Mean circulatory filling pressure: potential problems with measurement

1986 ◽  
Vol 251 (4) ◽  
pp. H857-H862 ◽  
Author(s):  
M. L. Gaddis ◽  
C. F. Rothe ◽  
R. S. Tunin ◽  
M. Moran ◽  
C. L. MacAnespie
Keyword(s):  
Venous Pressure ◽  
Accurate Estimate ◽  
Filling Pressure ◽  
Physiological Status ◽  
Pressure Potential ◽  
Volume Depletion ◽  
Experimental Conditions ◽  
Mean Circulatory Filling Pressure ◽  
Repeated Use ◽  
The Mean

Three experimental series using 22 acutely splenectomized mongrel dogs were completed to 1) compare fibrillation (Fib) and acetylcholine (ACh) injection as methods to stop the heart for the mean circulatory filling pressure (Pmcf) maneuver, and 2) test whether Pmcf equals portal venous pressure 7 s after heart stoppage (Pportal7s). Blood volume changes of -10, -20, +10, or +20 ml/kg were imposed and Pmcf and Pportal measurements were obtained. Pportal7s and Pmcf were significantly different with volume depletion but were similar under control conditions. Pmcf with ACh and Pmcf with Fib were significantly different only after a volume change of -20 ml/kg. However, severe pulmonary congestion and atelectasis were detected in animals where Ach was used to stop the heart. In some cases (with injection directly into the pulmonary artery) the damage was severe enough to cause irreversible arterial hypoxia. Thus we conclude that the repeated use of ACh may exert a detrimental influence on pulmonary function, changing the physiological status of the experimental animal. Also, the central venous pressure at 7 s of heart stoppage (Pcv7s) is not a fully accurate estimate of the true mean circulatory filling pressure during the Pmcf maneuver, because Pcv7s did not equal the Pportal7s under all experimental conditions.

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.

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.

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.

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.

Blood reservoir function in patients with Fontan circulation and asplenia syndrome

2019 ◽  
Vol 29 (8) ◽  
pp. 1016-1019
Author(s):  
Michitaka Fuse ◽  
Kenji Sugamoto ◽  
Seiko Kuwata ◽  
Rika Sekiya ◽  
Kohei Kawada ◽  
...  
Keyword(s):  
Blood Volume ◽  
Filling Pressure ◽  
Fontan Circulation ◽  
Splanchnic Circulation ◽  
Venous Capacitance ◽  
Mean Circulatory Filling Pressure ◽  
Hepatic Congestion ◽  
The Mean ◽  
Asplenia Syndrome ◽  
Blood Reservoir

AbstractSplanchnic circulation constitutes a major portion of the vasculature capacitance and plays an important role in maintaining blood perfusion. Because patients with asplenia syndrome lack this vascular bed as a blood reservoir, they may have a unique blood volume and distribution, which may be related to their vulnerability to the haemodynamic changes often observed in clinical practice. During cardiac catheterisation, the mean circulatory filling pressure was calculated with the Valsalva manoeuvre in 19 patients with Fontan circulation, including 5 patients with asplenia syndrome. We also measured the cardiac output index and circulatory blood volume by using a dye dilution technique. The blood volume and the mean circulatory filling pressure and the venous capacitance in patients with asplenia syndrome were similar to those in the remaining patients with Fontan circulation (85 ± 14 versus 77 ± 18 ml/kg, p = 0.43, 31 ± 8 versus 27 ± 5 mmHg, p = 0.19, 2.8 ± 0.6 versus 2.9 ± 0.9 ml/kg/mmHg, p = 0.86). Unexpectedly, our data indicated that patients with asplenia syndrome, who lack splanchnic capacitance circulation, have blood volume and venous capacitance comparable to those in patients with splanchnic circulation. These data suggest that (1) there is a blood reservoir other than the spleen even in patients with asplenia; (2) considering the large blood pool of the spleen, the presence of a symmetrical liver may represent the possible organ functioning as a blood reservoir in asplenia syndrome; and (3) if this is indeed the case, there may be a higher risk of hepatic congestion in patients with Fontan circulation with asplenia syndrome than in those without.

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.

Problems associated with the measurement of mean circulatory filling pressure by the atrial balloon technique in anaesthetized rats

1992 ◽  
Vol 70 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Linong Cheng ◽  
Andrew J. Rankin
Keyword(s):  
Portal Vein ◽  
Blood Volume ◽  
Volume Expansion ◽  
Inferior Vena ◽  
Vena Cava ◽  
Filling Pressure ◽  
Volume Depletion ◽  
Portal Vein Pressure ◽  
Mean Circulatory Filling Pressure ◽  
Pressure Equilibrium

