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The Egyptian Journal of Critical Care Medicine (2014) xxx, xxx–xxx
No. of Pages 6
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The Egyptian College of Critical Care Physicians
The Egyptian Journal of Critical Care Medicine
http://ees.elsevier.com/ejccm
www.sciencedirect.com
ORIGINAL ARTICLE
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Assessment of hypotension during dialysis
as a manifestation of myocardial ischemia
Q1 in patients with chronic renal failure
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Q2
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a
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Randa Aly Soliman
Q3
b
a,*
, Mohamed Fawzy a, Hussein Kandil b, Alia Abd el Fattah
a
The Critical Care Department, Cairo university, Egypt
The Critical Department in the National Liver Institute, Egypt
Received 4 September 2013; revised 3 May 2014; accepted 15 May 2014
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KEYWORDS
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Intradialytic hypotension
(IDH);
With chronic renal failure
(CRF);
Myocardial perfusion;
Imaging (MPI)
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Abstract Introduction: Intradialytic hypotension (IDH) remains to be a major complication of
hemodialysis occurring in nearly 25% of dialysis sessions. It is a significant independent factor
affecting mortality in hemodialysis patients. Autonomic nervous system dysfunction, blood sequestration in the setting of hypovolemia, cardiovascular diseases and increased plasma level of end
products of nitric oxide metabolism are possible causes. In this controlled prospective study we
examined patients with chronic renal failure and intradialytic hypotension to evaluate the relationship between this hypotension and myocardial ischemia after controlling other possible causes.
Materials and methods: Thirty patients with chronic renal failure who are on regular dialysis
were enrolled. Before dialysis, patients were subjected to history taking and clinical examination.
Echocardiography and several lab tests were done. Glomerular filtration rate (GFR) was calculated
using Cockcroft’s and Gault formula. Autonomic dysfunction was also assessed. The dialysis session was standardized in all patients. Intradialytic blood pressure was monitored and hypotension
was classified as mild (SBP > 100 mmHg), moderate (SBP 80–100) or severe (SBP < 80). After
dialysis, myocardial ischemia was assessed using stress myocardial perfusion imaging (MPI) (Pharmacologic stress testing using Dipyridamole) and is further classified as mild, moderate or severe
ischemia. Patients with sepsis, hemoglobin level less than 9 g/dL, diabetes mellitus, low cardiac output, coronary artery disease, significant valvular lesion or body weight below the dry weight of the
patient were excluded from the study. Bronchial asthma, emphysema and severe COPD are contraindications to Dipyridamole and thus were also excluded from the study.
Results: Twenty patients had no or mild intradialytic hypotension whereas ten patients had
* Corresponding author. Address: 20 Abou Hazem st., Madkour,
Haram, Giza, Egypt. Tel.: +20 1222402018.
E-mail address: randaalysoliman@hotmail.com (R.A. Soliman).
Peer review under responsibility of The Egyptian College of Critical
Care Physicians.
Production and hosting by Elsevier
2090-7303 2014 Production and hosting by Elsevier B.V. on behalf of The Egyptian College of Critical Care Physicians.
http://dx.doi.org/10.1016/j.ejccm.2014.05.001
Please cite this article in press as: Soliman RA et al. Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in
Q1 patients with chronic renal failure, Egypt J Crit Care Med (2014), http://dx.doi.org/10.1016/j.ejccm.2014.05.001
EJCCM 25
9 June 2014
No. of Pages 6
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R.A. Soliman et al.
moderate or severe hypotension. Among the first group, only two patients (10%) were found to
have myocardial ischemia, while in the latter group, seven patients (70%) had myocardial ischemia
that is mostly moderate (p = 0.002). Stress induced LV dysfunction was also significantly prevalent
in patients with moderate or severe intradialytic hypotension as opposed to the other group
(p = 0.002) LVED.
Conclusions: Patients with CKD and regular hemodialysis who experience moderate or severe
intradialytic hypotension have significantly higher prevalence of myocardial ischemia and stress
induced myocardial dysfunction, than those who experience no or mild intradialytic hypotension.
