Relevant bibliographies by topics / Intravascular volume

Academic literature on the topic 'Intravascular volume'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "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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Dissertations / Theses on the topic "Intravascular volume"

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Yang, Kimberly. "Correlating IVC Measurements with Intravascular Volume Changes at Three Distinct Measurement Sites." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/315932.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
Bedside ultrasound of the inferior vena cava (IVC) has grown to be an important tool in the assessment and management of critically ill patients. This study endeavors to examine which location along the IVC is most highly correlated with changes in intravascular volume status: (1) the diaphragmatic juncture (DJ) (2) two centimeters caudal to the hepatic vein juncture (2HVJ) or (3) left renal vein juncture (LRVJ). Data was collected in this prospective observational study on patients in the emergency department who were at least 16 years of age, being treated with intravenous fluids (IVF). Measurements of the IVC were recorded at each site during standard inspiratory and expiratory cycles, and again with the patient actively sniffing to decrease intrapleural pressures. IVF was then administered per the patient’s predetermined treatment, and the same six measurements were repeated after completion of fluid bolus. The difference in caval index (dCI) was calculated for all six data sets and correlated with the mL/kg of IVF administered. There was a statistically significant correlation between mL/kg of IVFs administered and dCI at all three sites (DJ: r = 0.354, p value = 0.0002; 2HVJ: r = 0.334, p value = 0.0003; LRVJ: r = 0.192, p value = 0.03). The greatest correlation between amount of fluids administered and dCI was observed along the IVC at the site 2 cm caudal to the juncture of the hepatic veins (2HVJ). This site is also where the largest change in diameter can be appreciated on ultrasound during intravascular volume resuscitation. Our data also suggests that every mL/kg of IVFs administered should change the dCI by 0.86-1.00%. This anticipated change in IVC diameter can be used to gauge a patient’s response to intravascular volume repletion.
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Gordon, Christopher, and res cand@acu edu au. "Hydrostatic and thermal influences on intravascular volume determination during immersion: quantification of the f-cell ratio." Australian Catholic University. School of Exercise Science, 2001. http://dlibrary.acu.edu.au/digitaltheses/public/adt-acuvp4.14072005.

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Previous data have shown that the most prevalent, indirect plasma volume (PV) measurement technique, which utilises changes in haematocrit (Hct) and haemoglobin concentration ([Hb]), underestimates actual PV changes during immersion, when compared to a direct tracer-dilution method. An increase in the F-cell ratio (whole-body haematocrit (Hctw) to large-vessel haematocrit (Hctv) ratio) has been purported as a possible explanation, probably due to hydrostatic and thermally-mediated changes during water immersion. Previous investigators have not quantified the F-cell ratio during immersion. Therefore, this study sought to determine the effect of the F-cell ratio on the indirect method during both, thermoneutral and cold-water immersions. Seven healthy males were tested three times, seated upright in air (control: 21.2°C SD ±1.1), and during thermoneutral (34.5oC SD ±0.2) and cold-water immersion (18.6oC SD ±0.2), immersed to the third intercostal space for 60 min. Measurements during the immersion tests included PV (Evans blue dye column elution, Evans blue dye computer programme, and Hct [Hb]), red cell volume (RCV; sodium radiochromate), cardiac frequency (fc) and rectal temperature (Tre). Plasma volume during the control trial remained stable, and equivalent across the three tests. There was a hydrostatically-induced increase in PV during thermoneutral immersion, when determined by the Evans blue dye method (16.2%). However, the Hct/[Hb] calculation did not adequately reflect this change, and underestimated the relative PV change by 43%. In contrast, PV decreased during cold immersion when determined using the Evans blue dye method by 17.9% and the Hct/[Hb] calculation by 8.0%, respectively, representing a 52% underestimation by the latter method. There was a non-significant decline in RCV during both immersions. Furthermore, an increase (8.6%) and decrease (-14.4%) in blood volume (BV) was observed during thermoneutral and cold-water immersions, respectively. The decline in RCV during thermoneutral immersion attenuated the BV expansion. Despite the disparity between the PV methods, there was no increase in the F-cell ratio during either immersion. In contrast, there was a significant decline in the F-cell ratio during the control: air and thermoneutral immersion, which may indicate that other, undefined variables may impact on the stability of the red cell compartment. The current study is the first to show that the Hct/[Hb] method clearly underestimates PV changes during both thermoneutral and cold-water immersion. Furthermore, RCV was shown, for the first time, to decline during both immersions. However, the changes in the F-cell ratio during this study, did not account for the underestimation of PV change using the Hct/[Hb] method.
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Chimabucuro, Wilson Kohama. "Isquemia mesentérica e reposição do volume intravascular. Estudo comparativo entre duas soluções salinas com diferentes concentrações de cloreto de sódio nos eventos desencadeados pela reperfusão intestinal. Um modelo experimental em ratos." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5159/tde-10062010-143136/.

