Hyperkalemia Induced by the Sequential Administration of Metoprolol and Carvedilol

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Abstract

This report describes the occurrence of asymptomatic hyperkalemia induced by the sequential administration of metoprolol and carvedilol in an 81-year-old man with type II diabetes and stable stage III renal insufficiency. The potassium level rose to 5.6–5.7 mEq/L with metoprolol and normalized when the agent was discontinued. However, the potassium level rose again to 5.6 mEq/L after the administration of carvedilol but the level normalized by halving the dose. The observations of hyperkalemia induced by two different β-blocker drugs in the same patient confirm that this side effect is common to all β-blocker drugs.

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Hyperkalemia complicating propranolol treatment of an infantile hemangioma.

Helena Pavlakovic, Max Lakomek, Silke Kietz … (2010)

Propranolol treatment was recently reported to be successful for the management of severe infantile hemangioma. Known adverse effects of propranolol treatment include transient bradycardia, hypotension, hypoglycemia, and bronchospasm (in patients with underlying spastic respiratory illnesses), which led to a general recommendation to gradually increase propranolol dosage and closely monitor patients' hemodynamics at the onset of therapy. To date, no serious or unexpected adverse effects that required specific intervention have been reported. In this report, we describe the case of a 17-week-old female preterm infant who presented with a large, ulcerated, cutaneous-subcutaneous hemangioma of the right lateral thoracic wall, which we treated successfully with propranolol. A few days into therapy, a potentially life-threatening adverse effect, severe hyperkalemia, was observed and required treatment with loop diuretics, fluids, and nebulized salbutamol to normalize her serum potassium levels. This therapy could be gradually tapered and finally discontinued only after several weeks of propranolol treatment. Our case report indicates that, at least during the initial phase of the propranolol treatment of infantile hemangioma, close monitoring of serum electrolytes, besides the monitoring of hemodynamics and blood glucose, is necessary.

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Resting skeletal muscle membrane potential as an index of uremic toxicity. A proposed new method to assess adequacy of hemodialysis.

J R Cotton, T D Woodard, N W Carter … (1979)

Electrochemical disturbances of skeletal muscle cells in untreated uremia are characterized by an increase in the intracellular sodium and chloride content, a decrease in intracellular potassium, and a low resting membrane potential. In this study, we have reexamined the foregoing and, in addition, have examined the effects of hemodialysis. Three groups of patients were studied. In the first group of 22 uncomplicated uremic patients, whose creatinine clearance (Ccr) ranged from 2 to 12 cm(3)/min per 1.73 m(2), resting transmembrane potential difference (Em) of skeletal muscle cells was measured. In each of the nine patients whose Ccr ranged between 6.3 and 12 cm(3)/min, the Em was normal (i.e., -90.8+/-0.9 mV, mean+/-SEM). However, as Ccr dropped below 6.3 cm/min, the Em became progressively reduced and assumed a linear relationship with the Ccr. In the second study, nine individuals with end-stage renal disease, whose mean Ccr was 4.3 cm(3)/min, underwent measurement of Em and intracellular electrolyte concentration before and after 7 wk of hemodialysis. Before dialysis, the Em was -78.5+/-2.1 mV, intracellular sodium and chloride were elevated, and the intracellular potassium was reduced. After 7 wk of hemodialysis the Em rose to -87.8+/-1.3 mV, and the intracellular sodium, chloride, and potassium became normal. In the third study, seven patients who were stable on 6-h thrice-weekly dialysis were studied before and after reduction of dialysis to 6 h twice weekly. In those individuals whose Em remained normal after 6 wk, dialysis time was reduced further. On thrice-weekly dialysis the Em was -91.2+/-1.0 mV. With reduced dialysis, the Em fell to -80.1+/-0.8 mV (P < 0.001). In each case, the Em became abnormal before significant signs or symptoms of uremia were noted. These findings demonstrate that end-stage renal disease is associated with serious electrochemical changes in the muscle cell which are reversed by hemodialysis and recur when dialysis time is reduced. Thus, serial observations of muscle Em may be a potentially powerful tool to assess adequacy of dialysis therapy.

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Carvedilol-induced hyperkalemia in a patient with chronic kidney disease.

Lindsay Hahn, Martin E Hahn (2015)

A 69-year-old male was admitted to the hospital with a chief complaint of abdominal pain, nausea, and vomiting. He had an extensive past medical history, including diabetes mellitus type 2 and chronic kidney disease stage III. Prior to admission, the patient was taking carvedilol 3.125 mg twice daily with no abnormality in his serum potassium. During hospitalization, his carvedilol was increased to 6.25 mg twice daily. The patient's serum potassium then rose from 4.8 to 6.7 mEq/L, with no improvement following administration of sodium polystyrene sulfonate. Nephrology concluded the carvedilol could be contributing to the hyperkalemia. The dose was decreased back to 3.125 mg twice daily, leading to the potassium normalizing to 4.4 mEq/L. The reported incidence of beta-blocker-induced hyperkalemia is less than 5%. A literature search revealed several cases of beta-blocker-induced hyperkalemia, but to the authors' knowledge, this is the first case describing carvedilol specifically. Utilization of the Naranjo probability scale indicated a possible probability that the carvediol was the cause.

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Author and article information

Contributors

S. Serge Barold:

ORCID: http://orcid.org/0000-0003-4951-6465

Journal

Journal ID (nlm-ta): Case Rep Cardiol

Journal ID (iso-abbrev): Case Rep Cardiol

Journal ID (publisher-id): CRIC

Title: Case Reports in Cardiology

Publisher: Hindawi

ISSN (Print): 2090-6404

ISSN (Electronic): 2090-6412

Publication date Collection: 2018

Publication date (Electronic): 15 October 2018

Volume: 2018

Electronic Location Identifier: 7686373

Affiliations

¹Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA

²San Diego Internal Medicine and Pediatrics Associates, San Diego, CA, USA

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Academic Editor: Magnus Baumhäkel

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S. Serge Barold http://orcid.org/0000-0003-4951-6465

Article

DOI: 10.1155/2018/7686373

PMC ID: 6205312

SO-VID: 4010a7b5-8086-4493-9515-d01eedc1db8b

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This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Hyperkalemia Induced by the Sequential Administration of Metoprolol and Carvedilol

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Most cited references 12

Hyperkalemia complicating propranolol treatment of an infantile hemangioma.

Resting skeletal muscle membrane potential as an index of uremic toxicity. A proposed new method to assess adequacy of hemodialysis.

Carvedilol-induced hyperkalemia in a patient with chronic kidney disease.

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