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2014 Production and hosting by Elsevier B.V. on behalf of The Egyptian College of Critical Care
Physicians.
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1. Introduction
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Intradialytic hypotension (IDH) remains to be a major complication of hemodialysis. It occurs in nearly 25% of dialysis sessions [1] and often requires aggressive resuscitative measures
and sometimes premature termination of hemodialysis. It is
also a significant independent factor affecting mortality in
hemodialysis patients [2].
Despite the advances of machines with ultrafiltration control devices, modifying dialysate composition, temperature
control, correction of nutritional deficiencies and treatment
of anemia with erythropoietin therapy, many patients still have
episodes of intradialytic hypotension. Among other factors,
the major pathophysiology of these episodes is the removal
of large volume of blood water and solutes over a short period
of time, overwhelming normal compensatory mechanisms,
which include plasma refilling and reduction of venous capacity (due to reduction of pressure transmission to veins).
In some patients, a seemingly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, decreased transmission of
pressure to veins with corresponding increase in venous capacity. Increased sequestration of blood in veins under conditions
of hypovolemia reduces cardiac filling, cardiac output and ultimately blood pressure. Hypotensive episodes during hemodialysis in patients with end stage renal disease in the absence of
inadequate maintenance of the plasma volume, pre-existence
of cardiovascular disease, or autonomic nervous system dysfunction are accompanied by increased plasma concentrations
of the end-products of nitric oxide metabolism (above the
expected levels, based on the reduction of urea [3]).
In this controlled prospective study, patients with chronic
renal failure and intradialytic hypotension episodes were thoroughly investigated, to evaluate the relationship between hypotension and myocardial ischemia after controlling other
possible causes.
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2. Patients and methods
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This prospective study was conducted in King Fahd Hemodialysis unit in Kasr Al-Aini hospital, Hemodialysis Unit in AlZahraa hospital and Critical Care Medicine Department in
Kasr Al-Aini hospital over the time period from February
2010 to June 2011. All patients included in the study provided
informed written consent. The study includes 30 patients with
chronic renal failure who receive regular hemodialysis sessions.
Twenty patients developed hypotension during hemodialysis
session, and the remaining 10 patients did not develop hypo-
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Table 1
Baseline characteristics of the study group (n = 30).
Parameter
Value [N (%) or mean ± SD]
Age (years)
Weight (Kg)
Male
44 ± 13
66 ± 10
12 (40)
Clinical
Smokers
Hypertension
History of chest pain
Family history of IHD
Autonomic neuropathy
AV fistula
Duration of hemodialysis (years)
7 (23)
12 (40)
6 (20)
9 (30)
9 (30)
23 (77)
3.7 ± 2.1
ECG and ECHO
Arrhythmia in ECG
LVH in ECG
RWMA
LVEDD (mm)
LVESD (mm)
EF (%)
4 (13)
6 (20)
5 (17)
49.7 ± 5.4
32.4 ± 4
62.3 ± 7.6
Grades of Albuminuria*
(+)
(++)
(+++)
Urine specific gravity*
6 (20)
7 (23)
2 (7)
1009 ± 2.1
Labs
Hb (g/dL)
Hct (%)
TLC (103 cells/cmm)
FBS (mg/dL)
PPBS (mg/dL)
HB A1C (mg/dL)
Serum Triglycerides (mg/dL)
Serum Cholesterol (mg/dL)
Serum Urea (mg/dL)
Serum Creatinine (mg/dL)
GFR (ml/min/1.73 m2)
Serum Sodium (mEq/L)
Serum Potassium (mEq/L)
10.5 ± 0.73
32.6 ± 2.9
6.1 ± 2.1
70.2 ± 11.2
123.5 ± 15.2
5 ± 0.59
109.7 ± 43
151 ± 60
129.8 ± 29.7
7.9 ± 2.1
11 ± 4.2
138 ± 5.8
5.2 ± 0.63
IHD, ischemic heart disease; LVH, left ventricular hypertrophy;
RWMA, regional wall motion abnormalities; LVEDD, left ventricle end-diastolic diameter; LVESD, left ventricle end-systolic
diameter; EF, ejection fraction Hb, hemoglobin; Hct, hematocrit;
TLC, total leukocytic count; FBS, fasting blood sugar; PPBS, post
prandial blood sugar; HB A1C, hemoglobin A1C; GFR, glomerular
filtration rate.