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A isquemia do intestino delgado ocorre nas oclusões arteriais dos vasos mesentéricos ou associada à baixa perfusão tecidual causada por choque circulatório. Seus efeitos deletérios locais e sistêmicos frequentemente agravam a evolução clínica de muitas doenças. Este estudo experimental investiga como a reposição do volume intravascular utilizando duas soluções salinas com diferentes concentrações de sódio (solução salina fisiológica e solução 7,5% de cloreto de sódio) modifica a resposta inflamatória e o estresse oxidativo causados pela isquemia do intestino delgado. Ratos Wistar, machos, peso corporal entre 250 e 300 g, número total =102, foram submetidos à oclusão transitória da artéria mesentérica superior durante 45 minutos. No protocolo utilizado, os animais foram sorteados para inclusão em um de quatro grupos experimentais: isquemia falsa (IF), isquemia intestinal seguida da infusão de solução salina hipertônica 7.5% em volume de 4 ml/kg de peso (SH), isquemia intestinal seguida da infusão de solução salina 0.9% em volume de 33 ml/kg de peso (SF) e isquemia intestinal sem reposição do volume intravascular (ST). Quando apropriado, as soluções foram administradas lentamente (5 minutos) pela veia jugular externa imediatamente antes da reperfusão intestinal. Em cada grupo experimental, logo após a reperfusão intestinal, os animais foram sorteados para tempo de sobrevida: 2 horas, 4 horas ou 6 horas após a reperfusão. Amostras de sangue foram colhidas pela veia jugular externa em vários períodos: imediatamente após a liberação da oclusão da artéria mesentérica, 2 horas, 4 horas e 6 horas após a reperfusão intestinal. O plasma foi separado e foram realizadas as dosagens de interleucinas (IL-6 e IL-10). No tempo determinado, os animais foram submetidos à eutanásia em condições humanamente aceitáveis e, então, nesse momento, foram colhidas amostras de tecidos (intestino, fígado e pulmão) para posterior quantificação das concentrações de malondialdeído (MDA) e interleucinas (IL-6 e IL-10). A atividade da mieloperoxidase (MPO) também foi avaliada nessas amostras. Os animais que não receberam tratamento apresentaram uma taxa de mortalidade maior do que os demais grupos. Os grupos de animais tratados com reposição de volume intravascular apresentaram uma taxa de mortalidade semelhante ao grupo de isquemia falsa. Os animais que receberam reposição de volume intravascular com soluções cristalóides (SH ou SF) apresentaram concentrações de MDA, MPO, IL-6 e IL-10 nos tecidos (intestino, fígado e pulmão) comparáveis ao grupo de animais com isquemia falsa. Em todos os momentos, esses valores foram mais elevados no grupo que não recebeu tratamento. As concentrações plasmáticas da IL-6 e da IL-10 foram mais elevadas nos animais tratados com SH. As análises mostram que a simples abertura da cavidade abdominal causa um trauma cirúrgico relevante aos animais e é responsável pelas alterações observadas no grupo de isquemia falsa. Os resultados sugerem que a isquemia intestinal transitória (45 minutos) realizada por oclusão da artéria mesentérica superior em ratos representa um modelo experimental de moderada gravidade. Dessa maneira, o modelo é adequado aos estudos das alterações bioquímicas e celulares que ocorrem a curto, médio e longo tempo de sobrevida. Este estudo foi elaborado para análise dos fatores relativos ao estresse oxidativo e reação inflamatória que ocorrem nas primeiras horas que seguem a reperfusão intestinal. De uma maneira geral, os animais foram beneficiados pela reposição do volume intravascular com soluções cristalóides. A solução salina fisiológica foi utilizada em volume aproximadamente oito vezes superior à solução hipertônica 7,5% de cloreto de sódio. Comparativamente, a atenuação similar das respostas deletérias após a reperfusão intestinal atingida com o uso de menor volume da solução hipertônica 7,5% de cloreto de sódio representa um fator positivo para a mesma. Considera-se que a maior concentração plasmática das interleucinas (IL-6 e IL-10) encontrada nos animais tratados com solução hipertônica7,5% de cloreto de sódio esteja relacionada ao aumento de permeabilidade da microcirculação associado às soluções hipertônicas
Gut ischemia is responsible for both local and systemic deleterious events. Since reperfusion occurs in a previous ischemic superior mesenteric artery territory (SMA), a succession of harmful mechanisms begins in the luminal epithelium that quickly lengthens the limits of the intestinal tract. Depending on the extension of the intestinal system involved in the ischemic/reperfusion injury there will be severe repercussion to distant organs in response to SMA occlusion. Several diseases could be associated with variables degrees of intestinal ischemia. Even minor intensity of intestinal ischemia had deleterious systemic effects and often aggravates the clinical outcome of many diseases. Our study investigates how different forms of volume restoration could modify two important mechanisms of injury after intestinal ischemia: oxidative stress and inflammatory responses. Wistar rats (n=102) were submitted to transient superior mesenteric artery occlusion (SMAo). After randomization, animals were divided in four groups: Sham intestinal ischemia; infusion of small volume of 7.5% hypertonic saline (HS), or infusion of high volume of 0.9% saline (NS) just prior reperfusion, and animals that did not receive intra vascular volume treatment (NT). At sequential times, the animals were euthanatized and tissue samples (lung, liver, and intestine) were collected to Malondialdehyde (MDA) dosage and myeloperoxidase (MPO) activity. Also, sequential plasmatic concentration of IL-6 and IL-10 were done. Animals treated with both forms of volume infusion showed lower levels of tissue MDA, MPO, IL-6, and IL-10 than found in NT group. Plasmatic concentration of IL-6 and IL-10 were higher in animals treated with HS. Positive correlation was found between tissue concentration of IL-10 and IL-6. The mortality rate was similar between the treated rats and the group of sham ischemia. The mortality rate was higher in the non treated animals. In this rat model of transient intestinal ischemia, adequate maintenance of intravascular volemia decreases oxidative stress and synthesis of inflammatory markers. Small volume of 7.5% HS (4ml/Kg body weight) and high amounts of NS ( 33 ml/Kg body weight) had similar effects in attenuation of these responses. In this study, 7.5% HS attenuates deleterious effects found after intestinal ischemia with the main advantage of the smallest volume utilized when compared with NS solution. Plasmatic concentrations of IL-6 and IL-10 were higher in HS treated animals. This observation is supported by action of hypertonic/hyperosmotic solutions at the microcirculatory level. These solutions increase the local vascular permeability. This characteristic of 7.5% HS solution could facilitate the passage of the locally produced interleukin to the systemic circulation
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Gomes, Carlos Filipe Vieira. "Avaliação do volume intravascular e da capacidade de resposta a fluidos." Master's thesis, 2014. http://hdl.handle.net/10400.6/5010.

