Central venous blood flow

Central venous blood flow is subject to intrathoracic pressure changes due to respiration (Gosselin et al. 2004). In the setting of CM-enhanced CT, this may be particularly harmful if a patient performs an ambitious Valsalva maneuver during breath holding. During a Valsalva maneuver, the intrathoracic pressure increases, which causes a temporary interruption of venous return from the superior vena cava and a temporary increase of (un-opacified) venous blood flow from the inferior vena cava. The effect of this flow alteration is a temporary decrease of vascular opacification. In some cases (especially with fast scan times), this may cause non-diagnostic opacification of the entire pulmonary arterial tree. 

A highly complex network of arteries, arterioles, and capillaries penetrates the dermis from below and extends up to the surface of, but not actually into, the epidermis. A matching venous system siphons the blood and returns it to the central circulation. Blood flow through the vasculature is linked to the production and movement of lymph through a complementary dermal lymphatic system. The dermis is laced with tactile, thermal, and pain sensors. 

The venous anatomy is very variable. Venous blood flows centrally via the deep cerebral veins and peripherally via the superficial cerebral veins into the dural venous sinuses, which lie between the outer and meningeal inner layer of the dura and drain into the internal jugular veins (Stam 2005) (Fig. 4.4). The cerebral veins do not have valves and are thin walled, and the blood flow is often in the same direction as in neighboring arteries. There are numerous venous connections between the cerebral veins and the dural sinuses, the venous system of the meninges, skull, scalp, and nasal sinuses, allowing infection or thrombus to propagate between these vessels. 

Erection occurs as a result of increased pressure in the corpora cavernosa, which translates into penile rigidity. The pressure increase is caused by three synergistic processes (i) relaxation of the smooth muscles of the corpora cavernosa (2)increase in arterial blood flow to the penis and (5) restriction of the venous blood flow out of the penis. Both central and peripheral mechanisms contribute to the process of penile erection. At the central level, the psychological component of penile erection is controlled by the hypothalamic and limbic systems (140). At the peripheral level, both sympathetic and parasympathetic pathways as well as several mediators are involved. Psychogenic and local stimulation results in the release of neurotransmitters from the cavemosal nerve terminals and smooth muscle endothelium. Factors that mediate the corpus cavemosum relaxation include nitric oxide (NO), vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP), and prostaglandin. 

Vasodilators are a group of dtugs, which relax the smooth muscle cells of the blood vessels and lead to an increased local tissue blood flow, a reduced arterial pressure and a reduced central venous pressure. Vasodilators reduce the cardiac pre-load as well as after-load and thereby reduce cardiac work. They are used in a variety of conditions including hypertension, cardiac failure and treatment/prevention of angina pectoris. Major groups are Ca2+-channel blockers (e.g. dihydropyridines), NO-donators (e.g. organic nitrates), K+-channel openers (minoxidil), phosphodiesterase inhibitors (e.g. sildenafil), Rho-kinase inhibitors (e.g. Y27632) or substances with unknown mechanism of action (e.g. hydralazine). Inhibitors of the... 

Central PN refers to the administration of PN via a large central vein, and the catheter tip must be positioned in the vena cava. Central PN allows the infusion of a highly concentrated, hypertonic nutrient admixture. The typical osmolarity of a central PN admixture is about 1500 to 2000 mOsm/L. Central veins have much higher blood flow, and the PN admixture is diluted rapidly on infusion, so phlebitis is usually not a concern. Patients who require PN administration for longer periods of time (greater than 7 days) should receive central PN. One limitation of central PN is the need for placement of a central venous catheter and an x-ray to confirm placement of the catheter tip. Central venous catheter placement may be associated with complications, including pneumothorax, arterial injury, air embolus, venous thrombosis, infection, chylothorax, and brachial plexus injury.1,20... 

