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.

scholarly journals A Comparison between Ketamine and Diazepam as Induction Agents for Pericardiectomy

1978 ◽  
Vol 6 (1) ◽  
pp. 66-70 ◽  
Author(s):  
H. G. G. Kingston ◽  
K. W. Bretherton ◽  
A. M. Holloway ◽  
and J. W. Downing
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiac Index ◽  
Central Venous Pressure ◽  
Systemic Vascular Resistance ◽  
Venous Pressure ◽  
Significant Rise ◽  
Central Venous ◽  
Induction Of Anaesthesia ◽  
Induction Agents

Ketamine 1 · 0 mg/kg and diazepam 0 · 3 mg/kg was used to induce anaesthesia in patients requiring pericardiectomy. A significant rise in blood pressure in patients receiving ketamine was noted. In contrast, a fall in blood pressure was seen when diazepam was administered. Changes in cardiac output, cardiac index, central venous pressure and systemic vascular resistance are discussed. Ketamine appears to be a more satisfactory agent for induction of anaesthesia in patients for pericardiectomy, whereas diazepam should be used with caution.

Role of venoconstriction in the cardiovascular responses of ducks to head immersion

1983 ◽  
Vol 244 (2) ◽  
pp. R292-R298
Author(s):  
B. L. Langille
Keyword(s):  
Cardiac Output ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Venous Blood ◽  
Cardiovascular Responses ◽  
Energy Requirements ◽  
Similar Increase ◽  
Low Oxygen ◽  
Central Venous

Central venous pressure of ducks rose from resting values of 0.31 +/- 0.16 (SE) to 1.75 +/- 0.20 kPa during forced head immersion. Because a similar increase in mean circulatory pressure (Pmc) was also observed (0.71 +/- 0.16 to 2.15 +/- 0.20 kPa) the rise in central venous pressure was attributed to a venoconstrictor mechanism. When this venoconstrictor-induced rise in central venous pressure was prevented by graded withdrawal of venous blood, then immersion bradycardia was inhibited, and the reduced cardiac output associated with head immersion was largely the result of reduced stroke volume. When compared with normal dives, this intervention resulted in greater myocardial energy requirements, as assessed by the pressure-rate product. It is concluded that venoconstriction increases central venous pressure during head immersion. The increase in central venous pressure alters cardiac function through the Frank-Starling mechanism such that myocardial energy requirements are minimized during this period of low oxygen availability.

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.

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.

ANP-mediated volume depletion attenuates renal responses in humans

1992 ◽  
Vol 263 (6) ◽  
pp. R1303-R1308 ◽  
Author(s):  
T. J. Ebert ◽  
L. Groban ◽  
M. Muzi ◽  
M. Hanson ◽  
A. W. Cowley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Central Venous Pressure ◽  
Sodium Excretion ◽  
Healthy Subjects ◽  
Venous Pressure ◽  
Urine Volume ◽  
Positive Pressure ◽  
Plasma Norepinephrine ◽  
Central Venous

Brief low-dose infusions of atrial natriuretic peptide (ANP) that emulate physiological plasma concentrations in humans have little if any effect on renal excretory function. This study explored the possibility that ANP-mediated reductions in cardiac filling pressures (through ANP's rapid effect on capillary dynamics) could attenuate its purported renal effects. Protocol A consisted of 16 healthy subjects (ages 19-27 yr old) who underwent three consecutive 45-min experimental sequences: 1) placebo, 2) ANP (10 ng.kg-1 x min-1), and 3) ANP alone (n = 8) or ANP with simultaneous lower body positive pressure (LBPP, n = 8). Electrocardiogram and direct measures of arterial and central venous pressures were continuously monitored. Blood was sampled at the end of each 45-min sequence before subjects stood to void. Compared with control (placebo), ANP produced a hemoconcentration and increased plasma norepinephrine, but did not change heart rate, blood pressure, plasma levels of renin, aldosterone, or vasopressin, or renal excretion of volume or sodium. In subjects receiving LBPP to maintain central venous pressure during the last 45 min of ANP infusion, norepinephrine did not increase and urine volume and sodium excretion increased (P < 0.05). In a second study (protocol B), five healthy subjects received a placebo infusion for 45 min followed by two consecutive 45-min infusions of ANP (10 ng.kg-1 x min-1). Central venous pressure was maintained (LBPP) at placebo baseline throughout the two ANP infusion periods. Urine volume and sodium excretion rates increased progressively and significantly during both ANP infusion periods (P < 0.05) without significant changes in creatinine clearance, blood pressure, or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Heat-stress-induced changes in central venous pressure do not explain interindividual differences in orthostatic tolerance during heat stress

2011 ◽  
Vol 110 (5) ◽  
pp. 1283-1289 ◽  
Author(s):  
R. Matthew Brothers ◽  
David M. Keller ◽  
Jonathan E. Wingo ◽  
Matthew S. Ganio ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Central Venous Pressure ◽  
Blood Pressure Control ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Pressure Control ◽  
Stress Index ◽  
Central Venous ◽  
The Difference

The extent to which heat stress compromises blood pressure control is variable among individuals, with some individuals becoming very intolerant to a hypotensive challenge, such as lower body negative pressure (LBNP) while heat stressed, while others are relatively tolerant. Heat stress itself reduces indexes of ventricular filling pressure, including central venous pressure, which may be reflective of reductions in tolerance in this thermal condition. This study tested the hypothesis that the magnitude of the reduction in central venous pressure in response to heat stress alone is related to the subsequent decrement in LBNP tolerance. In 19 subjects, central hypovolemia was imposed via LBNP to presyncope in both normothermic and heat-stress conditions. Tolerance to LBNP was quantified using a cumulative stress index (CSI), and the difference between normothermic CSI and heat-stress CSI was calculated for each individual. The eight individuals with the greatest CSI difference between normothermic and heat-stress tolerances (LargeDif), and the eight individuals with the smallest CSI difference (SmallDif), were grouped together. By design, the difference in CSI between thermal conditions was greater in the LargeDif group (969 vs. 382 mmHg × min; P < 0.001). Despite this profound difference in the effect of heat stress in decreasing LBNP tolerance between groups, coupled with no difference in the rise in core body temperatures to the heat stress (LargeDif, 1.4 ± 0.1°C vs. SmallDif, 1.4 ± 0.1°C; interaction P = 0.89), the reduction in central venous pressure during heat stress alone was similar between groups (LargeDif: 5.7 ± 1.9 mmHg vs. SmallDif: 5.2 ± 2.0 mmHg; interaction P = 0.85). Contrary to the proposed hypothesis, differences in blood pressure control during LBNP are not related to differences in the magnitude of the heat-stress-induced reductions in central venous pressure.

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