Changes in venous return parameters associated with univentricular Fontan circulations

2000 ◽  
Vol 279 (5) ◽  
pp. H2335-H2343 ◽  
Author(s):  
Loïc Macé ◽  
Patrice Dervanian ◽  
Armand Bourriez ◽  
Guy M. Mazmanian ◽  
Virginie Lambert ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Venous Return ◽  
Correlation Coefficients ◽  
Volume Loading ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Artery Pressure ◽  
Straight Lines ◽  
Proportional Decrease

To clarify the physiology of venous return (Qvr) in Fontan circulations, venous return conductance ( Gvr) and mean circulatory filling pressure (Pmcf) were determined in pentobarbital sodium-anesthetized pigs. Relationships between Qvrand right (biventricular, n = 8) or left (Fontan, n = 8) filling pressures are described by straight lines with significant correlation coefficients. Estimated Pmcfvalues were correlated with observed Pmcfvalues in either circulations ( P ≤ 0.02). Gvrwas smaller in Fontan than in biventricular circulations (4.51 ± 0.36 vs. 7.83 ± 0.69 ml · min−1· kg−1· mmHg−1, P = 0.002) and inversely correlated with pulmonary vascular resistances in Fontan circulations ( P = 0.01). Estimated Pmcf(20.5 ± 1.4 vs. 11.1 ± 0.9 mmHg, P = 0.001) and observed Pmcf(21.8 ± 1.3 vs. 10.6 ± 0.8 mmHg, P < 0.001) were higher in Fontan versus biventricular circulations, respectively. Pulmonary artery pressure in Fontan circulations was correlated with either Pmcf( P ≤ 0.04). We conclude that in Fontan circulations 1) pulmonary vascular resistances induce a proportional decrease in Gvr; and 2) volume loading, while increasing Pmcf(similar to pulmonary artery pressure), allows the gradient for Qvrto increase and maintains systemic blood flow at a biventricular level.

The peculiarities of pulmonary macro- and microhemodynamics changes after treatment with agonists and blockers of cholinoceptors

2021 ◽  
Vol 20 (4) ◽  
pp. 35-44
Author(s):  
Vadim I. Evlakhov ◽  
Ilya Z. Poyassov ◽  
Tatiana P. Berezina
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Venous Return ◽  
Filtration Coefficient ◽  
Artery Pressure ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient ◽  
Pulmonary Microcirculation

Background. The pulmonary arterial and venous vessels are innervated by parasympathetic cholinergic nerves. However, the studies, performed on the isolated rings of pulmonary vessels, can not give answer to the question about the role of cholinergic mechanisms in the changes of pulmonary circulation in full measure. Aim. The comparative analysis of the changes of the pulmonary macro- and microhemodynamics after acetylcholine, atropine, pentamine and nitroglycerine treatment. Materials and methods. The study was carried out on the anesthetized rabbits in the condition of intact circulation with the measurement of the pulmonary artery pressure and flow, venae cavae flows, cardiac output, and also on isolated perfused lungs in situ with stabilized pulmonary flow with measurement of the perfused pulmonary artery pressure, capillary hydrostatic pressure, capillary filtration coefficient and calculation of the pulmonary vascular resistance, pre- and postcapillary resistances. Results. In the conditions of intact circulation after acetylcholine, pentamine and nitroglycerine treatment the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance did not change as a result of decreasing of pulmonary artery flow and left atrial pressure due to diminution of venous return and venae cavaе flows. On perfused isolated lungs acetylcholine caused the increasing of pulmonary artery pressure, capillary hydrostatic pressure, pulmonary vascular resistance, pre- and postcapillary resistance and capillary filtration coefficient. After M-blocker atropine treatment the indicated above parameters of pulmonary microcirculation increased, on the contrary, after N-blocker pentamine treatment they decreased. Nitroglycerine infusion caused less decreasing of the parameters of pulmonary microcirculation in comparison with effects of pentamine, but capillary filtration coefficient decreased to a greater extent. These data indicate that nitroglycerine decreases endothelial permeability of pulmonary microvessels. Conclusion. After activation or blockade of cholinergic mechanisms in the condition of intact circulation the calculated parameter of pulmonary vascular resistance is depended from the ratio of the pulmonary artery pressure and flow and left atrial pressure, which are determined by the venous return. The different character of the changes of pulmonary microcirculatory parameters after M-blocker atropine and N-blocker pentamine treatment is evidence of reciprocal relations of M- and N-cholinoceptors in the nervous regulation of the pulmonary microcirculatory bed.

