Journal articles: 'Intravascular volume'

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Vallet, Benoit. "Intravascular Volume Expansion." Anesthesia & Analgesia 112, no. 2 (February 2011): 258–59. http://dx.doi.org/10.1213/ane.0b013e3182066299.

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Brock, H., C. Gabriel, D. Bibl, and S. Necek. "Monitoring intravascular volumes for postoperative volume therapy." European Journal of Anaesthesiology 19, no. 04 (April 2002): 288. http://dx.doi.org/10.1017/s0265021502000467.

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Brock, H., C. Gabriel, D. Bibl, and S. Necek. "Monitoring intravascular volumes for postoperative volume therapy." European Journal of Anaesthesiology 19, no. 4 (April 2002): 288–94. http://dx.doi.org/10.1097/00003643-200204000-00007.

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Rector, William G., and Fernando Ibarra. "Intravascular volume in cirrhosis." Digestive Diseases and Sciences 33, no. 4 (April 1988): 460–66. http://dx.doi.org/10.1007/bf01536032.

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Marx, Gernot, Achim W. Schindler, Christoph Mosch, Joerg Albers, Michael Bauer, Irmela Gnass, Carsten Hobohm, et al. "Intravascular volume therapy in adults." European Journal of Anaesthesiology 33, no. 7 (July 2016): 488–521. http://dx.doi.org/10.1097/eja.0000000000000447.

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Duarte, Alexander G. "Radiographic Assessment of Intravascular Volume." Chest 122, no. 6 (December 2002): 1879–81. http://dx.doi.org/10.1378/chest.122.6.1879.

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Holte, Kathrine, Nicolai B. Foss, Christer Svensén, Claus Lund, Jan L. Madsen, and Henrik Kehlet. "Epidural Anesthesia, Hypotension, and Changes in Intravascular Volume." Anesthesiology 100, no. 2 (February 1, 2004): 281–86. http://dx.doi.org/10.1097/00000542-200402000-00016.

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Background The most common side effect of epidural or spinal anesthesia is hypotension with functional hypovolemia prompting fluid infusions or administration of vasopressors. Short-term studies (20 min) in patients undergoing lumbar epidural anesthesia suggest that plasma volume may increase when hypotension is present, which may have implications for the choice of treatment of hypotension. However, no long-term information or measurements of plasma volumes with or without hypotension after epidural anesthesia are available. Methods In 12 healthy volunteers, the authors assessed plasma (125I-albumin) and erythrocyte (51Cr-EDTA) volumes before and 90 min after administration of 10 ml bupivacaine, 0.5%, via a thoracic epidural catheter (T7-T10). After 90 min (t = 90), subjects were randomized to administration of fluid (7 ml/kg hydroxyethyl starch) or a vasopressor (0.2 mg/kg ephedrine), and 40 min later (t = 130), plasma and erythrocyte volumes were measured. At the same time points, mean corpuscular volume and hematocrit were measured. Systolic and diastolic blood pressure, heart rate, and hemoglobin were measured every 5 min throughout the study. Volume kinetic analysis was performed for the volunteers receiving hydroxyethyl starch. Results Plasma volume did not change per se after thoracic epidural anesthesia despite a decrease in blood pressure. Plasma volume increased with fluid administration but remained unchanged with vasopressors despite that both treatments had similar hemodynamic effects. Hemoglobin concentrations were not significantly altered by the epidural blockade or ephedrine administration but decreased significantly after hydroxyethyl starch administration. Volume kinetic analysis showed that the infused fluid expanded a rather small volume, approximately 1.5 l. The elimination constant was 56 ml/min. Conclusions Thoracic epidural anesthesia per se does not lead to changes in blood volumes despite a reduction in blood pressure. When fluid is infused, there is a dilution, and the fluid initially seems to be located centrally. Because administration of hydroxyethyl starch and ephedrine has similar hemodynamic effects, the latter may be preferred in patients with cardiopulmonary diseases in which perioperative fluid overload is undesirable.

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Rutlen, D. L., F. G. Welt, and A. Ilebekk. "Passive effect of reduced cardiac function on splanchnic intravascular volume." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 5 (May 1, 1992): H1361—H1364. http://dx.doi.org/10.1152/ajpheart.1992.262.5.h1361.

