Blood volume, the venous system, preload, and cardiac output

1986 ◽  
Vol 64 (4) ◽  
pp. 383-387 ◽  
Author(s):  
Clive V. Greenway ◽  
W. Wayne Lautt
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Venous Pressure ◽  
Venous System ◽  
Right Atrial ◽  
Total Blood Volume ◽  
Total Blood ◽  
Stressed Volume ◽  
Unstressed Volume ◽  
Ventricular Compliance

Cardiac output is determined by heart rate, by contractility (maximum systolic elastance, Emax) and afterload, and by diastolic ventricular compliance and preload. These relationships are illustrated using the pressure–volume loop. Diastolic compliance and Emax place limits determined by the heart within which the pressure–volume loop must lie. End-diastolic and end-systolic pressures and hence the exact position of the loop within these limits are determined by the peripheral circulation. In the presence of minimal sympathetic tone, some 60% of total blood volume is hemodynamically inactive and constitutes a blood volume reserve (the unstressed volume). The remainder of the blood volume (the stressed volume) and the compliance of the venous system determine the venous pressure. This venous pressure together with venous resistance determines venous return, right atrial pressure, cardiac preload, and hence cardiac output. Venoconstriction causes conversion of unstressed volume to the stressed volume, the blood volume reserve is converted into hemodynamically active blood volume. After hemorrhage this replaces the lost stressed volume, while in other situations where total blood volume is not reduced, it allows a sustained increase in cardiac output. The major blood volume reserve is in the splanchnic bed: the liver and intestine, and in animals but not man, the spleen. A major unsolved problem is how the conversion of unstressed volume to stressed volume by venoconstriction is reflexly controlled.

Mechanism for decrease in cardiac output with atrial natriuretic peptide in dogs

1989 ◽  
Vol 256 (3) ◽  
pp. H760-H765 ◽  
Author(s):  
R. W. Lee ◽  
S. Goldman
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Right Atrial ◽  
Total Blood Volume ◽  
Total Blood ◽  
Atrial Natriuretic

To examine the mechanism by which atrial natriuretic peptide (ANP) decreases cardiac output, we studied changes in the heart, peripheral circulation, and blood flow distribution in eight dogs. ANP was given as a bolus (3.0 micrograms/kg) followed by an infusion of 0.3 microgram.kg-1.min-1. ANP did not change heart rate, total peripheral vascular resistance, and the first derivative of left ventricular pressure but decreased mean aortic pressure from 91 +/- 4 to 76 +/- 3 mmHg (P less than 0.001) and cardiac output from 153 +/- 15 to 130 +/- 9 ml.kg-1.min-1 (P less than 0.02). Right atrial pressure and left ventricular end-diastolic pressure also decreased. Mean circulatory filling pressure decreased from 7.1 +/- 0.3 to 6.0 +/- 0.3 mmHg (P less than 0.001), but venous compliance and unstressed vascular volume did not change. Resistance to venous return increased from 0.056 +/- 0.008 to 0.063 +/- 0.010 mmHg.ml-1.kg.min (P less than 0.05). Arterial compliance increased from 0.060 +/- 0.003 to 0.072 +/- 0.004 ml.mmHg-1.kg-1 (P less than 0.02). Total blood volume and central blood volume decreased from 82.2 +/- 3.1 to 76.2 +/- 4.6 and from 19.8 +/- 0.8 to 17.6 +/- 0.6 ml/kg (P less than 0.02), respectively. Blood flow increased to the kidneys. We conclude that ANP decreases cardiac output by decreasing total blood volume. This results in a lower operating pressure and volume in the venous capacitance system with no significant venodilating effects. Cardiac factors and a redistribution of flow to the splanchnic organs are not important mechanisms to explain the decrease in cardiac output with ANP.

