Serum Calcium Increases the Incidence of Arrhythmias During Acetate Hemodialysis

Serum Calcium Increases the Incidence of Arrhythmias During Acetate Hemodialysis Masato Nishimura, MD, Tadashi Nakanishi, MD, Akiyasu Yasui, MD, Yasuhiro Tsuji, MD, Hiroshi Kunishige, MD, Masami Hirabayashi, MD, Hakuo Takahashi, MD, and Manabu Yoshimura, MD • We investigated the occurrence of arrhythmias during maintenance acetate hemodialysis (HD) using a 24-hour continuous electrocardiogram recording system. Three of 22 patients showed augmented increases in both ventricular premature beats and supraventricular premature beats during HD. When we changed the dialysate from one with a Ca 2 + concentration of 1.75 mmol/L (3.5 mEq/L), to one with a Ca 2 + concentration of 1.25 mmol/L (2.5 mEq/L), the elevation of serum ca 2+ concentration during HD was abolished and the increases in both ventricular premature beats and supraventricular premature beats were significantly decreased. The elevation of serum Ca 2+ concentration during HD might induce either extracellular or intracellular increase in Ca 2 + concentration in the heart and elicit either reentryor triggered-activity types of arrhythmias during HD. The present results indicate that the dialysate with a lower Ca 2 + concentration is advisable to use in patients with underlying cardiac diseases. © 1992 by the National Kidney Foundation, Inc. INDEX WORDS: Hemodialysis; acetate-buffer; ventricular premature beats; supraventricular premature beats; serum electrolytes; calcium.

A

RRHYTHMIAS are one of the major cardiovascular complications during maintenance hemodialysis (HD), because their occurrence might result in severe cardiovascular conditions and sudden death. When acetate is used as a buffer, the appearance of arrhythmias will worsen the cardiac and systemic conditions, because acetate buffer may cause a decrease in blood pressure during HD.l There are some reports of the occurrence of life-threatening and complex arrhythmias during HD.2-7 These reports attributed the main causes of arrhythmias to the changes in serum electrolytes, as well as hemodynamics. Because abrupt and various changes in both hemodynamic and humoral factors are expected during HD, these changes may affect cardiovascular regulatory systems and increase the incidence of arrhythmias. One of the main causes of arrhythmias is a disturbance of peripheral autonomic nervous activities. 8 However, autonomic nervous functions in HD patients are reported to be lower than in healthy persons. 9 Therefore, the changes in humoral factors, as well as hemodynamic factors, might be a direct pathogenesis in arrhythmias during HD. The aim of the present study was to assess the effects of the changes in humoral factors, including serum electrolytes, on the occurrence of arrhythmias during HD. SUBJECTS AND METHODS Twenty-two patients on HD were selected (13 men, nine women; aged 53 ± 16 years) (Table I). Basal renal diseases

of these patients were as follows: chronic glomerulonephritis (II patients), toxic nephropathy by streptomycin sulfate (three), gouty kidney (two), toxemia of pregnancy (two), diabetic nephropathy (two), and polycystic kidney (two). No severe abnormalities were found on physical examinations, which included chest x-ray, standard electrocardiogram (ECG), and two-dimensional echocardiogram. However, hypertension, left ventricular hypertrophy, and mild cardiomegaly were noted in 7, 12, and 7 patients, respectively. These three abnormalities are common complications in HD patients.

Protocol A continuous 24-hour ambulatory ECG (Holter-ECG) was monitored by a portable two-channel electrocardiorecorder (Marquette 8500, Marquette Electronics, Milwaukee, WI) on the day of HD, and ECG tapes were analyzed by Marquette 8000(T. Serum concentrations of Na+, K+, Cl-, Ca2+, phosphorus, magnesium, urea nitrogen, creatinine, uric acid, and plasma concentrations of epinephrine and norepinephrine were measured before HD, during HD at I, 2, 3, and 4, hours, and I hour after HD. As a high-Ca2+ dialysate, we used Kindaly-3 (Na+ 132, K+ 2.0 mmol/L [mEqjL), Ca2+ 1.75 mmoljL [3.5 mEqjL), Mg2+ 0.75 mmol/L [1.5 mEqjL], Cl- 104 mmol/L [mEqjL), CH)COO- 35 mmol/L [mEqjL), glucose 11.1 mmoljL [201