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It has been hypothesized that lowered cardiac output due to heart failure results in passive redistribution of intravascular volume from the peripheral circulation to the central circulation and that this redistribution acts to support cardiac output. To test this hypothesis, acute heart failure was induced by rapid atrial pacing to raise heart rate from 148 +/- 6 to 232 +/- 1 beats/min for 5 min, while splanchnic intravascular volume was assessed with radionuclide imaging in eight anesthetized pigs that had undergone prior carotid denervation and vagotomy. Cardiac output decreased from 3,350 +/- 410 to 2,170 +/- 290 ml/min (P less than 0.001), mean arterial pressure decreased from 103 +/- 5 to 84 +/- 4 mmHg (P less than 0.001), left atrial pressure increased from 5.9 +/- 0.6 to 10.8 +/- 0.9 mmHg (P less than 0.001), right atrial pressure increased from 2.4 +/- 0.5 to 4.8 +/- 0.9 mmHg (P less than 0.001), total splanchnic intravascular volume did not change (0 +/- 2 ml), splenic intravascular volume decreased 11 +/- 3% (P less than 0.001), hepatic intravascular volume increased 12 +/- 2% (P less than 0.001), and mesenteric intravascular volume did not change (-3 +/- 2%). Thus, when cardiac output is lowered with pacing-induced acute heart failure, lowered perfusion pressure acts to lower splenic intravascular volume and increased central venous pressure acts to increase hepatic intravascular volume; however, total splanchnic intravascular volume does not decrease to support cardiac filling and cardiac output.

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Nakanishi, Rine, Anas Alani, Suguru Matsumoto, Dong Li, Michael Fahmy, Jeby Abraham, Christopher Dailing, et al. "Changes in Coronary Plaque Volume: Comparison of Serial Measurements on Intravascular Ultrasound and Coronary Computed Tomographic Angiography." Texas Heart Institute Journal 45, no. 2 (April 1, 2018): 84–91. http://dx.doi.org/10.14503/thij-15-5212.

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Serial measurements of coronary plaque volume have been used to evaluate drug efficacy in atherosclerotic progression. However, the usefulness of computed tomography for this purpose is unknown. We investigated whether the change in total plaque volume on coronary computed tomographic angiography is associated with the change in segment plaque volume on intravascular ultrasound. We prospectively enrolled 11 consecutive patients (mean age, 56.3 ± 5 yr; 6 men) who were to undergo serial invasive coronary angiographic examinations with use of grayscale intravascular ultrasound and coronary computed tomography, performed <180 days apart at baseline and from 1 to 2 years later. Subjects underwent 186 serial measurements of total plaque volume on coronary computed tomography and 22 of segmental plaque volume on intravascular ultrasound. We used semiautomated software to examine percentage relationships and changes between total plaque and segmental plaque volumes. No significant correlations were found between percentages of total coronary and segment coronary plaque volume, nor between normalized coronary plaque volume. However, in the per-patient analysis, there were strong correlations between the imaging methods for changes in total coronary and segment coronary plaque volume (r=0.62; P=0.04), as well as normalized plaque volume (r=0.82; P=0.002). Per-patient change in plaque volume on coronary computed tomography is significantly associated with that on intravascular ultrasound. Computed tomographic angiography may be safer and more widely available than intravascular ultrasound for evaluating atherosclerotic progression in coronary arteries. Larger studies are warranted.

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Sánchez-Tamayo, Marcelino, Miguel Liván Sánchez-Martín, Eivet García-Real, and Milagro de la Caridad Garcés-Tamayo. "Essential aspects during the resuscitation of intravascular volume in polytraumatized patients." Medwave 20, no. 03 (April 28, 2020): e7879-e7879. http://dx.doi.org/10.5867/medwave.2020.03.7879.

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Brightman, R. P., G. L. Rea, C. A. Miller, and W. E. Hunt. "Intravascular volume expansion affecting blood flow." Neurosurgery 22, no. 1 Pt 1 (January 1988): 160???1. http://dx.doi.org/10.1097/00006123-198801010-00032.

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Della Rocca, G., M. G. Costa, C. Coccia, L. Pompei, F. Ruberto, M. Rossi, P. Pietropaoli, and R. Cortesini. "Intravascular blood volume in cirrhotic patients." Transplantation Proceedings 33, no. 1-2 (February 2001): 1405–7. http://dx.doi.org/10.1016/s0041-1345(00)02529-x.

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Kaufman, Susan. "CONTROL OF INTRAVASCULAR VOLUME DURING PREGNANCY." Clinical and Experimental Pharmacology and Physiology 22, no. 2 (February 1995): 157–63. http://dx.doi.org/10.1111/j.1440-1681.1995.tb01973.x.

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Brightman, R. P., G. L. Rea, C. A. Miller, and W. E. Hunt. "Intravascular volume expansion affecting blood flow." Neurosurgery 22, no. 1 Pt 1 (January 1988): 160–1. http://dx.doi.org/10.1227/00006123-198801010-00032.

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Abd el-Hamid, A. M., M. A. Khashaba, and S. M. Twfik. "Intravascular Volume Assessment What Is New?" Benha Journal of Applied Sciences 6, no. 4 (August 1, 2021): 43–47. http://dx.doi.org/10.21608/bjas.2021.189512.

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Mailloux, Patrick, and William McGee. "STROKE VOLUME VARIABILITY, SVO2 AND INTRAVASCULAR VOLUME DURING CVVHD." Critical Care Medicine 34 (December 2006): A174. http://dx.doi.org/10.1097/00003246-200612002-00602.

