YOU'RE ASSESSING your patient, Roger Stratton, 62, when he suddenly slumps over. You rapidly assess him and verify that he's unresponsive, apneic, and pulseless. You call a code, then start CPR. Within minutes, the code team arrives and verifies Mr. Stratton's cardiac rhythm as pulseless electrical activity (PEA). As soon as I.V. access is established, you give 1 mg of epinephrine I.V. push and continue CPR. (Epinephrine can be repeated every 3 to 5 minutes.) Once endotracheal tube placement is confirmed, you send stat blood work to the lab. Because the PEA rate is slow, you also give 1 mg atropine I.V. push, while searching for contributing factors to the PEA. Atropine can be repeated every 3 to 5 minutes up to 3 doses.
What's the situation?
Mr. Stratton arrived at the ED about 10 minutes ago with complaints of generalized fatigue, severe weakness, and palpitations. When you took his history, he denied any other significant acute or chronic medical problems, and said he hadn't seen a health care provider in over 25 years.
His stat serum electrolyte panel shows a potassium level of 7.6 mEq/L (normal range, 3.5 to 5 mEq/L); serum blood urea nitrogen (BUN) level of 80 mg/dL (normal, 7 to 20 mg/dL); and creatinine of 5 mg/dL (normal, 0.6 to 1.2 mg/dL).
What's your assessment?
Mr. Stratton has hyperkalemia, or a serum potassium level greater than 5 mEq/L, probably secondary to the acute renal failure indicated by his elevated BUN and creatinine levels. Significant hyperkalemia (a level greater than 7.5 mEq/L) can lead to cardiac dysrhythmias (as in Mr. Stratton's case) and sudden death.
What must you do immediately?
Your first priority is to rapidly reduce Mr. Stratton's serum potassium level. Immediately prepare and administer 10% calcium chloride solution, 1,000 mg via slow I.V. push. Although calcium chloride won't lower Mr. Stratton's serum potassium level, it antagonizes the toxic effects of hyperkalemia at the cell membrane. Calcium chloride's onset of effect is 1 to 3 minutes and its effect lasts 30 to 60 minutes. The dosage can be repeated if necessary.
To shift potassium into the cells, you also administer 50 mEq of sodium bicarbonate by slow I.V. push. This will help to reduce the hyperkalemia that caused Mr. Stratton's PEA and also will help correct the metabolic acidosis often associated with hyperkalemia.
Prepare to administer 10 units of I.V. regular insulin, to shift potassium back into the cell, and 50 mL of 50% dextrose (25 g), to prevent hypoglycemia. Soon after he receives these medications, Mr. Stratton's PEA converts to sinus bradycardia with return of a pulse and BP of 90/50 mm Hg.
What should be done later?
Once he's stabilized, Mr. Stratton is transferred to the cardiac ICU for continuous monitoring, additional hyperkalemia management, and a renal consult. He'll need dialysis to replace his inadequate renal function and control his serum potassium level. Further management will depend on the underlying cause of his acute renal failure.