A 72-year-old woman came to the hemodialysis center after the long interdialytic period of the weekend, reporting generalized muscle weakness to the point of preventing ambulation.
She had stage V CRE on regular hemodialysis for four years.
She had unilateral atrial septal defect due to chronic atrial fibrillation with recurrent bradycardia.
Among his other antecedents, type 2 diabetes mellitus stood out in treatment with oral antidiabetics and arterial hypertension.
Its usual medications included: amiodarone, acetylsalicylic acid (no effects on potassium homeostasis).
Adherence to medical treatment was low and frequent transgressive eating disorders were common.
Physical examination was normal except for muscle weakness.
The constants were correct and the patient was normoglycemic.
The electrocardiogram (ECG) showed rhythm of seizures, with no other abnormalities.
Urgent blood tests revealed a potassium level of 8.2 mEq/l.
Pending the hemodialysis session, conventional treatment of hyperkalemia was initiated, establishing calcium gluconate, intravenous salbutamol and insulin and glucose infusion.
Minutes after starting this treatment, the patient presented a sudden decrease in the level of consciousness, with undetectable blood pressure and signs of peripheral hypoperfusion.
At that time, the ECG showed ventricular capture failure.
Urgent hemodialysis was performed, reversing both the clinical and electrocardiographic changes rapidly and completely.
