INTRADIALYTIC DOPAMINE THERAPY IN MAINTENANCE HEMODIALYSIS PATIENTS WITH PERSISTENT HYPOTENSION

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1 Original Article 22 INTRADIALYTIC DOPAMINE THERAPY IN MAINTENANCE HEMODIALYSIS PATIENTS WITH PERSISTENT HYPOTENSION Wen-Yuan Chiu, Horng-Rong Chang *, Zyh-Zan Lin **, Enny Halim, Jong-Da Lian * Intradialytic hypotension (IDH) is a common and frustrating complication of hemodialysis. Certain hemodialysis patients persistently manifest this problem. Both patient-specific factors (autonomic insufficiency, cardiac dysfunction) and dialysis treatment-related factors (ultrafiltration, increased core temperature) are thought to have significant causative roles. A variety of maneuvers have been used for the treatment of IHD with variable success. However, there are still a subgroup of patients that suffer from IHD. We report our experience of 8 persistent IDH patients treated with intravenous dopamine infusion during a hemodialysis session. After dopamine was intravenously infused during the entire hemodialysis session, there were uniform improvements in the lowest intradialytic blood pressure, as well as the postdialytic blood pressure. Predialysis blood pressures were similar before and after dopamine therapy. The mean lowest intradialytic SBP (from ± 7.19 to ± 9.03 mmhg, P < 0.001) and lowest intradialytic MAP (from ± 4.56 to ± 5.89 mmhg, P < 0.001) were significantly better after dopamine therapy compared with before dopamine therapy. The same was true for the postdialysis SBP (from ± to ± 6.25 mmhg, P < 0.001), MAP (from ± 6.90 to ± 9.03 mmhg, P < 0.001) and DBP (from ± 7.96 to ± 5.93 mmhg, P < 0.001) after dopamine therapy compared with before dopamine therapy. The mean frequency of hypotension episodes significantly decreased following dopamine treatment (from 1.06 ± 0.49 to 0.31 ± 0.47/session, P < 0.001). The mean required Trendelenburg s position decreased from a mean of 0.79 time per dialysis session per patient to a mean of 0.14 time per dialysis session per patient following dopamine therapy (from 0.79 ± 0.59 to 0.14 ± 0.35/session, P < 0.001). The mean required saline infusion decreased from 136 ml per dialysis session per patient to 34 ml per dialysis per patient (from ± to ± ml, P < 0.001). The mean required 50% glucose water infusion decreased from 8.0 to 2.25 ml per dialysis session per patient (from 8.0 ± 9.60 to 2.25 ± 6.16 ml, P < 0.001). Subjective symptoms of IHD improvement were found in all patients (4 marked, 2 moderate, 2 mild). Kt/V values before and after dopamine therapy were similar. The amount of fluid removal following dopamine therapy was higher than that before dopamine therapy to a statistically significant level (from 2.52 ± 0.25 to 2.91 ± 0.26 Kg, P < 0.05). No significant adverse effects were noted. In summary, dopamine therapy for IDH patients during dialysis session seems to be effective and safe in this small number and short-period study. (Acta Nephrologica 2007; 21: 22-29) Key words: intradialytic hypotension, dopamine Introduction Intrdialytic hypotension (IDH) is a common complication in hemodialysis patients which typically occurs during the latter stage of dialysis. It is estimated that hypotension occurs as many as 20-50% of patients during hemodialysis. 1 During the past 10 years, despite the improvements in dialysis technology, the frequency of IDH continue to increase due to an increasing number of older, more severely ill patients and diabetic patients. 2 Patients subgroups most likely to have IDH include those with diabetes, poor nutrition, anemia, autonomic dysfunction, left ventricular dysfunction, age 65 and predialysis systolic blood pressure < 100 mmhg. 2 Factors implicated in the pathogenesis of IHD are: (a) hypovolemia, due to ultrafiltration and solute removal, Bodhi Hospital, Chung-Shan Medical University Hospital*, Cheng-Ching Hospital**, Taichung, Taiwan Received: July, 2006 Revised: September, 2006 Accepted: Nvember, 2006 Address reprint requests to: Dr. Jong-Da Lian, 110, Sec. 1, Chien-Kuo North Rd, Chung-Shan Medical University Hospital, Taichung, Taiwan Tel: ext Fax: ext cshy590@csh.org.tw indd /3/16 11:56:04 AM

