Effects of hemodialysis on myocardial performance index
Melek UluçamAylin Yı́ldı́rı́rHaldun MüderrisoğluÜlkem YakupoğluMehmet Erdi KorkmazNurhan ÖzdemirBülent ÖzinEgemen Tayfun
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Preload
Hypervolemia
Uremia
Chronic renal failure
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Contractility
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Hypervolemia was produced in dogs by infusion of matched whole blood or of red cells suspended in dextran. In the dogs which had received matched whole blood, bleeding with simultaneous volume replacement with dextran produced acute hypervolemic anemia. This was associated with increased cardiac output, whereas no increase of cardiac output was seen in the same animals with a comparable amount of hypervolemia without anemia. The results suggest that anemia rather than hypervolemia was the important factor in causing an increase of cardiac output in these experiments.
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Purpose of review To summarize the relevant peer-reviewed publications over the past year that addressed issues of when to give (or not give) fluid to the critically ill patient. Recent findings Clinical data from several studies underscore the inability of measures of ventricular filling to assess either preload or preload responsiveness. Whereas less invasive monitoring techniques than pulmonary arterial catheterization demonstrate better discrimination with estimates of both preload and preload responsiveness. Measuring dynamic changes in stroke volume, descending aortic flow, and both superior and inferior vena caval diameters during ventilation provides good predictive value in defining preload responsiveness. One study demonstrated that resuscitation protocols keyed to esophageal flow measures improved outcome in postoperative cardiac surgery patients. Summary Preload is not preload responsiveness. Functional measures of preload responsiveness exist and are superior to traditional measures of filling pressures in driving resuscitation in critically ill patients.
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Hypervolemia is a condition with an excess of total body water and when sodium (Na) intake exceeds output. It can have different causes, such as hypervolemic hyponatremia (often associated with decreased, effective circulating blood volume), hypervolemia associated with metabolic alkalosis, and end-stage renal disease. The degree of hypervolemia in critically ill children is a risk factor for mortality, regardless of disease severity. A child (under 18 years of age) with hypervolemia requires fluid removal and fluid restriction. Diuretics are able to increase or maintain urine output and thus improve fluid and nutrition management, but their benefit in preventing or treating acute kidney injury is questionable.
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Objective To study the effect of intermedin 1-47 on cardiac function in isoproterenol induced myocardial injury in rats and ischemia/reperfusion(I/R) in isolated rat hearts.Mothod The myocardial Injury model was induced by isoproterenol in rats and ischemia/reperfusion in isolated rat heart.The mean arterial blood pressure(MBP), heart rate(HR),left ventricular systolic pressure(LVSP),diastolic pressure(LVDP),maximal velocity of increase and decrease of left ventriclar pressure(±dp/dt_(max)) was monitored on a BL-410.Results Compared with the normal control group,LVESP and MAP of the ISO group was decreased 41.1% and 19.7%,respectively,±dp/dt_(max) decreased 20% and 25.2%,respectively,LVEDP increased 517%.Compared with the ISO group,±dp/dt_(max) increased 8.7%,24%,respectively,in rats given with the treat of low-dose IMD 1-47 group(5 nmol·kg~(-1)·d~(-1)),and LVEDP decreased 52.8%.±dp/dt_(max) increased 26.6% and 47.4%,respectively,LVEDP decreased 67% in rats given high dose IMD 1-47 group(20 nmol·kg~(-1)·d~(-1)).Cardiac I/R induced a marked inhibition of cardiac function and myocardial injury.Reperfusion with IMD 1-47 significantly ameliorated the cardiac function inhibition induced by I/R.Conclusion IMD 1-47 has cardioprotective effects against myocardial I/R injury.
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The prevalence and consequences of hypervolemia in kidney transplant recipients (KTRs) have not been investigated. Specifically, its impact on blood pressure (BP) and relationship with N-terminal fragment of prohormone B-type natriuretic peptide (NT-proBNP) are unknown. The objectives of this study were to establish the prevalence of hypervolemia among clinically stable KTRs, investigate the predictors of posttransplant hypervolemia, assess its impact on blood pressure, and determine its relationship with NT-proBNP.This single-center cross-sectional study enrolled 123 clinically stable KTRs. Extracellular volume status was determined by multifrequency bioimpedance analysis. Mild and severe hypervolemia were defined as percentage volume expansion of greater than 7% and greater than 15%, respectively. Systolic BP (SBP) and diastolic BP (DBP) were measured, with mean arterial pressure (MAP) calculated. Serum NT-proBNP was quantified using a noncompetitive immunoluminometric assay. Potential demographic, nutritional, and clinical predictors of extracellular volume status, BP, and NT-proBNP levels were assessed.Hypervolemia was present in 30% of KTRs, with 5% classified as severe hypervolemia. Significant predictors of volume expansion were increased sodium intake, advancing age, and reduced fat mass (P<0.01 for all associations). Hypervolemia was the only independent predictor of elevated MAP, SBP, and DBP (P<0.001 for all associations). Raised NT-proBNP levels were independently associated with both hypervolemia (P=0.01) and allograft dysfunction (P=0.03).Hypervolemia is unexpectedly common among clinically stable KTRs. It is closely associated with elevated BP. The relationship with increased sodium intake signals potential therapeutic focus. Further study is warranted to prospectively investigate objective measures of extracellular volume status among KTRs.
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Interest in the study of the features of metabolism in chronic renal failure is steadily increasing due to the improvement of methods of treatment of uremia patients. Under conditions of prolonged hemodialysis uremia various metabolic disorders are observed, in particular changes in carbohydrate metabolism. As shown by studies in recent years, the majority of patients with chronic renal failure have reduced glucose tolerance with a frequency of 54 to 100%, which served as the basis for the introduction of the term uremic-azotemic pseudodiabetes.
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Fluid overdose can be harmful in critically ill patients. Since central venous pressure (CVP) is currently considered to be an inappropriate indicator of preload, much attention is being given to predicting fluid responsiveness, i.e., the response of stroke volume (SV) or cardiac output (CO) to fluid challenge. However, when fluid responsiveness was evaluated in critically ill patients, including sepsis, only 40–50% of the patients responded. Moreover, most fluid responders do not show significant hemodynamic improvement after fluid administration. In this review, we discuss why fluid responsiveness based on the Starling mechanism did not work well in the clinical setting. According to the Starling mechanism, a patient whose SV/CO significantly increases after a fluid challenge is considered to be a fluid responder and judged to need fluid therapy. However, the currently recommended fluid challenge dose of crystalloid 250–500 mL has little effect on increasing blood volume and is not sufficient to increase the preload of the Starling curve. Especially in septic patients, due to their vascular hyperpermeability, increase in blood volume is even smaller. Furthermore, Infusion induced hemodilution is known to reduce blood viscosity and hematocrit, as a result, decreasing afterload. This indicates that the increased SV/CO after fluid challenge is caused not only by increased preload but also by decreased afterload. For these reasons, fluid responsiveness with small crystalloid challenge is questionable as a clinical indicator of fluid therapy.
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