THE CHANGES IN CARDIAC OUTPUT, RIGHT ATRIAL PRESSURE AND BLOOD VOLUME IN HAEMORRHAGIC ANAEMIAS IN UNANAESTHETIZED RABBITS

1954 ◽  
Vol 32 (2) ◽  
pp. 241-252 ◽  
Author(s):  
I Darian Smith ◽  
WJ Simmonds
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure

Control of fetal cardiac output during changes in blood volume

1980 ◽  
Vol 238 (1) ◽  
pp. H80-H86 ◽  
Author(s):  
R. D. Gilbert
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Volume ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Volume Changes ◽  
Fetal Sheep ◽  
Systemic Pressure ◽  
Mean Systemic Pressure

Changes in cardiac output (Qco), heart rate, right atrial pressure, (Pra), and mean systemic pressure (Pms) in response to blood volume changes were measured in chronically prepared fetal sheep. With a 10% decrease in blood volume, fetal cardiac output, measured with the microsphere technique, decreased significantly from 592 +/- 28 to 471 +/- 32 ml . min-1 . kg-1. Heart rate changed little from control animals (163 +/- 5) to those with decreased volume (161 +/- 10 beats/min). Right atrial pressure decreased significantly from 5.4 +/- 0.4 to 4.2 +/- 0.6 mmHg. Mean systemic pressure decreased from 13.8 +/- 0.3 to 10.5 +/- 0.6 mmHg. With a 10% increase in fetal blood volume, cardiac output rose insignificantly to 632 +/- 38 ml . min-1 . kg-1. However, right atrial pressure increased significantly to 8.9 +/- 0.6 mmHg and mean systemic pressure increased significantly to 16.5 +/- 0.8 mmHg with the increased volume. Heart rate again changed little (153 +/- 9 beats/min). The fact that cardiac output rose only a small amount, whereas right atrial pressure rose sharply with an increased blood volume, suggests that the fetal heart is operating near the upper limit of its Starling function curve. As a result, there is very limited cardiac reserve for increases in fetal cardiac output.

scholarly journals Understanding Guyton's venous return curves

2011 ◽  
Vol 301 (3) ◽  
pp. H629-H633 ◽  
Author(s):  
Daniel A. Beard ◽  
Eric O. Feigl
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Venous Return ◽  
Systemic Circulation ◽  
Back Pressure ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Simultaneous Increase ◽  
Venous Circulation

Based on observations that as cardiac output (as determined by an artificial pump) was experimentally increased the right atrial pressure decreased, Arthur Guyton and coworkers proposed an interpretation that right atrial pressure represents a back pressure restricting venous return (equal to cardiac output in steady state). The idea that right atrial pressure is a back pressure limiting cardiac output and the associated idea that “venous recoil” does work to produce flow have confused physiologists and clinicians for decades because Guyton's interpretation interchanges independent and dependent variables. Here Guyton's model and data are reanalyzed to clarify the role of arterial and right atrial pressures and cardiac output and to clearly delineate that cardiac output is the independent (causal) variable in the experiments. Guyton's original mathematical model is used with his data to show that a simultaneous increase in arterial pressure and decrease in right atrial pressure with increasing cardiac output is due to a blood volume shift into the systemic arterial circulation from the systemic venous circulation. This is because Guyton's model assumes a constant blood volume in the systemic circulation. The increase in right atrial pressure observed when cardiac output decreases in a closed circulation with constant resistance and capacitance is due to the redistribution of blood volume and not because right atrial pressure limits venous return. Because Guyton's venous return curves have generated much confusion and little clarity, we suggest that the concept and previous interpretations of venous return be removed from educational materials.

Capacitive function of the heart: influence of acute changes in heart volume on mean right atrial pressure

1997 ◽  
Vol 272 (1) ◽  
pp. H553-H558 ◽  
Author(s):  
D. D. Sheriff ◽  
Z. Luo
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Normal Sinus Rhythm ◽  
Mean Value ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Atrial Pacing ◽  
Normal Sinus ◽  
Rapid Pacing