2 Acta Nephrologica Intradialytic Dopamine 23 causing a decrease in filling pressure; (b) decrease in stroke volume due to altered myocardial contractility; (c) lack of compensatory vasoconstriction and tachycardia, and (d) paradoxical withdrawal of sympathetic activity. 3 A variety of maneuvers, including sodium modeling, cooling of dialysate, correcting low hematocrit, use of bicarbonate dialysis, appropriate adjustment of the antihypertensive drugs on the day of dialysis, and pharmacological agents (caffeine, vasopressin, ephedrine, phenylephrine) have been used for the treatment of IDH with variable success. 4-7 However, there are still subgroup of patients suffering from IDH despite the above regimens. Dopamine is a natural catecholamine which produces positive chronotropic and inotropic effects on the myocardium, resulting in an increased heart rate and cardiac contractility. Dopamine s onset of action occurs within five minutes of intravenous administration, and with dopamine s plasma half-life of about two minutes, the duration of action is less than ten minutes. The predominant effects of dopamine are dose-related. At low rates of infusion (0.5-2 ug/kg/min) dopamine causes vasodilatation. At intermediate rates of infusion (2-10 ug/kg/min) dopamine acts to stimulate the beta1-adrenoceptors, resulting in improved myocardial contractility. At higher rates of infusion (10-20 ug/kg/min) there is an effect on the alpha-adrenoceptors, with consequent vasoconstrictor effects and a rise in blood pressure. 8,9 Dopamine has been broadly used in hypotensive heart failure for a long time. 8,9 However, there was no experience with the use of this drug on dialysis. Therefore, we conduct a study to evaluate the efficacy of dopamine for the treatment of symptomatic IDH in a subgroup of hemodialysis patients suffering from persistent IDH. Materials and Method The study was performed from January 2004 to November To be included in the study, subjects must be experiencing end-stage renal disease (ESRD), have been on chronic hemodialysis for at least 3 months, and demonstrate persistent symptomatic intradialytic hypotension. Intradialytic hypotension (IDH) was defined as a decrease in systolic blood pressure (SBP) of 20 mmhg or more during hemodialysis in addition to the development of symptoms such as dizziness, nausea, vomiting, syncope, yawn, cramps and chest distress. Hypotension was considered to be persistent if the patient continued to have hypotension despite (1) improvement in hematocrit and albumin levels; (2) appropriate sodium modeling; (3) low temperature hemodialysis (35.5 ); (4) avoidance of large interdialysis weight gain and maintenance of slow ultrafiltration rates; (5) antihypertensive drugs withheld on the day of hemodialysis; (6) optimizing anti-anginal therapy in patients with ischemic heart disease; (7) researching for and treating pericardial effusion, (8) using bicarbonate hemodialysis (all patients in our unit were on bicarbonate dialysis), and (9) using pharmacological vasoactive medication (Risumic or Effortil ). The inclusion criteria for this study was the persistence of hypotension, even when these remedies were used. Eight patients fulfilling the criteria were enrolled. All patients were dialyzed on Althen hemodialysis machine and PMMA material dialyzers with surface area ranging from 1.3 to 1.5 m 2. The electrolyte concentration of the dialysate was sodium 142 meq/l, potassium 2 meq/l, calcium 3.5 meq/l and bicarbonate 39 meq/l. The temperature of the dialysis bath was maintained at 35.5 for all treatment. Dry weight was defined as the weight on which the patient had a heart size (chest X-ray) as close as possible to normal, which was clinically tolerated. Throughout the study, any possible factors such as dialysate sodium concentration, dialysate temperature, buffer, ultrafltation rate, antihypertensive medication that may have interfered with the hemodynamics were controlled as far as possible. Likewise, dialysis procedures and materials of dialyzers which may affect hemodynamics were also controlled. Patients were asked to avoid excess interdialysis weight gain and food intake during dialysis. Hematocrit level was determined weekly, and clinical biochemical variables values were determined monthly for each patient. Kt/V was calculated by Gotch s equation. Blood pressure and pulse rate were measured by arm cuff with the patient in the supine position immediately prior to each dialysis session, at 30-minute intervals during dialysis, and at the end of dialysis session with the patient in the supine position. The predialysis