Disease relevance of Central Venous Pressure

• AVP in a dose of 0.4 ng/kg/min, which raised plasma level of AVP to 24 +/- 4 pg/ml, a value known to have a significant antidiuretic effect, had little hemodynamic effect, producing only mild bradycardia and a slight increase in central venous pressure [1].
• A posteriori analysis of the data by correlation analysis revealed that the fetal ACTH, vasopressin, and renin responses to the hemorrhage were more highly correlated to the changes in fetal arterial pH than to changes in fetal mean arterial pressure or central venous pressure [2].
• Beck's triad (low blood pressure, raised central venous pressure, and distant cardiac sounds) was recorded in 77% of the cases with proven tamponade, but pulsus paradoxus in only 11% [3].
• Mean arterial pressure (MAP), central venous pressure (CVP), heart rate (HR), PR, QT and QTc intervals, and left ventricular ejection fraction (LVEF) were measured, as well as daily body weight, blood glucose and potassium [4].
• Treatment of hepatorenal syndrome as defined by the international ascites club by albumin and furosemide infusion according to the central venous pressure: a prospective pilot study [5].

High impact information on Central Venous Pressure

• This position significantly reduced central venous pressure, diastolic pulmonary artery pressure, the number of isosorbide dinitrate tablets taken sublingually, and the number of angina episodes per night [6].
• MEASUREMENTS: Oxygen saturation, intra-arterial blood pressure, central venous pressure, chest wall movement, electrocardiography, electromyography, electroencephalography, electro-oculography, minute ventilation, arterial blood gases, and serum theophylline levels [7].
• Before converting-enzyme inhibition, group B patients received higher doses of furosemide (p less than 0.02) and had lower central venous pressures (p less than 0.05) than group A patients [8].
• Group 2 patients had higher postoperative central venous pressures (17.8 versus 14.1 mm Hg, P < .001) and oxygen saturations (86% versus 81%, P < .001) than did group 1 patients [9].
• LBNP produced similar decreases in central venous pressure in all groups before and after drug administration [10].

Chemical compound and disease context of Central Venous Pressure

• There was no evidence of complications caused by hypovolemia in the low (< or = 7 mm Hg) central venous pressure group, who had lower inotrope requirements (P = .02) and lower creatinine levels (P = .013) [11].
• 3 Increasing the halothane concentration of 3% led to marked myocardial depression as evidenced by reduced cardiac output and increased central venous pressure with increasing arterial hypotension [12].
• Volume expansion was produced by infusing the rats with isotonic saline equal to 10% of their body weight for 10 min, which significantly increased central venous pressure [13].
• Acute dimethyl sulfoxide therapy in experimental brain edema: part 2. Effect of dose and concentration on intracranial pressure, blood pressure, and central venous pressure [14].
• Embolism of CO2 occurs when central venous pressure is decreased by blood loss or distal compression [15].

Biological context of Central Venous Pressure

• LBNP alone (cardiac reflex) did not alter blood pressure or heart rate but decreased central venous pressure by 2.5 +/- 0.1 mm Hg (mean +/- SEM, p less than 0.05) and increased MSNA by 92 +/- 22% over the control value [16].
• To assess the magnitude of reflex forearm vasoconstriction triggered by decreased central venous pressure after sublingual nitroglycerin, lower body negative pressure (LBNP) was applied to produce a comparable decrease in central venous pressure to that after nitroglycerin [17].
• Atrial natriuretic peptide decreased mean circulatory filling pressure, central venous pressure, and blood volume by 0.9 mm Hg, 1.7 mm Hg, and 8.0 ml/kg, respectively, and displaced the pressure-volume relationship toward the pressure axis by decreasing extrapolated unstressed volume [18].
• Pulmonary capillary wedge pressure and central venous pressure, an index of preload, were decreased slightly in the nipradilol group [19].
• At exhaustion in both trials, systemic VO(2) declined in parallel with a similar fall in stroke volume and central venous pressure; yet the brain uptake of O(2), glucose and lactate increased [20].