From the Department ofClinical Laboratory and Medicine. Kyoto Pref ectural University o f Medicine. Kyoto. Japan; the Department of Renal Failure. and the Third Department of Internal Medicine. Matsushita M em orial Hospital. Moriguchi City, Osaka, Japan; and the Department of Internal Medicine. Nagitsuji Hospital. Kyoto. Japan. Address reprint requests to Masato Nishimura. MD. Department of Clinical Laboratory and M edicine. Kyoto Prefectural University of Medicine. 465 Kajii-cho. KawaramachiHirokoji. Kamikyo-Ku. Kyoto 602, Japan. © 1992 by the National Kidney Foundation. Inc. 0272-6386/ 92/1902-0007$3.00/ 0

American Journal of Kidney Diseases, Vol XIX. No 2 (February), 1992: pp 149-155

149

150

NISHIMURA ET AL Table 1. Characteristics of 22 Patients Subjected to This Study

Patient No.

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22

Age/Sex

Renal Disease

HD Period (mo)

BP (mmHg)

ECG

CTR (%)

Ht (%)

57/M 281M 52/M 44/F 63/M 78/F 26/F 36/F 51/M 44/M 62/F 59/M 54/M 43/M 59/M 44/F 46/M 831M 60/M 86/F 50/F 31/F

CGN CGN CGN CGN GK TN CGN TP TN TN ON CGN PK CGN ON TP GK CGN CGN CGN PK CGN

128 44 32 11 20 78 26 36 95 156 110 99 15 115 1 15 102 9 9 82 18 19

122/70 150/100 172/98 106/60 140/80 180170 144/104 170/100 130174 120170 160/60 144/74 88/60 140/90 170/80 112/70 112/70 104/70 112/60 180/60 136/80 142/80

LVH LVH LVH WNL RV pacing LVH LVH LVH Dextrocardia WNL LVH WNL LVH LVH LVH WNL LVH WNL WNL LVH WNL WNL

58 46 46 52 48 58 60 35 60 44 55 48 51 62 58 52 44 55 42 59 46 48

27.2 26.6 20.6 21.9 26.9 21.9 18.2 19.7 29.5 28.8 21.0 37.1 18.4 34.7 25.1 19.7 20.4 19.3 20.2 18.1 20.0 21.8

Abbreviations: BP, blood pressure; CTR, cardiothoracic ratio; Ht, hematocrit; CGN, chronic glomerulonephritis; GK, gouty kidney; TN, toxic nephropathy; TP, toxemia of pregnancy; ON, diabetic nephropathy; PK, polycystic kidney; LVH, left ventricular hypertrophy; WNL, within normal limits; RV pacing, right ventricular pacing.

mg/dL] , 287 mmol/L, Fuso Pharmaceutical Industry, Ltd, Osaka, Japan). As a low-Ca2+ dialysate, we used Kindaly-2 (Na+ 134, K+ 2.0 mmol/L [mEq/L], Ca2+ 1.25 mmol/L [2.5 mEq/L], Mg2+ 0.75 mmol/L [1.5 mEq/L], Cl- 104 mmol/L [mEq/L], CH 3COO- 33 mmol/L [mEq/L], glucose Il.l mmol/L [201 mg/dL], 285 mmol/L).

Statistical Analysis Ail values are expressed as the mean ± SD. One-way analysis of variance was used to evaluate the changes in humoral factors during HD. Duncan's mUltiple range test was applied to determine the differences from the values before HD. The difference between the two groups was evaluated using Student's t test. The criterion for statistical significance was P < 0.05.

