Measurement of limb venous compliance in humans: technical considerations and physiological findings

1999 ◽  
Vol 87 (4) ◽  
pp. 1555-1563 ◽  
Author(s):  
John R. Halliwill ◽  
Christopher T. Minson ◽  
Michael J. Joyner
Keyword(s):  
Cuff Pressure ◽  
Venous Pressure ◽  
Regression Line ◽  
Random Order ◽  
Sympathetic Activation ◽  
Quadratic Regression ◽  
Venous Compliance ◽  
Sympathetic Control ◽  
Unstressed Volume ◽  
Ischemic Handgrip Exercise

We conducted a series of studies to develop and test a rapid, noninvasive method to measure limb venous compliance in humans. First, we measured forearm volume (mercury-in-Silastic strain gauges) and antecubital intravenous pressure during inflation of a venous collecting cuff around the upper arm. Intravenous pressure fit the regression line, −0.3 ± 0.7 + 0.95 ± 0.02 ⋅ cuff pressure ( r = 0.99 ± 0.00), indicating cuff pressure is a good index of intravenous pressure. In subsequent studies, we measured forearm and calf venous compliance by inflating the venous collecting cuff to 60 mmHg for 4 min, then decreasing cuff pressure at 1 mmHg/s (over 1 min) to 0 mmHg, using cuff pressure as an estimate of venous pressure. This method produced pressure-volume curves fitting the quadratic regression (Δlimb volume) = β0 + β1 ⋅ (cuff pressure) + β2 ⋅ (cuff pressure)2, where Δ is change. Curves generated with this method were reproducible from day to day (coefficient of variation: 4.9%). In 11 subjects we measured venous compliance via this method under two conditions: with and without (in random order) superimposed sympathetic activation (ischemic handgrip exercise to fatigue followed by postexercise ischemia). Calf and forearm compliance did not differ between control and sympathetic activation ( P > 0.05); however, the data suggest that unstressed volume was reduced by the maneuver. These studies demonstrate that venous pressure-volume curves can be generated both rapidly and noninvasively with this technique. Furthermore, the results suggest that although whole-limb venous compliance is under negligible sympathetic control in humans, unstressed volume can be affected by the sympathetic nervous system.

scholarly journals Venous response to orthostatic stress

2008 ◽  
Vol 295 (4) ◽  
pp. H1587-H1593 ◽  
Author(s):  
Ineke Krabbendam ◽  
Loes C. A. Jacobs ◽  
Fred K. Lotgering ◽  
Marc E. A. Spaanderman
Keyword(s):  
Supine Position ◽  
Sympathetic Activity ◽  
Autonomic Function ◽  
Cuff Pressure ◽  
Venous Occlusion ◽  
Quadratic Regression ◽  
Venous Compliance ◽  
Time Curve ◽  
Pressure Time ◽  
Head Up Tilt

Head-up tilt (HUT) induces a reduction in preload, which is thought to be restored through sympathetic venoconstriction, reducing unstressed volume (Vu) and venous compliance (VeC). In this study, we assessed venous inflow and outflow responses and their reproducibility and determined the relation with autonomic function during HUT. Eight healthy non-pregnant women were subjected to 20° head-down tilt to 60° HUT at 20° intervals. At each rotational step, we randomly assessed forearm pressure-volume (P-V) curves (venous occlusion plethysmography) during inflow (VeCIN) and outflow [venous emptying rate (VEROUT)]. VeCIN was defined as the ratio of the slope of the volume-time curve and pressure-time curve, with direct intravenous pressure measurement. VEROUT was determined using the derivate of a quadratic regression model using cuff pressure. We defined Vu as the y-intercept of the P-V curve. We calculated, for both methods, the coefficients of reproducibility (CR) and variation (CV). Vascular sympathetic activity was determined by spectral analysis. VeCIN decreased at each rotational step compared with the supine position ( P < 0.05), whereas VEROUT increased. CR of VeCIN was higher in the supine position than VEROUT but lower during HUT. CV varied between 19% and 25% (VeCIN) and between 12% and 21% (VEROUT). HUT decreased Vu. The change in VeCIN and VEROUT correlated with the change in vascular sympathetic activity ( r = −0.36, P < 0.01, and r = 0.48, P < 0.01). This is the first study in which a reproducible reduction in VeCIN and Vu and a rise in VEROUT during HUT are documented. The alterations in venous characteristics relate to changes in vascular sympathetic activity.

