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.

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.

Acute plasma expansion: left ventricular hemodynamics and endocrine function during exercise

1992 ◽  
Vol 73 (5) ◽  
pp. 1791-1796 ◽  
Author(s):  
I. L. Kanstrup ◽  
J. Marving ◽  
P. F. Hoilund-Carlsen
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Healthy Subjects ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Endocrine Function ◽  
Plasma Expansion ◽  
Central Venous ◽  
Mean Pressure ◽  
Dextran Solution

In 11 healthy subjects (8 males and 3 females, age 21–59 yr) left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volumes were measured in the supine position by isotope cardiography at rest and during two submaximal one-legged exercise loads before and 1 h after acute plasma expansion (PE) by use of a 6% dextran solution (500–750 ml). After PE, blood volume increased from 5.22 +/- 0.92 to 5.71 +/- 1.02 (SD) liters (P < 0.01). At rest, cardiac output increased 30% (5.3 +/- 1.0 to 6.9 +/- 1.6 l/min; P < 0.01), stroke volume increased from 90 +/- 20 to 100 +/- 28 ml (P < 0.05), and LVEDV increased from 134 +/- 29 to 142 +/- 40 ml (NS). LVESV was unchanged (44 +/- 11 and 42 +/- 14 ml). Heart rate rose from 60 +/- 7 to 71 +/- 10 beats/min (P < 0.01). The cardiac preload [central venous pressure (CVP)] was insignificantly elevated (4.9 +/- 2.1 and 5.3 +/- 3.0 mmHg); systemic vascular resistance and arterial pressures were significantly reduced (mean pressure fell from 91 +/- 11 to 85 +/- 11 mmHg, P < 0.01). Left ventricular peak filling and peak ejection rates both increased (19 and 14%, respectively; P < 0.05). During exercise, cardiac output remained elevated after PE compared with the control situation, predominantly due to a 10- to 14-ml rise in stroke volume caused by an increased LVEDV, whereas LVESV was unchanged. CVP increased after PE by 2.1 and 3.0 mmHg, respectively (P < 0.05).2+ remained unchanged during exercise compared with rest after PE in

Central venous pressure in space

1996 ◽  
Vol 81 (1) ◽  
pp. 19-25 ◽  
Author(s):  
J. C. Buckey ◽  
F. A. Gaffney ◽  
L. D. Lane ◽  
B. D. Levine ◽  
D. E. Watenpaugh ◽  
...  
Keyword(s):  
Central Venous Pressure ◽  
Space Shuttle ◽  
Venous Pressure ◽  
Life Sciences ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Fluid Distribution ◽  
Central Venous ◽  
Cardiac Filling Pressure ◽  
Cardiac Filling

Gravity affects cardiac filling pressure and intravascular fluid distribution significantly. A major central fluid shift occurs when all hydrostatic gradients are abolished on entry into microgravity (microG). Understanding the dynamics of this shift requires continuous monitoring of cardiac filling pressure; central venous pressure (CVP) measurement is the only feasible means of accomplishing this. We directly measured CVP in three subjects: one aboard the Spacelab Life Sciences-1 space shuttle flight and two aboard the Spacelab Life Sciences-2 space shuttle flight. Continuous CVP measurements, with a 4-Fr catheter, began 4 h before launch and continued into microG. Mean CVP was 8.4 cmH2O seated before flight, 15.0 cmH2O in the supine legs-elevated posture in the shuttle, and 2.5 cmH2O after 10 min in microG. Although CVP decreased, the left ventricular end-diastolic dimension measured by echocardiography increased from a mean of 4.60 cm supine preflight to 4.97 cm within 48 h in microG. These data are consistent with increased cardiac filling early in microG despite a fall in CVP, suggesting that the relationship between CVP and actual transmural left ventricular filling pressure is altered in microG.

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

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.

Systemic filling pressure in intact circulation determined on basis of aortic vs. central venous pressure relationships

1994 ◽  
Vol 267 (6) ◽  
pp. H2255-H2258 ◽  
Author(s):  
E. A. Den Hartog ◽  
A. Versprille ◽  
J. R. Jansen
Keyword(s):  
Central Venous Pressure ◽  
Flow Resistance ◽  
Venous Pressure ◽  
Aortic Pressure ◽  
Filling Pressure ◽  
Central Venous ◽  
Mean Systemic Filling Pressure ◽  
Systemic Filling ◽  
The Mean ◽  
Systemic Filling Pressure

In the intact circulation, mean systemic filling pressure (Psf) is determined by applying a series of inspiratory pause procedures (IPPs) and using Guyton's equation of venous return (Qv) and central venous pressure (Pcv): Qv = a - b x Pcv. During an IPP series, different tidal volumes are applied to set Pcv at different values. From the linear regression between Qv and Pcv, Psf can be calculated as Psf = a/b. Guyton's equation can also be written as Qv = (Psf - Pcv)/Rsd, where Rsd is the flow resistance downstream of the places where blood pressure is equal to Psf. During an IPP, a steady state is observed. Therefore, we can also formulate the following equation for flow: Qs = (Pao - Psf)/Rsu, where Qs is systemic flow, Rsu is the systemic flow resistance upstream to Psf, and Pao is aortic pressure. Because both flows (Qs and Qv) are equal, it follows that Pao = Psf(1 + Rsu/Rsd) - Rsu/Rsd x Pcv. This equation implies a method to determine mean systemic filling pressure on the basis of Pao measurements instead of flow determinations. Using 22 IPPs in 10 piglets, we determined the mean systemic filling pressure, and we compared the values obtained from the flow curves with those obtained from the aortic pressure curves. The mean difference between the two methods was 0.03 +/- 1.16 mmHg. With the use of Pao measurements, the Psf can be estimated as accurately as in using flow determinations. The advantage of the new method is that estimation of cardiac output is not required.

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