RESULTS

Incidence ofArrhythmias During HD

Of 22 patients in this study, the occurrence of ventricular premature beats (VPB) was increased in three patients (13.6%, no. 13, 14, and 20 of Table 1). These three patients showed further increases in supraventricular premature beats (SVPB). Ventricular tachycardia was seen in one patient (4.5%, no. 13) and supraventricular

tachycardia in two patients (9.1 %, no. 13, and 14). In these three patients (no. 13, 14, and 20), the increases in both VPB and SVPB during HD were reproducible in three Holter ECG recordings. We observed transient atrial fibrillation in two patients (9.1 %), sinus arrhythmia in one patient (4.5%), and PQ prolongation over 0.2 seconds in two patients (9.1%) during HD. Background Factors

We investigated the difference in background factors between the three patients who had increases in both VPB and SVPB during HD (arrhythmia group) and the other 19 patients (nonarrhythmia group). As shown in Table 2, the patients in the arrhythmia group were older on average, had been well treated on HD for a longer time, had a larger cardiothoracic ratio (CTR), and had a higher incidence of left ventricular hypertrophy in ECG than patients in the nonarrhythmia group. However, the differences in background factors were not statistically significant

ARRHYTHMIAS DURING HEMODIALYSIS

151

Table 2. Differences in Clinical Parameters Between Arrhythmia and Nonarrhythmia Groups Arrhythmia Group (n = 3)

Male/Female Age (yr) HO periods (mo) Mean SP (mm Hg) ECG LVH Ischemic changes CTR(%) % FS in LV Hematocrit (%) T Chol (mmol/L) PTH-C (ng/mL) Calcitonin (pg/mL) Digitalization

61 71 92

2/1 ± 22 ± 51 ± 20

3 (100%) 1 (33%) 57 ± 5.7 41 ± 9.4 24 ± 9.5 4.1 ± 1.22 3.1 ± 2.52 204 ± 113.4 0(0%)

Nonarrhythmia Group (n = 19)

PValue

11/8 ± 15 ±47 ±15

NS NS NS

51 48 98

9 (47%) 2 (11%) 50 ± 6.9 40 ± 8.2 24 ± 4.8 4.5 ± 1.07 5.7 ± 4.41 225 ± 83.1 2 (10.5%)

NS NS NS NS NS NS

NOTE. Values are expressed as the mean ± SO. NS, P ~ 0.05. Abbreviations: SP, blood pressure; LVH, left ventricular hypertrophy; CTR, cardiothoracic ratio; % FS in LV, percent of fractional shortening in left ventricle using (two)-dimensional ultrasonic echocardiography; T Chol, serum concentration of total cholesterol; PTH-C, plasma concentration of C-terminal of parathyroid hormone; calcitonin, plasma concentration of calcitonin.

between the arrhythmia and nonarrhythmia groups. In addition, there were no significant differences in blood pressure, percent of fractional shortening in the left ventricle using two-dimensional ultrasonic echocardiography, hematocrit, and serum total cholesterol levels between the two groups. Both groups had high plasma levels of C-terminal of parathyroid hormone and calcitonin (Table 2). The increases in plasma parathyroid hormone and calcitonin suggest the existence of secondary hyperparathyroidism. In addition, none of the three patients of the arrhythmia group had ever taken digitalis-glycoside before or during the study. Effects of Serum Ca 2 + on the Occurrence ofArrhythmias

Serum concentration of Ca2+ was increased during HD using the high-Ca2 + dialysate, Kindaly-3. When we changed the dialysate to the lowCa2 + dialysate, Kindaly-2, the increase in serum Ca2+ concentration disappeared (Fig 1), and the increased occurrences of VPB and SVPB were also inhibited during HD in three patients of the arrhythmia group. Figure 2 shows the degree of reduction in the occurrences of VPB and SVPB in the arrhythmia group. Figure 3 shows individual recording charts of the changes in the occurrence of VPB.