A further analysis of why pulmonary venous pressure rises after the onset of LV dysfunction

2009 ◽  
Vol 106 (1) ◽  
pp. 81-90 ◽  
Author(s):  
S. Magder ◽  
S. Veerassamy ◽  
J. H. T. Bates
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Computational Model ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Venous Compliance ◽  
Stressed Volume ◽  
Lv Dysfunction ◽  
Arterial Blood ◽  
Unstressed Volume

Based on a dynamic computational model of the circulation, Burkhoff and Tyberg ( Am J Physiol Heart Circ Physiol 265: H1819–H1828, 1993) concluded that the rise in pulmonary venous pressure (Pvp) with left ventricular (LV) dysfunction requires a decrease in vascular capacitance and transfer of unstressed volume to stressed volume (ν). We argue that the values they used for venous resistance (Rvs), venous compliance (Cvs), and ν were too low, and changing these values significantly changes the conclusion. We used a computational model of the circulation that was similar to theirs, but we made Rvs four times higher (0.06 versus 0.015 mmHg·s·ml−1), Cvs larger (110 versus 70 ml/mmHg), and ν larger (1,400 versus 750 ml); all other parameters, including those for the heart, were essentially the same. We simulated left ventricular dysfunction by decreasing end-systolic elastance (Eeslv) as they did and examined changes in cardiac output, arterial blood pressure, and Pvp. We then examined the effect of changes in Rvs, heart rate, and ν when Eeslv was depressed with and without pericardial constraint. In contrast to their findings, with our parameters the model predicts that decreasing Eeslv substantially increases Pvp. Furthermore, increasing systemic vascular resistance or decreasing Rvs or heart rate produces large increases in Pvp when Eeslv is reduced. Pericardial constraint limits the changes in Pvp. In conclusion, when Rvs and Cvs are increased, baseline ν must be higher to maintain normal cardiac output. This increased volume can shift between compartments under flow conditions and account for the increase in Pvp with decreased left ventricular function even without recruitment of unstressed volume.

ANF does not increase total body venous compliance in conscious rats with myocardial infarction

1992 ◽  
Vol 262 (2) ◽  
pp. H432-H436 ◽  
Author(s):  
Y. Chien ◽  
B. L. Pegram ◽  
M. B. Kardon ◽  
E. D. Frohlich
Keyword(s):  
Myocardial Infarction ◽  
Blood Volume ◽  
Venous Pressure ◽  
Filling Pressure ◽  
Coronary Artery Ligation ◽  
Venous Compliance ◽  
Artery Ligation ◽  
Conscious Rats ◽  
Unstressed Volume ◽  
Total Body

To test the hypothesis that atrial natriuretic factor (ANF) increases total body venous compliance through venodilation and thereby reduces cardiac preload, we compared the systemic hemodynamic effects of ANF (99-126) with the venodilator nitroglycerin in conscious rats with myocardial infarction (mean infarct size 25%) induced by coronary artery ligation 3 wk previously. A 30-min ANF infusion (0.5 microgram.kg-1.min-1) decreased mean arterial pressure, central venous pressure, and blood volume by 11 mmHg, 0.8 mmHg, and 3 ml/kg, respectively (P less than 0.02). Nitroglycerin (10 micrograms.kg-1.min-1) similarly reduced arterial and venous pressures (7 and 0.6 mmHg; P less than 0.02) but increased blood volume by 2 ml/kg (P less than 0.05). Both ANF and nitroglycerin reduced mean circulatory filling pressure (MCFP) by 1 mmHg (P less than 0.05). Compared with vehicle infusion, nitroglycerin increased total body vascular compliance as derived from serial MCFP measurements taken during 10% blood volume changes (2.09 +/- 0.12 vs. 2.76 +/- 0.32 ml.kg-1.mmHg-1; P less than 0.05) and reduced extrapolated unstressed volume (34.96 +/- 1.10 vs. 23.79 +/- 3.80 ml/kg; P less than 0.02). In contrast, ANF had no effect on either measurement. These data suggest that ANF and nitroglycerin reduced cardiac filling pressure through different mechanisms; the lack of effects of ANF on total body venous compliance and unstressed volume does not support its venodilating effect in these rats postmyocardial infarction.

