A 70 yo man with a h/o DM, HTN, CAD, chronic renal insufficiency and recent NonSTEMI with pulmonary edema who is on carvedilol and amlodipine called 911 for weakness. His pulse was 40. BP was about 100 systolic.
Here is his prehospital ECG:
Bradycardia and large T-waves should immediately make you want to know the K. The K was 6.8 mEq/L. Creatinine was elevated at 5.0 mg/dl and the patient stated his urine output was low. He also had melena and a low hemoglobin. We placed a dialysis catheter and he went to the ICU for dialysis. The next AM this ECG was recorded:
Learning point: Bradycardia should always make you think of hyperkalemia, especially when on beta blockers and/or calcium channel blockers.
Here is his prehospital ECG:
There is sinus bradycardia with Giant T-waves. |
Bradycardia and large T-waves should immediately make you want to know the K. The K was 6.8 mEq/L. Creatinine was elevated at 5.0 mg/dl and the patient stated his urine output was low. He also had melena and a low hemoglobin. We placed a dialysis catheter and he went to the ICU for dialysis. The next AM this ECG was recorded:
Normal sinus rhythm and normal T-waves. |
Learning point: Bradycardia should always make you think of hyperkalemia, especially when on beta blockers and/or calcium channel blockers.
In patients receiving one or more agents that depress SA node and atrioventricular (AV) node function, a syndrome of bradycardia, renal failure, AV block, shock, and hyperkalemia (BRASH), has been described. Patients with BRASH are generally taking therapeutic doses of SA and AV node blocking medications, and the level of hyperkalemia may be mild. However, the severity of bradycardia (caused by sinus arrest and/or AV block) is generally greater than expected for either the dose/level of SA and AV node blocker or the level of hyperkalemia.
Dr. Smith, in first ECG there is ST elevation in V2-V5 but return to isoelectric after dialysis. Is it due to hyperkalemia, or else?
ReplyDeleteYes, all due to hyperkalemia!
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