Observations on Cardiac Output and ”Pulmonary Blood Volume” in Normal Man by External Recording of the Intracardiac Flow of 131I Labelled Albumin

1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Normal Subjects ◽  
Published Data ◽  
Total Blood Volume ◽  
Total Blood ◽  
Pulmonary Blood Volume ◽  
Intracardiac Flow ◽  
Normal Man ◽  
Mean Circulation

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.

Circulation of sympathectomized dogs under pentobarbital anesthesia

1965 ◽  
Vol 208 (4) ◽  
pp. 790-794
Author(s):  
Shu Chien ◽  
Shunichi Usami
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Blood Volume ◽  
Total Blood Volume ◽  
Central Blood Volume ◽  
Total Blood ◽  
Pentobarbital Anesthesia ◽  
Blood Flows ◽  
The Mean ◽  
Mean Circulation

In sympathectomized-splenectomized dogs under pentobarbital anesthesia, the total blood volume averaged 78 ml/kg, with 20% in the splanchnic circulation and 28% in the central blood volume. These values are almost the same as those found in the splenectomized (control) dogs with the sympathetic system intact. The over-all and the splanchnic Fcells factors are also not significantly different between these two groups. The sympathectomized animals had lower arterial pressure, cardiac output, and splanchnic blood flow, but the resistances calculated for the total and the splanchnic circulations were not significantly different from those of the control dogs. The mean circulation times for the total, the central, and the splanchnic circulations were all longer in the sympathectomized dogs. The data indicate that, under pentobarbital anesthesia, sympathectomized dogs are characterized by slower blood flows without any significant changes in either the blood volume or vascular resistance.

The Meaning of Dopamine β-Hydroxylase in Essential Hypertension

1975 ◽  
Vol 49 (6) ◽  
pp. 573-579
Author(s):  
J. M. Alexandre ◽  
G. M. London ◽  
C. Chevillard ◽  
P. Lemaire ◽  
M. E. Safar ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Healthy Subjects ◽  
Volume Ratio ◽  
Total Blood Volume ◽  
Total Blood ◽  
Hypertensive Patients ◽  
Borderline Hypertension ◽  
Haemodynamic Parameters ◽  
Apparently Healthy

1. Resting plasma dopamine β-hydroxylase (DBH) activity and haemodynamic parameters were studied in untreated borderline (twenty-nine) and permanent (twenty-seven) essential hypertensive patients. DBH was also measured in sixty-three apparently healthy subjects. 2. Mean DBH values were not significantly different between the groups. 3. Cardiac output, cardiopulmonary blood volume and the cardiopulmonary blood volume/total blood volume ratio (CPBV/TBV) were significantly higher in borderline than in permanent hypertensive patients. 4. In borderline hypertensive patients, plasma DBH activity was directly correlated with diastolic arterial pressure and with values of cardiac output, cardiopulmonary blood volume and CPBV/TBV ratio. No such correlations could be observed in the permanent hypertensive group. 5. These results suggest that plasma DBH activities in borderline hypertension mainly depend on the sympathetic activity responsible for the haemodynamic variations. Contrariwise, plasma DBH activities in permanent essential hypertensive patients appear to reflect other factors.

scholarly journals Venous return and clinical hemodynamics: how the body works during acute hemorrhage

2015 ◽  
Vol 39 (4) ◽  
pp. 267-271 ◽  
Author(s):  
Tao Shen ◽  
Keith Baker
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Venous Return ◽  
Venous Pressure ◽  
The Body ◽  
Venous System ◽  
Effective Mechanism ◽  
Acute Hemorrhage ◽  
Two Factors ◽  
Circulating Volume

Venous return is a major determinant of cardiac output. Adjustments within the venous system are critical for maintaining venous pressure during loss in circulating volume. This article reviews two factors that are thought to enable the venous system to compensate during acute hemorrhage: 1) changes in venous elastance and 2) mobilization of unstressed blood volume into stressed blood volume. We show that mobilization of unstressed blood volume is the predominant and more effective mechanism in preserving venous pressure. Preservation of mean circulatory filling pressure helps sustain venous return and thus cardiac output during significant hemorrhage.