When one patient (no. 14, arrhythmia group) had been orally administered verapamil (a Ca2 + channel blocker), the occurrences of VPB and SVPB were reduced by 97% and 75%, respectively, despite using high-Ca2 + dialysate. On the contrary, no increases in VPB, SVPB, or other arrhythmias were noted in 10 patients of the nonarrhythmia group who had performed HD using low-Ca2 + dialysate. Changes in Other Humoral Factors During HD Using Either High-C«+ or Low-Ca2 + Dialysate

Serum concentrations of both Na+ and cr did not change throughout HD using either high-Ca2+ dialysate (Na+, 141 ± 3.0 mmol/L before HD and 142 ± 1.6 mmol/L after HD [n = 12]; Cl-, 103 ± 3.2 mmol/L before HD and 101 ± 2.9 mmol/L after HD [n = 12]) or low-Ca2+ dialysate (Na+, 141 ± 2.9 mmol/L before HD and 140 ± 1.4 mmol/L after HD [n = 8]; Cl-, 104 ± 4.9 mmol/L before HD and 101 ± 2.3 mmol/L after HD [n = 8]). Serum K+ concentration was normalized within 3 hours after beginning HD, and there were no differences in the pattern of the decrease in serum K+ between HD using highCa2+ dialysate (5.0 ± 0.8 mmol/L before HD, 3.4 ± 0.7 mmol/L at 3 hours of RD, and 3.4 ± 0.6 mmol/L after HD, P < 0.01 compared with the value before HD, n = 12) and HD using low-

NISHIMURA ET AL

152 3.4 C

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3.2

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3.0

00

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2.8

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2.6

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**

CD

u-

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:::I

~

en

2.2

tt

.-.. .l:.-.J-..-..l-..~-. . .l before HD

1

2

3

4

after HD

Time (hour) Fig 1. Changes in serum Ca 2 + concentration (mmol/ L) before maintenance hemodialysis (HD), during HD at 1, 2, 3, and 4 hours, and after HD using either Kindaly3 (high-Ca2 + dialysate, n = 12) or Kindaly-2 (low-Ca 2+ dialysate, n = 8). *P < 0.05, **P < 0.01 compared with the values before HD. tP < 0.05, ttP < 0.01 compared with the values in low-Ca2 + dialysate.

concentration was unchanged throughout HO using either dialysate (high-Ca2 +, 1.26 ± 0.238 mmol/L [3.1 ± 0.6 mg/dL] before HO and 1.19 ± 0.149 mmol/L [2.9 ± 0.4 mg/dL] after HO [n = 12]; low-Ca2+, 1.26 ± 0.130 mmol/L [3.1 ± 0.3 mg/dL] before HO and 1.17 ± 0.105 mmol/L [2.8 ± 2.4 mg/dL] after HO [n = 8]) . No significant changes in plasma epinephrine concentration were observed during HO using either high-Ca2+ dialysate (180 ± 122.8 pmol/L [33 ± 22.5 pg/mL] before HO and 136 ± 120.6 pmol/L [25 ± 22.1 pg/mL] after HO, n = 11) or low-Ca2+ dialysate (82 ± 82.9 pmol/L [15 ± 15.2 pg/mL] before HO and 202 ± 225 pmol/L [37 ± 41.2 pg/mL] after HO, n = 8). However, there