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A administração de fluidos com o objectivo de aumentar o débito cardíaco é uma prática comum e um recurso valioso na abordagem ao doente hemodinamicamente instável. Contudo, recentemente, têm sido demonstrados diversos efeitos prognósticos adversos da utilização excessiva de fluidos, e da sua aplicação em doentes incapazes de converter o aumento do volume intravascular em aumento do débito cardíaco. Classicamente, parâmetros estáticos, como a pressão venosa central e a pressão de oclusão da artéria pulmonar, foram utilizados na avaliação do estado de volume intravascular. Contudo, diversos estudos evidenciaram a alta ineficácia destes indicadores em predizer a capacidade de resposta à administração de fluidos. Consequentemente, nos últimos anos, têm sido propostos diversos parâmetros dinâmicos, que apresentam maiores valores preditivos. Os métodos dinâmicos procuram identificar variações do volume de ejecção, utilizando métodos invasivos e não invasivos, em resposta a mudanças da pré-carga, como são as induzidas pela ventilação, pela elevação passiva dos membros inferiores e pela administração de pequenos volumes de fluidos. Estes métodos são baseados no conceito de capacidade de resposta à administração de fluidos que designa os indivíduos cujo coração se encontra a operar na parte de maior declive da curva de Frank-Starling. Cada um dos métodos recorre a um procedimento que induz a alteração da pré-carga e a um processo de estudo que, directa ou indirectamente, avalia a variação do volume de ejecção resultante. Assim, cada método apresenta vantagens e limitações próprias, as quais devem ser reconhecidas pelo médico na sua aplicação clínica.
Fluid administration intended to raise cardiac debit is a common practice and a valuable resource in the approach of hemodynamically unstable patients. However, recently various adverse effects have been demonstrated, from both the use of excessive fluids and their use in patients unable to raise the cardiac debit after increasing intravascular volume. Classically, static parameters, such as the central venous pressure and the pulmonary artery occlusion pressure, were used for intravascular volume assessment, and thus, as indicators of need for fluid administration. However, several studies have demonstrated the high ineffectiveness of these indicators in predicting fluid responsiveness. Consequently, over the last years, various dynamic parameters with higher predictive values have been proposed. The dynamic methods seek to identify variations in stroke volume, using both invasive and noninvasive methods, in response to changes in preload, as are those caused either by ventilation, by passive leg raising or by intravenous infusion of small fluid volumes. These methods are based on the concept of fluid responsiveness, which designates individuals whose heart is operating at the higher slope of the Frank-Starling curve. Each method uses a procedure for inducing a change in preload and a manner of studying that directly or indirectly measures the change in stroke volume variation. Thus, each method has its own advantages and limitations, which shall be recognized by the physician upon their clinical application.
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Buntman, Ari Jack. "Intravascular dehydration and changes in blood pressure in ultra-marathon runners." Thesis, 1997. http://hdl.handle.net/10539/21783.

