Recurrent Life‐Threatening Hyperkalemia without Electrocardiographic Changes

1North Central Bronx Hospital, Bronx, NY
2Freeman Health System, Joplin, MO
3Charleston Area Medical Center, Charleston, WV

Meeting: Hospital Medicine 2010, April 8-11, Washington, D.C.

Abstract number: 285

Case Presentation:

We report a case of profound recurrent hyperkalemia with no associated EKG changes in an 84‐year‐old female patient with normal baseline renal functions. Her past medical history was significant for hypertension, CHF, pulmonary hypertension, CVA, and multiple nodules in the liver and lungs with unknown primary malignancy. The patient was admitted with poor oral intake and dehydration. On initial assessment, she was found to be hemodynamically stable, with normal cardiopulmonary and abdominal exam. Initial lab work revealed K 10.1 mEq/L, Na 134 mEq/L, C1 111 mEq/L, HCO3 16.1 mEq/L, BUN 71 mg/dL, Cr 1.4 mg/dL, Ca 9.9 mg/dL, Mg 2.3 mg/dL, and PQ4 4.3 mg/dL. ABG analysis revealed metabolic acidosis with pH 7.22, O2; partial pressure 71 mm Hg, and CO2 partial pressure 36 mm Hg. Chest x‐ray was consistent with cardiomegaly and right‐sided pleural effusion. EKG showed NSR at 96 bpm, left axis deviation, and left ventricular hypertrophy by voltage criteria with normal PR interval and QRS complex. T waves were not tall or tented. Hyperkalemia was attributed to dehydration and type IV RTA. The treatment of hyperkalemia was initiated with calcium gluconate, insulin with dextrose, Kayexalate and bicarbonate infusion. Subsequently, K levels trended down to 4.8 mEq/L with BUN of 18 mg/dL and creatinine 0.9 mg/dL. The patient had repeat EKGs during the course of treatment to monitor for the signs of hyperkalemia, but interestingly none of the repeat EKG recordings had any manifestations of hyperkalemia. She was admitted twice in next 4 months and had high K exceeding 8.5 mEq/L with essentially no associated EKG changes. She was ruled out for pseudohyperkalemia and tumor lysis syndrome. Further workup of the patient revealed metastatic adenocarcinoma of the lung with aldosterone deficiency.


There is a predictable sequence of EKG changes with increasing hyperkalemia when the serum K exceeds 6.5‐7 mEq/L and it has been shown that high levels of K > 8 mEq/L are almost always associated with the classic EKG manifestations. Profound hyperkalemia has invariably been associated with peaked T waves, a prolonged PR interval, followed by increased QRS durations to a sine wave, although in patients with ESRD, the usual EKG manifestations of hyperkalemia could be less pronounced than those with normal renal functions, possibly because of variations in serum Ca concentration. The other possible reason for attenuation of cardiotoxic EKG manifestations of hyperkalemia in these patients could be the slow rate of rise in serum potassium in patients with chronic renal failure. Our case is unique, as it illustrates the lack of correlation between severe hyperkalemia and associated EKG changes, even with normal renal function.


Life‐threatening elevations of serum K can be seen in the absence of typical EKG findings; therefore, caution should be exercised in excluding the presence of hyperkalemia or monitoring the response to its therapy.

Author Disclosure:

S. Khalid, North Central Bronx Hospital, H. Khattak, Freeman Health System, K. Manzoor, Charleston Area Medical Center.

To cite this abstract:

Khalid S, Khattak H, Manzoor K. Recurrent Life‐Threatening Hyperkalemia without Electrocardiographic Changes. Abstract published at Hospital Medicine 2010, April 8-11, Washington, D.C. Abstract 285. Journal of Hospital Medicine. 2010; 5 (suppl 1). Accessed October 17, 2019.

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