V PBs during HD

SVPBs during HD

beats 2

Ca + dialysate (5.2 ± 0.4 mmol/L before HO, 3.4 ± 0.3 mmol/L ad hours of HO, and 3.2 ± 0.2 mmol/L after HO, P < 0.01 compared with the value before HO, n = 8). Serum concentrations of phosphorus, urea nitrogen, creatinine, and uric acid were decreased gradually through HO using either high-Ca2 + dialysate (phosphorus, 2.98 ± 0.865 mmol/L [9.2 ± 2.7 mg/dL] before HO and 1.13 ± 0.264 mmol/L [3.5 ± 0.8 mg/dL] after HO, P < 0.01 [n = 12]; urea nitrogen, 25.9 ± 4.82 mmol/L [73 ± 14 mg/dL] before HO and 9.5 ± 3.40 mmol/L [27 ± 6 mg/dL] after HO, P < 0.01 [n = 12]; creatinine, 1.2 ± 0.59 mmol/L [13.6 ± 6.7 mg/dL] before HO and 0.5 ± 0.17 mmol/L [5.7 ± 1.9 mg/dL] after HO, P < 0.01 [n = 12]; uric acid, 453 ± 109.0 ~mol/L [7.6 ± 1.8 mg/dL] before HO and 161 ± 51.3 ~mol/ L [2.7 ± 0.9 mg/dL] after HO, P < 0.01 [n = 12]) or low-Ca2+ dialysate (phosphorus, 2.30 ± 0.672 mmol/L [7.1 ± 2.1 mg/dL] before HO and 0.92 ± 0.154 mmol/L [2.8 ± 0.5 mg/dL] after HO, P < 0.01 [n = 8]; urea nitrogen, 31.9 ± 5.32 mmol/ L [89 ± 15 mg/dL] before HO and 10.5 ± 2.90 mmol/L [29 ± 8 mg/dL] after HO, P < 0.01 [n = 8]; creatinine, 1.3 ± 0.25 mmol/L [14.7 ± 2.8 mg/dL] before HO and 0.5 ± 0.11 mmol/L [5.7 ± 1.2 mgjdL] after HO, P < 0.01 [n = 8]; uric acid, 562 ± 88.7 ~mol/L [9.4 ± 1.5 mgjdL] before HO and 172 ± 45.3 ~mol/L [2.9 ± 0.8 mg/dL] after HO, P < 0.01 [n = 8]). Serum magnesium

2350 230 2250 2200 2150 2100

beats

\

150 100 50 0 "I. change

100 90

5000 4000 3000

.

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2000 1000

Kindoly-3

0

Kindaly-2

change 100 90

%

80 70

80 70

60 50

60 50

40

40

30 20 10 0

30"1 20 J 10 0

Fig 2. Degree of reduction in the occurrence of ventricular premature beats (VPBs) and supraventricular premature beats (SVPBs) in the arrhythmia group when the dialysate was changed from Kindaly-3 (high-Ca2 + dialysate) to Kindaly-2 (low-Ca2 + dialysate). The upper two panels show the number of occurrence of either VPBs or SVPBs during maintenance hemodialysis (HD). and the lower panels show the percent reduction rates of either VPBs or SVPBs during HD.

153

ARRHYTHMIAS DURING HEMODIALYSIS

VPBs / hr

HBs/hr

'000

' 000

Sep. 18

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8000

6000

'000

'000 500

1000

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B

: OCI . 14 T . S

54M (Kindaly-2)

Fig 3. Changes in heart beats (HBs) and ventricular premature beats (VPBs) in the patient who had the increase in VPBs during maintenance hemodialysis (HD). The upper lines show heart beats in each hour (MBs/h) and lower lines the number of occurrences of VPBs in each hour (VPBs/h). BP refers to systolic blood pressure (mm Hg). (A) High-Ca2 + dialysate, Kindaly-3, was used; (B) low-Ca 2 + dialysate, Kindaly-2, was used. When a dialysate was changed from Kindaly-3 to Kindaly-2, the increase in VPBs during HD was significantly inhibited.

was a gradual decrease in plasma norepinephrine concentration in HD using a low-Ca 2 + dialysate (3.2 ± 1.24 nmol/L [546 ± 209.3 pg/mL] before HD and 2.1 ± 0.49 pmol/L [363 ± 84.1 pg/mL] after HD, P < 0.05, n = 8). No change in plasma norepinephrine was seen in the patients treated with a high-Ca2+ dialysate (2.3 ± 0.89 pmol/L [381 ± 158.3 pg/mL] before HD and 2.0 ± 0.91 pmol/L [343 ± 153.7 pg/mL] after HD, n = It). DISCUSSION

We reported in a previous study that the occurrence of VPB was increased during and after HD in maintenance HD patients, but VPB was not increased by either the extracorponeal ultrafiltration method (ECUM) or hemofiltration