Net transfer of blood volume into or out of the cardiac chambers should have the same effect on central venous pressure as does transfer of an equal volume of blood to or from peripheral organs (e.g., spleen, or liver). We studied five pentobarbital sodium-anesthetized open-chest pigs (20-23 kg) to determine whether a reduction in the time-averaged volume of blood contained in the heart, induced by rapid atrial pacing, can raise right atrial pressure. A central premise of our study is that the mean value of right atrial pressure is acutely governed by the volume of blood that distends the central veins, and that atrial contractions primarily determine how atrial pressure varies about its mean value. To prevent changes in cardiac output from altering central blood volume and pressure, cardiac output during rapid pacing (2.36 +/- 0.18 l/min) was made to equal the resting output (2.35 +/- 0.16 l/min). This was achieved by selecting a rate of pacing at which the tendency for more frequent cardiac contractions to raise cardiac output was counterbalanced by the decrease in stroke volume induced by rapid pacing. Autonomic reflex mechanisms were attenuated by pharmacological blockade. Mean arterial pressure was minimally affected in the transition from a normal sinus rhythm (89 +/- 6 beats/min) to rapid atrial pacing (165 +/- 7 beats/min) in four pigs. Mean right atrial pressure rose abruptly from 2.8 +/- 0.5 mmHg during normal sinus rhythm to 3.5 +/- 0.5 mmHg (P = 0.015) at the onset of rapid pacing in these four pigs, presumably owing to decreased cardiac blood volume and a reciprocal expansion of central venous volume. In the fifth pig, a reduction in cardiac output induced by tachycardia led to a larger rise in mean right atrial pressure than did a reduction in cardiac output induced by bradycardia, presumably because tachycardia reduces cardiac blood volume whereas bradycardia raises cardiac volume. We conclude that the heart may play an important role in maintaining or raising its own filling pressure when heart rate rises.

Starling's "Law of the Heart": Rise and Fall of the Descending Limb

Physiology ◽  
1992 ◽  
Vol 7 (3) ◽  
pp. 134-137 ◽  
Author(s):  
Gijs Elzinga
Keyword(s):  
Cardiac Output ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Starling’S Law ◽  
Original Meaning ◽  
The Law

The descending limb of Starling's relationship between right atrial pressure and cardiac output was the cornerstone of his "law of the heart"; it was widely accepted in physiology. However, the original meaning of the law faded away over the years; the descending limb proved to be an experimental artefact.

Atrial dynamics, atrial natriuretic factor, tachycardia, and blood volume in anesthetized rabbits

1991 ◽  
Vol 261 (1) ◽  
pp. H22-H28 ◽  
Author(s):  
K. A. King ◽  
J. R. Ledsome
Keyword(s):  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Left Atrial ◽  
Wall Stress ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Atrial Wall ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The effects of tachycardia and a slow (1%/min) 20% reduction and elevation of blood volume (BV) on right atrial pressure (RAP), right atrial dimension (RAD), and plasma immunoreactive atrial natriuretic factor (IR-ANF) were examined in anesthetized rabbits. Plasma IR-ANF was significantly increased during pacing at 6 Hz in the presence of high BV but not at low BV. Mean RAP increased with expansion of BV, but this change was not associated with significant changes in IR-ANF. There were no statistically significant changes in systolic or diastolic RAD with alterations in BV or with tachycardia. Tachycardia had no effect on left atrial dimension. Diastolic right atrial wall stress (DRAS) and minute DRAS increased with a 20% increase in BV, but changes in BV did not affect systolic right atrial wall stress (SRAS) or minute SRAS. Tachycardia decreased DRAS at high BV and significantly increased SRAS and minute SRAS. The increases in SRAS and minute SRAS were greater during tachycardia at high BV, suggesting that an interaction between BV and tachycardia results in potentiation of SRAS and minute SRAS. The results suggest that systolic RAS is a significant factor in ANF release during tachycardia at high BV.

Mechanism of decrease in cardiac output caused by opening the chest

1964 ◽  
Vol 207 (5) ◽  
pp. 1112-1116 ◽  
Author(s):  
Jose D. Fermoso ◽  
Travis Q. Richardson ◽  
Arthur C. Guyton
Keyword(s):  
Cardiac Output ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Cardiopulmonary Function ◽  
Lower Cardiac Output

The cardiac output in ten dogs fell an average of 18.8% (±1.1 sem) when the chest was opened. Opening the chest, which increased the extracardiac pressure, shifted the cardiopulmonary-function curve (relating right atrial pressure to cardiac output) toward higher atrial pressure levels. This caused the cardiopulmonary curve to equate with the animal's systemic-function curve at a lower cardiac output; the greater the extracardiac pressure the lower the output. Thus, changes in extracardiac pressure can alter cardiac output even though the pumping ability of the heart is not altered.

