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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 2  |  Page : 339-341
Hyperkalemia presenting as wide-complex tachycardia in a dialysis patient

Department of Nephrology, All India Institute of Medical Sciences, New Delhi, India

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Date of Web Publication9-Mar-2010

How to cite this article:
Gupta A, Bhatt AP, Khaira A, Bhowmik DM, Tiwari SC. Hyperkalemia presenting as wide-complex tachycardia in a dialysis patient. Saudi J Kidney Dis Transpl 2010;21:339-41

How to cite this URL:
Gupta A, Bhatt AP, Khaira A, Bhowmik DM, Tiwari SC. Hyperkalemia presenting as wide-complex tachycardia in a dialysis patient. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2023 Feb 9];21:339-41. Available from: https://www.sjkdt.org/text.asp?2010/21/2/339/60207
To the Editor,

The diagnosis and management of wide com­plex tachycardia often proves challenging. We report to you unusual presentation of hyperka­lemia as wide complex tachycardia in a dialysis patient. Its prompt treatment with calcium glu­conate and hemodialysis completely reversed this life threatening condition. Hyperkalemia should be considered in differential diagnosis of wide complex tachycardia in patients at risk.

Hyperkalemia constitutes a medical emergen­cy, primarily due to its effects on the heart. Cardiac arrythmias associated with hyperkalemia include sinus bradycardia, sinus arrest, slow idio­ventricular rhythm, ventricular tachycardia, ven­tricular fibrillation and asystole. The usual cli­nical scenario is of hyperkalemia presenting as bradycardia. We report a 23-year-old man with chronic kidney disease stage 5 on maintenance hemodialysis thrice weekly for 2 months with unusual presentation of hyperkalemia. This young man missed his one dialysis session and pre­sented the next day to emergency room with palpitations for an hour. He was conscious with heart rate of 158/min and a supine blood pres­sure of 166/76 mmHg. Jugular venous pulse was raised with cannon waves. Variation in beat to beat intensity of first heart sound was present on auscultation. Oxygen saturation was 98%. An urgent 12 lead electrocardiogram (ECG) and arterial blood gas (ABG) was done along with bio-chemistry profile. ECG showed a wide complex tachycardia [Figure 1]. ABG revealed metabolic acidosis with potassium (K + ) of 8.6 mmol/L. A 10 mL of 10% calcium gluconate was given intravenously and the patient underwent hemodialysis. His Heart rate settled to 132/min by the time he reached the dialysis room. He­modialysis was done under cardiac monitoring and started with a dialysate K + bath of 1 mmol/L. Biochemistry showed a serum K + of 8.5 mmol/ L with no other significant electrolyte abnor­mality. Cardiac enzymes were normal. Three hours later, heart rate came down to 84/min and ECG showed a normal sinus rhythm. Dialysate K + was raised to 2 mmol/L and dialysis was completed for 4 hours. A post dialysis serum K + was 4.6 mmol/L. A 2D-echocardiography done after stabilization revealed concentric left ven­tricular hypertrophy with ejection fraction of 60% and no regional motion abnormality.

Hyperkalemia accounts for 1.9% to 5% of deaths among patients with end- stage renal fai­lure (ESRF). It is the reason for emergency he­modialysis in 24% patients with ESRF on he­modialysis. [1] The differential diagnosis of a wide complex tachycardia in hyperkalemia can be particularly problematic. Though there are feline models of such a presentation, but hyperkale­mia and wide QRS complex tachycardia in a dialysis patient is rare. [2],[3] Its treatment could prove rather challenging. Procainamide and li­docaine are probably the most effective agents for acute therapy in ventricular tachycardias. However, hyperkalemia potentiates the blocking effect of lidocaine on cardiac sodium channel and may precipitate asystole or ventricular fi­brillation. [4] Contrary to the management of wide complex tachycardia of other etiologies, injec­table calcium preparations would form the first line of treatment. Subsequently, hemodialysis with a low K + dialysate followed by a graded approach can be adopted once the acute arrhy­thmia has resolved. With such timely manage­ment progression to sine wave pattern, ventricu­lar fibrillation or asystole can be averted.

To conclude, hyperkalemia should always be considered in differential for etiologies of wide­complex tachycardia in a dialysis patient. Early recognition and prompt treatment with calcium gluconate and hemodialysis can completely re­verse this life threatening condition.

   References Top

1.Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial 2001;14:348-56.  Back to cited text no. 1  [PUBMED]    
2.Norman BC, Cote E, Barrett KA. Wide-complex tachycardia associated with severe hyperkalemia in three cats. J Feline Med Surg 2006;8:372-8.  Back to cited text no. 2      
3.Podbevsek D. Hyperkalemia and wide QRS complex tachycardia in a dialysis patient. Lijec Vjesn 2005;127:58-9.  Back to cited text no. 3      
4.McLean SA, Paul ID, Spector PS. Lidocaine­induced conduction disturbance in patients with systemic hyperkalemia. Ann Emerg Med 2000; 36:615-8.  Back to cited text no. 4  [PUBMED]    

Correspondence Address:
Ankur Gupta
Department of Nephrology, All India Institute of Medical Sciences, New Delhi
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Source of Support: None, Conflict of Interest: None

PMID: 20228526

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