Static filling pressure in patients during induced ventricular fibrillation

2003 ◽  
Vol 285 (6) ◽  
pp. H2510-H2515 ◽  
Author(s):  
J. D. Schipke ◽  
G. Heusch ◽  
A. P. Sanii ◽  
E. Gams ◽  
J. Winter
Keyword(s):  
Blood Pressure ◽  
Time Constant ◽  
Pressure Difference ◽  
Venous Pressure ◽  
Venous Blood ◽  
Central Venous ◽  
Equilibrium Pressure ◽  
Arterial Blood ◽  
Cardiac Pumping ◽  
Blood Pressure Difference

The static pressure resulting after the cessation of flow is thought to reflect the filling of the cardiovascular system. In the past, static filling pressures or mean circulatory filling pressures have only been reported in experimental animals and in human corpses, respectively. We investigated arterial and central venous pressures in supine, anesthetized humans with longer fibrillation/defibrillation sequences (FDSs) during cardioverter/defibrillator implantation. In 82 patients, the average number of FDSs was 4 ± 2 (mean ± SD), and their duration was 13 ± 2 s. In a total of 323 FDSs, arterial blood pressure decreased with a time constant of 2.9 ± 1.0 s from 77.5 ± 34.4 to 24.2 ± 5.3 mmHg. Central venous pressure increased with a time constant of 3.6 ± 1.3 s from 7.5 ± 5.2 to 11.0 ± 5.4 mmHg (36 points, 141 FDS). The average arteriocentral venous blood pressure difference remained at 13.2 ± 6.2 mmHg. Although it slowly decreased, the pressure difference persisted even with FDSs lasting 20 s. Lack of true equilibrium pressure could possibly be due to a waterfall mechanism. However, waterfalls were identified neither between the left ventricle and large arteries nor at the level of the diaphragm in supine patients. We therefore suggest that static filling pressures/mean circulatory pressures can only be directly assessed if the time after termination of cardiac pumping is adequate, i.e., >20 s. For humans, such times are beyond ethical options.

The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

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.

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.

Haemodynamic Monitoring in Theatre

2003 ◽  
Vol 4 (1) ◽  
pp. 10-16 ◽  
Author(s):  
Heidi Clinton
Keyword(s):  
Blood Pressure ◽  
Pulmonary Artery ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Haemodynamic Monitoring ◽  
Pressure Monitoring ◽  
Central Venous ◽  
Noninvasive Measurements ◽  
Non Invasive ◽  
Arterial Blood

AbstractThe number of devices available to monitor the haemodynamic status of patients is increasing. Practitioners need to be aware of the non-invasive and invasive methods available in order to care for their patients safely and effectively. This article reviews a number of noninvasive measurements of haemodynamic function, in addition to invasive methods such as arterial blood pressure, central venous pressure and pulmonary artery pressure monitoring. It is argued that using these methods in combination provides a comprehensive haemodynamic assessment.

Monitoring and equipment

2014 ◽  
Author(s):  
Anthea Hatfield
Keyword(s):  
Blood Pressure ◽  
Recovery Room ◽  
Venous Pressure ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Central Venous ◽  
Comprehensive Description ◽  
Arterial Blood ◽  
Routine Monitoring ◽  
Additional Monitoring

Routine monitoring is an essential part of recovery room procedure. Respiration, a vital concern while awakening after anaesthesia, is given specific attention with reference to modern capnography. This chapter also describes additional monitoring in detail: pulse oximetry, blood pressure, central venous pressure, and arterial blood gases are clearly described. A comprehensive description of electrocardiography guides the student through this complicated subject. The monitoring of temperature and warming blankets, with suggestions for purchasing equipment, are included.

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.

Sign in / Sign up

Export Citation Format

Share Document