Veins central venous pressure

The central venous pressure is the hydrostatic pressure generated by the blood in the great veins. It can be used as a surrogate of right atrial pressure (mmHg). 

GTN is a nitrate. This class of drugs are potent vasodilators. At therapeutic doses the main effect of nitrates is to act on vascular smooth muscle to dilate the veins, thus reducing central venous pressure (preload) and ventricular end-diastolic volume. The overall effect is to lower myocardial contraction, wall stress and oxygen demand, thereby relieving the angina. Nitrates also promote vasodilation of the coronary blood vessels. 

The most frequent cause of posthepatic portal hypertension is right ventricular insufficiency. The central venous pressure is transferred to the hepatic veins and the sinusoids. Constrictive pericarditis leads to a state of pronounced posthepatic portal hypertension with the early development of ascites. Severe tricuspid valve incompetence also culminates in this condition. A membranous obstruction of the inferior vena cava was likewise described in 1968 as a genetically determined cause of posthepatic portal hypertension (S. Yamamoto et al.). Three variants can be distinguished by angiography, depending on the different ways in which the hepatic veins are involved or whether they are affected at all. Thrombosis of the inferior vena cava can develop either from thrombosis of the pelvic veins or independently in the presence of predisposing factors. 

Rise in blood pressure Distended neck veins Elevated central venous pressure Convulsions... 

C. Secure venous access. Antecubital or forearm veins are usually easy to cannulate. Alternative sites include femoral, subclavian, internal jugular, or other central veins. Access to central veins is technically more difficult but allows measurement of central venous pressure and placement of a pacemaker or pulmonary artery lines. 

There are several contraindications for TIPS absolute contraindications consist of right-sided heart failure with elevated central venous pressure, polycystic liver disease, and severe hepatic failure (Shiffman et al. 1995). The latter contraindication is based on the fact that the TIPS shunts blood away from the liver, thus further compromising liver function. Relative contraindications consist of active or systemic infection, as TIPS makes use of a foreign device that could act as a colonization site for bacteria, severe hepatic encephalopathy poorly controlled by medical therapy and portal vein thrombosis. 

Lung transplant patients appear to be at increased risk of air embolism from catheters perhaps because of the considerable negative intrathoracic pressure that can develop when the diseased lung is replaced with a normal lung. Lung transplant patients are often also emaciated and have little subcutaneous tissue, allowing for a short tract from the central venous line insertion site to the opening of the central vein. 

The perivascular fibrous capsule (R Glisson, 1654) commences in the hepatic porta as a tree-like branching framework of connective tissue surrounding the interlobular vessels. It also surrounds the central hepatic vein and its small tributaries, which are joined to the parenchyma by radial fibres as well as being established in the portal tracts. This prevents a suction-induced collapse of the venous vessels as a result of respiration-dependent negative pressure in the pleural cavity. The perivascular connective tissue, known as Glisson s capsule, extends fine secondary trabeculae into the parenchyma. They contain the intralobular biliary, lymphatic and blood capillaries. 

Volume replacement Adequate volume replacement, when possible through two venous entry points, is initially of utmost importance. A central vein entry point is strongly recommended to facilitate the constant monitoring of pressure changes (CVP). 

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)... 

Invasive hemodynamic monitoring usually is performed with a flow-directed pulmonary artery (PA) or Swan-Ganz catheter placed percutaneously through a central vein and advanced through the right side of the heart and into the PA. Inflation of a balloon proximal to the end port allows the catheter to wedge, yielding the PAOP, which estimates the pulmonary venous (left atrial) pressure and, in the absence of intracardiac shunt or mitral valve or pulmonary disease, left ventricular diastolic pressure. Additionally, cardiac output may be measured and systemic vascular resistance (SVR) calculated. Normal values for hemodynamic parameters are listed in Table 14—12. 

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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