Control of right atrial pressure at constant cardiac output suppresses volume natriuresis in anesthetized rats

1984 ◽  
Vol 62 (7) ◽  
pp. 798-801 ◽  
Author(s):  
U. Ackermann ◽  
J. R. Rudolph
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Control Value ◽  
Volume Load ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Blood Volume Expansion

The blood volume of anesthetized rats was expanded acutely by 33% with donor blood while a caval snare was gradually tightened so that right atrial pressure (RAP) was prevented from rising (n = 6). In control experiments (n = 5) an aortic snare was used to hold mean arterial blood pressure near the values found in the experimental series. However, RAP was allowed to change freely and increased by 1.6 ± 0.4 mmHg (1 mmHg = 133.322 Pa) during volume expansion. When the two groups were compared, there were no significant differences between their mean arterial blood pressures (near 110 mmHg) or in their cardiac outputs (near 0.25 mL∙min−1∙g body weight−1). There were, however, significant differences between their renal responses to the volume load. When RAP was free to change, the rate of volume excretion [Formula: see text] increased to 30 ± 15 (SEM) μL∙min−1∙g kidney weight−1 (KW) from its control value of 3.49 ± 0.31 and the rate of sodium excretion [Formula: see text] increased to 3.59 ± 0.20 μequiv.∙min−1∙g KW−1 from its preinfusion value of 0.42 ± 0.10. When RAP was not allowed to increase during volume loading, [Formula: see text] and [Formula: see text] did not change from their respective preinfusion values (2.99 ± 0.46 μL∙min−1∙g KW−1 and 0.35 ± 0.10 μequiv.∙min−1∙g KW−1). The results imply that during acute blood volume expansion increased central vascular pressure is a prerequisite for the homeostasis of body water and salt.

scholarly journals Effect of Exercise on Cerebral Circulation

1983 ◽  
Vol 3 (3) ◽  
pp. 287-290 ◽  
Author(s):  
Mordecai Globus ◽  
Eldad Melamed ◽  
Andre Keren ◽  
Dan Tzivoni ◽  
Chaim Granot ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Physical Exercise ◽  
Normal Subjects ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Inhalation Technique ◽  
Cerebrovascular Autoregulation ◽  
Cerebrovascular Resistance

The effect of supine physical exercise on cerebral blood flow (CBF) was measured in 30 normal subjects with the 133Xe inhalation technique. The CBF measurements were correlated to changes in Pco2, heart rate, and blood pressure, and to cardiac output and right atrial pressure in 10 of the subjects who underwent Swan-Ganz catheterization. No significant change was found in CBF during physical exercise, although a marked increase in cardiac output, blood pressure, and right atrial pressure and a mild decrease in PCO2 were found. Cerebrovascular resistance increased by 38%, in contrast to a decrease of 33% in the peripheral vascular resistance. The factors that affect the mechanism of cerebrovascular autoregulation during exercise are discussed.

scholarly journals Right Atrial Pressure During Exercise Predicts Survival in Patients With Pulmonary Hypertension

2020 ◽  
Vol 9 (22) ◽  
Author(s):  
Mona Lichtblau ◽  
Patrick R. Bader ◽  
Stéphanie Saxer ◽  
Charlotte Berlier ◽  
Esther I. Schwarz ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Right Heart Catheterization ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Heart Catheterization ◽  
Right Heart ◽  
Risk Of Death ◽  
Exercise Induced

Background We investigated changes in right atrial pressure (RAP) during exercise and their prognostic significance in patients assessed for pulmonary hypertension (PH). Methods and Results Consecutive right heart catheterization data, including RAP recorded during supine, stepwise cycle exercise in 270 patients evaluated for PH, were analyzed retrospectively and compared among groups of patients with PH (mean pulmonary artery pressure [mPAP] ≥25 mm Hg), exercise‐induced PH (exPH; resting mPAP <25 mm Hg, exercise mPAP >30 mm Hg, and mPAP/cardiac output >3 Wood Units (WU)), and without PH (noPH). We investigated RAP changes during exercise and survival over a median (quartiles) observation period of 3.7 (2.8–5.6) years. In 152 patients with PH, 58 with exPH, and 60 with noPH, median (quartiles) resting RAP was 8 (6–11), 6 (4–8), and 6 (4–8) mm Hg ( P <0.005 for noPH and exPH versus PH). Corresponding peak changes (95% CI) in RAP during exercise were 5 (4–6), 3 (2–4), and −1 (−2 to 0) mm Hg (noPH versus PH P <0.001, noPH versus exPH P =0.027). RAP increase during exercise correlated with mPAP/cardiac output increase ( r =0.528, P <0.001). The risk of death or lung transplantation was higher in patients with exercise‐induced RAP increase (hazard ratio, 4.24; 95% CI, 1.69–10.64; P =0.002) compared with patients with unaltered or decreasing RAP during exercise. Conclusions In patients evaluated for PH, RAP during exercise should not be assumed as constant. RAP increase during exercise, as observed in exPH and PH, reflects hemodynamic impairment and poor prognosis. Therefore, our data suggest that changes in RAP during exercise right heart catheterization are clinically important indexes of the cardiovascular function.

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