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Anwar Habib1, Mohd Aslam2, Muhammad Uwais Ashraf2*, Shadab A Khan2
1Department of Medicine, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard. New Delhi, India.
2Department of Medicine, JN Medical College, AMU, Aligarh, UP, India.

Volume 3, Issue 1, Page 55-57, January-April 2015.

Article history
Received: 15 March 2015
Revised: 25 March 2015
Accepted: 15 April 2015
Early view: 20 April 2015

*Author for correspondence


Hyperkalemia is a common clinical condition associated with serious cardiac arrhythmias and at times may lead to death. Timely detection of hyperkalemia in a susceptible patient is crucial for patient survival. The emergence of new medications that specifically target hyperkalaemia could lead to new therapeutic horizons. Also, the prevention of severe episodes of hyperkalemia in high-risk patients requires measures aimed at the longterm normalization of potassium homeostasis. We present here an interesting case of Chronic Kidney Disease presenting with life threatening arrhythmia secondary to hyperkalemia. Prompt treatment of hyperkalemia reverted the arrhythmia in our patient and saved the life of a patient.

Keywords: Chronic Kidney Disease, Hyperkalemia


Hyperkalemia is a common clinical condition associated with serious cardiac arrhythmias and at times may lead to death. Timely detection of hyperkalemia in a susceptible patient is crucial for patient survival. Hyperkalaemia is common in patients with chronic kidney disease (CKD), in part because of the effects of kidney dysfunction on potassium homeostasis and in part because of the cluster of comorbidities (and their associated treatments) that occur in CKD. Due to its electrophysiological effects, hyperkalemia stands out as a medical emergency that should be treated promptly. Also, the prevention of severe episodes of hyperkalemia in high-risk patients requires measures aimed at the long-term normalization of potassium homeostasis (An et al., 2012). The effective and safe medical interventions for restoring chronic potassium balance are very few, and the management of hyperkalaemia on a long-term basis is primarily limited to the correction of modifiable exacerbating factors (Yelena Mushiyakh et al., 2011. The emergence of new medications that specifically target hyperkalaemia could lead to new therapeutic horizons, and the preventive aspects as well as the management of incidentally discovered elevations in serum potassium levels cannot be over-emphasised (Ahee et al., 2000).


55 year old male, known diabetic, CKD patient on maintenance haemodialysis for the last two years was brought to emergency department with complaints of vomitings and extreme weakness since morning. He had undergone haemodialysis two days before. On examination he was conscious but confused, his pulse was feeble and blood pressure was unrecordable. His JVP was not raised, there was no jaundice, pallor, sweating or breathlessness. His chest was clear. Respiratory rate was 22/mt. Cardiac auscultation revealed feeble heart sounds. Per Abdomen examination was normal and there was no organomegaly. There was no cyanosis or peripheral oedema. His nurological examination was normal with depressed reflexes. His ECG (Fig. 1) showed broad QRS complexes (224 mseconds) coming at wide intervals. He was immediately shifted to ICCU where cardiac monitor showed a heart rate of 15-20/min. Suspecting hyperkalemia we gave him 20 ml of Calcium gluconate, 50 ml of sodium bicarbonate, 100 ml of 25% dextrose with insulin and 0.6 mg of atropine. He responded a little to this regime and his heart rate went up to 45/min, his radial pulse became palpable, his BP was recordable at 100/50 and he also became oriented and alert. By this time his lab report had come which showed serum potassium of 9.4meq/l. He was subjected to Haemodialysis with potassium free dialysate. After haemodialysis the patient fully improved and his potassium came down to 5.8 meq/l. His ECG also improved, HR became 60/min and QRS became 120 ms. His cardiac enzymes were found to be within normal limits and echocardiographic examination also revealed normal Left Ventricular functions. He was discharged in a stable condition and is coming for regular haemodialysis. We could not ascertain the cause for his hyperkalemia. Neither drugs (he is on amlodipine, calcitriol, sevelamer, calcium Carbonate and pantoprazole) nor dietary history indicated anything significant. It is possible that in his previous dialysis he may have been dialysed with inappropriate potassium concentration in the dialysate.


Hyperkalemia is a common cause of the cardiac arrhythmias seen in clinical practice. The challenge in managing hyperkalemia is that it can be difficult, and at times, impossible, to identify the condition solely on the basis of electrocardiographic information. Patients who present with hyperkalemia may have a normal electrocardiogram or have changes that are so subtle that physicians frequently have difficulty attributing these changes to increased potassium levels. In a study conducted at the University of Pittsburgh Medical Center, it was seen that, 46% of patients who had potassium levels greater than 6.0 mEq/L had electro-cardiographic changes, and only 55% of patients with potassium levels greater than 6.8 mEq/L had changes consistent with hyperkalemia (Martinez-Vea et al., 1999). In fact, there have been several reports in the literature of patients who had potassium levels greater than 7.5 mEq/L with no electrocardiographic manifestations of hyperkalemia (Ettinger et al., 1974). It has been seen that, even if there is some evidence of hyperkalemia on a patient’s electrocardiogram, physicians often tend to miss the diagnosis. Wrenn and colleagues conducted a study to ascertain the ability of physicians to predict the presence of hyperkalemia solely on the basis of their patients’ electrocardiograms (Fisch, 1973). In this study, the physicians were able to predict hyperkalemia with a sensitivity of 35% to 43% and a specificity of 85% to 86%. This study emphasizes how difficult it can be to diagnose hyperkalemia. Still, hyperkalemia can manifest with classical electrocardiographic changes which directly point to the diagnosis.

Figure 1. ECG at the time of presentation.
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Figure 2. ECG before discharge.
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As our case illustrates, at times it may be difficult to diagnose hyperkalemia. Patients presenting with severe hyperkalemia may at times have normal electrocardiograms or electrocardiographic abnormalities that are difficult to attribute to hyperkalemia. The diagnosis of hyperkalemia may be suspected in any patient with clinical risk factors that would predispose them. More often, patients with hyperkalemia have underlying renal dysfunction or are taking a medication known to increase serum potassium concentrations. The treatment of hyperkalemia must be prompt and immediate to prevent the development of fatal cardiac arrhythmias. If a patient has electrocardiographic manifestations of hyperkalemia, or his serum potassium level is greater than 6.5 mEq/L, the first drug to be administered should be calcium. The reason behind this is that calcium has rapid onset of action and it has ability to stabilize myocyte electrical activity. Insulin with dextrose infusion, and ß2 agonists should then be quickly administered to decrease extracellular potassium levels. Hemodialysis is the most effective tool to decrease systemic potassium levels. Sodium bicarbonate therapy has limited role in the routine treatment of hyperkalemia unless severe metabolic acidosis is present. It is therefore suggested that physicians should perform a thorough search to identify the cause of the hyperkalemia in order to prevent a recurrence.

None declared.


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