scholarly journals Clinical review: Guyton - the role of mean circulatory filling pressure and right atrial pressure in controlling cardiac output

Critical Care ◽  
2010 ◽  
Vol 14 (6) ◽  
pp. 243 ◽  
Author(s):  
William R Henderson ◽  
Donald EG Griesdale ◽  
Keith R Walley ◽  
A William Sheel
Keyword(s):  
Cardiac Output ◽  
Clinical Review ◽  
Filling Pressure ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Mean Circulatory Filling Pressure

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.

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.

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.

Cardiovascular function and norepinephrine-thermogenesis in cold-acclimatized rats

1963 ◽  
Vol 204 (5) ◽  
pp. 888-894 ◽  
Author(s):  
Eugene Evonuk ◽  
John P. Hannon
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Room Temperature ◽  
Metabolic Response ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Systemic Resistance

The cardiovascular and metabolic actions of norepinephrine (NE) and their inter-relationships were studied at normal room temperature in anesthetized, warm-acclimatized (W-A) (26 ± 1 C) and cold-acclimatized (C-A) (3 ± 1 C) rats. The cardiac output, heart rate, stroke volume, arterial pressure, right atrial pressure, and systemic resistance were measured prior to NE infusion; during NE infusion (2 µg/min) at the 25, 50, 75, and 100% levels of increased metabolism; and after infusion of NE had ceased. Norepinephrine caused a greater increase in the cardiac output, heart rate, stroke volume, and right atrial pressure in the C-A animals than it did in W-A animals. During the early metabolic response to NE (i.e., up to 25% increase in O2 consumption) there was a marked increase in the arterial pressure of both W-A and C-A rats, with the latter showing the greater maximum response. Beyond the 25% level of increased metabolism the arterial pressure and concomitantly the systemic resistance of the C-A animals declined sharply to the preinfusion levels where they remained throughout the course of infusion. In contrast to this, the arterial pressure and systemic resistance of the W-A animals remained high. It was concluded that norepinephrine-calorigenesis in the C-A rat is supported by a greater capacity to increase the cardiac output and an ability to preferentially reduce the systemic resistance to actively metabolizing areas (i.e., the viscera).

Effect of diaphragm contraction on canine heart and pericardium

1983 ◽  
Vol 54 (5) ◽  
pp. 1261-1268 ◽  
Author(s):  
T. C. Lloyd ◽  
J. A. Cooper
Keyword(s):  
Cardiac Output ◽  
Left Atrial ◽  
Servo Control ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Abdominal Pressure ◽  
Canine Heart ◽  
Pressure Changes

Pericardiophrenic attachments transmit diaphragm contraction to the pericardium. We investigated this in two ways. 1) We replaced the hearts of externally perfused dogs with a balloon from which we measured pressure changes. Diaphragm contraction increased pressure from 4.6 to 5.5 Torr, equivalent to an isobaric volume decrease of 1.5%, and decreased volumetric compliance by 3%. 2) We selectively servo controlled right atrial pressure, left atrial pressure, or cardiac output in open-chest dogs and monitored the effect of diaphragm contraction on cardiovascular and abdominal pressures, cardiac output, and the volume of blood added to or withdrawn from the circulation to achieve servo control. Diaphragm contraction decreased left atrial pressure 0.4 Torr when right atrial pressure was controlled and right atrial pressure increased 0.2 Torr while controlling left atrial pressure, but there were no significant changes in cardiac output. Atrial pressure did not change significantly when output was controlled. Servo control required removal of approximately 50 ml of blood, presumably reflecting a decreased splanchnic vascular capacity at the higher abdominal pressure. We conclude that the diaphragm may slightly tense the pericardium, but this has no important primary effect on the heart.