Norepinephrine on venous compliance and unstressed volume in cat liver

1985 ◽  
Vol 248 (4) ◽  
pp. H468-H476 ◽  
Author(s):  
C. V. Greenway ◽  
K. L. Seaman ◽  
I. R. Innes
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Hepatic Veins ◽  
Venous Compliance ◽  
Inferior Vena Caval ◽  
Unstressed Volume ◽  
True Blood ◽  
The Central Nervous System ◽  
Infusion Of Norepinephrine

Hemodynamic relationships between flows, pressures, and blood volume have been examined in the denervated liver of cats anesthetized with pentobarbital. Portal and hepatic lobar venous pressures, portal and total hepatic flows, and hepatic blood volume were recorded when portal flow was varied from 0 to 240 ml X min-1 X 100 g liver-1 and when hepatic outflow pressure was varied from 0 to 9.5 mmHg, before, during, and after intravenous infusion of norepinephrine (2 micrograms X min-1 X kg body wt-1). Portal pressure was 1-2 mmHg higher than lobar venous pressure and 8-9 mmHg higher than inferior vena caval pressure, showing that the major site of resistance in the portal circuit was in the large hepatic veins. Intrahepatic pressure was linearly related to total hepatic flow, and norepinephrine increased the intercept but not the slope of this relationship. Hepatic blood volume was linearly related to intrahepatic pressure with a calculated compliance of 2.5-3.0 ml X mmHg-1 X 100 g liver-1 and a calculated unstressed volume at zero pressure of 10-15 ml/100 g liver. Norepinephrine did not significantly change vascular compliance but caused a marked reduction of 15-20 ml/100 g liver in calculated unstressed volume. Thus norepinephrine reduced hepatic blood volume by 15-20 ml/100 g liver at any given intrahepatic pressure. It is concluded that venoconstriction in the hepatic bed occurs by a decrease in unstressed volume with little change in compliance. Unstressed volume represents a true blood volume reserve, independent of passive influences, which can be mobilized by the central nervous system.

Effects of hemorrhage and hepatic nerve stimulation on venous compliance and unstressed volume in cat liver

1987 ◽  
Vol 65 (11) ◽  
pp. 2168-2174 ◽  
Author(s):  
C. V. Greenway
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Nerve Stimulation ◽  
Marked Decrease ◽  
Venous Compliance ◽  
Remarkable Feature ◽  
Unstressed Volume ◽  
Passive Response ◽  
The Relationship ◽  
Blood Volumes

Intrahepatic blood volume–pressure relationships were studied using plethysmography to measure hepatic blood volume and a hepatic venous long-circuit to control intrahepatic pressure. In cats anesthetized with pentobarbital or with ketamine–chloralose, hemorrhage (to reduce hepatic blood flow to 60% of control) caused marked reductions in hepatic blood volume and intrahepatic pressure but did not significantly change hepatic blood volume–pressure relationships. We were unable to demonstrate an active reflex venous response to hemorrhage in these preparations, although a large passive response occurred. The volume–pressure relationships in innervated livers were different from those in denervated livers: apparent venous compliance was much greater and apparent unstressed volume was zero or negative. Hepatic nerve stimulation in denervated livers caused a marked decrease in hepatic blood volume at low intrahepatic pressures but failed to alter hepatic blood volumes at high intrahepatic pressures (15 mmHg) (1 mmHg = 133.3 Pa). This resulted in large apparent compliances and apparently negative unstressed volumes, as seen in the innervated livers. Thus blood volume–pressure relationships in innervated livers may not give valid measurements of compliance and unstressed volume. A remarkable feature in all these experiments was the linearity of the relationship between hepatic blood volume and intrahepatic pressure. Exudation of fluid begins at higher intrahepatic pressures in innervated compared with denervated livers.

Effects of natriuretic peptides and nitroprusside on venous function in trout

1997 ◽  
Vol 273 (2) ◽  
pp. R527-R539 ◽  
Author(s):  
K. R. Olson ◽  
D. J. Conklin ◽  
A. P. Farrell ◽  
J. E. Keen ◽  
Y. Takei ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Aortic Pressure ◽  
Systemic Resistance ◽  
Venous Compliance ◽  
Venous Capacitance ◽  
Unstressed Volume ◽  
Ventral Aorta

