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of diaphragm contraction on cardiovascular and abdominal pressures, cardiac output, and the volume of blood added to or withdrawn from the circulation to achieve servo control.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.

Development of a circulatory mock loop for biventricular device testing with various heart conditions

2020 ◽  
Vol 43 (9) ◽  
pp. 600-605 ◽  
Author(s):  
Yuichiro Kado ◽  
Takuma Miyamoto ◽  
David J Horvath ◽  
Shengqiang Gao ◽  
Kiyotaka Fukamachi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Left Atrial ◽  
Aortic Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Artery Pressure

This study aimed to evaluate a newly designed circulatory mock loop intended to model cardiac and circulatory hemodynamics for mechanical circulatory support device testing. The mock loop was built with dedicated ports suitable for attaching assist devices in various configurations. This biventricular mock loop uses two pneumatic pumps (Abiomed AB5000™, Danvers, MA, USA) driven by a dual-output driver (Thoratec Model 2600, Pleasanton, CA, USA). The drive pressures can be individually modified to simulate a healthy heart and left and/or right heart failure conditions, and variable compliance and fluid volume allow for additional customization. The loop output for a healthy heart was tested at 4.2 L/min with left and right atrial pressures of 1 and 5 mm Hg, respectively; a mean aortic pressure of 93 mm Hg; and pulmonary artery pressure of 17 mm Hg. Under conditions of left heart failure, these values were reduced to 2.1 L/min output, left atrial pressure = 28 mm Hg, right atrial pressure = 3 mm Hg, aortic pressure = 58 mm Hg, and pulmonary artery pressure = 35 mm Hg. Right heart failure resulted in the reverse balance: left atrial pressure = 0 mm Hg, right atrial pressure = 30 mm Hg, aortic pressure = 100 mm Hg, and pulmonary artery pressure = 13 mm Hg with a flow of 3.9 L/min. For biventricular heart failure, flow was decreased to 1.6 L/min, left atrial pressure = 13 mm Hg, right atrial pressure = 13 mm Hg, aortic pressure = 52 mm Hg, and pulmonary artery pressure = 18 mm Hg. This mock loop could become a reliable bench tool to simulate a range of heart failure conditions.

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.

Reference sites not influenced by hydrostatic pressure for right and left atrial pressures

1964 ◽  
Vol 207 (2) ◽  
pp. 357-360 ◽  
Author(s):  
George G. Armstrong ◽  
John C. Hancock
Keyword(s):  
Hydrostatic Pressure ◽  
Reference Point ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Lateral Border ◽  
Zero Reference ◽  
The Right ◽  
Made In

Simultaneous recordings of left and right atrial pressures made in dogs being rotated into all positions in space allowed the location of rotational axes where right or left atrial pressure became independent of hydrostatic pressure. Utilization of these axes as zero reference levels made possible the measurement of right or left atrial pressure without the influence of hydrostatic factors. The right zero reference point lay 62.8% of the distance from the manubrium to the xiphoid, 61.2% of the posterior to anterior thoracic diameter, and 47.7% of the greatest transverse thoracic diameter as measured from the right lateral border. The left atrial zero reference point lay 62.1% of the manubrium to xiphoid distance, 57.2% of the posterior to anterior diameter of thorax, and 53.0% of the greatest transverse thoracic diameter as measured from the right lateral border. When referred to the anatomy of the dog, these points lay in the immediate vicinity of the right and left atrioventricular valves, respectively.

Furosemide reduces lung fluid filtration in lambs with lung microvascular injury from air emboli

1989 ◽  
Vol 67 (5) ◽  
pp. 1990-1996 ◽  
Author(s):  
M. E. Berner ◽  
W. G. Teague ◽  
R. G. Scheerer ◽  
R. D. Bland
Keyword(s):  
Cardiac Output ◽  
Left Atrial ◽  
Balloon Catheter ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Protein Ratio ◽  
Fluid Filtration ◽  
Lung Lymph ◽  
Lung Lymph Flow

To study the effects of furosemide on the neonatal pulmonary circulation in the presence of lung injury, we measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma of nine lambs that received furosemide, 2 mg/kg iv, during a continuous 8-h intravenous infusion of air. Air embolism increased pulmonary vascular resistance by 71% and nearly tripled steady-state lung lymph flow, with no change in lymph-to-plasma protein ratio. These findings reflect an increase in lung vascular protein permeability. During sustained lung endothelial injury, diuresis from furosemide led to a rapid reduction in cardiac output (average 29%) and a 2-Torr decrease in left atrial pressure. Diuresis also led to hemoconcentration, with a 15% increase in both plasma and lymph protein concentrations. These changes were associated with a 27% reduction in lung lymph flow. In a second set of studies, we prevented the reduction in left atrial pressure after furosemide by inflating a balloon catheter in the left atrium. Nevertheless, lymph flow decreased by 25%, commensurate with the reduction in cardiac output that occurred after furosemide. In a third series of experiments, we minimized the furosemide-related decrease in cardiac output by opening an external fistula between the carotid artery and jugular vein immediately after injection of furosemide. In these studies, the reduction in lung lymph flow (average 17%) paralleled the smaller (17%) decrease in cardiac output. These results suggest that changes in lung vascular filtration pressure probably do not account for the reduction in lung lymph flow after furosemide in the presence of lung vascular injury.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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