Central venous pressure (CVP) The usual CVP trace should be drawn on at a pressure of 5-10 mmHg. The c wave occurs during IVC owing to bulging of the closed tricuspid as the ventricle begins to contract. The y descent occurs immediately following IVR as the tricuspid valve opens and allows free flow of blood into the near empty ventricle. 

Lignocaine s clearance by the liver is flow dependent. In heart failure cardiac output may be very low and therefore hepatic blood flow through both the hepatic artery and the portal venous system is also low. This meant a lower extraction of the drug from the blood and accumulation of lignocaine until the high plasma concentration produced the central nervous system toxicity. 

Modern monitoring by both invasive and non-invasive techniques is complex and is undertaken in units dedicated to and, equipped for, this activity. The present comment is an overview. Monitoring will normally require close attention to heart rate and rhythm, blood pressure, fluid balance and urine flow, pulmonary gas exchange and central venous pressure. The use of drugs in shock is secondary to accurate assessment of cardiovascular state (especially of peripheral flow) and to other essential management, treatment of infection and maintenance of intravascular volume. 

Fig. 2.13 Diagram of the classic hepatic lobule (I), the portal vein lobule (II) and the hepatic acinus (III) CV = central vein ( ), P = portal tract ( ). Flow direction venous blood (= blue arrow), arterial blood (= red arrow) and bile (= green arrow), with the microcirculatory acinus zones 1, 2, 3. (cf. W Ekataksin et af, 1992 the microvascular unit is regarded as an area in which all hver cells receive blood from a common terminal vessel)...

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)... 

Corticosteroids are used in clinical practice to relieve pressure symptoms caused by many tumor types, notably intracerebral tumors but also those causing airway or central venous obstruction. Their mode of action has been studied in animals (57) and humans (58), and is thought to involve first constriction of tumor vascular volume and then a reduction in water content. Reduced interstitial pressure should increase perfusion and extravascular diffusion rates, and high doses of steroids have been shown to increase blood flow in human colonic tumors transplanted into mice. Uptake of antibody into tumors has been assessed before and after administration of high-dose dexamethasone to decrease tumor interstitial pressure and thus increase antigen accessibility. Three patients with recurrent colorectal carcinoma had two antibody scans each, 72 h apart, and the injected dose was the same for all scans (20 mg). Dexamethasone was started 24 h before the second dose of antibody, with an initial iv dose of 10 mg followed by 4 mg four times daily orally for 48 h. 

Thrombotic complications are common with catheter use. The development of a fibrin sheath is a near universal occurrence on intravascular devices such as central venous (Hoshal et al., 1971) and hemodialysis catheters, and can have a profound effect upon blood flow in the device (Trerotola, 2000). This sheath can be removed either by stripping (Rockall et al., 1997 Crain et al., 1996) or fibrinolytic medical therapy (Twardowski et al., 1998), or the catheter can be replaced to restore adequate flow performance. Recent randomized controlled clinical trials have revealed improved long-term outcomes with catheter exchange versus fibrin sheath stripping (Merport, 2000), while no outcome differences were realized in patients randomized to either fibrin sheath stripping or thrombolytic therapy (Gray, 2000). 

According to some recommendations [36] if osmolarity of the infusion is higher than 500 mOsmol/1, administration should occur via a central venous catheter that is inserted in a vessel with high blood flow such as the vena subclavia, proximal axillary vein or superior vena cava. 

Fig. 11.10a,b. Abnormal liver hemodynamics in the acute phase of Budd-Chiari syndrome, a Due to the hepatic venous flow obstruction there is rising pressure in the portal system resulting in reduced intrahepatic portal venous flow and a compensatory increase of the arterial flow. Since there is a normal pressure gradient between the arterial and portal systems, functional AP shunts are used leading to total inversion of the direction of the blood flow within the main portal vein that acts as a draining vein, b In the arterial phase of liver enhancement, iodinated blood conveyed by the hepatic artery perfuses the central areas of the liver. Due to the complete flow reversal within the portal vein early and isolated enhancement is observed... 

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