Active venous regulation of cardiovascular function is well known in mammals but has not been demonstrated in fish. In the present studies, the natriuretic peptides (NP) rat atrial natriuretic peptide (ANP) and trout ventricular natriuretic peptide (VNP), clearance receptor inhibitor SC-46542, and sodium nitroprusside (SNP) were infused into unanesthetized trout fitted with pressure cannulas in the ventral aorta, dorsal aorta, and ductus Cuvier, and a ventral aorta (VA) flow probe was used to measure cardiac output (CO). In another group, in vivo vascular (venous) capacitance curves were obtained during ANP or SNP infusion. The in vitro effects of NP on vessels and the heart were also examined. ANP, VNP, and SC-46542 decreased central venous pressure (PVen), CO, stroke volume (SV), and gill resistance (RG), whereas systemic resistance (RS) and heart rate (HR) increased. Dorsal aortic pressure (PDA) transiently increased and then fell even though RS remained elevated. ANP decreased mean circulatory filling pressure (MCFP), increased vascular compliance at all blood volumes, and increased unstressed volume in hypovolemic fish. ANP had no direct effect on the heart. ANP responses in vivo were not altered in trout made hypotensive by prior treatment with the angiotensin-converting enzyme inhibitor lisinopril. SNP reduced ventral aortic pressure (PVA), PDA, and RS, increased CO and HR, but did not affect PVen, SV, or RG. SNP slightly decreased MCFP but did not affect compliance or unstressed volume. In vitro, large systemic arteries were more responsive than veins to NP, whereas SNP relaxed both. These results show that, in vivo, NP decrease venous compliance, thereby decreasing venous return, CO, and arterial pressure. Conversely, SNP hypotension is due to decreased RS. This is the first evidence for active regulation of venous capacitance in fish, which probably occurs in small veins or venules. The presence of venous baroreceptors is also suggested.

Effect of hypoxic hypoxia on systemic vasculature

1984 ◽  
Vol 56 (5) ◽  
pp. 1403-1410 ◽  
Author(s):  
J. Malo ◽  
H. Goldberg ◽  
R. Graham ◽  
H. Unruh ◽  
C. Skoog
Keyword(s):  
Arterial Pressure ◽  
Inferior Vena ◽  
Superior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Venous Drainage ◽  
Hypoxic Hypoxia ◽  
Venous Compliance ◽  
Flow Curves ◽  
Pressure Flow

Effects of hypoxic hypoxia (HH) on cardiac output (CO), CO distribution, arterial and venous pressure-flow curves, vascular compliance, vascular time constant (tau), and resistance to venous return (RVR) were evaluated on six dogs. The vascular bed was isolated into four compartments depending on venous drainage: superior vena cava (SVC), splanchnic, renal and adrenal, and the remainder of the inferior vena cava (IVC). Low arterial O2 content and PO2 produced a threefold increase in CO at the same mean arterial pressure and a significant redistribution of CO to the SVC. Arterial pressure-flow curves decreased their slope (i.e., flow resistance) by a factor of two in the IVC and renal beds and by a factor of three in the splanchnic and SVC beds. Venous pressure-flow curves for the animal also decreased their slope significantly. HH causes a twofold increase in venous compliance and in mean venous pressure; tau did not change, but RVR halved. Seventy percent of the CO increase is explained by the increase in mean venous pressure and 30% by the reduction in RVR.

scholarly journals Venous compliance and clinical implications

2018 ◽  
Vol 7 (2) ◽  
Author(s):  
Paolo Zamboni ◽  
Valentina Tavoni ◽  
Francesco Sisini ◽  
Massimo Pedriali ◽  
Erika Rimondi ◽  
...  
Keyword(s):  
Venous Pressure ◽  
Vena Cava ◽  
Cross Sectional Area ◽  
Venous System ◽  
Clinical Implications ◽  
Sectional Area ◽  
Venous Compliance ◽  
Cross Sectional ◽  
The Cross ◽  
Deformable System

Compliance is a characteristic of every deformable system. Compliance is very clear concept in physics and mechanics but in clinics, perhaps, is not the same. However, in veins compliance fits perfectly with the function of drainage of the venous system. Volumetric increase (dV) of the content is correlated with pressure increase (dP) inside the vein according to the equation C’= dV/dP. In humans 75% of the blood is located in the venous system, primarily because the molecular components of a vein media layer is significantly more compliant to that of arteries. This property is fundamental to understanding the change in blood volume in response to a change in posture. Measurements of venous compliance in clinical practice can be done by the means of ultrasound, as well as with the plethysmography. Ultrasound methods assimilate the cross sectional area to the volume of the vein, because it reflects the blood content. Changes in cross sectional area can be reliably measured in response to a change in posture, while pressure can be derived from the hydrostatic pressure changes. Venous compliance is of paramount importance also in pulsatile veins such as the inferior or superior vena cava and the jugular veins, where high resolution ultrasound may accurately derive the cross sectional area. Clinical implications of the mechanical properties of the venous wall are extensively discussed, including the need of dedicated venous stenting, which takes into account venous compliance as the main parameter of the venous function. In addition, venous compliance is the interpretative key for a better understanding of plethysmography curves, as well as of varicose veins and of their return to normal cross sectional area following ambulatory venous pressure reduction.

