Outflow vein

A well-functioning VA provides the prescribed blood flow (without recirculation) that ranges from 200 to 500 ml/min during dialysis treatment. Over 90% of VA dysfunction is a result of stenotic problems developing in the access circuit. Manifestation of dysfunction depends on the location of stenosis in the circuit, its diameter relative to volume of blood flow and the outflow pattern [11]. A stenosis located in the juxta-anastomotic artery or vein tends to reduce inflow. A stenosis located in the outflow vein beyond the needling segment tends to in-... 

For AVG, NFK-KDOQI recommends PE for access monitoring. It lists use of intra-access flow, direct or derived static venous pressures and US as preferred techniques for access surveillance. For AVF, direct flow measurements, physical findings of persistent swelling of the arm, presence of collateral veins, prolonged bleeding on needle withdrawal, altered characteristics of pulse or thrill in the outflow vein and US are preferred techniques of surveillance [17]. 

The patient should be involved in the dialysis process and not allow alarms to be ignored. High venous pressure may indicate clotting of the coil leading to blood loss. Persisting high venous pressure is suspicious for the presence of outflow vein stenosis. Blood pressure should be kept stable during dialysis. 

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. 

The pressure gradient, or the inflow pressure minus the outflow pressure, is determined by the pressure at the beginning of the venous system (Pv) and right atrial pressure (Prblood flow the slightly stiffer large veins offer a small degree of resistance (Rv). 

There are many different procedures used for pancreas transplantation, and there is no one standard protocol used in all transplant centers. The important considerations, however, are that the arterial blood flow supply to the pancreas and duodenal segment, and venous outflow from the pancreas via the portal vein should be adequate. The recipient s right common or external iliac artery is used to restore vascularization of the artery in the pancreas. The Y graft of the tissue is anastomosed end-to-side and the venous vascularization is performed either systemically or portally, but mostly it is done with systemic venous drainage. 

The statistical moment parameters for the outflow pattern of a bolusly administered drag from the portal vein are defined as follows ... 

Even if spatial and contrast resolution of these imaging modalities will increase in the future, it might be difficult to differentiate the artery from the vein on the anterior surface of the cord. The anterior spinal artery and vein run very close together. The branching of a radicular artery or vein has a very similar hairpin-configuration, and the level at which a segmental in- or outflow occurs cannot be predicted in a given case. 

Sympathomimetic agents, such as brimonidine tartrate, apraclonidine, adrenaline and dipivefrine hydrochloride, which is a prodrug for adrenaline), act on a-adrenoreceptors to induce dilation of the veins to reduce IOP. They also induce mydriasis (dilation of the pupils). Adrenaline may reduce the rate of formation of the aqueous humour, which in turn reduces the IOP it may also increase the outflow through the trabecular meshwork. Stimulation of alpha-2-adrenoreceptor (c -adrenoreceptor) by drugs such as brimonidine and apraclonidine on the adrenergic neurons supplying the ciliary body can also result in reduction of secretion of aqueous humour. 

In one case priapism followed the use of first risperidone and then ziprasidone YET TO start HERE(197). In two other cases, presumed to be due to risperidone (198,199), penile irrigation with isotonic saline and phenylephrine injection resulted in detumescence. Risperidone has a high affinity for alpha-1 adrenoceptors, and alpha-1 blockade leads to direct arteriolar dilatation, which results in increased blood inflow and reduced outflow secondary to effacement and subsequent obstruction of emissary veins. 

The hepatic blood flow is decreased in chronic heart insufficiency, and there is disturbed venous outflow, i. e. cardiac output is diminished. There is also a pressure increase in the splanchnic nerve area with subsequent blood pooling as a result of the rise in CVP. The markedly reduced hepatic blood flow at first evokes an increase in oxygen extraction, but after its elimination, hypoxia with centrilobular cell necroses follows. The elevated CVP extends as far as the central veins, so that dilatation and hyperaemia of the sinusoids occur. Pericentral atrophy in the liver cell trabeculae develops at a later stage, (s. tab. 39.1) (s. fig. 39.3)... 

Computer tomography, especially when coupled with a contrast medium and in the form of CTAP, is an excellent tool for analyzing the venous blood flow and detecting any disturbances in inflow or outflow. Thrombosed hepatic veins are not visible the parenchyma is characterized by an inhomogeneous, patch-like enhancement. (s. fig. 39.6) MRI provides reliable evaluation by means of multiphase, contrast-enhanced, three-dimensional MR angiography. 

The portal circulation handles aU of the venous outflow of the GI tract, the spleen, the pancreas, and the gallbladder (Figure 47-11). The portal vein is formed by the union of the splenic vein and the superior mesenteric vein. Portal flow is normally 1000 to 1200mL/min with a pressure of 5 to 7 mm... 

Ingested protein is digested in a stepwise fashion in the stomach, small intestinal lumen, and small intestinal mucosal cells (Chapter 12). Peptides formed in the intestinal lumen are absorbed into the mucosal cells and degraded to free amino acids. The outflow of amino acids to the portal vein does not reflect the amino acid composition of the ingested protein. Thus, alanine levels increase two-to fourfold, and glutamine, glutamate, and aspartate are absent. These changes arise from amino acid interconversions within the intestinal cell. 

As in the management for CRVO, the purpose of such a procedure is to reestablish venous outflow by creating a chorioretinal anastomosis distal to the site of obstruction, to attempt to improve visual acuity by decreasing macular edema, and to decrease the conversion from nonischemic to ischemic vein occlusion. Fekrat and de Juan (77) reported on six eyes with branch vein occlusion of whom, three had successful anastomoses. Of the six eyes, the visual acuity improved one to three lines in two, remained unchanged in one, and decreased in three. This result does not appear to be significantly better than the natural history of visual acuity loss due to BRVO. 

Alpha agonists, nonselective Epinephrine, dipivefrin Increased outflow, probably via the uveoscleral veins Topical drops... 

Arterioles and Veins constriction CNS Postsynaptic Terminals i sympathetic outflow from brain Urinary Bladder Sphincter contraction (urine retention)... 

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