Anatomical context of Central Venous Pressure

• Although not statistically identical, measurements of "central" venous pressure in the inferior vena cava and right atrium correlated well (r2 = .87 for mechanical ventilation; r2 = .83 for spontaneous ventilation) [21].
• During severe exercise, a reduction in cardiac filling may result in a fall in central venous pressure and stimulate baroreceptor vasoconstrictor reflexes [22].
• The sensitivity of the aortic-cardiac baroreflex was determined during a steady-state phenylephrine-induced increase in mean arterial pressure combined with lower body negative pressure to counteract central venous pressure increases and neck pressure to offset the increased carotid sinus transmural pressure [23].
• MEASUREMENTS AND RESULTS: In addition to the primary goals PCWP and ITBVI, at defined temperatures, central venous pressure (CVP), extravascular lung water index, the number of infusions, and packed RBCs, as well as serum lactate level, norepinephrine dosage, and levels of liver enzymes, bilirubin, creatinine, and urea were measured [24].
• RS-1893, an orally active cardiotonic agent, has been suggested to dilate venous blood vessels, because it markedly decreases central venous pressure in anesthetized dogs [25].

Associations of Central Venous Pressure with chemical compounds

• Central venous pressure was held at control levels by LBNP during phenylephrine and saline infusion during nitroprusside [26].
• Digitalis and dobutamine produced similar increases in baseline mean arterial pressure and decreases in central venous pressure and MSNA [10].
• Decreases in central venous pressure with LBNP-10 were nearly identical before compared with after nifedipine [27].
• First, we recorded muscle SNA before and during brief infusions of ANF, vehicle (saline solution), and sodium nitroprusside, titrated to achieve reductions similar to those produced by ANF in diastolic pressure and central venous pressure, and we also assessed the effect of ANF on sympathetic nerve responses to a cold pressor test (CPT) [28].
• Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency X amplitude) and expressed as units [29].

Gene context of Central Venous Pressure

• Conversely, an increase in central venous pressure was accompanied by a reduction in plasma renin activity [30].
• Prior intravenous protamine, central venous pressure prior to protamine, preoperative ejection fraction and the need for inotropes when coming off bypass did not exhibit statistically significant associations with events (all p > 0.15) [31].
• Simultaneously, an i.c. pressure-derived collateral flow index (CFI, no unit) was determined as the ratio between distal occlusive minus central venous pressure divided by the mean aortic minus central venous pressure [32].
• Candoxatril lowered central venous pressure (P < .001) and increased systolic pressure (from 116 +/- 6 to 120 +/- 7 mm Hg; P < .05), endothelin (from 4.6 +/- 1.1 to 6.8 +/- 3.2 pmol/L; P < .02), and epinephrine (P < .05), without affecting any other variables [33].
• In fact, in rats infused with 100 ng endothelin there was a progressive decline in central venous pressure and a raised hematocrit, even in the splenectomized group, suggesting a loss of plasma volume [34].

Analytical, diagnostic and therapeutic context of Central Venous Pressure

• Increasing levels of lower body negative pressure (LBNP) (-10 and -40 mm Hg) induced a progressive decrease in central venous pressure (CVP) and an increase in FVR [35].
• There were no significant increases in either cerebral perfusion pressure, central venous pressure, PaCO2, or serum norepinephrine concentration to account for the cerebral effects; however, serum epinephrine concentrations increased by 61% [36].
• The effects of iv succinylcholine (SCh) on the electroencephalogram (EEG), cerebral blood flow (CBF), cerebral metabolic rate (CMRO2), intracranial pressure (ICP), central venous pressure (CVP), and mean arterial pressure (MAP) were tested in halothane-anesthetized dogs [37].
• Systolic, diastolic, and central venous pressures were measured before fentanyl administration, before cardiopulmonary bypass (CPB), and after separation from CPB [38].
• Patients taking propranolol who require general anesthesia for delivery should have continuous monitoring of electrocardiogram and central venous pressure [39].

References