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 ::  Introduction
 ::  Case report
 ::  Discussion
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ARTICLE
Year : 1979  |  Volume : 25  |  Issue : 3  |  Page : 174-176

A case of hypokalaemia simulating hyperkalaemia


Department of Medicine, Seth G. S. Medical College and K.E.M. Hospital, Parel, Bombay-400 012, India

Correspondence Address:
N C Talwalkar
Department of Medicine, Seth G. S. Medical College and K.E.M. Hospital, Parel, Bombay-400 012
India
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Source of Support: None, Conflict of Interest: None


PMID: 529171

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 :: Abstract 

A case of chronic renal failure with hypokalaemia presenting electrographically as tall `U' waves simulating tall `T' waves of hyperkalaemia is described. The differentiating points between hypokalaemia and hyperkalaemia on ECG have been highlighted.



How to cite this article:
Talwalkar N C, Chawla KP, Mehta P J, Gandhi A K, Thacker U M, Acharya VN. A case of hypokalaemia simulating hyperkalaemia. J Postgrad Med 1979;25:174-6

How to cite this URL:
Talwalkar N C, Chawla KP, Mehta P J, Gandhi A K, Thacker U M, Acharya VN. A case of hypokalaemia simulating hyperkalaemia. J Postgrad Med [serial online] 1979 [cited 2023 May 31];25:174-6. Available from: https://www.jpgmonline.com/text.asp?1979/25/3/174/42137



 :: Introduction Top


Electrocardiographic changes of hypo­kalemia are very well described. How­ever, occurrance of tall `U' waves falling on `T' waves and giving an appearance of tall `T' waves is rather unusual. But it is important to diagnose such a condition, otherwise it may be mistaken for tall `T' waves characteristic of hyperkalaemia and wrongly treated with fatal results. We publish below a case of hypokalaemia which presented with tall `U' waves simulating tall `T' waves of hyperkalae­mia.


 :: Case report Top


Mrs. V. N., a thirty-six year old female patient was admitted to the K.E.M. Hospital, Bombay with a history of severe diarrhoea and vomiting for a period of two days.

She was a known case of chronic pyelonephri­tis and chronic renal failure for the last 10 months and was on diuretics since then. She was well controlled on conservative line of treatment, without requiring any dialyses and maintained at a level of serum Creatinine of 6 mg% and BUN of 51 mg%.

The present episode of diarrhoea was a severe one, with 10-12 watery stools per day. Vomit­ing was moderate, three to four times a day and was bilious in nature. Along with this she had oliguria and difficulty in breathing.

On examination, she was found to be average­ly built and nourished. She had pallor and grade III dehydration, with pulse of 100 per minute and blood pressure of 100/77 mm of Hg­A few irregular beats were noted in her pulse. She was obviously acidotic but otherwise her chest was clear. Her cardiovascular and alimen­tary system did not reveal any abnormalities, except occasional irregular heart beats. She was drowsy but otherwise there were no focal ab­normalities in her central nervous system. She did not have manifest tetany.

On investigations, following profile was noted. Haemogram; Haemoglobin was 8 gm%; Total WBC Count was 9800/cu. mm. with Neutro­phils-60%, Lymphocytes-32%, Eosinophils-6%, Monocytes-2%; ESR was 25 mm/1st hr. (Westergren). Her urine examination could not be done immediately as she remained anuric for almost 12 hours. Her blood biochemistry done on the next three successive days was as shown below in [Table 1].

Her total serum protein was 4.2 gms% with albumin of 1.8 gms% and globulins 2.4 gms % Serum Calcium was 7.6 mg.%; Phosphorus was 5 mg% Alkaline Phosphatase was 9 Bodan­sky units. Her electrocardiogram done at this stage is shown in [Figure 1]. Her serial electro­cardiograms done on the next two days are shown in [Figure 2] and [Figure 3] (See [Figure 1],[Figure 2] and [Figure 3] on page 176A).

Her infusion pyelograms done in 1976 had shown bilaterally small contracted kidneys with poor function on either side. Patient was treat­ed with intravenous potassium chloride (KCI), calcium gluconate and sodabicarb and on the second day she was taken up for peritoneal dialysis in view of her azotemia and electrolyte disturbances. However, patient expired within 4 days of dialysis.