Role of β-adrenergic agonists in the control of vascular capacitance

1990 ◽  
Vol 68 (5) ◽  
pp. 575-585 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Peripheral Resistance ◽  
Filling Pressure ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Central Venous ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance

The role of β-adrenergic agonists, such as isoproterenol, on vascular capacitance is unclear. Some investigators have suggested that isoproterenol causes a net transfer of blood to the chest from the splanchnic bed. We tested this hypothesis in dogs by measuring liver thickness, cardiac output, cardiopulmonary blood volume, mean circulatory filling pressure, portal venous, central venous, pulmonary arterial, and systemic arterial pressures while infusing norepinephrine (2.6 μg∙min−1∙kg−1), or isoproterenol (2.0 μg∙min−1∙kg−1), or histamine (4 μg∙min−1∙kg−1), or a combination of histamine and isoproterenol. Norepinephrine (an α- and β1-adrenergic agonist) decreased hepatic thickness and increased mean circulatory filling pressure, cardiac output, cardiopulmonary blood volume, total peripheral resistance, and systemic arterial and portal pressures. Isoproterenol increased cardiac output and decreased total peripheral resistance, but it had little effect on liver thickness or mean circulatory filling pressure and did not increase the cardiopulmonary blood volume or central venous pressure. Histamine caused a marked increase in portal pressure and liver thickness and decreased cardiac output, but it had little effect on the estimated mean circulatory filling pressure. Isoproterenol during histamine infusions reduced histamine-induced portal hypertension, reduced liver size, and increased cardiac output. We conclude that the β-adrenergic agonist, isoproterenol, has little influence on vascular capacitance or liver volume of dogs, unless the hepatic outflow resistance is elevated by agents such as histamine.Key words: β-adrenergic agonists, vascular capacitance, mean circulatory filling pressure, isoproterenol, histamine, liver sphincters.

scholarly journals Right atrial pressure and venous return during cardiopulmonary bypass

2017 ◽  
Vol 313 (2) ◽  
pp. H408-H420 ◽  
Author(s):  
Per W. Moller ◽  
Bernhard Winkler ◽  
Samuel Hurni ◽  
Paul Philipp Heinisch ◽  
Andreas Bloch ◽  
...  
Keyword(s):  
Venous Return ◽  
Filling Pressure ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Pump Speed ◽  
Mean Systemic Filling Pressure ◽  
Upstream Pressure ◽  
Systemic Filling ◽  
Systemic Filling Pressure

The relevance of right atrial pressure (RAP) as the backpressure for venous return (QVR) and mean systemic filling pressure as upstream pressure is controversial during dynamic changes of circulation. To examine the immediate response of QVR (sum of caval vein flows) to changes in RAP and pump function, we used a closed-chest, central cannulation, heart bypass porcine preparation ( n = 10) with venoarterial extracorporeal membrane oxygenation. Mean systemic filling pressure was determined by clamping extracorporeal membrane oxygenation tubing with open or closed arteriovenous shunt at euvolemia, volume expansion (9.75 ml/kg hydroxyethyl starch), and hypovolemia (bleeding 19.5 ml/kg after volume expansion). The responses of RAP and QVR were studied using variable pump speed at constant airway pressure (PAW) and constant pump speed at variable PAW. Within each volume state, the immediate changes in QVR and RAP could be described with a single linear regression, regardless of whether RAP was altered by pump speed or PAW ( r2 = 0.586–0.984). RAP was inversely proportional to pump speed from zero to maximum flow ( r2 = 0.859–0.999). Changing PAW caused immediate, transient, directionally opposite changes in RAP and QVR (RAP: P ≤ 0.002 and QVR: P ≤ 0.001), where the initial response was proportional to the change in QVR driving pressure. Changes in PAW generated volume shifts into and out of the right atrium, but their effect on upstream pressure was negligible. Our findings support the concept that RAP acts as backpressure to QVR and that Guyton’s model of circulatory equilibrium qualitatively predicts the dynamic response from changing RAP. NEW & NOTEWORTHY Venous return responds immediately to changes in right atrial pressure. Concomitant volume shifts within the systemic circulation due to an imbalance between cardiac output and venous return have negligible effects on mean systemic filling pressure. Guyton’s model of circulatory equilibrium can qualitatively predict the resulting changes in dynamic conditions with right atrial pressure as backpressure to venous return.

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