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| Year : 2010 | Volume
: 21
| Issue : 2 | Page : 339-341 |
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| Hyperkalemia presenting as wide-complex tachycardia in a dialysis patient |
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Ankur Gupta, Anil P Bhatt, Ambar Khaira, Dipankar M Bhowmik, Suresh C Tiwari
Department of Nephrology, All India Institute of Medical Sciences, New Delhi, India
Click here for correspondence address and email
| Date of Web Publication | 9-Mar-2010 |
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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 | |  |
| 1. | Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial 2001;14:348-56.  [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. |
| 3. | Podbevsek D. Hyperkalemia and wide QRS complex tachycardia in a dialysis patient. Lijec Vjesn 2005;127:58-9. |
| 4. | McLean SA, Paul ID, Spector PS. Lidocaineinduced conduction disturbance in patients with systemic hyperkalemia. Ann Emerg Med 2000; 36:615-8. [PUBMED] |
Correspondence Address:
Ankur Gupta
Department of Nephrology, All India Institute of Medical Sciences, New Delhi
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 20228526 
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