Evaluation of mean systemic filling pressure from pulse contour cardiac output and central venous pressure

2011 ◽  
Vol 25 (3) ◽  
pp. 193-201 ◽  
Author(s):  
Jacinta J. Maas ◽  
Bart F. Geerts ◽  
Jos R. C. Jansen
Keyword(s):  
Cardiac Output ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Pulse Contour ◽  
Filling Pressure ◽  
Central Venous ◽  
Mean Systemic Filling Pressure ◽  
Systemic Filling ◽  
Systemic Filling Pressure ◽  
Pulse Contour Cardiac Output

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.

scholarly journals Central venous pressure and cardiac function during spaceflight

1998 ◽  
Vol 85 (2) ◽  
pp. 738-746 ◽  
Author(s):  
Ronald J. White ◽  
C. Gunnar Blomqvist
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Shape Change ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Reference Measurements

Early in spaceflight, an apparently paradoxical condition occurs in which, despite an externally visible headward fluid shift, measured central venous pressure is lower but stroke volume and cardiac output are higher, and heart rate is unchanged from reference measurements made before flight. This paper presents a set of studies in which a simple three-compartment, steady-state model of cardiovascular function is used, providing insight into the contributions made by the major mechanisms that could be responsible for these events. On the basis of these studies, we conclude that, during weightless spaceflight, the chest relaxes with a concomitant shape change that increases the volume of the closed chest cavity. This leads to a decrease in intrapleural pressure, ultimately causing a shift of blood into the vessels of the chest, increasing the transmural filling pressure of the heart, and decreasing the central venous pressure. The increase in the transmural filling pressure of the heart is responsible, through a Starling-type mechanism, for the observed increases in heart size, left ventricular end-diastolic volume, stroke volume, and cardiac output.

scholarly journals Hubungan Volume Cairan dengan Cardiac Output dan Venous Return pada Pasien Kritis

2019 ◽  
Vol 11 (3) ◽  
pp. 164-177
Author(s):  
Listiana Dewi Sartika ◽  
Erwin Pradian ◽  
Nurita Dian ◽  
Reza W Sudjud ◽  
Ricky Aditya
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Venous Return ◽  
Filling Pressure ◽  
Mean Systemic Filling Pressure ◽  
Systemic Filling ◽  
Systemic Filling Pressure

Pemberian cairan merupakan salah satu intervensi medis yang sering dilakukan pada pasien kritis di intensif care unit (ICU). Perkembangan ilmu mengenai cairan tubuh dulu lebih menitikberatkan pada fisiologi jantung kiri. Cardiac output, pada mulanya lebih dikenal sebagai fungsi jantung kiri dimana cardiac output ditentukan oleh jumlah darah yang dipompa dari ventrikel kiri dalam semenit (stroke volume) dan heart rate. Namun demikian, ternyata pemahaman fisiologi kardiovaskular tidak sesederhana itu. Menurut Starling, jantung hanya akan memompa darah yang masuk ke dalam jantung kanan. Dengan demikian, jumlah darah yang masuk ke jantung kanan harus sama dengan jumlah darah yang dipompa oleh jantung kiri, dimana keduanya adalah cardiac output. Ini kemudian diteliti lagi oleh Guyton. Guyton mencoba memandang cardiac output sebagai darah yang masuk ke jantung kanan (venous return). Terdapat banyak faktor yang menentukan kembalinya cairan ke jantung kanan. Faktor perbedaan tekanan antara mean systemic filling pressure (MSFP) dengan tekanan atrium kanan, serta faktor resistensi vena merupakan faktor penentu dalam fungsi venous return. Guyton juga mencari hubungan antara fungsi jantung dengan fungsi venous return. Pemahaman cardiac output secara utuh baik sebagai fungsi jantung dan sebagai venous return ini dapat menjelaskan banyak hal yang berhubungan dengan disfungsi kardiovaskular maupun gangguan ekstra kardiak pada pasien kritis dengan kondisi syok. Oleh karena itu, sangat penting bagi klinisi untuk memahami hubungan antara cairan tubuh dengan cardiac output dan venous return.

Cardiovascular actions of histamine and potassium

1959 ◽  
Vol 197 (5) ◽  
pp. 1005-1007 ◽  
Author(s):  
Calvin Hanna ◽  
Patricia B. McHugo ◽  
William H. MacMillan
Keyword(s):  
Cardiac Output ◽  
Central Venous Pressure ◽  
Potassium Chloride ◽  
Venous Pressure ◽  
Plasma Potassium ◽  
Dilution Method ◽  
Cardiac Rate ◽  
Central Venous ◽  
Arterial Blood ◽  
Cardiovascular Actions

The cardiovascular actions of intravenous histamine, in doses from 2.5 to 20 µg/kg of the free base, were studied in the pentobarbitalized dog using the dye dilution method. With the small dose there was a consistent but small initial increase in cardiac output and with the larger doses there was a biphasic change in output. Cardiac rate, central venous pressure, central blood volume, hematocrit and the mean circulation time were essentially unchanged. Infusions of histamine and of potassium chloride at the rate of 1 µg and 1 mg/kg/min., respectively, moderately increased the cardiac output. Potassium chloride had no effect on the arterial blood pressure, cardiac rate and central venous pressure. Both the infusion of potassium chloride and injection of histamine produced a comparable elevation of the plasma potassium. It is possible that the actions of histamine to increase the plasma potassium contribute to the cardiovascular actions of this amine, especially on the cardiac output.

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