blood pressure, lowest intradialytic blood pressure, post dialysis blood pressure, and corresponding pulse rate, predialysis weight, and postdialysis weight were recorded for 10 consecutive hemodialysis sessions prior to the initiation of dopamine therapy. Dopamine infusion fluid was prepared as 200 mg of dopamine added in 100 ml of normal saline. Dopamine infusion began at the initiation of hemodialysis for 4 hours during each dialysis using an intravenous infusion pump. For nursing cares convenience, we started dopamine infusion at a rate of 10 microdrips per minute (approximately 5 ug/min/kg for a 70-Kg patient). The goal was to maintain systolic blood pressure above 120 mmhg. If the goal was achieved, we continued the concurrent dose; if the systolic blood pressure dropped below 120 mmhg, we increased the dose of dopamine at an interval of 10 minutes at the rate of 5 microdrips per minute increment to a maximal dose of 40 microdrips per minute (approximately 20 ug/min/kg for a 70-Kg indd /3/16 11:56:04 AM

3 24 W. Y. CHIU, H. R. CHANG, Z. Z. LIN, E. HALIM, J. D. LIAN Vol. 21, No. 1, 2007 patient). If systolic blood pressure was greater than 180 mmhg, diastolic blood pressure (DBP) was greater than 120 mmhg, heart beats were greater than 120/min or there was any effect that the patient couldn t tolerate, dopamine infusion was withheld at the initiation of hemodialysis or during hemodialysis in order to prevent undesired complications such as a cerebral vascular accident, myocardial ischemia or even lethal dysrhythmias. However, this was not required in any of these patients. The same parameters for blood pressure, pulse rate, and weight were recorded for 10 consecutive hemodialysis session following the initiation of dopamine therapy. Predialysis blood pressure (SBP, DBP, mean arterial pressure [MAP]), lowest intradialysis blood pressure and postdialysis blood pressure before dopamine therapy were compared with predialysis blood pressure, lowest intradialysis blood pressure and postdialysis blood pressure following dopamine therapy. Pulse rates before and after dopamine therapy were also compared. The frequency of hypotension episodes before and after dopamine therapy were compared. Nursing interventions (volume of replacement fluid such as normal saline, 50% glucose water infusion and Trendelenburg s position) and patient symptoms were recorded during each treatment and were compared before and after dopamine administration. The amount of fluid removal, Kt/ V before and after dopamine therapy were recorded and compared. The various subjective symptoms of intradialytic hypotension (dizziness, nausea, vomiting, syncope, yawn, cramps and chest distress) were recorded by dialysis nurse during the dialysis period and were compared before and after dopamine administration. At the end of the treatment, a global opinion of improvement of these symptoms (marked, moderate or mild improvement, unchanged, worsened) in comparison with baseline period (before dopamine therapy was viewed as baseline) were made. All patients had an echocardiogram prior to the study (within 4 weeks before starting dopamine) as part of routine workup to exclude significant cardiac causes, such as pericardial effusion, for the hypotensive episodes on hemodialysis. M-mode and Doppler echocardiogram were performed using Hewlett Packard M2410A. The echocardiograms were carried out and interpreted by the same cardiologist (Dr. Zyh-Zan Lin). The readings did not take place in a blinded fashion. The M-mode echocardiogram was recorded from the left margin of the third or forth intercostal sternum to measure the interventricular septum (IVS), posterior wall (PW), left atrium (LA), left ventricular end-systolic dimension (LVDs), left ventricular end-diastolic dimension (LVDd), aorta (Ao) as recommended by the International Society and Federation of Cardiology/World Health Organization (ISFC/WHO). Fraction shortening was calculated from LVDs and LVDd. The ejection fraction was also calculated. The Doppler echocardiography was measured simultaneously with the M-mode echocardiogram. The early diastolic filling wave (E wave) and early late diastolic filling wave (A wave), and the E/A ratio were also measured from transmitral Doppler recordings. We didn t perform cardiac output, peripheral resistance or autonomic function tests due to facilities limitation. All numerical values