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Hilsted, J., N. J. Christensen, and S. Larsen. "Effect of Catecholamines and Insulin on Plasma Volume and Intravascular Mass of Albumin in Man." Clinical Science 77, no. 2 (August 1, 1989): 149–55. http://dx.doi.org/10.1042/cs0770149.

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1. The effect of intravenous catecholamine infusions and of intravenous insulin on plasma volume and intravascular mass of albumin was investigated in healthy males. 2. Physiological doses of adrenaline (0.5 μg/min and 3 μg/min) increased peripheral venous packed cell volume significantly; intravenous noradrenaline at 0.5 μg/min had no effect on packed cell volume, whereas packed cell volume increased significantly at 3 μg of noradrenaline/min. No significant change in packed cell volume was found during saline infusion. 3. During adrenaline infusion at 6 μg/min, packed cell volume increased, plasma volume decreased and intravascular mass of albumin decreased significantly. During noradrenaline infusion at 6 μg/min, packed cell volume increased and plasma volume decreased, but intravascular mass of albumin did not change. 4. Application of a hyperinsulinaemic, euglycaemic glucose clamp led to an increase in transcapillary escape rate of albumin and a decrease in intravascular mass of albumin. Packed cell volume remained constant, while plasma volume, measured by radiolabeled albumin, decreased. 5. We conclude that the previously reported changes in packed cell volume, plasma volume, intravascular mass of albumin and transcapillary escape rate of albumin during hypoglycaemia may be explained by the combined actions of adrenaline and insulin.

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Müller-Suur, Niels, Peter P. Kleeman, Frank Brost, and Miklos P. B. Halmagyi. "Blood Volume Substitutes in Emergency Care." Prehospital and Disaster Medicine 1, S1 (1985): 173–75. http://dx.doi.org/10.1017/s1049023x00044332.

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Volume substitutes for restoring circulating blood volume are eminently important for emergency care. In addition to side effects, the intravascular volume effect immediately after infusion and the duration of this volume effect are determining factors for the selection of volume replacement solutions available on the market today. Therefore, we controlled the intravascular volume effect of 16 test solutions, immediately as well as 90 and 240 min after the end of infusion.

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Dries, David J. "Blood transfusion and acute intravascular volume loss." Air Medical Journal 17, no. 3 (July 1998): 108–10. http://dx.doi.org/10.1016/s1067-991x(98)90105-5.

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Diringer, Michael N., Kathy Wu, Jeffrey Kirsch, Cecil Borel, and Daniel Hanley. "REGULATION OF INTRAVASCULAR VOLUME FOLLOWING SUBARACHNOID HEMORRHAGE." Critical Care Medicine 18, Supplement (December 1990): S202. http://dx.doi.org/10.1097/00003246-199012001-00052.

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Fleming, S. J., J. S. Wilkinson, E. N. Greenwood, L. R. I. Baker, and W. E. Cattell. "Dialysate Composition and Change in Intravascular Volume." Clinical Science 69, s12 (December 1, 1985): 66P—67P. http://dx.doi.org/10.1042/cs069066pb.

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Roberti, Andrea, and Massimo Girardis. "Extravascular lung water and intravascular volume monitoring." Intensive Care Medicine 28, no. 12 (December 1, 2002): 1832. http://dx.doi.org/10.1007/s00134-002-1541-x.

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Ricci, Zaccaria, Stefano Romagnoli, and Claudio Ronco. "Perioperative intravascular volume replacement and kidney insufficiency." Best Practice & Research Clinical Anaesthesiology 26, no. 4 (December 2012): 463–74. http://dx.doi.org/10.1016/j.bpa.2012.11.001.

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Bell, Leonard, and David L. Rutlen. "Quantitative radionuclide assessment of total pulmonary vascular volume changes." Canadian Journal of Physiology and Pharmacology 68, no. 6 (June 1, 1990): 727–32. http://dx.doi.org/10.1139/y90-110.

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Current techniques do not permit continuous and noninvasive assessments of changes in total pulmonary intravascular volume. Hence, the present study was undertaken to determine whether quantitative radionuclide imaging can be used to determine the direction and estimate the magnitude of total pulmonary vascular volume changes. The pulmonary circulation was separately perfused at a constant rate via the pulmonary artery and drained at a constant pressure via the left atrium in nine dogs. Changes in pulmonary intravascular volume were recorded as reciprocal changes in extracorporeal reservoir volume during phenylephrine or isoproterenol administration, a 20% increase in pulmonary artery flow or a 5 mmHg (1 mmHg = 133.32 Pa) decrease in left atrial pressure. Erythrocytes were labeled with technetium-99 m and pulmonary volume changes were determined from tissue attenuation, blood radioactivity, and changes in total pulmonary radioactivity obtained with a γ-camera. During each of the interventions, count changes correlated with volume changes (r ≥ 0.75). The technique reliably detected volume changes as small as 10 mL. For all 531 individual pairs of radionuclide- and reservoir-determined volume changes, the correlation between reservoir-determined and radionuclide-estimated pulmonary intravascular volume changes was 0.87. The standard error of the radionuclide estimate was 21 mL. Hence, the present study demonstrates that quantitative radionuclide imaging can be used to continuously and noninvasively determine total pulmonary vascular volume changes.Key words: pulmonary circulation, intravascular volume, radionuclide imaging, capacitance vasculature.