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A research report submitted to the Faculty of Medicine, University of the Witwatersrand, in partial fulfilment of the requirements for the degree of Master of Science in Medicine in Applied Physiology. Johannesburg, 1997.
A post-exercise reduction in blood pressure (BP) may be the primary reason that athletes suffer from exerclse-assoclated collapse (EAC) at the end ot ultra-endurance running ever.s. Plasma volume decreases, possibly caused by dehydration, may be the cause of the decrease til blood pressure, In order to determine whether there is a correlation between plasma volume changes and the post-exercise BP drop, this study evaluated alterations in pre- and post-race blood pressures and changes in blood and plasma volumes, It found that compared to resting values, systolic, dlastollc and mean arterial blood pressures (mmHg) fell significantly from 119 ± 4, mean ± standard deviation, 74 ± 8, and 88 ± 5 respectively to '106 ± 14, 62 ± 12 and 77 ± 10 (ps 0,05), whereas pulse pressure failed to change, Compared to pre-race values, plasma and blood volume were found not to have changed significantly, During the race plasma urea (U) and creatinine (C) concentrations increased significantly, whereas body mass and body mass index both fell significantly. Haernatocrlt, haemoglobin, mean cell volume, red blood cell number, mean cell haemoglobin concentration, the mean cell haemoglobin, plasma sodium, potassium, chloride and protein concentrations, the U:C ratio and osmolality remained constant. There were no significClnt correlations between changes in plasma or blood volume and changes in blood pressure, These data support the Idea that a post-race decrease in blood pressure does not result primarily from an intravascular fluid loss, It is likely therefore that athletes who collapse at the end of ultraendurance races due to EAC do so as a result of 'post-exercise hypotension' secondary to venous pooling, and not as a result of a reduction in plasma volume,
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Books on the topic "Intravascular volume"