scholarly journals Understanding basic vein physiology and venous blood pressure through simple physical assessments

2019 ◽  
Vol 43 (3) ◽  
pp. 423-429 ◽  
Author(s):  
Etain A. Tansey ◽  
Laura E. A. Montgomery ◽  
Joe G. Quinn ◽  
Sean M. Roe ◽  
Christopher D. Johnson
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Central Venous Pressure ◽  
Venous Return ◽  
Venous Pressure ◽  
Venous Blood ◽  
Venous System ◽  
Arterial System ◽  
Right Atrial ◽  
Central Venous

An understanding of the complexity of the cardiovascular system is incomplete without a knowledge of the venous system. It is important for students to understand that, in a closed system, like the circulatory system, changes to the venous side of the circulation have a knock-on effect on heart function and the arterial system and vice versa. Veins are capacitance vessels feeding blood to the right side of the heart. Changes in venous compliance have large effects on the volume of blood entering the heart and hence cardiac output by the Frank-Starling Law. In healthy steady-state conditions, venous return has to equal cardiac output, i.e., the heart cannot pump more blood than is delivered to it. A sound understanding of the venous system is essential in understanding how changes in cardiac output occur with changes in right atrial pressure or central venous pressure, and the effect these changes have on arterial blood pressure regulation. The aim of this paper is to detail simple hands-on physiological assessments that can be easily undertaken in the practical laboratory setting and that illustrate some key functions of veins. Specifically, we illustrate that venous valves prevent the backflow of blood, that venous blood pressure increases from the heart to the feet, that the skeletal muscle pump facilitates venous return, and we investigate the physiological and clinical significance of central venous pressure and how it may be assessed.

Alterations in Cardiac Function and Cardiopulmonary Blood Volume in Chronic Sodium Depletion in Dogs

1980 ◽  
Vol 59 (s6) ◽  
pp. 393s-395s ◽  
Author(s):  
M. P. Lynn ◽  
F. Fouad ◽  
S. A. Cook ◽  
Carmen A. Napoli ◽  
C. M. Ferrario
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Pressor Response ◽  
Vagal Afferents ◽  
Dietary Sodium ◽  
Total Blood Volume ◽  
Sodium Depletion ◽  
Vagus Nerves ◽  
Total Blood ◽  
Ventricular Performance

1. Chronic sodium depletion in dogs is associated with a blunting of the pressor response to carotid occlusion. After section of the vagus nerves this pressor response reverts to normal although atropine is without effect, suggesting a possible role for increased activity of cardiopulmonary vagal afferents in suppressing sympathetic outflow. Since increases in central blood volume stimulate vagal afferents, cardiopulmonary haemodynamics were studied by radioisotope dilution before and after 3 and 4 weeks of dietary sodium restriction together with frusemide. 2. Sodium depletion was associated with significant decreases in cardiac output, ejection fraction and total blood volume; the cardiopulmonary blood volume increased but the change was not statistically significant (P<0.2). These changes were accompanied by a significant increase in the ratio cardiopulmonary blood volume/total blood volume and a decrease in the ratio cardiac output/cardiopulmonary blood volume. 3. Results indicate that sodium depletion may be accompanied by a paradoxical translocation of blood to the cardiopulmonary region in part due to depressed ventricular performance.

A588 DETERMINATION OF TOTAL BLOOD VOLUME (TBV) FROM CARDIAC OUTPUT AND MEAN CIRCULATION TIME

1997 ◽  
Vol 87 (Supplement) ◽  
pp. 588A
Author(s):  
Gotz Wietasch ◽  
Thomas Scheeren ◽  
Andreas Hoeft ◽  
Joachim O. Arndt
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Circulation Time ◽  
Total Blood Volume ◽  
Total Blood ◽  
Mean Circulation
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