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 reentry-
or 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 car-

diovascular complications during mainte-
nance hemodialysis (HD), because their occur-
rence 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 re-
ports 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 hemo-
dynamics. 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 ac-
tivities. 8 However, autonomic nervous functions
in HD patients are reported to be lower than in
healthy persons. 9 Therefore, the changes in hu-
moral 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 fac-
tors, including serum electrolytes, on the occur-
rence 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), di-
abetic 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, hyperten-
sion, left ventricular hypertrophy, and mild cardiomegaly were
noted in 7, 12, and 7 patients, respectively. These three ab-
normalities 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+, phos-
phorus, 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. De-
partment of Clinical Laboratory and M edicine. Kyoto Prefec-
tural University of Medicine. 465 Kajii-cho. Kawaramachi-
Hirokoji. 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

HD
Patient Renal Period BP CTR Ht
No. Age/Sex Disease (mo) (mmHg) ECG (%) (%)

1 57/M CGN 128 122/70 LVH 58 27.2

2 281M CGN 44 150/100 LVH 46 26.6
3 52/M CGN 32 172/98 LVH 46 20.6
4 44/F CGN 11 106/60 WNL 52 21.9
5 63/M GK 20 140/80 RV pacing 48 26.9
6 78/F TN 78 180170 LVH 58 21.9
7 26/F CGN 26 144/104 LVH 60 18.2
8 36/F TP 36 170/100 LVH 35 19.7
9 51/M TN 95 130174 Dextrocardia 60 29.5
10 44/M TN 156 120170 WNL 44 28.8
11 62/F ON 110 160/60 LVH 55 21.0
12 59/M CGN 99 144/74 WNL 48 37.1
13 54/M PK 15 88/60 LVH 51 18.4
14 43/M CGN 115 140/90 LVH 62 34.7
15 59/M ON 1 170/80 LVH 58 25.1
16 44/F TP 15 112/70 WNL 52 19.7
17 46/M GK 102 112/70 LVH 44 20.4
18 831M CGN 9 104/70 WNL 55 19.3
19 60/M CGN 9 112/60 WNL 42 20.2
20 86/F CGN 82 180/60 LVH 59 18.1
21 50/F PK 18 136/80 WNL 46 20.0
22 31/F CGN 19 142/80 WNL 48 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 de-
termine the differences from the values before HD. The dif-
ference 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 in-
creases 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 record-
ings. We observed transient atrial fibrillation in
two patients (9.1 %), sinus arrhythmia in one pa-
tient (4.5%), and PQ prolongation over 0.2 sec-
onds in two patients (9.1%) during HD.
Background Factors
We investigated the difference in background
factors between the three patients who had in-
creases in both VPB and SVPB during HD (ar-
rhythmia group) and the other 19 patients (non-
arrhythmia 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 hyper-
trophy in ECG than patients in the nonarrhyth-
mia group. However, the differences in back-
ground factors were not statistically significant
ARRHYTHMIAS DURING HEMODIALYSIS 151

Table 2. Differences in Clinical Parameters Between Arrhythmia and Nonarrhythmia Groups

Arrhythmia Group Nonarrhythmia Group
(n = 3) (n = 19) PValue

Male/Female 2/1 11/8

Age (yr) 61 22 51 15 NS
HO periods (mo) 71 51 48 47 NS
Mean SP (mm Hg) 92 20 98 15 NS
ECG
LVH 3 (100%) 9 (47%)
Ischemic changes 1 (33%) 2 (11%)
CTR(%) 57 5.7 50 6.9 NS
% FS in LV 41 9.4 40 8.2 NS
Hematocrit (%) 24 9.5 24 4.8 NS
T Chol (mmol/L) 4.1 1.22 4.5 1.07 NS
PTH-C (ng/mL) 3.1 2.52 5.7 4.41 NS
Calcitonin (pg/mL) 204 113.4 225 83.1 NS
Digitalization 0(0%) 2 (10.5%)