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Weinstock, Barry S. Influence of verapamil on total and regional intravascular volume in the dog. [New Haven: s.n.], 1987.

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Freely Jr, John J., and Michel Sabbagh. Pyloric Stenosis. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0083.

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Pyloric stenosis is one of the most common surgical conditions affecting neonates and young infants. Hypertrophy of the pyloric muscular layers results in gradual gastric outlet obstruction. Persistent episodic projectile vomiting and dehydration as well as hypochloremic, hypokalemic metabolic alkalosis are cardinal features. Definitive treatment is surgical pyloromyotomy, but it is not a surgical emergency. Emergency medical intervention is often required to correct intravascular volume depletion and electrolyte disturbances. Morbidity and mortality should be limited due to advancements in surgical and perioperative care. Morbidity can occur due to poor preoperative resuscitation, anesthetic management difficulties, or postoperative complications. The following manuscript is a review of current evidence-based perioperative care of infants with pyloric stenosis. It reviews the pathophysiology that results in metabolic disturbances and intravascular volume depletion. It focuses on preoperative assessment and correction of electrolyte abnormalities and anesthetic technique including airway management and postoperative analgesia.
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Stewart, Douglas, Gaurav Shah, Jeremiah R. Brown, and Peter A. McCullough. Contrast-induced acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0246.

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Contrast-induced acute kidney injury (CI-AKI) occurs because all forms of intravascular contrast contain iodine and their biochemical structures induce immediate changes in systemic and renal vasoreactivity. In the kidneys, contrast induces a transient decrease in renal blood flow. This is more pronounced in patients with chronic kidney disease and diabetes mellitus. The reduction in blood flow allows slowed transit of contrast and reabsorption by the proximal tubular cells where contrast is directly toxic resulting in tubular cell dysfunction and death. When there is considerable damage, a transient rise in serum creatinine and reduction in urine output will be observed in the hours to days after contrast exposure. Principles to reduce CI-AKI include limiting the amount of contrast used, intravascular volume expansion to maximize renal blood flow and speed transit of contrast, and possibly agents to reduce the oxidative damage caused by the contrast agents themselves.
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Delaney, Anthony. Physiology of body fluids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0068.

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An understanding of the physiology of body fluids is essential when considering appropriate fluid resuscitation and fluid replacement therapy in critically-ill patients. In healthy humans, the body is composed of approximately 60% water, distributed between intracellular and an extracellular compartments. The extracellular compartment is divided into intravascular, interstitial and transcellular compartments. The movement of fluids between the intravascular and interstitial compartments, is classically described as being governed by Starling forces, leading to a small net efflux of fluid from the intravascular to the interstitial compartment. More recent evidence suggests that a model incorporating the effect of the endothelial glycoclayx layer, a web of glycoproteins and proteoglycans that are bound on the luminal side of the vascular endothelium, better explains the observed distribution of fluids. The movement of fluid to and from the intracellular compartment and the interstitial fluid compartment, is governed by the relative osmolarities of the two compartments. Body fluid status is governed by the difference between fluid inputs and outputs; fluid input is regulated by the thirst mechanism, with fluid outputs consisting of gastrointestinal, renal, and insensible losses. The regulation of intracellular fluid status is largely governed by the regulation of the interstitial fluid osmolarity, which is regulated by the secretion of antidiuretic hormone from the posterior pituitary gland. The regulation of extracellular volume status is regulated by a complex neuro-endocrine mechanism, designed to regulate sodium in the extracellular fluid.
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Wijdicks, Eelco F. M., and Sarah L. Clark. Fluid Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0014.