 :: Discussion Top


This patient's E.C.G. taken on admis­sion showed tall 'T' wave like appear­ance. However these were quite wide and showed a slurring especially in lead V 5 (see [Figure 1] on page 176A). The E.C.G. also showed multiple ventricular premature heats. The QT interval was normal (0.4 sees). With clinical setting and such E.C.G. findings, it was obvious that these were tall 'U' waves in the E.C.G. which were simulating tall 'T' waves, and in fact this was hypokalaemia and not hyperka­laemia. This was confirmed by the serum electrolyte report [Table 1]. On correct­ing the hypokalaemia, both the serum electrolytes and E.C.G. picture improved and the tall 'U' waves disappeared (see [Figure 2] and [Figure 3] on page 176A).

It is known that hypokalaemia can give rise to tall 'U' waves which may be occasionally mistaken for tall 'T' waves of hyperkalaemia. [3],[5],[6],[7] Sama [5] has described tall 'U' waves simulating 'T' waves in 2 cases with hypokalaemia, hypochloraemia and metabolic alkalosis due to pyloric stenosis. In both the cases there was severe hypochloraemia and he attributed these 'U' wave changes to hypokalaemia and hypochloraemia.

In the present case also the patient did have moderate hypochloraemia [Table 1]. However, she had predominant meta­bolic acidosis and not alkalosis as in the cases reported by Sarma. [5] The role of chloride ions causing such changes is not reported elsewhere.

A phenomenon of T-U wave alternance causing tall 'U' waves in alternating beats has been reported. Kimura et al [4] believe that it is due to hypocalcaemia and Dolora and Pazzi [2] believe that both hypocalcaemia and hypokalaemia may be responsible. In this patient the levels of serum calcium and ionised serum calcium were low (serum albumin was 1.8 gm%) and this could have re­sulted in tall 'U' waves. As the patient was treated with calcium gluconate and potassium, it is difficult to say which of the two (or both the ions) was respon­sible for such a phenomenon. Hypo­magnesaemia also may be responsible in producing tall 'U' waves and 'U' wave alternance as reported by Bashour et al. [1] In this patient, measurement of serum magnesium could not be done.

Thus it is important to realise that tall 'U' waves may mimic tall `T' waves and a wrong diagnosis of hyperkalaemia may be made. Important points of differentia­tion are: (i) Clinical setting; (ii) Broad slurred 'U' waves; (iii) Ectopic activity which suggests hypokalaemia rather than hyperkalaemia, as potassium pro­tects the myocardium from ectopic acti­vity. [3] In our case, all these criteria were fulfilled.


 :: Acknowledgement Top


We express our thanks to the Dean, K.E.M. Hospital, Bombay for his kind permission to publish this case.

 
 :: References Top

1.Bashour, T., Rios, J. C. and Gorman, P. A.: U wave alternans and increased ven­tricular irritability. Chest, 64: 377-379, 1973.  Back to cited text no. 1    
2.Dolora, A. and Pozzi, L.: Electrical alter­nation of T wave without change in QRS complex. Brit. Heart J., 33: 161-163, 1971.  Back to cited text no. 2    
3.Hurst, J. W., Logue, R. B., Schlant, R. C. and Wenger, N. K.: "The Heart, Arteries and Veins". 3rd edition McGraw Hill, Koga Kusha Ltd., A Blackiston Publication, New York, St Louis, San Fransisco, Auckland, London, Toronto. Tokyo etc., 1974, p. 1500.  Back to cited text no. 3    
4.Kimura, E. and Yoshida, K.: A case showing electrical alternans of the T wave without change in the QRS complex. Amer. Heart J., 56: 391-393, 1963.  Back to cited text no. 4    
5.Sarma, R. N.: Unusually tall and narrow U waves simulating hyperkalemic T waves -Report of 2 cases of hypochloremic alkalosis with hypokalemia. Amer. Heart J., 70: 397-401, 1965.  Back to cited text no. 5    
6.Schamroth, L.: "The Disorders of Car­diac Rhythm". Blackwell Scientific Publi­cations, Oxford and Edinburgh, 1971, p. 504.  Back to cited text no. 6    
7.Schamroth, L.: Drug and Electrolyte effect. In, "An Introduction to Electro­cardiography". 5th Edition, Blackwell Scientific Publications, Oxford, Edinburgh and Melbourne, 1976, p. 82.  Back to cited text no. 7    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1]



 

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