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      Effects of the Intermittent Pneumatic Circulator on Blood Pressure during Hemodialysis

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          Abstract

          Hypotension is frequently reported during hemodialysis. This study aimed to examine the effect of the intermittent pneumatic circulator on blood pressure during hemodialysis. Sixteen subjects with chronic hemodialysis were recruited. Each subject randomly received two test conditions on separate days, hemodialysis with and without the circulator. The circulator was applied to the subject on lower extremities during 0.5–1 hr, 1.5–2 hr, 2.5–3 hr, and 3.5–4 hr of hemodialysis. Systolic and diastolic blood pressures (SBP and DBP) and heart rate (HR) were analyzed at pre-dialysis, 1 hr, 2 hr, and 3 hr of hemodialysis. Stroke volume (SV) and cardiac output (CO) were evaluated between 2.5 and 3.0 hr of hemodialysis. Blood chemicals (sodium, calcium, potassium, and phosphorous) and Kt/V before and after each hemodialysis session were analyzed. The number of episodes of hypotension was also recorded. The circulator intervention significantly improved SBP and DBP across all time points (P = 0.002 for SBP; P = 0.002 for DBP). The frequency of hypotension was significantly decreased (P = 0.028). SV and CO were significantly improved with the circulator intervention (P = 0.017 for SV; P = 0.026 for CO) and no statistical significances were found on blood chemicals or Kt/V analyses. The results suggested that the circulator intervention helps stabilize blood pressure and appears to be a practical treatment. Future studies are suggested to develop new circulator innovations with sensor feedback systems to enhance safety and maximize treatment efficiency.

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          Most cited references37

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          Hemodialysis-induced cardiac injury: determinants and associated outcomes.

          Hemodialysis (HD)-induced myocardial stunning driven by ischemia is a recognized complication of HD, which can be ameliorated by HD techniques that improve hemodynamics. In nondialysis patients, repeated ischemia leads to chronic reduction in left ventricular (LV) function. HD may initiate and drive the same process. In this study, we examined the prevalence and associations of HD-induced repetitive myocardial injury and long-term effects on LV function and patient outcomes. Seventy prevalent HD patients were assessed for evidence of subclinical myocardial injury at baseline using serial echocardiography and followed up after 12 mo. Intradialytic blood pressure, hematologic and biochemical samples, and patient demographics were also collected at both time points. Sixty-four percent of patients had significant myocardial stunning during HD. Age, ultrafiltration volumes, intradialytic hypotension, and cardiac troponin-T (cTnT) levels were independent determinants associated with its presence. Myocardial stunning was associated with increased relative mortality at 12 mo (P = 0.019). Cox regression analysis showed increased hazard of death in patients with myocardial stunning and elevated cTnT than in patients with elevated cTnT alone (P < 0.02). Patients with myocardial stunning who survived 12 mo had significantly lower LV ejection fractions at rest and on HD (P < 0.001). HD-induced myocardial stunning is common, and may contribute to the development of heart failure and increased mortality in HD patients. Enhanced understanding of dialysis-induced cardiac injury may provide novel therapeutic targets to reduce currently excessive rates of cardiovascular morbidity and mortality.
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            Pathophysiology of dialysis hypotension: an update.