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Administration of intravenous fluids for maintenance and the more consequential fluid resuscitation are common therapeutic interventions in the neurosciences intensive care unit. Intravenous fluids are provided to ensure adequate hydration because acutely ill neurologic patients often cannot swallow safely. There is a reason to use certain types of fluids and certain measures to maintain an adequate fluid balance specifically in patients admitted to the neurosciences ICU. This chapter covers the regulation of fluid status and the effect of certain fluids on intravascular volume. Daily fluid requirements and the best methods of resuscitation are discussed. The chapter also outlines fluid solutions and the infusion rate associated with different techniques. The side effects of large-volume resuscitation are emphasized.
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Newcomer, Anne, and Michael Gropper. Diabetic Ketoacidosis. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0030.

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Perioperative clinicians caring for patients with diabetes should understand the underlying mechanisms, diagnosis, and treatment of hyperglycemic crises. Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) require prompt recognition and treatment. Disturbances such as these can create acute problems associated with intravascular volume and electrolyte abnormalities, as well as effect postoperative recovery and wound healing. Common precipitants, clinical manifestations, and basic treatment algorithms aimed at safely correcting the underlying cause, as well as the associated problems, are described in this chapter. Perioperative glycemic control is an area of recent intense investigation, and specific recommendations are provided herein.
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Wijdicks, Eelco F. M., and Sarah L. Clark. Osmotic Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0005.

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Osmotic drugs are ubiquitously used in neurocritically ill patients. Mannitol and hypertonic saline are readily available in emergency departments and intensive care units to reduce intracranial pressure. Mannitol depletes and hypertonic saline expands the volume status. Hyperosmolar fluids increase the intravascular osmolality, draw water from the brain, reduce or temporize shift, and reduce globally increased intracranial pressure from any cause. These osmotic fluids change fluid compartments and cannot be used indiscriminately. Particularly when they are administered regularly, close monitoring is needed and target goals should be set. This chapter discusses triggers for the use of these osmotic agents, how to judge their effect, and how to dose adequately.
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Wijdicks, Eelco F. M., and Sarah L. Clark. Vasopressors and Inotropes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0012.

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Vasopressors and inotropes are used in the neurosciences intensive care unit to treat hypotension and to augment blood pressure. Hypotension can be attributed to abnormal cardiac output, abnormal intravascular volume or abnormal systemic vascular resistance. Vasopressors are needed to manage hemodynamic augmentation in patients with severe cerebral vasospasm and aneurysmal subarachnoid hemorrhage, in patients with critical carotid or basilar artery stenosis producing marginal blood flow, or when patients are maintained in drug-induced comas. The main incentive is to maintain adequate perfusion pressure to the brain and vital organs, particularly the kidneys. This chapter provides the essentials of management of these complex drugs and how to avoid unintended side effects.
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Hoorn, Ewout J., and Robert Zietse. Approach to the patient with hyponatraemia. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0028.

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Hyponatraemia is the most common electrolyte disorder in hospitalized patients and is primarily a water balance disorder. Therefore, hyponatraemia is due to a relative excess of water in comparison with sodium in the extracellular fluid volume. Hyponatraemia is usually due to the release of vasopressin despite hypo-osmolality; this secretion is either ‘appropriate’ (i.e. due to a low intravascular volume) or ‘inappropriate’. The diagnostic approach to hyponatraemia relies on the assessment of the time of development, symptoms, and volume status, along with laboratory parameters such as urine sodium and urine osmolality. Complications are mainly neurological and usually depend on the rate of development and correction. If hyponatraemia develops acutely, treatment should be directed towards counteracting the water shift to or brain cells. Conversely, in more chronic cases of hyponatraemia, treatment should be directed at the underlying cause, while avoiding over-correction.
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Aguilar-Torres, Río. Assessment of left atrial function. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0010.