scholarly journals Correlation of Pulse Wave Transit Time with Pulmonary Artery Pressure in a Porcine Model of Pulmonary Hypertension

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1212
Author(s):  
Fabian Mueller-Graf ◽  
Jonas Merz ◽  
Tim Bandorf ◽  
Chiara Albus ◽  
Maike Henkel ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Transit Time ◽  
Pulse Wave ◽  
Correlation Coefficients ◽  
Physiological Basis ◽  
Artery Pressure ◽  
Hypoxic Vasoconstriction ◽  
Pulse Wave Transit Time

For the non-invasive assessment of pulmonary artery pressure (PAP), surrogates like pulse wave transit time (PWTT) have been proposed. The aim of this study was to invasively validate for which kind of PAP (systolic, mean, or diastolic) PWTT is the best surrogate parameter. To assess both PWTT and PAP in six healthy pigs, two pulmonary artery Mikro-Tip™ catheters were inserted into the pulmonary vasculature at a fixed distance: one in the pulmonary artery trunk, and a second one in a distal segment of the pulmonary artery. PAP was raised using the thromboxane A2 analogue U46619 (TXA) and by hypoxic vasoconstriction. There was a negative linear correlation between PWTT and systolic PAP (r = 0.742), mean PAP (r = 0.712) and diastolic PAP (r = 0.609) under TXA. During hypoxic vasoconstriction, the correlation coefficients for systolic, mean, and diastolic PAP were consistently higher than for TXA-induced pulmonary hypertension (r = 0.809, 0.778 and 0.734, respectively). Estimation of sPAP, mPAP, and dPAP using PWTT is feasible, nevertheless slightly better correlation coefficients were detected for sPAP compared to dPAP. In this study we establish the physiological basis for future methods to obtain PAP by non-invasively measured PWTT.

Effects of extracorporeal oxygenation of venous return on pulmonary artery pressure

1962 ◽  
Vol 202 (3) ◽  
pp. 510-514 ◽  
Author(s):  
William M. Chadduck
Keyword(s):  
Pulmonary Artery ◽  
Oxygen Saturation ◽  
Pulmonary Artery Pressure ◽  
Venous Return ◽  
Arterial Oxygen Saturation ◽  
Right Atrial ◽  
Arterial Oxygen ◽  
Artery Pressure ◽  
Pulmonary Arterial ◽  
Extracorporeal Oxygenation

Pulmonary arterial hyperoxemia was produced in anesthetized, open-chest dogs by means of an extracorporeal oxygenator with an inflow system which prevented right atrial pressure from exceeding 7–10 cm of blood. No significant changes in pulmonary artery pressure were found when pulmonary arterial oxygen saturation was elevated to 80–99%. The elevated pulmonary artery pressure associated with systemic arterial hypoxemia was reduced by extracorporeal oxygenation of venous return. The use of such a system for attainment of tolerable levels of systemic arterial oxygen saturation in patients with acute disorders of pulmonary alveolar-capillary gas exchange is discussed.

Inflammation and Congenital Heart Disease Associated Pulmonary Hypertension

2015 ◽  
Vol 18 (1) ◽  
pp. 038 ◽  
Author(s):  
Mete Gursoy ◽  
Ece Salihoglu ◽  
Ali Can Hatemi ◽  
A. Faruk Hokenek ◽  
Suleyman Ozkan ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Neutrophil To Lymphocyte Ratio ◽  
Cell Distribution ◽  
Inflammation Markers ◽  
Distribution Width ◽  
Artery Pressure ◽  
Lymphocyte Ratio ◽  
Mean Pulmonary Artery Pressure ◽  
Pulmonary Arterial