are expressed as mean ± SD. Symptoms of intradialytic hypotension were compared with Yates correction χ2 test. Hypotensive episode, times of Trendelenburg s position, dose of normal saline and 50% glucose were compared with paired-t test. Kt/V and amount of fluid removal before and after dopamine therapy were compared using Wilcoxon signed ranks test. Changes in blood pressure before and after dopamine therapy were compared with paired-t test. P value < 0.05 was regarded as statistical significance. Result Eight patients were enrolled into this study. There were 2 males and 6 females. Four patients had diabetes mellitus. The mean duration of hemodialysis was ± months (range months). The average age was ± 9.49 years (range years). The mean body weight was ± 6.39 Kg (range Kg). The laboratory and dialysis data are presented in Table 1. The echocardiogram results are presented in Table 2. The ejection fraction ranged from 33-55% with E/A ratio ranged from 0.6 to 1.3. Three patients had an ejection fraction less than 45% and 6 patients had E/A < 1.0. The mean dose of dopamine was 7.0 ± 1.7 ug/kg/min (range 5-12 ug/kg/min). There were uniform improvements Table 1. Laboratory data (mean ± standard deviation) BUN mg/dl ± Creatinine mg/dl 7.84 ± 1.44 Na meq/l ± 2.43 K meq/l 5.15 ± 0.40 Ca meq/l ± 0.24 P meq/l 5.88 ± 0.81 Alb g/dl 4.20 ± 0.28 Kt/V 1.45 ± 0.12 WBC ± Platelet ( 10 3 /ul) ± Hct % ± indd /3/19 10:11:09 AM

4 Acta Nephrologica Intradialytic Dopamine 25 Table 2. Echocardiogram findings of patients Patient LVDd LVDs IVS PW LA Ao EF FS E/A LVDd = left ventricular end-diastolic dimension, LVDs = left ventricular end-systolic dimension, IVS = interventricular septum, PW = left ventricular posterior wall, LA = left atrium, Ao= aorta, EF = ejection fraction, FS = fractional shortening, E/A = ratio of E to A in the lowest intradialytic blood pressure, as well as the postdialytic blood pressure. Predialysis blood pressures were similar before and after dopamine therapy. The mean lowest intradialytic SBP (from ± 7.19 to ± 9.03 mmhg, P < 0.001) and lowest intradialytic MAP (from ± 4.56 to ± 5.89 mmhg, P < 0.001) were significantly better following dopamine therapy compared with before dopamine therapy (Fig 1). The same was true for the postdialysis SBP (from ± to ± 6.25 mmhg, P < 0.001), MAP (from ± 6.90 to ± 9.03 mmhg, P < 0.001) and DBP (from ± 7.96 to ± 5.93 mmhg, P < 0.001) following dopamine therapy compared with before dopamine therapy (Fig 1). The pulse rates were similar before and after dopamine therapy (Fig 2). The mean frequency of hypotension episodes before and after dopamine treatment were compared. It was significantly decreased following dopamine treatment (from 1.06 ± 0.49 to 0.31 ± 0.47 episode/session, P < 0.001, Table 3). The mean required Trendelenburg s position to be decreased from 0.79 times per dialysis session per patient before dopamine treatment to 0.14 times per dialysis session per patient following the initiation of dopamine therapy (from 0.79 ± 0.59 to 0.14 ± 0.35 /session, P < 0.001, Table 3). Before dopamine treatment, the mean required saline infusion was 136 ml per dialysis session per patient. With dopamine therapy, the mean required saline infusion decreased to 34 ml per dialysis session per patient (from ± to ± ml, P < 0.001, Table 3). Following dopamine treatment, the mean dose of 50% glucose water infusion required decreased from 8.0 to 2.25 ml per dialysis session per patient (from 8.0 ± 9.60 to 2.25 ± 6.16 ml, P < 0.001, Table 3). Subjective symptoms of dialysis induced hypotension were reviewed (Table 4) and improvement of symptoms were found in all patients (4 marked, 2 moderate, 2 mild) No significant adverse effects were noted. One patient (patient 6) experienced palpitations that resolved over time. The amount of fluid removal after dopamine therapy was higher than that of before dopamine therapy with statistical significance (from 2.52 ± 0.25 to 2.91 ± 0.26 Kg, P < 0.05, Table 3). Kt/V before and after dopamine therapy were similar (Table 3). Discussion Intradialytic hypotension (IDH) is the most frequent adverse event of hemodialysis occurring in 20-50% of dialysis treatments. 