To examine the existence of pressure equilibrium between tributary veins and the central vena cava during the mean circulatory filling pressure manoeuvre, pressures in the hepatic portal vein, renal vein, and inferior vena cava were determined at 4-s intervals over a 20-s period of circulatory arrest induced by inflating a right atrial balloon in normal blood volume, 10% volume depletion, and 10% volume expansion states in urethane-anaesthetized rats. Portal vein pressure determined 8 s after arrest during volume depletion and expansion was significantly higher than vena caval pressure (6.2 ± 0.8 vs. 3.4 ± 0.2 and 7.7 ± 0.5 vs. 6.2 ± 0.4 mmHg (1 mmHg = 133.32 Pa), respectively; p < 0.01): this pressure disequilibrium continued for 16 s during volume expansion and for the entire 20 s during volume depletion. Renal vein pressure was equal to vena caval pressure during this manoeuvre. Portal vein pressure at normal blood volume was not significantly different from vena caval pressure following circulatory arrest (4.6 ± 0.3 vs. 3.8 ± 0.4 mmHg, respectively). Following ganglionic blockade, portal vein pressure was still significantly higher than vena caval pressure for 12 s during volume alterations. At the 8th s of the arrest the portal pressure determined in volume depletion was 3.6 ± 0.3 mmHg and the inferior vena caval pressure was 2.6 ± 0.4 mmHg (p < 0.05). Under the volume expansion condition, the respective values were 6.5 ± 0.3 and 5.3 ± 0.4 mmHg (p < 0.05). We conclude that, under conditions of blood volume alterations, there is no pressure equilibrium between the portal vein and the inferior vena cava when mean circulatory filling pressure is measured by this technique; a transhepatic barrier independent of reflex control during the measurement of mean circulatory filling pressure appears to play a role in obstructing the establishment of pressure equilibrium within the venous system.Key words: mean circulatory filling pressure, vascular capacitance, hepatic portal vein pressure, unstressed volume.

Compartmental vascular changes in dogs after nephrectomy, DOCA, and saline: effect of nifedipine

1987 ◽  
Vol 65 (9) ◽  
pp. 1891-1897 ◽  
Author(s):  
Richard I. Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Time Constant ◽  
Venous Return ◽  
Flow Distribution ◽  
Filling Pressure ◽  
Fast Time ◽  
Mean Circulatory Filling Pressure ◽  
Hypertensive Group ◽  
Arteriolar Resistance ◽  
The Mean ◽  
Overall Resistance

Hypertension (mean arterial pressure, (MAP) 131 ± 3 mmHg) developed in 18 dogs 4 weeks after left nephrectomy, deoxycorticosterone acetate (DOCA), 5 mg/kg sc twice weekly), and 0.5% NaCl drinking solution. This can be compared with MAP (95 ± 7 mmHg) of 13 dogs with nephrectomy alone and MAP (86 ± 4 mmHg) of 25 dogs without nephrectomy. The two-compartment model of the circulation revealed no differences in systemic vascular compliance, compartmental compliance, or flow distribution to the compartments. However, the time constant for venous return for the compartment with the rapid time constant was increased from 0.05 ± 0.004 min in control animals to 0.07 ± 0.006 min in the nephrectomy alone group and 0.09 ± 0.008 min in the hypertensive group (p < 0.001), as a result of an increase in venous resistance. Arteriolar resistance in this compartment was also increased in the hypertensive animals, as was the mean circulatory filling pressure and overall resistance to venous return. Nifedipine (0.025–0.05 mg/kg) reduced MAP by 15% in the nephrectomy alone group and by 22% in the hypertensive group, with reduction in arteriolar resistance only in the fast time constant compartment. In the slow time constant compartment, arteriolar resistance was increased by more than 100% and flow decreased by more than 50% after nifedipine. Unilateral nephrectomy, DOCA, plus NaCl resulted in hypertension by increasing arteriolar resistance in a vascular compartment with a fast time constant for venous return. Nifedipine countered this effect by inducing arteriolar vasodilation in this compartment. In addition, nifedipine reduced the mean circulatory filling pressure and overall resistance to venous return.

Mean circulatory filling pressure: its meaning and measurement

1993 ◽  
Vol 74 (2) ◽  
pp. 499-509 ◽  
Author(s):  
C. F. Rothe
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Muscle Tone ◽  
Rapid Change ◽  
Circulatory System ◽  
Filling Pressure ◽  
The Body ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

The volume-pressure relationship of the vasculature of the body as a whole, its vascular capacitance, requires a measurement of the mean circulatory filling pressure (Pmcf). A change in vascular capacitance induced by reflexes, hormones, or drugs has physiological consequences similar to a rapid change in blood volume and thus strongly influences cardiac output. The Pmcf is defined as the mean vascular pressure that exists after a stop in cardiac output and redistribution of blood, so that all pressures are the same throughout the system. The Pmcf is thus related to the fullness of the circulatory system. A change in Pmcf provides a uniquely useful index of a change in overall venous smooth muscle tone if the blood volume is not concomitantly changed. The Pmcf also provides an estimate of the distending pressure in the small veins and venules, which contain most of the blood in the body and comprise most of the vascular compliance. Thus the Pmcf, which is normally independent of the magnitude of the cardiac output, provides an estimate of the upstream pressure that determines the rate of flow returning to the heart.

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