<strong>Background:</strong> Increased blood flow may trigger pulmonary arterial wall inflammation, which may influence progression of pulmonary artery hypertension in patients with congenital heart disease. In this study, we aimed to investigate the correlation between preoperative inflammation markers and pulmonary arterial hypertension. <br /><strong>Methods:</strong> A total of 201 patients with pulmonary hypertension were enrolled in this study retrospectively; they had undergone open heart surgery between January 2012 and December 2013. Patients’ preoperative C-reactive protein (CRP), neutrophil to lymphocyte ratio, red blood cell distribution width, pulmonary pressures, and postoperative outcomes were evaluated.<br /><strong>Results:</strong> Patient age, neutrophil to lymphocyte ratio, red blood cell distribution width, and CRP were found to be significantly correlated with both preoperative peak and mean pulmonary artery pressures. These data were entered into a linear logistic regression analysis. Patient age, neutrophil to lymphocyte ratio, and CRP were found to be independently correlated with peak pulmonary pressure (P &lt; .001, P &lt; .001, and P = .004) and mean pulmonary artery pressure (P &lt; .001, P &lt; .001, and P = .001), whereas preoperative mean pulmonary artery pressure was found to be independently correlated with intensive care unit stay (P &lt; .001). No parameter was found to be significantly correlated with extubation time and mortality. Eighteen patients had experienced pulmonary hypertensive crisis; in this subgroup, patients’ mean pulmonary artery pressure and neutrophil to lymphocyte ratio were found to be significant (P = .047, P = .003). <br /><strong>Conclusion:</strong> Preoperative inflammation markers may be correlated with the progression of pulmonary hypertensive disease, but further studies with larger sample size are needed to determine the predictive role of these markers for postoperative outcomes.<br /><br />

scholarly journals Association of Admission Glucose Level and Improvement in Pulmonary Artery Pressure in Patients with Submassive-type Acute Pulmonary Embolism

2018 ◽  
Vol 57 (5) ◽  
pp. 647-654
Author(s):  
Masaomi Gohbara ◽  
Keigo Hayakawa ◽  
Azusa Hayakawa ◽  
Yusuke Akazawa ◽  
Yukihiro Yamaguchi ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Glucose Level ◽  
Acute Pulmonary Embolism ◽  
Artery Pressure ◽  
Admission Glucose

scholarly journals CHANGES IN PULMONARY ARTERY PRESSURE DURING CARDIOPULMONARY BYPASS

1958 ◽  
Vol 36 (4) ◽  
pp. 604-620
Author(s):  
James B. Littlefield ◽  
J. Francis Dammann ◽  
Phyllis R. Ingram ◽  
William H. Muller
Keyword(s):  
Cardiopulmonary Bypass ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Artery Pressure

Effect of acute lower respiratory tract infection on pulmonary artery pressure in children with post-tricuspid left-to-right shunt

2021 ◽  
pp. 1-5
Author(s):  
Sakshi Sachdeva ◽  
Shyam S. Kothari ◽  
Saurabh K. Gupta ◽  
Sivasubramanian Ramakrishnan ◽  
Anita Saxena
Keyword(s):  
Tract Infection ◽  
Pulmonary Artery ◽  
Respiratory Tract ◽  
Respiratory Tract Infection ◽  
Lower Respiratory Tract Infection ◽  
Pulmonary Artery Pressure ◽  
Lower Respiratory Tract ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Artery Pressure

Abstract We sought to examine the influence of clinically severe lower respiratory tract infection on pulmonary artery pressure in children having CHD with post-tricuspid left-to-right shunt, as it may have physiological and clinical implications. In a prospective single-centre observational study, 45 children with post-tricuspid left-to-right shunt and clinically severe lower respiratory tract infection were evaluated during the illness and 2 weeks after its resolution. Pulmonary artery systolic pressure was estimated non-invasively using shunt gradient by echocardiography and systolic blood pressure measured non-invasively. Median pulmonary artery systolic pressure during lower respiratory tract infection was only mildly (although statistically significantly) elevated during lower respiratory tract infection [60 (42–74) versus 53 (40–73) mmHg, (p < 0.0001)]. However, clinically significant change in pulmonary artery systolic pressure defined as the increase of >10 mmHg was present in only 9 (20%) patients. In the absence of hypoxia or acidosis, only a small minority (9%, n = 4) showed significant pulmonary artery systolic pressure rise >10 mmHg. In the absence of hypoxia or acidosis, severe lower respiratory tract infection in patients with acyanotic CHD results in only mild elevation of pulmonary artery systolic pressure in most of the patients.

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