1 For the hemodialysis patient, IHD can develop discomforts such as dizziness, nausea, vomiting, syncope, yawn, cramp and chest distress which require some form of intervention by the dialysis nurse. Symptomatic hypotension during hemodialysis is a disabling complication in ESRD for mild IDH, the patients may be reclined in the Trendelenburg s position. A more serious IDH patient requires administration of bolus saline or 50% glucose water injection, which negates the fluid removal functions of hemodialysis and contributes to increased cardiac overload and morbidity. Very serious IDH patients require the dialysis nurse to turn off the ultrafiltration or prematurely terminate the hemodialysis session. A variety of therapeutic options have been used to treat this problem with marginal success. In the past, bicarbonate dialysis (versus acetate), sequential ultrafiltration, isovolemic dialysis, increased duration of hemodi indd /3/16 11:56:05 AM

5 26 W. Y. CHIU, H. R. CHANG, Z. Z. LIN, E. HALIM, J. D. LIAN Vol. 21, No. 1, 2007 Fig. 1. Blood pressure before and after dopamine therapy (mean SD bars). ID BP, intradialytic blood pressure; HD hemodialysis (, SBP/before dopamine therapy;, MAP/before dopamine therapy;, DBP/before dopamine therapy;, SBP/after dopamine therapy;, MAP/after dopamine therapy;, DBP/after dopamine therapy; SBP, systolic blood pressure; MAP, mean arterial pressure; DBP, diastolic blood pressure, P < 0.001) Table 3. Comparison of mean episode of hypotension, Trendelenburg s position, dose of normal saline, 50% glucose water, Kt/V and amount of fluid removal before and after dopamine therapy Before After P value Hypotensive episode /session 1.06 ± ± 0.47 p < Trendelengburg s position /session 0.79 ± ± 0.35 p < Normal saline ml/session ± ± p < % glucose water ml/session 8.0 ± ± 6.16 p < Kt/V 1.45 ± ± 0.09 N.S UF amount Kg/session 2.52 ± ± 0.26 P < 0.05 Table 4. Comparison of episodes of symptoms of intradialytic hypotension before and after dopamine therapy Symptoms Before After P value Dizziness 18 7 p < 0.05 Nausea/vomit 16 3 p < 0.01 Syncope 7 0 p < 0.05 Yawn p < 0.01 Cramp 6 2 N.S Chest distress 11 2 p < indd /3/19 10:11:09 AM

6 Acta Nephrologica Intradialytic Dopamine (beats/minute) rate Pulse Predialytic pulse Intradialytic pulse Postdialytic pulse Fig. 2. Pulse rate before and after dopamine therapy(mean SD bars;, before dopamine therapy,, after dopamine therapy, NS). alysis, withholding blood pressure-lowering medications on the day of dialysis, and avoidance of food ingestion during dialysis have been attempted. 4-7 More recently ramped sodium modeling, 10 cooling of dialysate, 11 and administration of vasoactivating pharmacological agents such as midodrine have been applied. 12 Cooling of dialysate to 35.5 appears to hold the most promise for this problem, but is associated with patient intolerance due to the lower temperature. 11,13 Although some patients experience benefits from the above intervention, 14 a subgroup of patients still suffer from IDH and the associated morbidity. These included patients with diabetes, autonomic dysfunction and cardiac-compromised patients. 13 This subgroup of maintenance hemodialysis patients might have persistent hypotension during hemodialysis; in this situation any fluid removal during hemodialysis is poorly tolerated. A number of patient-specific and dialysis-associated factors typically conspire to create significant hypotension during dialysis. These factors include autonomic dysfunction, cardiac dysfunction (either systolic or diastolic dysfunction), vascular responsiveness, excessively rapid ultrafiltration rate, declining extracellular osmolality, an increased core temperature, and a paradoxical withdrawal of sympathetic activity. 3 Cardiac compromised patients are at higher risk for this problem. Symptomatic hypotension may occurs as a result of a decrease in blood volume and reduced vascular reactivity during dialysis in combination with structural abnormalities of the cardiovascular system The immediate cause of a decrease in blood pressure during hemodialysis is intravascular hypovolemia. Structural cardiovascular changes such as decreased left ventricular compliance (ie, diastolic dysfunction) or reduced myocardial contractility (ie, systolic dysfunction) may predispose a patient to symptomatic hypotension indd /3/16 11:56:07 AM