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The left atrium (LA) plays an important role in cardiovascular performance, not only as a mechanical contributor, elastic reservoir, and a primer for left ventricular filling, but also as a participant in the regulation of intravascular volume through the production of atrial natriuretic peptide.Although LA diameter in the parasternal long-axis view has been routinely employed, LA volume is a more robust marker for predicting events than LA areas or diameters. The assessment of LA performance based on two-dimensional volumetrics, Doppler evaluation of mitral, pulmonary vein flow, and annular tissue Doppler, as well as deformation imaging techniques, may provide incremental information for prognostic purposes and for the evaluation of severity and duration of conditions associated with LA overload.The aims of this chapter are to explain the basics of LA function, and to describe the role of Doppler echocardiography techniques, and how to implement them, for the non-invasive evaluation of LA in clinical practice.
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Book chapters on the topic "Intravascular volume"

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Citerio, G., C. Giussani, Hugo Sax, Didier Pittet, Xiaoyan Wen, John A. Kellum, Angela M. Mills, et al. "Intravascular and Extravascular Volume Monitoring at the Bedside." In Encyclopedia of Intensive Care Medicine, 1286–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_709.

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Citerio, G., C. Giussani, Hugo Sax, Didier Pittet, Xiaoyan Wen, John A. Kellum, Angela M. Mills, et al. "Intravascular Volume Assessment by Inferior Vena Cava Sonography." In Encyclopedia of Intensive Care Medicine, 1293–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_867.

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Dean, Anthony J. "Intravascular Volume Assessment by Ultrasound Evaluation of the Inferior Vena Cava." In Emergency Point-of-Care Ultrasound, 115–25. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119072874.ch10.

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Rasheed, Saad. "Is Normal Saline Solution the Best Crystalloid for Intravascular Volume Resuscitation?" In You’re Wrong, I’m Right, 55–56. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43169-7_16.

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Stratta, P., C. Canavese, L. Gurioli, M. Porcu, M. Dogliani, T. Todros, G. C. Mattone, O. Fianchino, L. Gagliardi, and A. Vercellone. "Intravascular Volume Expansion as Therapeutic Approach to the Underfill State of Preeclampsia." In Current Therapy in Nephrology, 111–13. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0865-2_28.

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Koratala, Abhilash. "Lung and Cardiac Ultrasound for Assessment of Intravascular Volume Status in Children." In Advances in Critical Care Pediatric Nephrology, 41–53. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4554-6_5.

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Aibiki, Mayuki, Shuji Kawaguchi, Osamu Umegaki, Shinji Ogura, Nobuyuki Kawai, Yoshihiro Kinoshita, and Satoshi Yokono. "Intravascular Volume Expansion During Therapeutic Moderate Hypothermia for Brain-Injured Patients: Preliminary Report." In Brain Hypothermia, 161–68. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66882-4_15.

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Lengyel, Jed, Donald P. Greenberg, Alan Yeung, Edwin Alderman, and Richard Popp. "Three-Dimensional Reconstruction and Volume Rendering of Intravascular Ultrasound Slices Imaged on a Curved Arterial Path." In Lecture Notes in Computer Science, 399–405. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-540-49197-2_50.

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Tomita, M., F. Gotoh, N. Tanahashi, M. Kobari, Y. Terayama, B. Mihara, and K. Ohta. "Intravascular RBC Aggregation and Transient Diminution of Cerebrovascular Volume Following Middle Cerebral Artery Occlusion in Cats." In Cerebral Ischemia and Hemorheology, 377–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71787-1_44.

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Buckmaster, Jonathan. "Intravascular Volume Depletion." In Critical Care Nephrology, 510–14. Elsevier, 2009. http://dx.doi.org/10.1016/b978-1-4160-4252-5.50101-5.

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Conference papers on the topic "Intravascular volume"

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Greitzer, Katya, and Ofer Barnea. "Intravascular blood volume estimation during fluid resuscitation." In 2012 IEEE 27th Convention of Electrical & Electronics Engineers in Israel (IEEEI 2012). IEEE, 2012. http://dx.doi.org/10.1109/eeei.2012.6377059.