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Hagberg, James M., Andrew P. Goldberg, Loretta Lakatta, Frances C. O’Connor, Lewis C. Becker, Edward G. Lakatta, and Jerome L. Fleg. "Expanded blood volumes contribute to the increased cardiovascular performance of endurance-trained older men." Journal of Applied Physiology 85, no. 2 (August 1, 1998): 484–89. http://dx.doi.org/10.1152/jappl.1998.85.2.484.

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To determine whether expanded intravascular volumes contribute to the older athlete’s higher exercise stroke volume and maximal oxygen consumption (V˙o 2 max), we measured peak upright cycle ergometry cardiac volumes (99mTc ventriculography) and plasma (125I-labeled albumin) and red cell (NaCr51) volumes in 7 endurance-trained and 12 age-matched lean sedentary men. The athletes had ∼40% higherV˙o 2 max values than did the sedentary men and larger relative plasma (46 vs. 38 ml/kg), red cell (30 vs. 26 ml/kg), and total blood volumes (76 vs. 64 ml/kg) (all P < 0.05). Athletes had larger peak cycle ergometer exercise stroke volume indexes (75 vs. 57 ml/m2, P < 0.05) and 17% larger end-diastolic volume indexes. In the total group,V˙o 2 maxcorrelated with plasma, red cell, and total blood volumes ( r = 0.61–0.70, P < 0.01). Peak exercise stroke volume was correlated directly with the blood volume variables ( r = 0.59–0.67, P < 0.01). Multiple regression analyses showed that fat-free mass and plasma or total blood volume, but not red cell volume, were independent determinants ofV˙o 2 max and peak exercise stroke volume. Plasma and total blood volumes correlated with the stroke volume and end-diastolic volume changes from rest to peak exercise. This suggests that expanded intravascular volumes, particularly plasma and total blood volumes, contribute to the higher peak exercise left ventricular end-diastolic volume, stroke volume, and cardiac output and hence the higherV˙o 2 max in master athletes by eliciting both chronic volume overload and increased utilization of the Frank-Starling effect during exercise.

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Bertram, T. A. "Intravascular Macrophages in Lungs of Pigs Infected with Haemophilus pleuropneumoniae." Veterinary Pathology 23, no. 6 (November 1986): 681–91. http://dx.doi.org/10.1177/030098588602300606.

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Pigs were inoculated intratracheally with a virulent or an avirulent isolate of Haemophilus pleuropneumoniae serotype 5 and sacrificed during the first 24 hours post-inoculation. Intravascular macrophages were examined by electron microscopic and morphometric techniques. Samples of lung were taken from regions with no macroscopic lesions (Zone 0), 2.5 to 3.0 cm from lesions (Zone 1), and from the immediate edge of lesions (Zone 2). Those pigs inoculated with the avirulent isolate did not develop lesions. Pigs given the virulent isolate consistently developed necrohemorrhagic lesions in the dorsolateral aspect of the caudal and middle lung lobes. Relative volumes of intravascular macrophages in Zones 1 and 2 increased with increased time post-inoculation; in pigs given the avirulent isolate, intravascular macrophage volume decreased with increased time post-inoculation. Cytoplasmic volume to nuclear volume ratios for macrophages in Zone 2 from pigs with necrohemorrhagic lesions progressively increased with increased time post-inoculation. Enlarged intravascular macrophages had large nuclei, prominent nucleoli, and abundant cytoplasm. Increased cytoplasmic volume was the result of increased numbers of lysosomes, phagosomes, rough and smooth endoplasmic reticulum, and large Golgi complexes. Pigs inoculated with the virulent bacteria had IV macrophages with large phagosomes that contained necrotic cell debris and fibrin. Macrophages with phagosomes were more frequent in the 6-, 9-, and 24-hour sample periods of pigs with lesions than in any other group. Intercellular adhesion plaques (ICAP) were present between IV macrophages and subjacent endothelial cells. ICAP's increased in length with increased time post-inoculation in Zones 1 and 2 from pigs with necrohemorrhagic lesions. In later sample periods, multiple closely associated and interlacing IV macrophages formed a discontinuous layer over endothelial cells in Zone 2 samples near necrohemorrhagic lesions. These results suggest that the intravascular macrophage population changes from immature macrophages to mature macrophages or immature epithelioid cells within 24 hours after inhalation of a virulent Haemophilus pleuropneumoniae. Furthermore, intravascular macrophages likely function to clear cellular and acellular debris from the blood in pneumonic conditions.

