CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 AFRICA 99 cardiac action potential and reduce the amplitude of the action potential in the atrioventricular (AV) node.7,8 It has also been shown that extremely low levels of sodium in the fluid perfusing isolated heart muscle can reduce the number of contractions as well as the excitability and conduction velocity.9 Remarkably, our patient developed various cardiac arrhythmias at different serum sodium concentrations. Clinical studies have suggested that hyponatraemia may cause atrial fibrillation (AF) episodes.10,11 Hyponatraemia due to water retention increases atrial wall stretch, which can increase vulnerability to atrial arrhythmia.12 A study on rabbit hearts demonstrated that hyponatraemia induced genesis of pulmonary vein burst firing, which may contribute to the high occurrence of AF.13 AF might also be due to a combined effect of electrolyte disturbance or induced by bradycardia during sinus arrest. However, AF induced by transient bradycardia is rare and its underlying mechanisms remain unclear.14 The patient was found to have peaked T waves on ECG during severe hyponatraemia (Fig. 1A). T-wave shape reverted to normal after the hyponatraemia was corrected. Although T-wave shape changes in hyperkalaemia are well known, peaked T waves are rare in hyponatraemia. It is recommended that ECG manifestations of peaked T waves should be clinically contextualised and not attributed only to hyperkalaemia. In the case presented here, the patient was admitted to hospital on foot and had no previous history of heart disease. Treatment of the patient with sinus arrest, AV block and AF was to stop diuresis and supply sodium only. As the patient’s sodium levels returned to normal, the clinical symptoms and ECG also improved and no further arrhythmia was identified at follow ups, which made us attribute the temporary changes in the ECG to low sodium levels. Our patient experienced hyperkalaemia during the treatment of hyponatraemia. After treatment with hypertonic saline on the first day, her potassium level reached 6.01 mmol/l. Three possible mechanisms could explain this phenomenon. Firstly, when the patient received a high dosage of sodium after severe hyponatraemia, there was a reduction in aldosterone secretion, which would tend to decrease the rate of potassium secretion and may consequently reduce urinary excretion of potassium.15 Secondly, the patient’s glomerular filtration rate was low, reducing distal tubular flow rates. The potassium concentration may have built up relatively early in the tubule and thus progressively decreased the electrochemical gradient principal Table 1. Changes in electrolyte levels and ECG manifestations Time Serum sodium (mmol/l) Serum potassium (mmol/l) Serum calcium (mmol/l) ECG 9 December 131 5.6 1.69 Normal sinus rhythm 14 December, 11:20 102 (↓) 5.14 1.71 Sinus arrest; junctional escape beat (Fig. 1A) 14 December, 16:40 114.8 (↓) 6.01 (↑) 1.75 Atrial fibrillation (Fig. 1B) 15 December, 10:38 118.9 (↓) 6.14 (↑) 1.72 Atrial fibrillation with second-degree AV block; ventricular premature beat (Fig. 1C) 15 December, 18:00 132 5.5 1.72 Normal sinus rhythm (Fig. 1D) 15 December, 23:00 127.9 (↓) 5.14 1.75 Normal sinus rhythm Fig. 1. Manifestations of the patient’s ECG. (A) Sinus arrest (the longest R-R interval was 3.8 s) and junctional escape beat with a sodium level of 102 mmol/l. (B) Atrial fibrillation (AF) when the sodium level reached 114.8 mmol/l. (C) AF with second-degree AV block and ventricular premature beat when the sodium level reached 118.9 mmol/l. (D) Normal sinus rhythm when the sodium level reached 132 mmol/l. A B C D
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