*
Done only for the 15 patients who were not anuric.
Please cite this article in press as: Soliman RA et al. Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in
Q1 patients with chronic renal failure, Egypt J Crit Care Med (2014), http://dx.doi.org/10.1016/j.ejccm.2014.05.001
EJCCM 25
9 June 2014
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Q1 Assessment of hypotension during dialysis as a manifestation of myocardial ischemia
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Figure 1 Myocardial ischemia diagnosed by MPI in patients with moderate or severe intradialytic hypotension, in comparison to those
with no or mild hypotension (p = 0.002).
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tension during the sessions. Myocardial ischemia was assessed
in all patients using stress myocardial perfusion imaging (MPI)
(Pharmacologic stress testing using Dipyridamole).
Patients with sepsis, hemoglobin level less than 9 g/dL,
diabetes mellitus, low cardiac output, acute coronary
syndrome, significant valvular lesion or body weight below
the dry weight of the patient were excluded from the study.
Bronchial Asthma, emphysema and severe COPD are
contraindications to Dipyridamole and thus were also
excluded from the study.
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2.1. Before dialysis
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All eligible patients were subjected to full history taking and
clinical examination. Serum Urea and Creatinine were measured. Glomerular filtration rate (GFR) was calculated using
Cockcroft’s and Gault equation. Autonomic dysfunction was
assessed using at least 2 of the following tests; blood pressure
(BP) response to standing, BP response to sustained handgrip,
Heart Rate (HR) response to standing, HR response to deep
breathing and HR response to valsalva. Positive result of
any test indicates autonomic dysfunction [4].
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2.2. During dialysis
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Dialysis was done via AV fistula (23 patients) or dialysis catheter (7 patients), using Fresenius 4008B, Nipro machine with
ultrafiltration volume control and polysulfone, Fresenius F6
filters. Temperature of dialysate was kept at 36 C. Blood
pump was kept between 250 and 350 ml/min except during
the hypotensive episodes during which the blood pump was
decreased to only 200 ml/min and not less to insure adequate
dialysis session. Dialysate flow was 500 ml/min. All dialysis
sessions lasted around 4 h.
BP is recorded using standard sphygmomanometer every
30 min in supine position. Each time the mean of 3 measurements is recorded. Intradialytic hypotension is defined as a
symptomatic decrease of more than 30 mmHg in systolic blood
pressure or as an absolute systolic blood pressure under
90 mmHg [5]. Hypotension is further classified as mild (Systolic Blood Pressure (SBP) > 100 mmHg), moderate (SBP
80–100 mmHg) and Severe (SBP < 80 mmHg) [6].
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Patients who required vasopressors were unstable and
accordingly were excluded from this study.
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2.3. After dialysis
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Within 2–5 h after dialysis, patients had both trans-thoracic
echocardiography and MPI. The echo was done using an
ATL machine HDI 5000 with the patient lying in the left lateral decubitus using a 3.5 MHZ probe. MPI was done at the
nuclear laboratory of the critical care medicine department,
Kasr Al-Aini hospital, Cairo University utilizing the ‘‘freeze
imaging protocol’’. The set of SPECT images was acquired
using a triple head Siemens gamma camera with high resolution collimators (model Symbia E). Pharmacological stress
testing using Dipyridamole was done as most patients with
CKD could not achieve target HR during treadmill stress testing due to marked physical limitations.
Patients were instructed to fast for at least 6–8 h, stop theophylline medications for at least 24 h and not to have any caffeinated drinks or beverages for at least 24 h prior to the study.