            Dialysis hypotension occurs because a large volume of blood water and solutes are removed over a short period of time, overwhelming normal compensatory mechanisms, including plasma refilling and reduction of venous capacity, due to reduction of pressure transmission to veins. In some patients, seemingly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, increased transmission of pressure to veins, and corresponding increase in venous capacity. Increased sequestration of blood in veins under conditions of hypovolemia reduces cardiac filling, cardiac output, and, ultimately, blood pressure. Adenosine release due to tissue ischemia may participate in reducing norepinephrine release locally, and activation of the Bezold-Jarisch reflex, perhaps in patients with certain but as yet undefined cardiac pathology, may be responsible for sudden dialysis hypotension. Patients with diastolic dysfunction may be more sensitive to the effects of reduced cardiac filling. The ultimate solution is reducing the ultrafiltration rate by use of longer dialysis sessions, more frequent dialysis, or reduction in salt intake. Increasing dialysis solution sodium chloride levels helps maintain blood volume and refilling but ultimately increases thirst and interdialytic weight gain, with a possible adverse effect on hypertension. Blood volume monitoring with ultrafiltration or dialysis solution sodium feedback loops are promising new strategies. Maintaining tissue oxygenation via an adequate blood hemoglobin level seems to be important. Use of adenosine antagonists remains experimental. Given the importance of sympathetic withdrawal, the use of pharmacologic sympathetic agonists is theoretically an attractive therapeutic strategy.
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              The effect of exercise during haemodialysis on solute removal.

              Urea rebound results as urea re-equilibrates between intracellular and intravascular compartments post haemodialysis. The mechanism of the rebound is thought to be due to either a reduced diffusion rate or blood flow. It is hypothesized that low blood flow in the skeletal muscles might be responsible. We tested this by studying the effect of exercise during dialysis on the removal of urea, creatinine and potassium. Eleven patients (aged 32-78 years) on haemodialysis (4-58 months) were studied on paired dialysis sessions; one with exercise and the other as a control. Patients pedalled on a cycle for 5-20 min at submaximal workload followed by 10 min rest to achieve a total of 60 min exercise. Plasma concentrations of urea, creatinine and potassium were measured pre-, post- and 30-min post dialysis. The post-dialysis rebound (% rebound) and reduction ratios (RR) of the solutes and equilibrated (two-pool) urea Kt/V were calculated for comparison. The rebound of all three solutes was reduced significantly following exercise. The rebound of urea decreased from 12.4 to 10.9% (median, P<0.01 Wilcoxon signed rank test), creatinine from 21.2 to 17.2% (P<0.001) and potassium from 62 to 44% (P<0.05). Kt/V and RR increased significantly as a result: Kt/V urea from 1.00 to 1.15 (P=0.001), RR urea from 0.63 to 0.68 (P<0.001); Kt/V creatinine from 0.71 to 0.84 (P<0.01); and RR creatinine from 0.51 to 0.57 (P<0.05). Exercise increased the efficiency of dialysis by reducing the rebound of solutes due to increased perfusion of the skeletal muscles.
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                Author and article information

                Journal
                Sensors (Basel)
                Sensors (Basel, Switzerland)
                Molecular Diversity Preservation International (MDPI)
                1424-8220
                2010
                9 November 2010
                : 10
                : 11
                : 10014-10026
                Affiliations
                [1 ] Department of Internal Medicine, Pao-Chien Hospital, Ping-Tung City, Taiwan; E-Mail: tc003022@ 123456ms34.hinet.net
                [2 ] Physical Therapy Department and Graduate Institute of Rehabilitation Science, Chang Gung University, Tao-Yuan, Taiwan; E-Mail: yjchang@ 123456mail.cgu.edu.tw
                [3 ] Department of Cardiology, Pao-Chien Hospital, Ping-Tung City, Taiwan; E-Mail: thinkingteam2000@ 123456yahoo.com
                [4 ] Department of Physical Therapy, College of Health Science, Kaohsiung Medical University, Kaohsiung, Taiwan
                [5 ] Department of Rehabilitation, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: mjhsu@ 123456kmu.edu.tw ; Tel.: +886-7-3121101-2673; Fax: +886-7-3215845.
                Article
                sensors-10-10014
                10.3390/s101110014
                3230995
                22163454
                00e843aa-1ce5-4108-bc9a-07c76a4374c9
                © 2010 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/.)

                History
                : 12 July 2010
                : 10 September 2010
                : 23 October 2010
                Categories
                Article

                Biomedical engineering
                mechanical pump,hemodialysis,dialysis,circulator,blood pressure
                Biomedical engineering
                mechanical pump, hemodialysis, dialysis, circulator, blood pressure

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