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Mahl, T. C. "Hetastarch versus albumin for intravascular volume support during large volume paracentesis." Gastroenterology 108, no. 4 (April 1995): A1116. http://dx.doi.org/10.1016/0016-5085(95)28764-7.

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RAGALLER, MAXIMILIAN J. R., HERMANN THEILEN, and THEA KOCH. "Volume Replacement in Critically Ill Patients with Acute Renal Failure." Journal of the American Society of Nephrology 12, suppl 1 (February 2001): S33—S39. http://dx.doi.org/10.1681/asn.v12suppl_1s33.

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Abstract. Maintenance and restoration of intravascular volume are essential tasks of critical care management to achieve sufficient organ function and to avoid multiple organ failure in critically ill patients. Inadequate intravascular volume followed by impaired renal perfusion is the predominate cause of acute renal failure. Crystalloid solutions are the first choice to correct fluid and electrolyte deficits in these patients. However, in case of major hypovolemia, particularly in situations of increased capillary permeability, colloid solutions are indicated to achieve sufficient tissue perfusion. Whereas albumin should be avoided for correction of intravascular hypovolemia, synthetic colloids can restore intravascular volume and stabilize hemodynamic conditions. In addition to a faster, more effective and prolonged restoration of intravascular volume, colloid solutions are able to improve microcirculation. Of the synthetic colloids, hydroxyethyl starch (HES) solutions with a low in vivo molecular weight, such as HES 200/0.5, offer the best risk/benefit ratio. These solutions are safe with respect to effects on coagulation, platelets, reticuloendothelial system, and renal function, if used below their upper dosage limits. For patients with acute renal dysfunction, daily monitoring of renal function is necessary if colloids are required to stabilize hemodynamic conditions. In these patients, measurement of the colloidal osmotic pressure and adequate amounts of crystalloid solutions will reduce the risk of hyperoncotic renal failure. Of all colloids, gelatin and HES solutions with low in vivo molecular weight are preferred in these cases. In the very specific situation of kidney transplantation, colloid solutions should be administered in a restricted manner to organ donors and kidney recipients.

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Corboy, John C., Robert J. Walker, Mark B. Simmonds, Gerard T. Wilkins, A. Mark Richards, and Eric A. Espiner. "Plasma Natriuretic Peptides and Cardiac Volume during Acute Changes in Intravascular Volume in Haemodialysis Patients." Clinical Science 87, no. 6 (December 1, 1994): 679–84. http://dx.doi.org/10.1042/cs0870679.

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1. Plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptides (BNP) were measured, along with left and right atrial and left ventricular volumes, in eight patients with chronic renal failure before and after the removal of 2.1 ± 0.61 of fluid by ultrafiltration and again during volume repletion with intravenous sodium chloride solution (150 mmol/l saline) to restore body weight plus 0.5 kg. 2. Baseline levels of ANP (46.0 ± 7.5 pmol/l) and BNP (22.0 ± 4.4 pmol/l) were elevated above normal. There was a significant reduction in plasma ANP (26.5 ± 4.7 pmol/l, P < 0.05) and BNP (19.1 ± 4.9 pmol/l, P < 0.05)) following ultrafiltration. Changes in plasma ANP during ultrafiltration correlated significantly with changes in left atrial volume (r = 0.643, P < 0.05). 3. During volume repletion there was an exaggerated release of ANP (mean level post repletion 71.3 ± 20.8 pmol/l) which was not paralleled by changes in BNP. Changes in BNP were small, showing no correlation with atrial or ventricular volumes during either ultrafiltration or volume repletion. 4. These findings indicate that in chronic renal failure without left ventricular dysfunction, moderate acute changes in volume status elict only small immediate responses in plasma BNP. Changes in plasma ANP are greater than BNP and more responsive to changes in left atrial volume.

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Freudenberg, S., P. Palma, K. Schuster, C. Mkony, and K. Waschke. "Small Volume Resuscitation with 7.5% Hypertonic Saline Solution — Treatment of Haemorrhagic Shock in the Tropics." Tropical Doctor 33, no. 3 (July 2003): 165–66. http://dx.doi.org/10.1177/004947550303300316.

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Rapid intravenous injection of 4 mL/kg body weight of a 7.5% hypertonic sodium chloride solution immediately increases intravascular osmotic pressure and intravascular volume after haemorrhage. This ‘small volume resuscitation’ rapidly improves blood pressure and microcirculatory perfusion in patients with hypovolaemic shock after large blood losses. Pathophysiological findings as well as practical application approaches are described. Small volume resuscitation is an effective and economic method in the first-line treatment of acute haemorrhagic shock.