7 28 W. Y. CHIU, H. R. CHANG, Z. Z. LIN, E. HALIM, J. D. LIAN Vol. 21, No. 1, 2007 Recent reports revealed that intradialytic hypotension appeared to result from the inability to adequately increase arteriolar tone and a reduction in left ventricular function. 19 Both vascular tone and left ventricular function appeared to be impaired by the dialysis procedure. Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. Dopamine s onset of action occurs within five minutes of intravenous administration, and with dopamine s plasma half-life of about two minutes, the duration of action is less than ten minutes. Therefore, intradialytic administration of dopamine seems to be appropriate in the treatment of IDH. In this study, we attempt to use dopamine infusion during the entire course of hemodialysis to maintain SBP greater than 120 mmhg to prevent IDH. To avoid undesired complications, dopamine infusion was withheld at the initiation of hemodialysis or during hemodialysis if systolic blood pressure was greater than 180 mmhg, diastolic blood pressure (DBP) was greater than 120 mmhg, heart beats were greater than 120/min or any effect that patient couldn t tolerate. However, this was not required in any patient. We set the infusion rate of 40 microdrips per minute as the maximal dose because dopamine doses greater than 20 ug/kg/min didn t provide a better effect to myocardium but increased the risks of vasoconstriction and ischemia. Experience with dopamine therapy in ESRD is limited. To date, there is no study reporting its use in persistent IDH patients. In this article, we made some influences and opened a new mellieu in the treatment of IDH. Administration of intradialytic dopamine infusion is an easy and convenient method for patients on maintenance hemodialysis. As compared with other high-end techniques (ramped sodium model, blood volume monitoring, cooling dialysis), the only gadget we need is the intravenous infusion pump. As compared with oral vasoactive agents, dopamine infusion can be more precisely adjust the dose of dopamine to counter the changes of blood pressures immediately during hemodialysis to prevent hypotension. There are some criticisms and limitations to this study. First, the pathogenesis of persistent IDH in our patients is undetermined. From the echocardiogram findings, we knew some of our patients with IDH had left ventricular systolic (ejection fraction < 45%), diastolic (E/A < 1.0) or combined dysfunction. However, we were unable to perform follow-up echocardiogram for all patients because some of these patients died of diseases other than cardiac dysfunction (one died of colon cancer due to massive lower GI bleeding 3 months later; the other died of sepsis 4 months later). Autonomic dysfunction, which occurs in over 50% of patients on maintenance dialysis, is thought to play a significant role in intradialytic hypotension. 20 Half of our patients had diabetes mellitus. The degree of autonomic insufficiency may be enhanced in diabetes. This defect may be most prominent in patients with severe recurrent IDH. Risumic, Effortil and midodrine were commonly used in the treatment for IDH. These oral vasoactive agents have been used in the treatment of IDH with/ without autonomic neuropathy. 12,21 If the causative factor of recurrent IDH in our patient was due to autonomic dysfunction. Avoiding intake before and during hemodialysis and oral vasoactive agents would solve this problem. 22 However, our patients didn t respond well to these managements. We don t know the reason for this as of yet. The dose of vasoactive agent (phenylephrine) necessary to increase systolic blood pressure in IDH patients by 20 mm Hg was nearly twice as high as in normotensive dialysis patients and healthy controls. 23 The dose of oral vasoactive agents in the treatment of IDH might be greater than we expected. Since we didn t perform cardiac output, peripheral resistance or autonomic function tests, we didn t know the pathogenesis of IDH in our patients. However, searching for the pathogenesis of IDH in our patients and the reason why these patients were resistant to most conventional treatment is beyond the scope of this article. Second, the mechanism of dopamine infusion in the treatment of IDH is unclear. Both alpha-adrenoceptors and beta1-adrenoceptors effect were found in the dose of dopamine we used, ranging from 5 to 15 ug/kg/min. Dopamine can increase alpha-adrenoceptors vasoconstriction effect and beta1- adrenoceptors myocardium contractility. Vasocontriction increases peripheral resistance of arterioles and venules which reduces venous pooling, and thereby increases cardiac