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.

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.

Cardiac output, GFR, and renal excretion rates during maintained volume load in rats

1978 ◽  
Vol 235 (6) ◽  
pp. H670-H676 ◽  
Author(s):  
U. Ackermann
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Renal Excretion ◽  
Venous Pressure ◽  
Circulating Blood Volume ◽  
Reservoir Volume ◽  
Volume Load ◽  
Blood Volume Expansion ◽  
Highly Correlated ◽  
Excretion Rates

The correlation among cardiac output (CO), glomerular filtration rate (GFR), fractional tubular sodium rejection (TFRNa), and renal excretion rates of water and salt was investigated during ischemic blood volume expansion in rats. Initially circulating blood volume was equilibrated isovolemically with a reservoir volume of 6% albumin solution equal to one-third the estimated blood volume. Later the equilibrated reservoir contents were infused intravenously. CO was measured by thermodilution, GFR by inulin clearance. Significant linear correlations existed between GFR and the rates of urine flow (r = 0.90), sodium excretion (r = 0.75) and potassium excretion (r = 0.76) that prevailed 5--10 min after a given GFR change. The increased GFR was highly correlated with CO (r = 0.94), probably correlated with mean central venous pressure (r = 0.45), but not correlated with mean abdominal aortic blood pressure. The correlation between CO and time-delayed (5--10 min) TRFNa was also highly significant (r = 0.98). The saluresis appears to have been caused initially by increased tubular load and subsequently by decreased absolute tubular reabsorption.

ASSESSMENT OF THE MATERNAL VENOUS CIRCULATION: WHY IS IT RELEVANT?

2013 ◽  
Vol 24 (3) ◽  
pp. 194-199
Author(s):  
KATHLEEN TOMSIN ◽  
WILFRIED GYSELAERS
Keyword(s):  
Cardiac Output ◽  
Organ Dysfunction ◽  
Venous Return ◽  
Cardiovascular Disorder ◽  
Systemic Circulation ◽  
Renal Vein Thrombosis ◽  
Venous System ◽  
Total Blood ◽  
Venous Circulation ◽  
Cardiovascular Assessment

The venous system is considered the main capacitor of the human body. Approximately 70% of the total blood volume resides in the venous bed, half of which circulates as venous return whereas the other half functions as reserve volume in the splanchnic veins. These veins are richly innervated and highly compliant, and communicate with the systemic circulation via capillaries (entrance) and portal vein and liver (exit). This constitution allows the venous compartment to balance circulating and stored blood volumes, and thus control cardiac output. Clinical conditions with reduced cardiac output are often associated with hampered venous return, resulting in visceral oedema, ascites or organ dysfunction. Organ dysfunction or failure may also result from (sub)obstructed venous outflow, as is illustrated in renal vein thrombosis or in the Nutcracker syndrome. Recently, the application of Doppler ultrasonography in the study of the maternal venous system illustrated that preeclampsia is another cardiovascular disorder with dysfunctional venous haemodynamics. In this opinion paper, we summarise results from Doppler studies of the maternal venous compartment, illustrating that performing venous haemodynamics function tests is to become a fundamental part of an integrated cardiovascular assessment of women with hypertension in pregnancy, facilitating an individualised diagnostic and therapeutic approach for every woman at risk for gestational hypertensive disease.

Atrial natriuretic peptide increases resistance to venous return in rats

1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Total Peripheral Resistance ◽  
Venous Return ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Atrial Natriuretic

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.

Contractility–afterload mismatch after the Fontan operation

2005 ◽  
Vol 15 (S3) ◽  
pp. 35-38 ◽  
Author(s):  
Gábor Szabó ◽  
Susanne Bährle
Keyword(s):  
Cardiac Output ◽  
Therapeutic Option ◽  
Fontan Operation ◽  
Venous Pressure ◽  
Peripheral Circulation ◽  
Good Prognosis ◽  
Fontan Circulation ◽  
The Body ◽  
Inadequate Response ◽  
Mechanical Coupling