scholarly journals Limb venous tone and responsiveness in hypertensive humans

2008 ◽  
Vol 105 (3) ◽  
pp. 894-901 ◽  
Author(s):  
Erin P. Delaney ◽  
Colin N. Young ◽  
Angela DiSabatino ◽  
Michael E. Stillabower ◽  
William B. Farquhar
Keyword(s):  
Repeated Measures ◽  
Muscle Tone ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Quadratic Regression ◽  
Venous Compliance ◽  
Venous Tone ◽  
Venous Capacitance ◽  
Regression Parameters ◽  
One Way Anova

Hypertensive (HTN) animal models demonstrate lower venous compliance as well as increased venous tone and responsiveness compared with normotensive (NTN) controls. However, the extent to which findings in experimental animals can be extended to humans is unknown. Forearm and calf venous compliance were quantified in 9 NTN (23 ± 1 yr) and 9 HTN (24 ± 1 yr) men at baseline, after administration of nitroglycerin (NTG), during a cold pressor test (CP), and post-handgrip exercise ischemia (PEI). Individual pressure-volume relationships from a cuff deflation protocol (1 mmHg/s) were modeled with a quadratic regression. Regression parameters β1 and β2 were used to calculate compliance. A one-way ANOVA was used to compare the beta parameters and a repeated-measures ANOVA was used to compare volumes across all pressures (between groups at baseline and within groups during perturbations). Limb venous compliance was similar between groups (forearm: NTN β1 = 0.11 ± 0.01 and β2 = −0.00097 ± 0.0001, HTN β1 = 0.10 ± 0.01 and β2 = −0.00088 ± 0.0001; calf: NTN β1 = 0.12 ± 0.01 and β2 = −0.00102 ± 0.0001, HTN β1 = 0.11 ± 0.01 and β2 = −0.00090 ± 0.0001). However, at baseline, volume across all pressures (i.e., capacitance) was lower in the forearm ( P ≤ 0.01) and tended to be lower in the calf ( P = 0.08) in HTN subjects. Venous compliance was not altered by any perturbation in either group. Forearm volume was increased during NTG in HTN subjects only. While venous compliance was similar between NTN and HTN adults, HTN adults have lower forearm venous capacitance (volume) which is increased with NTG. These data suggest that young HTN adults may have augmented venous smooth muscle tone compared with NTN controls.

Vascular perturbations in the chronic orthostatic intolerance of the postural orthostatic tachycardia syndrome

2000 ◽  
Vol 89 (4) ◽  
pp. 1505-1512 ◽  
Author(s):  
Julian M. Stewart ◽  
Amy Weldon
Keyword(s):  
Blood Flow ◽  
Orthostatic Intolerance ◽  
Venous Pressure ◽  
Fluid Collection ◽  
Lower Extremities ◽  
Postural Orthostatic Tachycardia Syndrome ◽  
Size Change ◽  
Venous Compliance ◽  
Edema Formation ◽  
Calf Blood Flow

Chronic orthostatic intolerance is often related to the postural orthostatic tachycardia syndrome (POTS). POTS is characterized by upright tachycardia. Understanding of its pathophysiology remains incomplete, but edema and acrocyanosis of the lower extremities occur frequently. To determine how arterial and venous vascular properties account for these findings, we compared 13 patients aged 13–18 yr with 10 normal controls. Heart rate and blood pressure were continuously recorded, and strain-gauge plethysmography was used to measure forearm and calf blood flow, venous compliance, and microvascular filtration while the subject was supine and to measure calf blood flow and calf size change during head-up tilt. Resting venous pressure was higher in POTS compared with control (16 vs. 10 mmHg), which gave the appearance of decreased compliance in these patients. The threshold for edema formation decreased in POTS patients compared with controls (8.3 vs. 16.3 mmHg). With tilt, early calf blood flow increased in POTS patients (from 3.4 ± 0.9 to 12.6 ± 2.3 ml · 100 ml−1 · min−1) but did not increase in controls. Calf volume increased twice as much in POTS patients compared with controls over a shorter time of orthostasis. The data suggest that resting venous pressure is higher and the threshold for edema is lower in POTS patients compared with controls. Such findings make the POTS patients particularly vulnerable for edema fluid collection. This may signify a redistribution of blood to the lower extremities even while supine, accounting for tachycardia through vagal withdrawal.

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