filling. Increased myocardial contractility further increased cardiac output. However, formal studies of cardiac output and peripheral vascular resistance have not been performed in our patients. As the mechanism of dopamine in the treatment of congestive heart failure, the beneficiary effect of dopamine infusion in our IDH patients might follow the same mechanism. Third, the number of patients we evaluated was small, and we didn t have a placebo run-in period. However, since patients served as their own controls, it seems unlikely that this might have changed the results significantly. In summary, the administration of dopamine during a dialysis session appears to be an effective and welltolerated therapy for the subgroup of patients with persistent symptomatic IDH. However, a prospective trial with a large sample and longer follow-up would be useful for evaluating the efficacy and safety of this drug in patient with IDH indd /3/16 11:56:07 AM

8 Acta Nephrologica Intradialytic Dopamine 29 Acknowledgement The authors wish to thank the dialysis nurses for their devotion to these patients and Miss Chiu-Chu Lin for her secretarial assistance. References 1. Sherman RA: The pathophysiologic basis for hemodialysisrelated hypotension. Semin Dial 1988; 1: Schreiber MJ: Setting the stage. Am J Kidney Dis 2001; 38: S Converse RL, Jacobsen TN, Jost CM, et al: Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension. J Clin Invest. 1992; 90: Anderson LE, Nixon JV, Henrich WL: Effects of acetate and bicarbonate dialysate on left ventricular performance. Am J Kidney Dis. 1987; 10: Daugirdas JT, Purandare VV, Ing TS, et al: Ultrafiltration hemodynamics in an animal model: Effect of a decreasing plasma sodium level. Trans Am Soc Artif Intern Organs 1984; 30: Jost CM, Agarwal R, Khair-el-Din T, et al: Effects of cooler temperature dialysis on hemodynamic stability in problem dialysis patients. Kidney Int 1993; 44: Daugirdas JT: Preventing and managing hypotension. Semin Dial 1994; 7: Reid PR, Thompson WL: The clinical use of dopamine in the treatment of shock. Johns Hoskins Med J 1975; 137: Bayram M, De Luca L, Massie MB, Gheorghiade M: Reassessment of dobutamine, dopamine, and milrinone in the management of acute heart failure syndromes. Am J Cardil 2005; 96: Henrich WL, Woodard TD, MaPhaul JJ: The chronic efficacy and safety of high sodium dialysate: Double-blind cross over study. Am J Kidney Dis 1982; 2: Sherman RA, Rubin MP, Cody RP, Eisinger RP: Amelioration of hemodialysis associated hypotension by the use of cool dialysate. Am J Kidney Dis 1985; 5: Cruz DN, Mahnensmith RL, Perazella MA: Intradialytic hypotension: Is midodrine beneficial in symptomatic hemodialysis patients? Am J Kidney Dis 1997; 30: van Der Sande FM, Kooman JP, Leunissen KM: Strategies for improving hemodynamic stability in cardiac-compromised dialysis patients. Am Kidney Dis 2000; 35: E Fine A, Penner B: The protective effect of cool dialysate is dependent on the patient s pre-dialysis temperature. Am J Kidney Dis 1996; 28: Aoki J, Ikari Y, Nakajima H, et al: Clinical and pathologic characteristics of dilated cardiomyopathy in hemodialysis patients. Kidney Int 2005; 67: Hung KC, Huang HL, Chu CM, et al: Effects of altered volume loading on left ventricular hemodynamics and diastolic filling during hemodialysis. Ren Fail 2004; 26: Hung KC, Huang HL, Chu MC, et al: Evaluating preload dependence of a novel Doppler application in assessment of left ventricular diastolic function during hemodialysis. Am J Kidney Dis 2004; 43: Wanic-Kossowska M, Lehmann P, Czekalski S: Left ventricular systolic and diastolic dysfunction in patients with chronic renal failure treated with hemodialysis. Pol Arch Med Wewn 2003; 109: Nette RW, van den Dorpel MA, Krepel HP, et al: Hypotension during hemodialysis results from an impairment of arteriolar tone and left ventricular function. Clin Nephrol 2005; 63: Kersh ES, Kronfield SJ, Unger A, et al: Autonomic insufficiency in uremia as a cause of hemodialysis-induced hypotension. N Engl J Med 1974; 290: Yang CS, Chen CM, Wu SC: Treatment of intradialytic hypotension with amezinium metilsulfate. Acta nephrologica ROC 1997; 11: Daugidas JT: Pathophysiology of dialysis hypotension: an update. Am J Kidney Dis 2001;38:S Daul AE, Wang XL, Michel MC, Brodde OE: Arterial hypotension in chronic hemodialyzed patients. Kidney Int 1987; 32: indd /3/16 11:56:07 AM