(HF).7 Because less changes in humoral factors were expected in both ECUM and HF than in usual HD, we considered that one of the main causes of arrhythmias during HD might be the abrupt changes in humoral factors during HD.7 In 1980, Morrison et al reported that frequent and complex arrhythmias had been observed during HD in nine of 23 HD patients, and suggested that either administration of digitalis-glycoside or hypokalemia might have been one of the causes of arrhythmias. 2 In addition, Weber et al reported that hypokalemia would be a main cause ofVPB during HD.4 On the contrary, Kyriakidis et al suggested that incomplete clearance of serum K+ would lead to the occurrence of VPB. 5 In the present study, the change in serum K + concentration apparently had no correlation with the occurrence of arrhythmias, because there was no difference in the change in serum K+ concentration during HD between the arrhythmia and nonarrhythmia groups and between HD using high-Ca2 + dialysate in which arrhythmias were augmented and HD using low-Ca2 + dialysate in which augmented arrhythmias were inhibited. Only the alteration in serum Ca2+ concentration during HD was different between HDs using either high-Ca2+ or 10w-Ca2+ dialysate among the humoral factors we investigated. Serum Ca2 + concentration was increased in accordance with the progression ofHD using high-Ca2+ dialysate, but it was not changed when low-Ca 2+ dialysate was used. In addition, the administration of a Ca2 + channel blocker inhibited the increase in both VPB and SVPB during HD in one patient. These results indicate that the increase in serum Ca2 + concentration is an important cause of arrhythmias during HD. Increased concentration of serum Ca2 + results in increased extracellular Ca2 + concentration in the heart. This would inhibit a fast Na+ current in the cardiac plasma membrane,1O and elicit an impaired conduction of electrical excitement in the heart. An impaired conduction of electrical excitement would probably induce the reentrytype of arrhythmias. In addition, the increase in extracellular ea2+ concentration could result in the increase in intracellular Ca2+ concentration, which could induce (1) an increase in intercellular electrical resistance,11 (2) an increase in K+ per-

154

NISHIMURA ET AL

meability in the plasma membrane, 12 and (3) delayed depolarization. 13 Both (1) and (2) may cause reentry-type arrhythmias, and (3) may elicit triggered-activity type arrhythmias in the heart. High serum concentration of Ca2+ (2.75 mmol/L [5.5 mEq/L]) was recorded after HD in one patient whose VPB lasted after HD, as well as during HD. On the contrary, the ranges of serum Ca2+ concentration after HD were 2.4 to 2.55 mmol/L [4.8 to 5.1 mEq/L] in the other two patients whose arrhythmias were increased only during HD. These results suggest that the clearance of Ca2 + from serum may be an important factor in the pathogenesis of postdialysis arrhythmias. There are some reports in which either administration of digitalis-glycoside or hypokalemia is described as one of the main causes of arrhythmias during HD.2.4 In the present study, both hypokalemia and administration of digitalis-glycoside had no relation to the occurrence of arrhythmias during HD. However, both digitalisglycoside and hypokalemia are considered to increase intracellular Ca2+ concentration by inhibiting Na+-K+ pump activity of the membrane. The inhibition of Na+-K+ pump activity would lead to the increase in intracellular Na+ concentration, and the increase in intracellular Na+ concentration would inhibit Na+-Ca2+ exchange, which must induce the increase in intracellular Ca2+ concentration. 14 Therefore, the increase in intracellular Ca2+ concentration is considered as one of the important pathogeneses in either hypokalemia- or digitalis-glycoside-induced arrhythmias. No difference could be seen in serum levels of urea nitrogen, creatinine, uric acid, and plasma epinephrine between HDs using either high-Ca2+ or low-Ca2 + dialysate. Plasma norepinephrine