During the past decades, different variants of the Fontan circulation have become the primary therapeutic option for physiological correction of congenital cardiac malformations in which restoration to biventricular circulations is impossible. Subsequent to creation of the Fontan circulation, the pulmonary and systemic circulations are in series, with only one pumping chamber. Thus, the functionally single ventricle must provide energy for flow of blood to the lungs, as well as to the body. Generally, patients who have undergone these procedures have a good prognosis, although they have subnormal cardiac output at rest, while their central venous pressure is significantly elevated. Despite an adequate haemodynamic situation at rest, exercise performance is usually reduced. Thus far, this reduction has been attributed to cardiac factors, such as the absence of the morphologically right ventricle, or impaired function of the morphologically left ventricle. Due to the mechanical coupling between the heart and the peripheral circulation, however, the inadequate response to exercise in terms of cardiac output might also be dependant on insufficient peripheral vascular adjustments. In this review, we assess the existing experimental and clinical studies which provide detailed analysis of ventriculo-arterial mechanics in the setting of the Fontan circulation.

Effects of heat stress on vascular capacitance

1994 ◽  
Vol 266 (5) ◽  
pp. H2122-H2129 ◽  
Author(s):  
A. Deschamps ◽  
S. Magder
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Heat Stress ◽  
Blood Volume ◽  
Adrenergic Receptor ◽  
Venous Return ◽  
Receptor Blockade ◽  
Ganglionic Blockade ◽  
Unstressed Volume ◽  
Adrenergic Receptor Blockade

In dogs and humans, heat stress is associated with an increase in cardiac output that sustains blood flow to heat-dissipating organs. Because cardiac output and venous return are equal in the steady state, the circulation must also adjust in heat stress to allow the venous return to increase. To analyze these adjustments, we measured blood volumes, unstressed volumes, blood flow distribution, venous compliance, venous resistance, and the time constant of venous drainage of the splanchnic and extrasplanchnic vascular beds in dogs anesthetized with alpha-chloralose at normal and at high core temperatures. We repeated the measurements at high core temperatures with ganglionic blockade, alpha-adrenergic receptor blockade, or beta-adrenergic receptor blockade to determine the efferent neurohumoral pathway. When core temperature was increased from 37.8 +/- 0.2 to 41.9 +/- 0.1 degrees C, total splanchnic blood volume decreased 23% (4.6 +/- 1.4 ml/kg) and splanchnic unstressed volume decreased 38.5%. None of the other determinants of venous return changed. Ganglionic blockade shifted the total and unstressed splanchnic blood volume during heat stress back to normothermic values. However, beta- and alpha-blockade did not affect splanchnic volumes. We conclude that a decrease in splanchnic unstressed volume is an important factor for the increased venous return during heat stress. Although mediated through sympathetic ganglions, this decrease is not abolished by alpha- or beta-receptor blockade.

Splanchnic and systemic haemodynamic response to volume changes in patients with cirrhosis and portal hypertension

1999 ◽  
Vol 96 (5) ◽  
pp. 475-481 ◽  
Author(s):  
Panagiotis VLAVIANOS ◽  
Padraik MAC MATHUNA ◽  
Roger WILLIAMS ◽  
David WESTABY
Keyword(s):  
Cardiac Output ◽  
Portal Hypertension ◽  
Systemic Vascular Resistance ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Haemodynamic Response ◽  
Volume Depletion ◽  
Compensated Cirrhosis

We investigated the haemodynamic response to volume depletion and subsequent repletion in patients with cirrhosis and portal hypertension. Twelve patients with compensated cirrhosis and portal hypertension were included in the study. The haemodynamic changes occurring after removal of approx. 15% of the blood volume, and subsequently after isovolume repletion with colloid, were assessed. Baseline haemodynamic measurements showed increased cardiac output and a systemic vascular resistance at the lower limit of normal. The hepatic venous pressure gradient (HVPG) was increased, at 18 mmHg. After depletion, arterial pressure, cardiac output and all right-heart-sided pressures decreased, and systemic vascular resistance increased. HVPG decreased to 16.0 mmHg. All the above changes were statistically significant. After blood volume restitution, the haemodynamic values returned to baseline. In particular, an increase in HVPG was shown in four out of the twelve patients (two with ascites and two without), which was small in three of them. However, HVPG remained the same as or lower than the baseline in the other eight patients. Patients with cirrhosis and portal hypertension exhibit an abnormal haemodynamic response to blood volume depletion. After volume repletion, no increase in the portal pressure was noted in this group of patients as a whole, although four out of the twelve patients did show an increase, possibly due to extensive collateral circulation.

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