Renal Disease Division, Department of Medicine, State University of New York Downstate Medical Center, Brooklyn, New York, USA
![]() |
Abstract |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Methods. Pre-dialysis serum potassium concentration and other electrolytes were measured and simultaneous 12-lead electrocardiogram obtained.
Results. The 74 study subjects (45 men, 29 women) comprised 63 blacks (85%), four Hispanics (6%), four whites (6%), and three Asians (4%) of mean±standard deviation age 55.5±14.7 years. Mean pre-dialysis potassium concentration was 4.9±0.71 mEq/l (range 3.36.7). No study subject evinced arrhythmia or any of the typical electrocardiographic changes associated with hyperkalaemia. There was no significant difference in T wave amplitude (F statistic=2.1; P=0.11) or T wave to R wave ratio (F statistic=2; P=0.12) between quartiles of serum potassium concentration. Also, T wave amplitude was equivalent in patients with serum potassium concentration >5.5 mEq/l (7.1±4.1 mm) or 5.5 mEq/l (5.2±3.5 mm) (P=0.13). Linear regression analysis showed that the total serum calcium concentration had an inverse relation with T wave amplitude (P=0.03) after adjustment for other factors (a high total serum calcium concentration was associated with a low T wave amplitude).
Conclusion. Haemodialysis patients with hyperkalaemia may not exhibit the usual electrocardiographic sequella of hyperkalaemia, possibly due in part to fluctuations in serum calcium concentration. Thus, the absence of electrocardiographic changes in hyperkalaemic haemodialysis patients should be interpreted with caution.
Keywords: arrythmia; calcium; chronic renal failure; ECG; ESRD; haemodialysis; hyperkalaemia; potassium; T wave
![]() |
Introduction |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Ascertaining whether electrocardiography (ECG) is a reliable tool to detect potentially lethal hyperkalaemia in haemodialysis patients is critical, because the course of immediate care proffered by clinicians in non-renal failure patients with hyperkalaemia is guided by the presence or absence of the ECG changes associated with hyperkalaemia, such as a tall peaked T wave.
Moreover, relying on symptoms of hyperkalaemia may not be helpful in determining whether hyperkalaemia is life threatening in ESRD. The most prominent adverse effects of hyperkalaemia are unpredictable and potentially lethal arrhythmias, respiratory depression, and weakness [5,6]. But, weakness in a haemodialysis patient may result from myriad other reasons and would not necessarily be primarily attributed to hyperkalaemia.
![]() |
Subjects and methods |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Serum potassium concentration, total serum calcium concentration, serum sodium concentration, and serum bicarbonate concentration were measured in a blood sample obtained immediately before a regular dialysis treatment. Laboratory measurement of serum electrolytes was performed in the central hospital laboratory within 1 h after blood drawing. A simultaneous 12-lead ECG was obtained in all subjects, by one investigator (S.A.). All ECGs were read by one investigator without knowledge of the serum potassium concentration. The same investigator also measured the pre-cordial lead T wave amplitude and calculated the T wave to R wave ratio for each patient.
Conventional dialysis was performed using modified cellulose acetate hollow-fibre dialyzers (Althin Medical Inc., Miami Lakes, FL, USA), a bicarbonate-based dialysate with sodium concentration of 140 mEq/l for 4 h thrice weekly.
Statistical analysis
The serum potassium concentration was sorted into quartiles and analysis of variance was used for between group comparisons of mean T wave amplitude and the T wave to R wave ratio. Tukey tests were used to test for differences between individual means. Multiple regression analysis was used to assess the independent association of T wave amplitude (outcome variable) with all other measured variables. Independent variables were age, duration of ESRD, pre-dialysis serum bicarbonate concentration, total serum calcium concentration, serum sodium concentration, and serum potassium concentration (5.5 vs >5.5 mEq/l). Multiple regression results include Beta, the standardized regression coefficient, and the standard error (SE). All P values are two-tailed. Plus/minus values are mean± standard deviation (SD). Computations were done in SPSS [7] (Statistics Program for Social Sciences version 8.0, 1997, SPSS Inc., Chicago, IL, USA).
![]() |
Results |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Mean serum total calcium concentration was 9.1±0.94 mg/dl (range 7.511.6), mean serum sodium concentration was 137±3.2 mEq/l (range 130143), and mean serum bicarbonate concentration was 22±3 mEq/l (range 1028).
No study subject evinced arrhythmia or any of the typical ECG changes associated with hyperkalaemia. There was no significant difference in T wave amplitude (F statistic=2.1; P=0.11) or T wave to R wave ratio (F statistic=2; P=0.12) between quartiles of serum potassium concentration (Table 1). T wave amplitude was equivalent in patients with serum potassium concentration >5.5 (7.1±4.1) or
5.5 mEq/l (5.2±3.5 mm) (P=0.13). Also, T wave to R wave ratio was equivalent in patients with serum potassium concentration >5.5 (2.8±3) or
5.5 mEq/l (1.9±2.7 mm) (P=0.37). Bivariate correlation analysis showed that the r value for the inverse correlation between serum calcium concentration and T wave amplitude was -0.32 (P=0.007; Figure 1
). Multiple linear regression analysis showed that total serum calcium concentration had an inverse relation with T wave amplitude (P=0.03) after adjustment for other factors (a high total serum calcium concentration was associated with a low T wave amplitude) (Table 2
).