concentration was decreased gradually during HD using low-Ca2 + dialysate, but it was not changed during HD using high-Ca2 + dialysate. Plasma norepinephrine concentration is a potential arrhythmogenic factor, but it does not seem that plasma norepinephrine is a key factor for the mechanism of arrhythmias in HD, because there was no change in plasma norepinephrine concentration during HD using high-Ca2+ dialysate in which the increases in both VPB and SVPB were observed. The present study suggests that serum Ca2+ concentration is one of the most important arrhythmogenic factors in HD. The use of a dialysate with high-Ca2+ concentration increases serum Ca2 + concentration and may induce lifethreatening and fatal arrhythmias during HD, especially when the patient has severe cardiovascular complications. In addition, the use of highCa2+ dialysate may increase the risk of hypercalcemia and ectopic calcification, which are serious complications of end-stage renal disease patients who are taking either calcium acetate or calcium carbonate as the major phosphate binders. 15.16 Therefore, the use of low-Ca2 + dialysate may be a better way not only to decrease arrhythmias during HD, but also to prevent hypercalcemia and ectopic calcification in HD patients. 17 In conclusion, it might be one of the treatments that should be tried either to change the dialysate to a 10w-Ca2+ one (1.25 mmol/L) or to administer a Ca2+ channel blocker when the patients have severe arrhythmias such as frequent SVPB, VPB, or ventricular tachycardia during HD. ACKNOWLEDGMENT The authors would like to express our gratitude to Dr Christine H . Block of the Cleveland Clinic Foundation for editorial assistance.

REFERENCES I. Chen TS, Friedman HS, Smith AJ, et al: Hemodynamic changes during hemodialysis: Role of dialyzate. Clin Nephrol 20:190-196, 1983 2. Morrison G, Michelson EL, Brown S, et al: Mechanism and prevention of cardiac arrhythmias in chronic hemodialysis patients. Kidney Int 17:811-819, 1980 3. Blumberg A, Hiiusermann M, Strub B, et al: Cardiac arrhythmias in patients on maintenance hemodialysis. Nephron 33:91-95, 1983 4. Weber H, Schwarzer C, Stummvoll HK, et al: Chronic

hemodialysis; high risk patients for arrhythmias? Nephron 37:180-185,1984 5. Kyriakidis M, Voudiclaris S, Kremastinos D, et al: Cardiac arrhythmias in chronic renal failure? Nephron 38:26-29, 1984 6. Wizemann V, Kramer W, Funke T, et al: Dialysis-induced cardiac arrhythmias; fact or fiction? Nephron 39:356360, 1985 7. Nakanishi T, Inoue D, Furukawa K, et al: The effects of hemodialysis on the occurrence of premature ventricular beats. Heart 9:944-949, 1985 8. Nakanishi T, Nishimura M, Mizoi Y, et al: Occurrence

ARRHYTHMIAS DURING HEMODIALYSIS

of ventricular premature beats is correlated with endogenous catecholamine levels in patients over 40 years of age. Proceedings of the Free Paper Sessions of the International Symposium on Cardiac Arrhythmias, Kanagawa, Japan, Excerpta Medica, 1986, pp 529-534 9. Bondia A, Tabernero JM, Macias JF, et al: Autonomic nervous system in hemodialysis. Nephrol Dial Transpant 2: 174-180,1988 10. Beeler GW, Reuter H: Voltage clamp experiments on ventricular myocardial fibers. J Physiol 207: 191-209, 1970 II. Kameyama M: Electrical coupling between ventricular paired cells isolated from guinea-pig heart. J PhysioI336:345357, 1983 12. Isenberg G: Cardiac purkinje fibers. [Ca2+1i controls the potassium permeability via the conductance components gK, and gK2 • Pfliigers Arch 371 :77-85, 1977

155 13. Hiraoka M, Okamoto Y, Sano T: Oscillatory afterpotentials in dog ventricular muscle fibers. Circ Res 48:510518, 1981 14. Blaustein MP, Mordecai MB: Sodium ions, calcium ions, blood pressure regulation and hypertension: A reassessment and hypothesis. Am J PhysioI232:CI65-CI73, 1977 15. Emmett M, Sirmon MD, Kirkpatrick WG, et al: Calcium acetate control of serum phosphorus in hemodialysis patients. Am J Kidney Dis 17:544-550, 1991 16. Ittel TH, Schafer C, Schmitt H, et a1: Calcium carbonate as a phosphate binder in dialysis patients: Evaluation of an enteric-coated preparation and effect of additional aluminium hydroxide on hyperaluminaemia. Klin Wochenschr 69:5967,1991 17. Slatopolsky E, Weerts C, Norwood K, et a1: Long-term effects of calcium carbonate and 2.5 mEqfliter calcium dialysate on mineral metabolism. Kidney Int 36:897-903,1989