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 dif-
ferences in blood pressure, percent of fractional
shortening in the left ventricle using two-dimen-
sional 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 cal-
citonin (Table 2). The increases in plasma para-
thyroid hormone and calcitonin suggest the ex-
istence of secondary hyperparathyroidism. In
addition, none of the three patients of the ar-
rhythmia 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, Kin-
daly-3. When we changed the dialysate to the low-
Ca2 + 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 individ-
ual recording charts of the changes in the occur-
rence 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%, respec-
tively, 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 nor-
malized within 3 hours after beginning HD, and
there were no differences in the pattern of the
decrease in serum K+ between HD using high-
Ca2+ 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-
152 NISHIMURA ET AL

3.4
_ _ Klndaly3 concentration was unchanged throughout HO
C .. -0 Klndaly-2
using either dialysate (high-Ca2 +, 1.26 0.238
:8 3.2
** mmol/L [3.1 0.6 mg/dL] before HO and 1.19
!! 3.0
C 0.149 mmol/L [2.9 0.4 mg/dL] after HO [n
CD
u-
C:::'
00
2.8 = 12]; low-Ca2+, 1.26 0.130 mmol/L [3.1 0.3
+U E
g 2.6 mg/dL] before HO and 1.17 0.105 mmol/L
'"'111
tt
U [2.8 2.4 mg/dL] after HO [n = 8]) .
E
:::I
~
en
2.4
.-.. .l:.-.J-..-..l-..~-. . .l No significant changes in plasma epinephrine
2.2 concentration were observed during HO using
either high-Ca2+ dialysate (180 122.8 pmol/L
before HD 1 2 3 4 after HD [33 22.5 pg/mL] before HO and 136 120.6
Time (hour) pmol/L [25 22.1 pg/mL] after HO, n = 11) or
low-Ca2+ dialysate (82 82.9 pmol/L [15 15.2
Fig 1. Changes in serum Ca 2 + concentration (mmol/ pg/mL] before HO and 202 225 pmol/L [37
L) before maintenance hemodialysis (HD), during HD at
1, 2, 3, and 4 hours, and after HD using either Kindaly- 41.2 pg/mL] after HO, n = 8). However, there
3 (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. V PBs during HD SVPBs during HD
beats beats

