Possible equilibration of portal venous and central venous pressures during circulatory arrest

1993 ◽  
Vol 264 (1) ◽  
pp. H259-H261 ◽  
Author(s):  
R. Tabrizchi ◽  
S. L. Lim ◽  
C. C. Pang
Keyword(s):  
Circulatory Arrest ◽  
Venous Pressure ◽  
Filling Pressure ◽  
Intravenous Bolus ◽  
Ang Ii ◽  
Central Venous ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Anesthetized Rats ◽  
Total Body

The mean circulatory filling pressure technique has been used to assess total body venous tone. It involves measuring central venous pressure (CVP) at 5-8 s following circulatory arrest. This study examines if CVP and portal venous pressure (PVP) equilibrate when circulation is stopped by inflating a balloon implanted in the right atrium. CVP and PVP were measured in the control condition and after intravenous bolus injections of norepinephrine (NE, 1.6 microgram/kg), angiotensin II (ANG II, 1.3 microgram/kg), and isoproterenol (Iso, 0.5 microgram/kg) in conscious and pentobarbital-anesthetized rats. In conscious rats, CVP was similar to PVP after circulatory arrest under conditions of normal, elevated, or reduced vascular tone. In anesthetized rats, CVP was similar to PVP in the control condition and after intravenous bolus injection of NE and Iso but was less than PVP after the administration of ANG II. Therefore, mean circulatory filling pressure may not fully reflect total body venous tone in anesthetized, surgically stressed rats.

Central venous pressure and mean circulatory filling pressure in the dogfish Squalus acanthias: adrenergic control and role of the pericardium

2006 ◽  
Vol 291 (5) ◽  
pp. R1465-R1473 ◽  
Author(s):  
Erik Sandblom ◽  
Michael Axelsson ◽  
Anthony P. Farrell
Keyword(s):  
Central Venous Pressure ◽  
Venous Return ◽  
Venous Pressure ◽  
Filling Pressure ◽  
Control Fish ◽  
Central Venous ◽  
Venous Capacitance ◽  
Mean Circulatory Filling Pressure ◽  
Adrenergic Control ◽  
Venous Vasculature

Subambient central venous pressure (Pven) and modulation of venous return through cardiac suction (vis a fronte) characterizes the venous circulation in sharks. Venous capacitance was estimated in the dogfish S qualus acanthias by measuring the mean circulatory filling pressure (MCFP) during transient occlusion of cardiac outflow. We tested the hypothesis that venous return and cardiac preload can be altered additionally through adrenergic changes of venous capacitance. The experiments involved the surgical opening of the pericardium to place a perivascular occluder around the conus arteriosus. Another control group was identically instrumented, but lacked the occluder, and was subjected to the same pharmacological protocol to evaluate how pericardioectomy affected cardiovascular status. Routine Pven was negative (−0.08 ± 0.02 kPa) in control fish but positive (0.09 ± 0.01 kPa) in the pericardioectomized group. Injections of 5 μg/kg body mass ( Mb) of epinephrine and phenylephrine (100 μg/kg Mb) increased Pven and MCFP, whereas isoproterenol (1 μg/kg Mb) decreased both variables. Thus, constriction and relaxation of the venous vasculature were mediated through the respective stimulation of α- and β-adrenergic receptors. α-Adrenergic blockade with prazosin (1 mg/kg Mb) attenuated the responses to phenylephrine and decreased resting Pven in pericardioectomized animals. Our results provide convincing evidence for adrenergic control of the venous vasculature in elasmobranchs, although the pericardium is clearly an important component in the modulation of venous function. Thus active changes in venous capacitance have previously been underestimated as an important means of modulating venous return and cardiac performance in this group.

scholarly journals Defining human mean circulatory filling pressure in the intensive care unit

2020 ◽  
Vol 129 (2) ◽  
pp. 311-316
Author(s):  
Marije Wijnberge ◽  
Jaap Schuurmans ◽  
Rob B. P. de Wilde ◽  
Martijn K. Kerstens ◽  
Alexander P. Vlaar ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intensive Care Unit ◽  
Intensive Care ◽  
Venous Pressure ◽  
Filling Pressure ◽  
Central Venous ◽  
Venous Compliance ◽  
Icu Patients ◽  
Mean Circulatory Filling Pressure ◽  
Arterial Blood

In a cohort of 311 intensive care unit (ICU) patients, median mean circulatory filling pressure (Pmcf) measured after cardiac arrest was 15 mmHg (interquartile range 12–18). In 48% of cases, arterial blood pressure remained higher than central venous pressure, but correction for arterial-to-venous compliance differences did not result in clinically relevant alterations of Pmcf. Fluid balance, use of vasopressors or inotropes, and being on mechanical ventilation were associated with a higher Pmcf.

