A 35-year-old man is brought to the emergency department due to generalized weakness. Medical history is significant for end-stage renal disease due to glomerulonephritis. The patient usually does peritoneal dialysis at home but has not had treatment for the past 2 days. Temperature is 37.3 C (99.1 F), and blood pressure is 80/60 mm Hg. Cardiopulmonary examination shows no murmurs, rubs, or gallops. The abdomen is soft and nontender. Bowel sounds are present. Pulses are palpable bilaterally. Muscle strength is 4/5 in all 4 extremities. ECG is shown in the exhibit. Which of the following is the most appropriate next step in management of this patient?
Clinical features of hyperkalemia | |
Sequence of |
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Cardiac membrane stabilization |
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Rapidly acting |
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Removal of potassium |
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This patient with end-stage renal disease has muscle weakness, hypotension, and an ECG notable for QRS complex widening, bradycardia, and a lack of P waves. This presentation is concerning for hyperkalemia (potassium >5.5 mEq/L), likely due to missed peritoneal dialysis, resulting in decreased potassium excretion. Among the most serious manifestations of hyperkalemia are muscle weakness and cardiac conduction abnormalities (eg, bradycardia with resulting hypotension) due to impaired neuromuscular transmission caused by the potassium imbalance. Although the classic ECG findings associated with hyperkalemia are peaked T waves, the sequence includes: peaked T waves (not seen in this patient) → progressive lengthening of the PR interval → absent/flattened (ie, low amplitude) P waves → QRS complex widening → sine wave pattern.
Once hyperkalemia is recognized, emergency treatment is indicated if there are attributable ECG changes. The most immediate intervention is intravenous calcium (chloride or gluconate) administration to stabilize the cardiac myocyte membrane and make it resistant to the effect of hyperkalemia for 30-60 minutes. Intravenous insulin (in combination with glucose) and/or beta-2 agonists (eg, albuterol) are used to transiently shift potassium intracellularly, which lowers the serum potassium level.
Definitive measures to reduce total body potassium are still required, including:
Reversal of correctable etiology (eg, intravenous fluids for prerenal azotemia)
Diuretics (avoided in patients with dehydration)
Cation exchangers to remove potassium via the gastrointestinal tract (effect takes hours)
Dialysis (eg, hemodialysis, peritoneal dialysis), which takes time to schedule and perform; emergency treatment with calcium administration takes precedence (Choice B).
(Choice A) Although hypotension and weakness in the setting of peritoneal dialysis are concerning for peritonitis and sepsis, this patient's lack of fever and abdominal symptoms (eg, pain, tenderness to palpation) makes peritonitis unlikely. Sepsis is also more likely to cause hypotension and tachycardia (not bradycardia).
(Choices C and E) Cardioversion is indicated for unstable arrhythmia (eg, ventricular tachycardia with hypotension) but not bradycardia. Pacing and vasopressor support (eg, dopamine) may be considered if the patient's bradycardia and hypotension persist, but potassium correction takes precedence.
(Choice F) Sodium bicarbonate is used in some patients with metabolic acidosis to raise pH, which can lead to intracellular potassium movement. However, efficacy is limited.
Educational objective:
Patients with hyperkalemia who develop arrhythmias or other significant ECG changes should be treated rapidly with intravenous calcium. Temporary measures (eg, intravenous insulin plus glucose) and definitive treatment (eg, dialysis) to reduce serum potassium should follow calcium administration.