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Vincent, Jean-Louis. "Intravascular Volume Assessment in the Critically Ill Patient." Clinical Journal of the American Society of Nephrology 15, no. 4 (December 3, 2019): 557–59. http://dx.doi.org/10.2215/cjn.10760919.

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Spronk, Peter E., Can Ince, Martin J. Gardien, Keshen R. Mathura, Heleen M. Oudemans-van Straaten, and Durk F. Zandstra. "Nitroglycerin in septic shock after intravascular volume resuscitation." Lancet 360, no. 9343 (November 2002): 1395–96. http://dx.doi.org/10.1016/s0140-6736(02)11393-6.

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Sanchez, Manuel, Manuel Jimenez, Manuel Cidoncha, Maria Jose Asensio, Raquel Herrero, Eva Herrero, Santiago Yus, and Eva Perales. "COMPARISON OF TWO METHODS FOR PREDICT INTRAVASCULAR VOLUME." Critical Care Medicine 32, Supplement (December 2004): A143. http://dx.doi.org/10.1097/00003246-200412001-00509.

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Marik, Paul E. "Assessment of intravascular volume: A comedy of errors." Critical Care Medicine 29, no. 8 (August 2001): 1635–36. http://dx.doi.org/10.1097/00003246-200108000-00024.

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BUNDGAARD-NIELSEN, M., C. C. JØRGENSEN, N. H. SECHER, and H. KEHLET. "Functional intravascular volume deficit in patients before surgery." Acta Anaesthesiologica Scandinavica 54, no. 4 (April 2010): 464–69. http://dx.doi.org/10.1111/j.1399-6576.2009.02175.x.

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Lange, Matthias, Christian Ertmer, Hugo Van Aken, and Martin Westphal. "Intravascular Volume Therapy With Colloids in Cardiac Surgery." Journal of Cardiothoracic and Vascular Anesthesia 25, no. 5 (October 2011): 847–55. http://dx.doi.org/10.1053/j.jvca.2010.06.005.

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Kaufman, S., and Y. Deng. "Splenic control of intravascular volume in the rat." Journal of Physiology 468, no. 1 (August 1, 1993): 557–65. http://dx.doi.org/10.1113/jphysiol.1993.sp019788.

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Killu, Keith, Mustafa Al-Jubouri, Mustafa Baldawi, Jenna Watson, Darlene Dereczyk, Greta Wenk, Victor Coba, and Dionne Blyden. "121: INTRAVASCULAR VOLUME ASSESSMENT BY SONOGRAPHY (VAS) SCORE." Critical Care Medicine 46, no. 1 (January 2018): 43. http://dx.doi.org/10.1097/01.ccm.0000528141.19087.25.

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Mathews, Donald M. "Epidural Anesthesia, Hypotension, and Changes in Intravascular Volume." Survey of Anesthesiology 49, no. 1 (February 2005): 43–44. http://dx.doi.org/10.1097/01.sa.0000151236.82877.83.

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De Backer, Daniel, and Diego Orbegozo Cortés. "Characteristics of fluids used for intravascular volume replacement." Best Practice & Research Clinical Anaesthesiology 26, no. 4 (December 2012): 441–51. http://dx.doi.org/10.1016/j.bpa.2012.10.005.

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Nguyen, Minhtri K., Vahram Ornekian, Liyo Kao, Anthony W. Butch, and Ira Kurtz. "Defining the role of albumin infusion in cirrhosis-associated hyponatremia." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 2 (July 15, 2014): G229—G232. http://dx.doi.org/10.1152/ajpgi.00424.2013.

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The presence of negatively charged, impermeant proteins in the plasma space alters the distribution of diffusible ions in the plasma and interstitial fluid (ISF) compartments to preserve electroneutrality and is known as Gibbs-Donnan equilibrium. In patients with hypoalbuminemia due to underlying cirrhosis, the decrease in the plasma water albumin concentration ([Alb−]pw) would be expected to result in a decrease in the plasma water sodium concentration ([Na+]pw) due to an alteration in the distribution of Na+ between the plasma and ISF. In addition, cirrhosis-associated hyponatremia may be due to the renal diluting defect resulting from the intravascular volume depletion due to gastrointestinal losses and overdiuresis and/or decreased effective circulatory volume secondary to splanchnic vasodilatation. Therefore, albumin infusion may result in correction of the hyponatremia in cirrhotic patients either by modulating the Gibbs-Donnan effect due to hypoalbuminemia or by restoring intravascular volume in patients with intravascular volume depletion due to gastrointestinal losses and overdiuresis. However, the differential role of albumin infusion in modulating the [Na+]pw in these patients has not previously been analyzed quantitatively. In the present study, we developed an in vitro assay system to examine for the first time the quantitative effect of changes in albumin concentration on the distribution of Na+ between two compartments separated by a membrane that allows the free diffusion of Na+. Our findings demonstrated that changes in [Alb−]pw are linearly related to changes in [Na+]pw as predicted by Gibbs-Donnan equilibrium. However, based on our findings, we predict that the improvement in cirrhosis-associated hyponatremia due to intravascular volume depletion results predominantly from the restoration of intravascular volume rather than alterations in Gibbs-Donnan equilibrium.