|
|
|
![]() |
Discussion |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Our results confirm and extend the findings of a case report by Szerlip et al. [1], of two renal failure patients with a serum potassium concentration >9 mEq/l who did not have ECG manifestations. Hyperkalaemia reduces the resting membrane potential, bringing it closer to threshold. It slows conduction velocity and increases the rate of repolarization due to increased membrane permeability for potassium [5]. As such, changes in repolarization that may manifest initially as tall peaked T waves in the pre-cordial leads of the ECG are early signs of hyperkalaemia [6]. Tall peaked T waves may be followed by decreased amplitude of the R wave, widened QRS complex, prolonged PR interval, and then decreased amplitude and disappearance of the P wave [6]. Finally, the QRS blends into the T wave, forming the classic sine wave [6]. Cardiac arrest or ventricular arrhythmia may occur at any point in this progression.
Once the typical ECG changes are detected in a person with hyperkalaemia, the immediate course of action is the administration of intravenous calcium gluconate. Calcium antagonizes the effect of hyperkalaemia on the membrane by reducing the threshold potential, thereby restoring the normal difference between the two potentials that is necessary for excitability.
We do not have a validated explanation for the absence of usual ECG findings of hyperkalaemia in ESRD. However, our finding of an inverse relation between total serum calcium concentration and T wave amplitude suggests that elevated serum calcium concentration in haemodialysis patients may blunt the cardiotoxic effects of hyperkalaemia [8]. Although secondary hyperparathyroidism, a common feature of ESRD, is usually associated with hypocalcaemia, total serum calcium levels in many haemodialysis patients is often above the average due to a regimen designed to increase serum calcium concentration and combat secondary hyperparathyroidism [9]oral calcium therapy, supplemental vitamin D, and treatment with a dialysate that often has as much as 3.5 mEq/l of ionized calcium.
Furthermore, while total body potassium is decreased in haemodialysis patients [10,11], elevated serum potassium concentration tells little about the ratio between intracellular and extracellular potassium, which is the critical factor in membrane depolarization. Complex electrolyte perturbations impinge on the stability of myocardial cells in partially corrected uraemia including fluctuations in calcium, magnesium, and pH, any of which may alter expression of hyperkalaemia.
It is also possible that cell membrane changes in ESRD, such as deposition of phospholipids may counteract any of the cardiac effects of hyperkalaemia. In addition, it is suggested that the rate of rise in serum potassium, which is slow in ESRD, may be more relevant than the actual level of serum potassium attained [12]. Thus, during a slow rise in serum potassium concentration, concurrent compensatory changes occur to counteract the effect of hyperkalaemia on membrane depolarization.
A limitation of our study is that we did not compare the study ECG to prior ECGs when patients were not hyperkalaemic and we did not measure ionized serum calcium. We acknowledge that as non-specific ECG changes including ischaemic-appearing changes of uncertain significance are common in the dialysis population [13,14], these may obscure the usual changes of hyperkalaemia.
Many ESRD patients receive concomitant care from generalist physicians and nephrologists. It should be recognized that the distribution of pre-dialysis serum potassium values in ESRD is different from that in health [2,15], with a mean and distribution curve shifted to the right (higher baseline potassium values). The majority of patients on haemodialysis have pre-dialysis serum potassium concentration >5 mEq/l [2,15], the upper limit of normal in persons without ESRD. In fact, as many as 19% of patients receiving haemodialysis may have pre-dialysis serum potassium values >6 mEq/l [2]. Therefore, an elevated serum potassium concentration in ESRD patients is bound to be frequently encountered by non-nephrologists or emergency room physicians when evaluating these patients for non-renal medical problems. We emphasize that despite the absence of ECG changes of hyperkalaemia in ESRD, hyperkalaemia is still a potentially life-threatening condition in ESRD [16]. In three haemodialysis patients whose deaths were attributed to hyperkalaemia by Siddiqui et al. [16], the serum potassium concentration was 8, 7.4, and 7.8 mEq/l, respectively, just before cardiac arrest. On the other hand, the two patients in the report by Szerlip et al. [1], with serum potassium concentrations of 9.2 and 10.2 mEq/l, respectively, did not manifest any specific symptom or ECG feature of hyperkalaemia. Thus, the conundrum, in the absence of ECG changes to guide therapy, the threshold serum potassium concentration that should trigger immediate potassium lowering measures or use of intravenous calcium gluconate in persons with ESRD is unclear.
Lacking any supportive scientific data, a common-sense approach to deciding what to in ESRD patients with elevated serum potassium without ECG changes would be to compare the value with the patient's usual serum potassium concentration and also take their general clinical condition into consideration. When uncertain of the importance of a raised potassium level, it is prudent to go ahead and administer calcium gluconate, as the downside risk is minimal.
Clearly, extrapolating usual ECG changes of hyperkalaemia in non-renal failure patients to persons with ESRD is an unreliable means of detecting potentially lethal hyperkalaemia. Thus, the absence of ECG changes in hyperkalaemic haemodialysis patients should be interpreted with caution.
![]() |
Notes |
---|
![]() |
References |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|