Department of Nephrology, Rabin Medical Center, Campus Golda, Petach Tikva, Israel
Sir,
We read, with interest, the article in the June edition of NDT regarding atrial fibrillation in dialysis patients [1].
We do feel, however, that a potentially important point was missing. Haemodialysis patients drop their serum potassium levels during a haemodialysis treatment session. When dialysed against a potassium concentration of 2 mEq/l, these patients will become relatively hypokalaemic during the last 2 h of a standard 4-h treatment. During this period atrial fibrillation commonly occurs. Also, Zebe rightly points out that atrial fibrillation ... as a rule stops spontaneously without therapeutic intervention 23 h after the dialysis session. Could this return to sinus rhythm be attributable, at least in part, to the sharp rise in serum potassium levels known to occur after dialysis has ended?
Hypokalaemia is considered to be an accepted risk factor for both ventricular and supraventricular arrhythmias [2]. This has been shown in patients on prolonged diuretic therapy [3], and hypokalaemia may actually be a serious problem in patients with either an acute myocardial infarction [4], or with a failing heart [5].
For this reason most of our dialysis patients who have a previous history of atrial fibrillation occurring during haemodialysis are subsequently dialysed against a dialysis potassium concentration of 3.0 mEq/l. This is irrespective if the patient is receiving digoxin or not.
Finally, it may be interesting to speculate whether intradialytic magnesium supplementation may help in ameliorating atrial fibrillation in these patients [6].
References