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Extracorporeal circuits

Figure 18.2 (a) Schematic of extracorporeal circuit in hemodialysis and hemodiafiltration. Substitution fluid is added only in the case of large UFflowrate, that is, in HDF. (b) Fresenius monitor 5008 used for HD or HDF. [Pg.413]

Figure 18.8 Hollow-fiber plasma filter with its extracorporeal circuit for plasma exchange. Figure 18.8 Hollow-fiber plasma filter with its extracorporeal circuit for plasma exchange.
As seen above, the artificial systems are only able to supply detoxication functions of the liver. In some cases, this might not be enough to save patients. An alternative is the design of bioartificial liver. A simplistic approach consists in considering such a device as a bioreactor based on synthetic elements able to offer an adequate environment to the liver cells. This environment would in turn lead to the maintenance of efficient functions of the cells aiming at liver supply, when placed in a bioreactor located in an extracorporeal circuit. The mandatory requirements for acceptable cell viability and functions in a bioartificial liver (BAL) are tentatively listed below, according to a biotechnological point of view ... [Pg.429]

Up to now, none of the presented system can claim its ability to fully replace all liver functions in an extracorporeal circuit. On the one hand, purely artificial techniques can only cover some detoxification aspects, which is already crucial in many clinical cases to save patients. On the other hand, bioartificial livers have not proven their full efficiency yet, mainly because both regulatory and logistic aspects limit, for the moment, the inclusion of significant numbers of patients to draw statistically relevant conclusions. [Pg.430]

Note X = ISO evaluation tests for consideration 0 = additional tests which may be applicable note + tissue includes tissue fluids and subcutaneous spaces note a for all devices used extracorporeal circuits. [Pg.816]

Vascular access thrombosis has been reported in up to 26% of patients treated with epoetin alfa (3,34,38). Most of the failures occurred in poljdetrafluoroethylene grafts. There was no comparison with patients not treated with epoetin. It has been suggested that the increased risk of extracorporeal circuit clotting and the higher heparin requirements during hemodialysis may not be due to a hypercoagulable state, but rather to an increase in erythrocyte mass and consequently in whole blood viscosity (66). [Pg.1245]

Annich GM, Meinhardt JP, Mowery KA, Ashton BA, Merz SI, et al. 2000. Reduced platelet activation and thrombosis in extracorporeal circuits coated with nitric oxide release polymers. Crit. Care Med. 28 915-20... [Pg.606]

HD relies on good vascular access to the circulation of the patient to enable blood to be pumped around the extracorporeal circuit at a rate in excess of 300 mL per minute. This ahflity was not introduced until the 1960s, Although Kolff in Groningen Hospital in the Netherlands performed the first dialysis experiments in humans in 1943, the problem of dialysis support with long-term vascular access was not solved until Scribner developed the arteriovenous cannula in 1960, This was followed by the development of the surgically... [Pg.1719]

Using an arteriovenous shunt model of thrombosis in the rat, compounds 4 and 7 were evaluated for their ability to maintain patency of the extracorporeal circuit which serves as a thrombogenic surface [76]. Table 2 shows that on a gravimetric basis r-hirudin and inhibitor 4, were equipotent [r-hirudin EDis = 1.4 mg/kg 4 EDi5= 1.2 mg/kg i.v. bolus]. The thrombin inhibitor 7 was less effective in this assay having an EDi5= 6.3 mg/kg. [Pg.278]

In contrast to the patient with CKD, the calcium balance is usually not an important issue for the ARF patient due to the limited duration of the iUness. One exception to this is in patients receiving continuous RRT that is anticoagulated with citrate. Citrate binds to serum calcium and without calcium, blood cannot form a clot. Citrate is typically infused as blood leaves the body. A calcium infusion must be administered either at the end of the extracorporeal circuit or centrally to provide sufficient unbound calcium to the patient. Insufficient calcium infusions wiU result in hypocalcemia, arrhythmias, and even death, so frequent monitoring of unbound serum calcium concentrations is essential. [Pg.794]

This syndrome may occur occasionally with the first use of a dialyzer, usually of the cuprophane type, and is an anaphylactic reaction with hypotension, wheezing, and flushing. Rarely it may be severe, resulting in death from marked bronchospasm and shock. In most cases the symptoms subside upon stopping the dialysis without returning the blood in the extracorporeal circuit to the patient, but a few patients require vigorous treatment for anaphylactic shock. [Pg.96]

Two control experiments determined that essentially no heparin was non-specifically removed from the extracorporeal circuit. Four experiments were then conducted on each of the three animals, and the model predictions are shown together with the experimental data in Fig. 13. In all cases, the model clearances were within a few percent of the experimentally determined values (47). [Pg.35]

Having demonstrated that PLA2-LDL was rapidly removed from the blood pool, an extracorporeal circuit containing an immobilized PLA2 reactor was then designed. [Pg.39]

Figure 1. Proposed heparin circuit. The extracorporeal device could be a renal dialysis unit or a pump-oxygenator. The heparinase reactor could be part of a blood filter to be used either continuously (in which case heparin would, be added, continuously at the start of the circuit) or at the end of an operation. Heparin could thus be confined to the extracorporeal circuit. Figure 1. Proposed heparin circuit. The extracorporeal device could be a renal dialysis unit or a pump-oxygenator. The heparinase reactor could be part of a blood filter to be used either continuously (in which case heparin would, be added, continuously at the start of the circuit) or at the end of an operation. Heparin could thus be confined to the extracorporeal circuit.
Fig. 1. Schematic of an extracorporeal circuit for blood purifi cation. Fig. 1. Schematic of an extracorporeal circuit for blood purifi cation.
Griffin, L. C., Tidmarsh, G. E., Bock, L. C., Toole, J. J., Keung, L. L. K. (1993). In vivo anticoagulant properties of a novel nucleoside-based thrombin inhibitor and demonstration of regional anticoagulation in extracorporeal circuits. Blood 81, 3271-3276. [Pg.27]

Saito, N., Motoyama, S., and Sawamoto, J., Effects of new polymer-coated extracorporeal circuits on biocompatibility during cardiopulmonary bypass, Artif. Organs, 2000 24(7) 547-554. [Pg.534]

Westaby S (1987) Organ dysfunction after cardiopulmonary bypass A systemic inflammatory reaction initiated by the extracorporeal circuit. Intensiv Care Med 13(2) 89-95... [Pg.1134]


See other pages where Extracorporeal circuits is mentioned: [Pg.428]    [Pg.296]    [Pg.297]    [Pg.217]    [Pg.70]    [Pg.2]    [Pg.349]    [Pg.284]    [Pg.1308]    [Pg.594]    [Pg.195]    [Pg.1013]    [Pg.512]    [Pg.210]    [Pg.222]    [Pg.484]    [Pg.224]    [Pg.250]    [Pg.972]    [Pg.342]    [Pg.142]    [Pg.512]    [Pg.513]    [Pg.527]    [Pg.548]    [Pg.43]    [Pg.131]    [Pg.423]    [Pg.438]    [Pg.558]   
See also in sourсe #XX -- [ Pg.425 ]

See also in sourсe #XX -- [ Pg.423 , Pg.425 , Pg.428 ]




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