Vascular capacitance following preoptic recess lesions

1993 ◽  
Vol 264 (2) ◽  
pp. H560-H566 ◽  
Author(s):  
S. L. Bealer
Keyword(s):  
Circulatory Arrest ◽  
Venous Pressure ◽  
Blocking Agent ◽  
Right Atrial ◽  
Significant Shift ◽  
Central Venous ◽  
Venous Tone ◽  
Vascular Capacitance ◽  
Electrolytic Ablation ◽  
Ganglionic Blocking

Vascular capacitance was studied in anesthetized control (CONT) animals and in rats after electrolytic ablation of the periventricular tissue surrounding the anteroventral third cerebral ventricle (AV3V-X). Blood volume (BV) was determined by use of radiolabeled serum albumin, and mean arterial pressure (MAP) and central venous pressure (CVP) were continuously measured. Mean circulatory filling pressure (MCFP) was calculated by use of MAP and CVP obtained during circulatory arrest induced by inflation of a right atrial balloon during BV expansion and contraction. MCFP-BV relationships were calculated to estimate vascular compliance. CONT and AV3V-X animals were tested after treatment with both vehicle and hexamethonium, a ganglionic blocking agent. BV, MAP, and CVP were similar between CONT and AV3V-X animals. However, MCFP was significantly lower in AV3V-X animals (4.6 +/- 0.3 mmHg) than in CONT rats (6.6 +/- 0.5 mmHg). Furthermore, AV3V ablation caused a significant shift of the MCFP-BV relationship toward the volume axis with no change in compliance, indicating decreased venous tone. Finally, hexamethonium treatment significantly reduced MCFP in CONT animals (3.8 +/- 0.7 mmHg) and shifted the MCFP-BV line toward the BV axis but had no effect on these measures in AV3V-X animals. These data indicate that electrolytic ablation of AV3V periventricular tissue significantly reduces venous tone by decreasing neurally mediated venoconstriction.

Measurement of mean circulatory filling pressure and vascular compliance in domestic pigs

1990 ◽  
Vol 258 (6) ◽  
pp. H1925-H1932 ◽  
Author(s):  
R. I. Ogilvie ◽  
D. Zborowska-Sluis ◽  
B. Tenaschuk
Keyword(s):  
Cardiac Arrest ◽  
Circulatory Arrest ◽  
Filling Pressure ◽  
Right Atrial ◽  
Base Line ◽  
Pentobarbital Sodium ◽  
Closed Chest ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Compliance ◽  
Venous Circulation

To measure mean circulatory filling pressure (Pmcf), a balloon was placed in the right atrium of seven pentobarbital sodium-anesthetized open-chest pigs for transient occlusion of flow combined with mechanical transfer of blood from the arterial to the venous circulation. Equilibration occurred within 6-8 s at a pressure at 12.3 +/- 0.3 (SE) mmHg after a 2.9 +/- 0.2 ml/kg transfer of blood. In another group of pentobarbital sodium-anesthetized closed-chest pigs, acetylcholine (ACh) was used to induce cardiac arrest. The Pmcf was 11.6 +/- 1.0 mmHg in the 7:17 pigs that arrested for 6-8 s. In four isoflurane-anesthetized closed-chest pigs, the Pmcf was 12.0 +/- 1.0 mmHg after terminal cardiac arrest induced by KCl. The pressure gradient for venous return [Pmcf--right atrial pressure (Pra)] averaged 5.9 +/- 0.2 mmHg. Total vascular compliance estimated from plots of Pmcf at base line, 5, and 10 ml/kg increases in circulating volume was 2.1 +/- 0.3 and 3.5 +/- 0.9 ml.kg-1.mmHg-1 in the balloon and ACh groups, respectively compared with 2.8 +/- 0.4 ml.kg-1.mmHg-1 using a volume infusion-withdrawal method without circulatory arrest. The use of ACh for the estimate of Pmcf in the pig is not recommended because of failure to consistently induce circulatory arrest and probable failure to achieve sufficient equilibrium of vascular pressures 6-8 s postarrest when it occurs.

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.

Functional Interaction between Angiotensin and Sympathetic Reflexes in Cats

1982 ◽  
Vol 62 (1) ◽  
pp. 51-56 ◽  
Author(s):  
R. Hatton ◽  
D. P. Clough ◽  
S. A. Adigun ◽  
J. Conway
Keyword(s):  
Blood Pressure ◽  
Central Venous Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Partial Recovery ◽  
Ang Ii ◽  
Central Venous ◽  
Efferent Nerve ◽  
Arterial Blood ◽  
Sympathetic Reflexes

1. Lower-body negative pressure (LBNP) was used to stimulate sympathetic reflexes in anaesthetized cats. At −50 mmHg for 10 min it caused transient reduction in central venous pressure and systemic arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. Central venous pressure showed only partial recovery. The resting level of plasma renin activity (PRA; 2.9–3.2 ng h−1 ml−1) did not change until approximately 5 min into the manoeuvre. 2. When converting-enzyme inhibitor (CEI) was given 75 s after the onset of suction it caused a greater and more sustained fall in arterial blood pressure than when administered alone. The angiotensin II (ANG II) antagonist [Sar1,Ala8]ANG II produced similar effects after a short-lived pressor response. 3. This prolonged fall in arterial blood pressure produced by CEI was not associated with reduced sympathetic efferent nerve activity. This indicates that the inhibitor affects one of the peripheral actions of angiotensin and in so doing produces vasodilatation of neurogenic origin. 4. These findings suggest that angiotensin, at a level which does not exert a direct vasoconstrictor action, interacts with the sympathetic nervous system to maintain arterial blood pressure when homeostatic reflexes are activated. A reduction in the efficiency of these reflexes by CEI may contribute to its hypotensive effect.

Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

1990 ◽  
Vol 68 (3) ◽  
pp. 384-391 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial Pao2 = 38 mmHg), hypercapnia (Paco2 = 72 mmHg), or hypoxic hypercapnia (Pao2 = 41; Paco2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.Key words: cardiovascular reflex, vascular capacitance, hypoxia, hypercapnia, mean circulatory filling pressure, venoconstriction.

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