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Venkat, Shruthi Kamal, Reshma Sattar, and Dinesh Kumar. "An unusual case of relative polycythemia with complication of pseudocyst of pancreas." International Surgery Journal 4, no. 2 (January 25, 2017): 816. http://dx.doi.org/10.18203/2349-2902.isj20170241.

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Relative polycythemia is a term used to describe an elevation of the hematocrit level either caused by an acute transient state of hemoconcentration associated with intravascular fluid depletion or a chronic sustained relative polycythemia caused by contraction of the plasma volume. Relative polycythemia can occur when the plasma volume is reduced due to intravascular volume depletion during acute pancreatitis episode, complicating as pseudocyst of pancreas. We report a case of Relative Polycythemia with pseudocyst of Pancreas a secondary complication of pancreatitis.

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Kalantari, Kambiz, Jamison N. Chang, Claudio Ronco, and Mitchell H. Rosner. "Assessment of intravascular volume status and volume responsiveness in critically ill patients." Kidney International 83, no. 6 (June 2013): 1017–28. http://dx.doi.org/10.1038/ki.2012.424.

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Montgomery, Leslie D., Richard W. Montgomery, Wayne A. Gerth, Michael Bodo, Julian M. Stewart, and Marty Loughry. "Segmental intracellular, interstitial, and intravascular volume changes during simulated hemorrhage and resuscitation: A case study." Journal of Electrical Bioimpedance 10, no. 1 (August 20, 2019): 40–46. http://dx.doi.org/10.2478/joeb-2019-0006.

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Abstract This paper describes a new combined impedance plethysmographic (IPG) and electrical bioimpedance spectroscopic (BIS) instrument and software that will allow noninvasive real-time measurement of segmental blood flow, intracellular, interstitial, and intravascular volume changes during various fluid management procedures. The impedance device can be operated either as a fixed frequency IPG for the quantification of segmental blood flow and hemodynamics or as a multi-frequency BIS for the recording of intracellular and extracellular resistances at 40 discrete input frequencies. The extracellular volume is then deconvoluted to obtain its intravascular and interstitial component volumes as functions of elapsed time. The purpose of this paper is to describe this instrumentation and to demonstrate the information that can be obtained by using it to monitor segmental compartment volume responses of a pig model during simulated hemorrhage and resuscitation. Such information may prove valuable in the diagnosis and management of rapid changes in the body fluid balance and various clinical treatments.

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Bell, L., and D. L. Rutlen. "Muscarinic regulation of pulmonary intravascular volume in isolated canine lungs." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 5 (November 1, 1988): H1219—H1226. http://dx.doi.org/10.1152/ajpheart.1988.255.5.h1219.

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The influence of acetylcholine on pulmonary intravascular volume has not been clearly identified. In 14 anesthetized dogs, the pulmonary circulation was separately perfused in situ at a constant rate and drained to an extracorporeal reservoir, so that changes in total pulmonary intravascular volume could be recorded as reciprocal changes in reservoir volume. In eight animals, acetylcholine at 100 micrograms/min for 20 min was associated with increases in pulmonary intravascular volume (PIV) and pulmonary arterial pressure of 41 +/- 5 (SE) ml (P less than 0.001) and 2.0 +/- 0.0 mmHg (P less than 0.001; 11 infusions), respectively. These responses were abolished after atropine (6 infusions). In six animals, pulmonary venous pressure was also measured, so that total pulmonary (TPR), pulmonary arterial (PAR), and pulmonary venous (PVR) resistances could be calculated. TPR and PVR increased from 21 +/- 2 to 24 +/- 3 (P less than 0.001) and from 7 +/- 1 to 11 +/- 1 mmHg.min.l-1 (P less than 0.001), respectively, while PAR did not change significantly (6 infusions). In three of the six animals, these changes were abolished by atropine (6 infusions). In the other three animals, PIV increased 56 +/- 11 ml (P less than 0.001) before and 47 +/- 6 ml (P less than 0.001) after indomethacin. The acetylcholine-associated increases in TPR and PVR were also not significantly attenuated after indomethacin. Hence, muscarinic receptor stimulation with acetylcholine is associated with an increase in pulmonary intravascular volume, which is mediated by an increase in resistance to pulmonary venous outflow. These changes are not due to release of prostanoids.(ABSTRACT TRUNCATED AT 250 WORDS)

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Gumeniuk, M. I., G. L. Gumeniuk, and S. G. Opimakh. "Anaphylactic shock infusion therapy." Infusion & Chemotherapy, no. 2 (June 24, 2020): 21–27. http://dx.doi.org/10.32902/2663-0338-2020-2-21-27.