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Xu, Mengdi, Jun Cheng, Jimmy Addison Lee, Damon Wing Kee Wong, Akira Taruya, Atsushi Tanaka, Nicolas Foin, and Philip Wong. "Automatic volume classification in intravascular optical coherence tomography images." In 2017 IEEE 2nd International Conference on Signal and Image Processing (ICSIP). IEEE, 2017. http://dx.doi.org/10.1109/siprocess.2017.8124532.

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Chen, Chi Hau, Labhesh Potdat, Rakesh Chittineni, Donald O. Thompson, and Dale E. Chimenti. "TWO NOVEL ACM (ACTIVE CONTOUR MODEL) METHODS FOR INTRAVASCULAR ULTRASOUND IMAGE SEGMENTATION." In REVIEW OF PROGRESS IN QUANTITATIVE NONDESTRUCTIVE EVALUATION VOLUME 29. AIP, 2010. http://dx.doi.org/10.1063/1.3362467.

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Latus, Sarah, Maximilian Neidhardt, Matthias Lutz, Nils Gessert, Norbert Frey, and Alexander Schlaefer. "Quantitative Analysis of 3D Artery Volume Reconstructions Using Biplane Angiography and Intravascular OCT Imaging." In 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857712.

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Malek, Adel M., and Alexandra Lauric. "CFD Challenge: Solutions Using the Commercial Finite Volume Solver Fluent on Tetrahedral and Polyhedral Meshes." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80938.

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Research by the Malek Computational Hemodynamics Laboratory has focused on using computational fluid dynamic (CFD) tools to gain an improved insight of the mechanical environment faced by endothelial cells in and around cerebrovascular atherosclerotic and aneurysmal lesions. More recently, we have been interested in studying the effect of endovascular therapies such as aneurysm-occluding coils and intravascular stents on local microhemodynamics.
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Dent, Paul, Bin Deng, Jerry Goodisman, Charles M. Peterson, Sriram Narsipur, and J. Chaiken. "Noninvasive in vivo plasma volume and hematocrit in humans: observing long-term baseline behavior to establish homeostasis for intravascular volume and composition." In SPIE Photonics Europe, edited by Jürgen Popp, Valery V. Tuchin, Dennis L. Matthews, and Francesco S. Pavone. SPIE, 2016. http://dx.doi.org/10.1117/12.2227981.

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Silva, Pedro L., Andreas Güldner, Christopher Uhlig, Nadja Cristinne S. Carvalho, Alessandro Beda, Ines Rentzsch, Michael Kasper, et al. "Effects Of Intravascular Volume Replacement On Lung Function And Damage In Non-Septic Experimental Lung Injury." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5238.

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Wu, Hao, Brendan L. Eck, Jacob Levi, Anas Fares, Hiram G. Bezerra, and David L. Wilson. "Quantitative estimation of flow rate to fill the intravascular volume (FRIV) for CT myocardial perfusion imaging." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor S. Gimi and Andrzej Krol. SPIE, 2020. http://dx.doi.org/10.1117/12.2549838.

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Klingensmith, Jon D., David G. Vince, Raj Shekhar, Barry D. Kuban, E. M. Tuzcu, and J. Fredrick Cornhill. "Quantification of coronary arterial plaque volume using 3D reconstructions formed by fusing intravascular ultrasound and biplane angiography." In Medical Imaging '99, edited by Chin-Tu Chen and Anne V. Clough. SPIE, 1999. http://dx.doi.org/10.1117/12.349604.

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Sun, Yi, and Ze Ye. "Distribution of intravascular and extravascular extracellular volume fractions for neovascularization assessment by dynamic contrast-enhanced magnetic resonance imaging." In 2012 IEEE Signal Processing in Medicine and Biology Symposium (SPMB). IEEE, 2012. http://dx.doi.org/10.1109/spmb.2012.6469466.

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