

I actually ordered potassium before the labs came back with a potassium of 6.3.  I had forgotten that hyperkalemia can also cause ST depression.  Fortunately the nurses had not give the potassium and I was able to cancel it.  Eventually we were able to determine that she was not only on HCTZ, which is famous for dropping K, but was also on losartan and spironolactone, both of which can increase K.

Looking more carefully at the morphology of the ST depression and T wave, both are more consistent with hyperkalemia than the typical scooped out ST depression of hypokalemia.   Here creatinine had risen from 0.8 to 1.5 as well, likely contributing to hyperkalemia.

Case lessons:

  1. Thought it may be safer to treat electrolyte issues suggested by the ECG without lab confirmation, especially if the patient has been fainting or is symptomatic or ECG changes are severe, consider waiting for labs if the patient has been asymptomatic and is stable.  Venous blood gas can give quicker results if you are in a rush.
  2. ST depression and QT prolongation can both be caused by either high or low potassium, which is definitely unfair.
  3. With high potassium the ST depression is usually flat and the QT prolongation is due to a long, flat ST segment as in this case.  Also the T wave is usually on the narrow side.  In this patient T waves were short but still narrow/spiky.
  4. With hypokalemia the ST depression is usually scooped out looking and the QT prolongation is due to a U wave or to TU fusion.  These look different so pay attention and do as I say not as I did.  Below is an ECG from a patient with a K of 2.4 for comparison.