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ABSTRACT. Anaphylactic shock is anaphylaxis with signs of critical organ hypoperfusion that threatens the patient’s life. For anaphylactic shock, the features of both distributive and hypovolemic shock are inherent. Distributive shock leads to the movement of fluid from the capillaries into the surrounding tissue, accompanied by inadequate perfusion of the tissues. The rapid recognition of anaphylaxis, the administration of epinephrine and the replacement of intravascular fluid are key factors in the successful outcome of the treatment of this potentially fatal event. The main principle that should be followed when carrying out infusion therapy of anaphylactic shock is the principle of small volume resuscitation (SVR), based primarily on the redistribution of endogenous fluid without the need for significant volumes of exogenous solutions. Hyperosmolar solutions used for SVR infusion therapy provide fluid return from the intercellular space to the vascular bed. The movement of fluid from the intercellular sector to the intravascular volume leads to an increase in the volume of circulating blood, contributes to the normalization of microcirculation and perfusion of tissues. SVR leads to an anti-shock effect due to a sharp increase in the intravascular volume of blood, and a decrease in edema improves microcirculation and perfusion of tissues and normalizes the water-electrolyte balance. Infusion therapy for anaphylactic shock is carried out by crystalloid solutions till hemodynamic stabilization. The choice of acceptable preparations for infusion varies among simple and balanced saline solutions, preparations based on polyhydric alcohols, taking into account the individual reaction of the patient to volume infusion.

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Park, Sang Jun, Shin Hyung Kim, Seon Ju Kim, Duck Mi Yoon, and Kyung Bong Yoon. "Comparison of Incidences of Intravascular Injection between Medial and Lateral Side Approaches during Traditional S1 Transforaminal Epidural Steroid Injection." Pain Research and Management 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/6426802.

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Purpose. Intravascular injection rates are higher during traditional S1 transforaminal epidural steroid injection (TFESI) compared with lumbar transforaminal injection. We compared the incidences of intravascular injection between the medial and lateral approaches to the S1 foramen during S1 TFESI. Materials and Methods. A total of 139 patients underwent one or more TFESIs (170 total injections). The patients received S1 TFESI by either medial or lateral side of S1 foramen under fluoroscopic anteroposterior view using digital subtraction method. The intravascular injection rates, epidural spread patterns, and contrast volumes required to reach the superior aspect of the L5-S1 intervertebral disc (SIVD) were compared between groups. Results. Intravascular injection rates during S1 TFESI were significantly lower in the medial approach compared with the lateral approach patients (4.9% versus 38.6%, resp., P<0.001). The medial approach group had more epidural spread to the L5-S1 SIVD than the lateral group (82.1% versus 58.8%, resp.); lower contrast volume amounts were required to extend the L5-S1 SIVD (1.46±0.48 versus 1.90±0.62, resp.). Conclusion. During S1 TFESI, approaching the needle towards the medial part of the S1 foramen may reduce intravascular injection risk.

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Norris, Susan O’brien. "Managing Low Cardiac Output States: Maintaining Volume after Cardiac Surgery." AACN Advanced Critical Care 4, no. 2 (May 1, 1993): 309–19. http://dx.doi.org/10.4037/15597768-1993-2008.

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Low cardiac output after cardiac surgery may be caused by hypovolemia, myocardial depression, vasoconstriction, and dysrhythmias. Postoperative hypovalemia occurs because of blood volume loss and decreased diastolic filling. Diuresis, intravascular fluid shift into the interstitium, hormonal influences, and bleeding deplete blood volume. Diastolic filling may be compromised by positive end-expiratory pressure, vasodilation, dysrhythmias, and venous return obstruction. The primary indicator of intravascular volume is ventricular preload, which may be measured indirectly with central venous pressure, left atrial pressure, or pulmonary capillary wedge pressure. Recognition of hypovolemia is aided through the use of cardiac pressure trend monitoring and evaluation of noninvasive indicators of hypovolemia. Nursing goals, in response to hypovolemia, are to increase the circulating volume, optimize oxygen delivery, stabilize hemodynamics, improve tissue perfusion, and prevent shock

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Hoeft, A., B. Schom, A. Weyland, M. Scholz, E. Stepanek, and W. Buhre. "A New Method for Bedside Measurement of Intravascular Volume." Anesthesiology 77, Supplement (September 1992): A492. http://dx.doi.org/10.1097/00000542-199209001-00492.

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Martin, Greg S., and E. Wesley Ely. "Underutilized Tools for the Assessment of Intravascular Volume Status." Chest 124, no. 1 (July 2003): 415–16. http://dx.doi.org/10.1378/chest.124.1.414.

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Journal articles on the topic 'Intravascular volume'

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