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 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.

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.

Cardiovascular actions of histamine and potassium

1959 ◽  
Vol 197 (5) ◽  
pp. 1005-1007 ◽  
Author(s):  
Calvin Hanna ◽  
Patricia B. McHugo ◽  
William H. MacMillan
Keyword(s):  
Cardiac Output ◽  
Central Venous Pressure ◽  
Potassium Chloride ◽  
Venous Pressure ◽  
Plasma Potassium ◽  
Dilution Method ◽  
Cardiac Rate ◽  
Central Venous ◽  
Arterial Blood ◽  
Cardiovascular Actions

The cardiovascular actions of intravenous histamine, in doses from 2.5 to 20 µg/kg of the free base, were studied in the pentobarbitalized dog using the dye dilution method. With the small dose there was a consistent but small initial increase in cardiac output and with the larger doses there was a biphasic change in output. Cardiac rate, central venous pressure, central blood volume, hematocrit and the mean circulation time were essentially unchanged. Infusions of histamine and of potassium chloride at the rate of 1 µg and 1 mg/kg/min., respectively, moderately increased the cardiac output. Potassium chloride had no effect on the arterial blood pressure, cardiac rate and central venous pressure. Both the infusion of potassium chloride and injection of histamine produced a comparable elevation of the plasma potassium. It is possible that the actions of histamine to increase the plasma potassium contribute to the cardiovascular actions of this amine, especially on the cardiac output.

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

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