Dipyridamole 0.56 mg/kg was diluted with 40 cc normal saline
and infused over 4 min. 2 min later, 20–25 mCi Tc-99 m Sestamibi were injected intravenously through a wide bore cannula followed by saline flush. Patients were monitored for at least 5 min
or till vital signs returned to baseline. Ambulant patients were
asked to walk for 4 min after Dipyridamole infusion.
Twenty projections were acquired (30 s for each frame) at
120 degree arc and total acquisition time of 12 min. SPECT
images were processed using the back-projection technique to
get trans-axial images then short axis, vertical long axis and
horizontal long axis cuts. The twenty-segment scoring system
was applied to estimate the Myocardium At Risk (MAR),
and the severity of perfusion defect was assessed for each segment using a ‘‘0–4’’ scoring system with ‘‘0’’ indicating normal
perfusion and ‘‘4’’ indicating no photon activity. The sum of
these scores is the Summed Stress Score (SSS).
Seventy two hours later, patients were re-injected with 20–
30 mCi Tc-99 m Sestamibi intravenously to acquire the second
set of SPECT images at rest, and to estimate the left ventricular ejection fraction (EF) utilizing the Gated SPECT technique. The severity of perfusion defects of MAR in this set
of SPECT images is assessed similarly and the sum of these
scores is the Summed Rest Score (SRS).
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Please cite this article in press as: Soliman RA et al. Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in
Q1 patients with chronic renal failure, Egypt J Crit Care Med (2014), http://dx.doi.org/10.1016/j.ejccm.2014.05.001
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Table 2
Comparison of demographic, clinical, laboratory and MPI data between the 2 study groups.
Parameter
Group A (n = 20)
Group B (n = 10)
Age (years)
Weight (Kg)
Male
43.5 (33–54)
65.5 (56–73)
9 (45)
47.5 (28–58)
67 (58–77)
3 (30)
0.63
0.81
0.69
Clinical
Smokers
Hypertension
Family history of IHD
Autonomic neuropathy
AV fistula
Duration of hemodialysis (years)
5 (25)
7 (35)
5 (25)
4 (20)
16 (80)
4 (3–6)
2 (20)
5 (50)
4 (20)
5 (50)
7 (70)
2.5 (1–4)
1.0
0.69
0.43
0.115
0.66
0.1
ECG and ECHO
Arrhythmia in ECG
LVH in ECG
RWMA
LVEDD (mm)
LVESD (mm)
EF (%)
1 (5)
3 (15)
2 (10)
52 (46.5–55)
32 (30–35)
63 (56–70)
3 (30)
3 (30)
3 (30)
44.5 (44–51)
31.5 (28–34)
59.5 (56–62)
0.095
0.37
0.30
0.046
0.63
0.19
Grades of Albuminuria*
(+)
(++)
(+++)
Urine specific gravity
n=8
5/8 (62.5)
3/8 (37.5)
0/8
1010 (1008–1010)
n=7
1/7 (14.3)
4/7 (57.1)
2/7 (28.6)
1009 (1005–1010)
0.12
Labs
Hb (g/dL)
Hct (%)
TLC (103 cells/cmm)
FBS (mg/dL)
PPBS (mg/dL)
HB A1C (mg/dL)
Serum Triglycerides (mg/dL)
Serum Cholesterol (mg/dL)
Serum Urea (mg/dL)
Serum Creatinine (mg/dL)
GFR (ml/min/1.73 m2)
Serum Sodium (mEq/L)
Serum Potassium (mEq/L)
10.4 (9.8–10.9)
31.9 (30.3–35)
5.4 (4.8–7.6)
71 (60–80)
123 (116–131)
4.9 (4.6–5.5)
90.5 (80–117)
135 (113–165)
138 (101–151)
8.4 (6.3–9.7)
10.2 (7.9–12.4)
138.5 (133–144)
5.2 (4.7–5.5)
10.5 (10.3–11.3)
33 (32.3–37)
5.2 (4–8)
69 (62–76)
119 (108–134)
4.8 (4.3–5.5)
97 (75–170)
117 (109–247)
121 (106–144)
7.7 (6.5–9)
9.5 (8.9–12.6)
138.5 (133–142)
5.3 (5–6.1)
0.15
0.098
0.74
0.88
0.58
0.42
0.75
0.55
0.4
0.63
0.55
1.0
0.094
MPI
Ischemia (total count)
Mild ischemia
Moderate ischemia
Scar
Stress induced LV dysfunction
2 (10)
1/1 (50)
1/1 (50)
0
2 (10)
7 (70)
1/7 (14.3)
6/7 (85.7)
2 (20)
7 (70)
0.002
0.417
0.092
0.103
0.002
Data are displayed as n (%) or median (inter-quartile range).
