Correlations between cardiac output, stroke volume, central venous pressure, intra-abdominal pressure and total circulating blood volume in resuscitation of major burns

Resuscitation ◽  
2006 ◽  
Vol 70 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Markus V. Küntscher ◽  
Günter Germann ◽  
Bernd Hartmann
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Blood Volume ◽  
Venous Pressure ◽  
Abdominal Pressure ◽  
Central Venous ◽  
Circulating Blood Volume

Does Central Venous Pressure Reflect the Circulating Blood Volume for the Decrement of Compliance Just After Esophagectomy?

Surgery Today ◽  
2000 ◽  
Vol 30 (1) ◽  
pp. 11-15 ◽  
Author(s):  
Satoru Motoyama ◽  
Michihiko Kitamura ◽  
Satoshi Kibira ◽  
Hiroyuki Suzuki ◽  
Shuichi Kamata ◽  
...  
Keyword(s):  
Central Venous Pressure ◽  
Blood Volume ◽  
Venous Pressure ◽  
Central Venous ◽  
Circulating Blood Volume

scholarly journals Central venous pressure and cardiac function during spaceflight

1998 ◽  
Vol 85 (2) ◽  
pp. 738-746 ◽  
Author(s):  
Ronald J. White ◽  
C. Gunnar Blomqvist
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Shape Change ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Reference Measurements

Early in spaceflight, an apparently paradoxical condition occurs in which, despite an externally visible headward fluid shift, measured central venous pressure is lower but stroke volume and cardiac output are higher, and heart rate is unchanged from reference measurements made before flight. This paper presents a set of studies in which a simple three-compartment, steady-state model of cardiovascular function is used, providing insight into the contributions made by the major mechanisms that could be responsible for these events. On the basis of these studies, we conclude that, during weightless spaceflight, the chest relaxes with a concomitant shape change that increases the volume of the closed chest cavity. This leads to a decrease in intrapleural pressure, ultimately causing a shift of blood into the vessels of the chest, increasing the transmural filling pressure of the heart, and decreasing the central venous pressure. The increase in the transmural filling pressure of the heart is responsible, through a Starling-type mechanism, for the observed increases in heart size, left ventricular end-diastolic volume, stroke volume, and cardiac output.

Effects of the Third (Aqueous) Extract of Ginseng on the Cardiovascular Dynamics of Dogs During Halothane Anesthesia

1978 ◽  
Vol 06 (03) ◽  
pp. 253-259
Author(s):  
DONALD H. CLIFFORD ◽  
DO CHIL LEE ◽  
CHONG YUL KIM ◽  
MYUNG O. LEE
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Aqueous Extract ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Central Venous ◽  
Cardiovascular Variables

An electromagnetic flowmeter probe was chronically implanted around the ascending aorta in a group of dogs. Subsequently, ten dogs were lightly anesthetized with halothane (0.75%), and a third (aqueous) extract of ginseng (40 mg/kg) was administered intravenously. Five dogs were anesthesized without the administration of ginseng. Eleven cardiovascular variables including cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2, and base deficit were compared. The cardiac output, stroke volume, and central venous pressure were decreased significantly, while total peripheral resistance was increased significantly following ginseng.

Changes in cardiac output, stroke volume, and central venous pressure induced by atropine in man

1959 ◽  
Vol 58 (2) ◽  
pp. 204-213 ◽  
Author(s):  
J.Norman Berry ◽  
Howard K. Thompson ◽  
D.Edmond Miller ◽  
Henry D. McIntosh
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Central Venous

Cardiac remodeling and increased central venous pressure underlie elevated stroke volume and cardiac output of seawater-acclimated rainbow trout

2017 ◽  
Vol 312 (1) ◽  
pp. R31-R39 ◽  
Author(s):  
Jeroen Brijs ◽  
Erik Sandblom ◽  
Esmée Dekens ◽  
Joacim Näslund ◽  
Andreas Ekström ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Gastrointestinal Blood Flow ◽  
Cardiac Filling

Substantial increases in cardiac output (CO), stroke volume (SV), and gastrointestinal blood flow are essential for euryhaline rainbow trout ( Oncorhyncus mykiss) osmoregulation in seawater. However, the underlying hemodynamic mechanisms responsible for these changes are unknown. By examining a range of circulatory and cardiac morphological variables of seawater- and freshwater-acclimated rainbow trout, the present study revealed a significantly higher central venous pressure (CVP) in seawater-acclimated trout (~0.09 vs. −0.02 kPa). This serves to increase cardiac end-diastolic volume in seawater and explains the elevations in SV (~0.41 vs. 0.27 ml/kg) and CO (~21.5 vs. 14.2 ml·min−1·kg−1) when compared with trout in freshwater. Furthermore, these hemodynamic modifications coincided with a significant increase in the proportion of compact myocardium, which may be necessary to compensate for the increased wall tension associated with a larger stroke volume. Following a temperature increase from 10 to 16.5°C, both acclimation groups exhibited similar increases in heart rate (Q10 of ~2), but SV tended to decrease in seawater-acclimated trout despite the fact that CVP was maintained in both groups. This resulted in CO of seawater- and freshwater-acclimated trout stabilizing at a similar level after warming (~26 ml·min−1·kg−1). The consistently higher CVP of seawater-acclimated trout suggests that factors other than compromised cardiac filling constrained the SV and CO of these individuals at high temperatures. The present study highlights, for the first time, the complex interacting effects of temperature and water salinity on cardiovascular responses in a euryhaline fish species.

scholarly journals Should we stop using the determination of central venous pressure as a way to estimate cardiac preload?

2012 ◽  
pp. 181-184 ◽  
Author(s):  
Johann Smith Ceron Arias ◽  
Manuel Felipe Muñoz Nañez
Keyword(s):  
Central Venous Pressure ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Pressure Change ◽  
Cardiac Preload ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Dynamic Variables

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.

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