\
2 2350 5000
Ca + dialysate (5.2 0.4 mmol/L before HO, 3.4
230
0.3 mmol/L ad hours of HO, and 3.2 0.2 2250 4000
mmol/L after HO, P < 0.01 compared with the 2200
value before HO, n = 8). Serum concentrations
2150 3000
of phosphorus, urea nitrogen, creatinine, and uric 2100
acid were decreased gradually through HO using
either high-Ca2 + dialysate (phosphorus, 2.98
.
,
2000
150
0.865 mmol/L [9.2 2.7 mg/dL] before HO 100 1000
and 1.13 0.264 mmol/L [3.5 0.8 mg/dL] 50
after HO, P < 0.01 [n = 12]; urea nitrogen, 25.9 0 0
4.82 mmol/L [73 14 mg/dL] before HO and Kindoly-3 Kindaly-2
"I. change % change
9.5 3.40 mmol/L [27 6 mg/dL] after HO, P 100 100
< 0.01 [n = 12]; creatinine, 1.2 0.59 mmol/L 90 90
[13.6 6.7 mg/dL] before HO and 0.5 0.17 80 80
mmol/L [5.7 1.9 mg/dL] after HO, P < 0.01 70 70
[n = 12]; uric acid, 453 109.0 ~mol/L [7.6 60 60
1.8 mg/dL] before HO and 161 51.3 ~mol/ 50 50
L [2.7 0.9 mg/dL] after HO, P < 0.01 [n = 12]) 40 40
or low-Ca2+ dialysate (phosphorus, 2.30 0.672 30 30"1
mmol/L [7.1 2.1 mg/dL] before HO and 0.92 20 20 J
0.154 mmol/L [2.8 0.5 mg/dL] after HO, P 10 10
< 0.01 [n = 8]; urea nitrogen, 31.9 5.32 mmol/ 0 0
L [89 15 mg/dL] before HO and 10.5 2.90
mmol/L [29 8 mg/dL] after HO, P < 0.01 [n Fig 2. Degree of reduction in the occurrence of ven-
= 8]; creatinine, 1.3 0.25 mmol/L [14.7 2.8 tricular premature beats (VPBs) and supraventricular
premature beats (SVPBs) in the arrhythmia group when
mg/dL] before HO and 0.5 0.11 mmol/L [5.7 the dialysate was changed from Kindaly-3 (high-Ca2 +
1.2 mgjdL] after HO, P < 0.01 [n = 8]; uric dialysate) to Kindaly-2 (low-Ca2 + dialysate). The upper
acid, 562 88.7 ~mol/L [9.4 1.5 mgjdL] before two panels show the number of occurrence of either
VPBs or SVPBs during maintenance hemodialysis (HD).
HO and 172 45.3 ~mol/L [2.9 0.8 mg/dL] and the lower panels show the percent reduction rates
after HO, P < 0.01 [n = 8]). Serum magnesium of either VPBs or SVPBs during HD.
ARRHYTHMIAS DURING HEMODIALYSIS
HBs/hr
'000
Sep. 18
T . S.
HBs/hr
"'t
B:!~
,, '
,,
8000
,,
6000
'000
1000
"~"':;::.: : .:m==:::::::=';="'}i.'m
:'.====,!.: ":'H :::-....Im.==~::Jll0 OOp.m
;-::--m----:.:-c"""
Oct. 15 : OCI . 14
B T . S
Fig 3. Changes in heart beats (HBs) and ventricular
premature beats (VPBs) in the patient who had the in-
crease 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 di-
alysate 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 oc-
currence of VPB was increased during and after
HD in maintenance HD patients, but VPB was
not increased by either the extracorponeal ultra-
filtration method (ECUM) or hemofiltration
153
(HF).7 Because less changes in humoral factors
were expected in both ECUM and HF than in
VPBs / hr
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
' 000 In 1980, Morrison et al reported that frequent
and complex arrhythmias had been observed
during HD in nine of 23 HD patients, and sug-
gested that either administration of digitalis-gly-
coside or hypokalemia might have been one of
~M (Kindaly-ll
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, Ky-
riakidis et al suggested that incomplete clearance
VPBs/hr 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
'000 was no difference in the change in serum K+ con-
500
centration during HD between the arrhythmia
and nonarrhythmia groups and between HD us-
. ing high-Ca2 + dialysate in which arrhythmias
were augmented and HD using low-Ca2 + dialy-
sate in which augmented arrhythmias were in-
54M (Kindaly-2)
hibited.
Only the alteration in serum Ca2+ concentra-
tion 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 ar-
rhythmias 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 reentry-
type 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
meability in the plasma membrane, 12 and (3) de-
layed depolarization. 13 Both (1) and (2) may cause
reentry-type arrhythmias, and (3) may elicit trig-
gered-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 clear-
ance of Ca2 + from serum may be an important
factor in the pathogenesis of postdialysis arrhyth-
mias.
There are some reports in which either ad-
ministration of digitalis-glycoside or hypokalemia
is described as one of the main causes of arrhyth-
mias during HD.2.4 In the present study, both
hypokalemia and administration of digitalis-gly-
coside had no relation to the occurrence of
arrhythmias during HD. However, both digitalis-
glycoside and hypokalemia are considered to in-
crease intracellular Ca2+ concentration by inhib-
iting Na+-K+ pump activity of the membrane.
The inhibition of Na+-K+ pump activity would
lead to the increase in intracellular Na+ concen-
tration, 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 hy-
pokalemia- or digitalis-glycoside-induced ar-
rhythmias.
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
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NISHIMURA ET AL
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 poten-
tial 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+ dialy-
sate 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 dia-
lysate with high-Ca2+ concentration increases
serum Ca2 + concentration and may induce life-
threatening and fatal arrhythmias during HD,
especially when the patient has severe cardiovas-
cular complications. In addition, the use of high-
Ca2+ dialysate may increase the risk of hypercal-
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a better way not only to decrease arrhythmias
during HD, but also to prevent hypercalcemia
and ectopic calcification in HD patients. 17 In
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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.
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