IHD, ischemic heart disease; LVH, left ventricular hypertrophy; RWMA, regional wall motion abnormalities; LVEDD, left ventricle enddiastolic diameter; LVESD, left ventricle end-systolic diameter; EF, ejection fraction; Hb, hemoglobin; Hct, hematocrit; TLC, total leukocytic
count; FBS, fasting blood sugar; PPBS, post prandial blood sugar; HB A1C, hemoglobin A1C; GFR, glomerular filtration rate.
*
Done only for the 15 patients who were not anuric.
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The difference between SSS and SRS is the Summed Difference Score (SDS). It is classified as follows; 0–4 indicates no
ischemia, 5–8 mild ischemia, 9–12 moderate ischemia and
more than 12 is severe ischemia.
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2.4. Statistical methods
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Statistical analysis was done using Statistical Package for
Social Sciences (SPSS) software, release 16.0.0 for Windows
(SPSS Inc., Chicago, Illinois).
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Categorical variables are described as frequency (n) and
percentage (%). Quantitative variables are described as
mean ± standard deviation (SD) whenever parametric. Nonparametric quantitative variables are described as median
and interquartile range (IQR). Bivariate analysis of categorical
variables was done using Chi-square test with Yates Continuity correction for 2 · 2 tables. Whenever cell frequency is <5,
Fisher’s Exact test is used.
Comparison of two groups of quantitative variables was
done using Independent-Samples Student’s t test for parametric data, and Mann–Whitney test for non-parametric data.
Please cite this article in press as: Soliman RA et al. Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in
Q1 patients with chronic renal failure, Egypt J Crit Care Med (2014), http://dx.doi.org/10.1016/j.ejccm.2014.05.001
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Figure 2 Stress induced LV dysfunction diagnosed by MPI in patients with moderate or severe intradialytic hypotension in comparison
to those with no or mild hypotension (p = 0.002).
Figure 3 Left ventricular end-diastolic diameter in patients with moderate or severe intradialytic hypotension (44.5 mm [44–51]) in
comparison to those with no or mild intradialytic hypotension (52 mm [46.5–55]) (p = 0.046).
In all cases, the 2-sided significance was always taken as p
value. p value <0.05 is considered statistically significant.
52 mm, IQR 46.5–55) than in Group B (44.5 mm, 44–50.75)
(p = 0.046) (Fig. 3).
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3. Results
4. Discussion
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Thirty patients were included in this study. Their baseline
characteristics are listed in Table 1.
We found that 70% (7/10) of patients who had moderate or
severe hypotension (Group B) had myocardial ischemia on
MPI, in comparison to 10% (2/20) of patients who experienced
no or mild intradialytic hypotension (Group A); a difference
that is statistically significant (p = 0.002) (Fig. 1).
Several other variables were compared across both study
groups (Table 2). It is to be noted that patients of Group B
were more likely to have stress induced LV dysfunction on
MPI (7/10, 70%) than patients of Group A (2/20, 10%)
(p = 0.002) (Fig. 2). LVED was wider in Group A (Median
Intradialytic hypotension (IDH) is a major complication of
hemodialysis. Two to four liters of fluid needs to be removed
during a regular session, equivalent to 40–80% of the blood
volume. It is therefore not surprising that hypotension occurs
so often. Although many factors – patient or treatment related
– play a role, a reduction of blood volume is crucial in its pathogenesis [1].
