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The authors work in the Department of Cardiology at the M.D. Anderson Cancer Center in Houston, Tex. They have indicated no relationships to disclose relating to the content of this article. Erich Fogg is Assistant Professor in and Program Director of the Physician Assistant Program at the College of Health Professions, University of New England, Portland, Me.

CASE

A 70-year-old man presents to his primary oncologist to consider new chemotherapy to treat relapsed chronic lymphocytic leukemia. During the assessment, a routine ECG reveals new-onset bradycardia. The patient is sent to our cardiology clinic for further evaluation. In our clinic, he describes a 1-day history of increasing exertional dyspnea, fatigue, bilateral flank pain, and dark tea-colored urine. He denies nausea, vomiting, chest pain, fever, or syncope. His medical history includes diabetes, hypertension, chronic renal insufficiency, heart failure, and the leukemia. Medications include enalapril, half a 5-mg tablet daily; spironolactone, half a 25-mg tablet daily; furosemide, 40 mg twice a day; isosorbide mononitrate, 30 mg daily; simvastatin, 40 mg daily; metformin, 500 mg twice a day; and metoprolol succinate, 100 mg daily.

Physical examination The patient appears somewhat somnolent, but he is responsive. His BP is 100/56 mm Hg; pulse, 48 beats per minute. The jugular venous pressure is elevated at 11 cm above the right atrium. Faint bibasilar crackles are heard on lung auscultation. Cardiac evaluation reveals a bradycardic rate but a regular rhythm; S1 and S2 sounds are normal, without an S3. A grade II/VI holosystolic murmur is noted at the apex. The abdomen is nondistended with active bowel sounds and tenderness at the bilateral flanks. There is no significant evidence of edema in the lower extremities. The ECG shows bradycardia (44 beats per minute) and a widened QRS complex (see Figure 1).

WHAT IS YOUR WORKING DIAGNOSIS?

DISCUSSION

The correct diagnosis is junctional escape rhythm secondary to acute hyperkalemic renal failure in the setting of concurrent beta-blocker therapy. Notable findings on the ECG include lack of P waves, widened QRS complexes, and peaked T waves. Laboratory test results reveal a potassium level of 6.5 mEq/L and a creatinine level of 3.3 mg/dL. Serial cardiac panels were negative for MI, and a urinalysis was negative for infection or myoglobinuria.

Hyperkalemia can manifest without symptoms or with nonspecific weakness and fatigue. Advanced findings can include muscle weakness in the lower extremities that progresses proximally, eventually leading to paralysis. The ECG in patients with hyperkalemia can show progressive findings that may initially reveal peaked T waves followed by an increase in the PR interval and QRS duration. Loss of the P waves, ventricular fibrillation, and even asystole will ensue if this electrolyte abnormality persists.

Treatment Management of hyperkalemia consists of multiple regimens.¹ Calcium gluconate directly antagonizes potassium’s effects on the cell membrane to protect the cardiac conduction in less than 5 minutes. Albuterol, insulin, and sodium bicarbonate shift the potassium into cells, thereby reducing the serum potassium concentration. When insulin is used to treat hyperkalemia, glucose should always be administered to prevent hypoglycemia. However, the above measures help only temporarily. For definitive treatment, excess potassium can be removed by use of sodium polystyrene sulfonate, loop diuretics, or hemodialysis. There is a potential for exacerbation of fluid overload when using polystyrene sulfonate or sodium bicarbonate in patients with severe heart or renal failure; therefore, these therapies should be used with caution.

Outcome The patient was immediately transferred to the emergency department. His cardiac medications were discontinued, and he received nebulized albuterol, calcium gluconate, and sodium polystyrene sulfonate. . Transcutaneous pacing was initiated, and the patient was admitted. Despite these measures, the bradycardia and other ECG changes did not completely resolve until after hemodialysis. The patient was discharged 2 days later in stable condition without any significant evidence of volume overload. The enalapril and spironolactone were not resumed, but the other medications were started again.

Comment Although ACE inhibitors and spironolactone are commonly used for management of heart failure, these drugs can precipitate hyperkalemia, especially in patients with underlying renal dysfunction or acute illness. Therefore, serum potassium, BUN, and creatinine levels must be monitored periodically.

REFERENCES

1. Kim HJ, Han SW. Therapeutic approach to hyperkalemia. Nephron. 2002;92(suppl 1):33-40.

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