CENTRAL VENOUS PRESSURE AND DIRECT SERIAL MEASUREMENTS AS GUIDES IN BLOOD-VOLUME REPLACEMENT

The Lancet ◽  
1966 ◽  
Vol 288 (7464) ◽  
pp. 609-614 ◽  
Author(s):  
Edward Friedman ◽  
Ernest Grable ◽  
Jacob Fine
2012 ◽  
pp. 181-184 ◽  
Author(s):  
Johann Smith Ceron Arias ◽  
Manuel Felipe Muñoz Nañez

The determination of the values of central venous pressure has long been used as a guideline for volumetric therapy in the resuscitation of the critical patient, but the performance of such parameter is currently being questioned as an effective measurement of cardiac preload. This has aroused great interest in the search for more accurate parameters to determine cardiac preload and a patient’s blood volume. Goals and Methodology: Based on literature currently available, we aim to discuss the performance of central venous pressure as an effective parameter to determine cardiac preload. Results and Conclusion: Estimating variables such as end-diastolic ventricular area and global end-diastolic volume have a better performance than central venous pressure in determining cardiac preload. Despite the best performance of these devices, central venous pressure is still considered in our setting as the most practical and most commonly available way to assess the patient’s preload. Only dynamic variables such as pulse pressure change are superior in determining an individual’s blood volume.


PEDIATRICS ◽  
1976 ◽  
Vol 58 (4) ◽  
pp. 484-493
Author(s):  
Roderic H. Phibbs ◽  
Paul Johnson ◽  
Joseph A. Kitterman ◽  
George A. Gregory ◽  
William H. Tooley ◽  
...  

We measured aortic and central venous pressures beginning soon after birth in 40 prematurely born infants with moderate or severe erythroblastosis fetalis, including 13 with severe and 10 with mild hydrops fetalis. All but four were asphyxiated at birth and this affected intravascular pressures. Before resuscitation, aortic or central venous pressure or both were elevated in more than one third. All but two of the remaining infants had normal initial pressures. Following resuscitation which relieved acidosis, hypoxia, and anemia, but did not reduce blood volume, the high pressures usually fell to normal and occasionally to subnormal levels, normal pressures fell to subnormal in almost one half, and those with initial subnormal pressures remained hypotensive. In all, 40% were hypotensive after resuscitation; treatment with blood volume expanders consistently returned these pressures to normal. Only two of the 13 severely hydropic infants and none of the mildly hydropic had findings indicative of hypervolemia and myocardial failure which persisted after treatment of asphyxia.


2005 ◽  
Vol 25 (1) ◽  
pp. 136-143 ◽  
Author(s):  
Timothy D Wilson ◽  
J Kevin Shoemaker ◽  
R Kozak ◽  
T-Y Lee ◽  
Adrian W Gelb

Adrenergic nerves innervate the human cerebrovasculature, yet the functional role of neurogenic influences on cerebral hemodynamics remains speculative. In the current study, regional cerebrovascular responses to sympathoexcitatory reflexes were evaluated. In eight volunteers, contrast-enhanced computed tomography was performed at baseline, –40 mmHg lower body negative pressure (LBNP), and a cold pressor test (CPT). Cerebral blood volume (CBV), mean transit time (MTT), and cerebral blood flow (CBF) were evaluated in cortical gray matter (GM), white matter (WM), and basal ganglia/thalamus (BGT) regions. Lower body negative pressure resulted in tachycardia and decreased central venous pressure while mean arterial pressure was maintained. Cold pressor test resulted in increased mean arterial pressure concomitant with tachycardia but no change in central venous pressure. Neither reflex altered end-tidal carbon dioxide. Cerebral blood volume was reduced in GM during both LBNP and CPT ( P<0.05) but was unchanged in WM and BGT. Mean transit time was reduced in WM and GM during CPT ( P<0.05). Cerebral blood flow was only modestly affected with either reflex ( P<0.07). The combined reductions in GM CBV (˜ –25%) and MTT, both with and without any change in central venous pressure, with small CBF changes (˜ –11%), suggest that active venoconstriction contributed to the volume changes. These data demonstrate that CBV is reduced during engagement of sympathoexcitatory reflexes and that these cerebrovascular changes are heterogeneously distributed.


1995 ◽  
Vol 82 (4) ◽  
pp. 975-982. ◽  
Author(s):  
Wolfgang Funk ◽  
Verena Baldinger

Background Because of the passage of water and salt molecules into the interstitial space, volume replacement with crystalloid solutions requires an amount at least four times that of lost blood. The resulting tissue edema may interfere with nutritive capillary perfusion and oxygen delivery. To prove this hypothesis, the effects of isovolemic hemodilution (hematocrit 30%) with Ringer's lactate solution or dextran 60 on tissue perfusion and oxygenation were investigated in awake Syrian golden hamsters. Methods Experiments were performed by using a chronic dorsal skinfold window giving access to skeletal muscle tissue (musculus cutaneus) with in vivo microscopy, quantitative video image analysis, and surface oxygen partial pressure electrodes. Central venous and arterial pressures were measured by means of chronically implanted jugular venous and carotid catheters. Results Isovolemic exchange of blood with dextran caused no significant changes in arterial or central venous pressure, heart rate, capillary flow velocity, functional capillary density, or surface oxygen partial pressure during the 1-h observation period. A volume of Ringer's solution equal to four times of the amount of blood lost maintained arterial pressure and heart rate when central venous pressure was kept at predilution control values. However, tissue perfusion determined by counting perfused capillaries per terminal arteriole was reduced by 62%, and mean tissue oxygen partial pressure decreased from 19 to 8 mmHg. Conclusions In this model, volume replacement with artificial colloids yielded hemodynamic stability and adequate tissue oxygen supply, whereas administration of crystalloids alone jeopardized tissue perfusion and oxygenation.


The Lancet ◽  
1970 ◽  
Vol 296 (7685) ◽  
pp. 1252
Author(s):  
H.E. Eliahou ◽  
U. Weinberg ◽  
E. Reisin ◽  
A. Iaina ◽  
M. Ziperkowski

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