Hypotension is one of the clinical presentations of CVD in
patients with CKD [7]. There are a number of possible explanations for the independent association of reduced GFR and
CVD outcomes. First, a reduced GFR may be associated with
an increased level of nontraditional CVD risk factors that fre-
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Please cite this article in press as: Soliman RA et al. Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in
Q1 patients with chronic renal failure, Egypt J Crit Care Med (2014), http://dx.doi.org/10.1016/j.ejccm.2014.05.001
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quently are not assessed in many studies. Second, reduced
GFR may be a marker of undiagnosed vascular disease or
alternatively a marker of the severity of diagnosed vascular
disease, especially in high or highest risk populations. Third,
reduced GFR may have had more severe hypertension or dyslipidemia and therefore have suffered more vascular damage
secondary to hypertension or dyslipidemia. Fourth, recent
studies have suggested that subjects with reduced GFR are less
likely to receive medications or therapies such as angiotensin
converting enzyme inhibitors, ß-blockers, aspirin, platelet
inhibitors, thrombolytics, or percutaneous intervention than
patients with preserved GFR. Perhaps as important was the
fact that in the same studies, patients with reduced GFR
who did receive the above interventions obtained similar benefit as patients with preserved GFR. Finally, decreased GFR
itself may be a risk factor for progression of ventricular remodeling and cardiac dysfunction [7].
Different studies stated that, during hemodialysis, patients
are particularly susceptible to myocardial ischemia for number
of reasons including: LV hypertrophy [8], intradialytic hypotension and instability [9], high prevalence of decreased coronary flow reserve even in the absence of coronary vessel
stenosis [10,11].
Hakeem et al. [12] reported that in patients with CKD 40%
of perfusion scans were abnormal (SSS P 4) with 20% mild
defects and 20% moderated to severe defects.
Q4
In line with Hakeem’s result, we found that patients who
experience moderate or severe intradialytic hypotension have
significantly higher prevalence of myocardial ischemia (70%,
7/10), in comparison to those who have no or mild intradialytic hypotension (10%, 2/20) (p = 0.002).
Paoletti et al. [13] stated that there is growing evidence that
patients with CKD have unrecognized LV dysfunction, both
systolic and diastolic. They also pointed at the importance of
LV dysfunction (LV ejection fraction <40%) as a predictor
of cardiac death in patients with CKD.
We similarly found that CKD patients who develop moderate or severe intradialytic hypotension, have significantly
higher prevalence of stress induced LV dysfunction (70%, 7/
10) than those who have no or mild hypotensive episodes
(10%, 2/20) (p = 0.002).
Deterioration of renal function in CKD may lead to dyslipidemia or accumulation of uremic toxins, which can stimulate
oxidative stress and inflammation, which in turn contributes to
endothelial dysfunction and progression of atherosclerosis
[14]. Renal failure causes changes in plasma components and
endothelial structure and function that favor vascular injury,
which may play a role as a trigger for inflammatory response.
Dyslipidemia associated with CKD contributes to the inflammatory response in renal failure [15]. However, in our study
we found that levels of serum cholesterol and triglycerides were
not significantly different between the two study groups, a
finding probably attributed to the small number of the study
group and the relatively low economic standard of those
patients.
Patients with CKD also have a high prevalence of arteriosclerosis and remodeling of large arteries. Remodeling may
be due to either pressure overload – which is distinguished
by wall hypertrophy and an increased wall-to-lumen ratio –
or flow overload, which is characterized by a proportional
increase in arterial diameter and wall thickness [16].
R.A. Soliman et al.
In conclusion, we found that patients with CKD and regular hemodialysis who experience moderate or severe intradialytic hypotension have significantly higher prevalence of
myocardial ischemia and stress induced myocardial dysfunction, than those who experience no or mild intradialytic
hypotension.
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Please cite this article in press as: Soliman RA et al. Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in
Q1 patients with chronic renal failure, Egypt J Crit Care Med (2014), http://dx.doi.org/10.1016/j.ejccm.2014.05.001
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