scholarly journals Pulmonary Artery Pressure and Alveolar Gas Exchange in Man during Acclimatization to 12,470 ft

1971 ◽  
Vol 50 (4) ◽  
pp. 827-837 ◽  
Author(s):  
Richard S. Kronenberg ◽  
Peter Safar ◽  
Joseph Lee ◽  
Fred Wright ◽  
William Noble ◽  
...  
2020 ◽  
Vol 105 (9) ◽  
pp. 1648-1659
Author(s):  
Joseph W. Duke ◽  
Kara M. Beasley ◽  
Julia P. Speros ◽  
Jonathan E. Elliott ◽  
Steven S. Laurie ◽  
...  

Thorax ◽  
2001 ◽  
Vol 56 (7) ◽  
pp. 524-528
Author(s):  
B Schönhofer ◽  
T Barchfeld ◽  
M Wenzel ◽  
D Köhler

BACKGROUNDIt is not known whether long term nocturnal mechanical ventilation (NMV) reduces pulmonary hypertension in patients with chronic respiratory failure (CRF).METHODSPulmonary haemodynamics, spirometric values, and gas exchange were studied in 33 patients requiring NMV due to CRF (20 with thoracic restriction, 13 with chronic obstructive pulmonary disease (COPD)) at baseline and after 1 year of NMV given in the volume cycled mode. Patients with COPD also received supplemental oxygen.RESULTSLong term NMV improved gas exchange while lung function remained unchanged. Mean pulmonary artery pressure at rest before NMV was higher in patients with thoracic restriction than in those with COPD (33 (10) mm Hgv 25 (6) mm Hg). After 1 year of NMV mean pulmonary artery pressure decreased in patients with thoracic restriction to 25 (6) mm Hg (mean change –8.5 mm Hg (95% CI –12.6 to –4.3), p<0.01) but did not change significantly in patients with COPD (mean change 2.2 mm Hg (95% CI –0.3 to 4.8)).CONCLUSIONSLong term NMV in CRF improves pulmonary haemodynamics in patients with thoracic restriction but not in patients with COPD.


2016 ◽  
Vol 27 (3) ◽  
pp. 428 ◽  
Author(s):  
Jon Andrews ◽  
Stefanie Martina ◽  
Michael Natoli ◽  
Nicole Harlan ◽  
Luke Neilans ◽  
...  

1975 ◽  
Vol 39 (3) ◽  
pp. 469-474 ◽  
Author(s):  
J. C. Cruz ◽  
L. H. Hartley ◽  
J. A. Vogel

The supine pulmonary venous admixture (shunt) has been measured at Cerro de Pasco, 4,350 m altitude in eight subjects native to high altitude (HAN) under resting condition. Alveolar-arterial O2 tension difference (AaDO2) was also determined at rest and during exercise. The same subjects were studied again after 10 days' sojourn at sea level in Lima at 150 m altitude. They were compared with four subjects from sea level (SLN) who were studied first at Lima and after 2 and 10 days at Cerro de Pasco. At altitude, AaDO2 was smaller in HAN than SLN both at rest and during exercise. Shunt was the same in both groups. It is concluded that HAN show more even ventilation/perfusion relationship (VA/Q) at altitude, probably due to their high pulmonary artery pressure. On the contrary, SLN show less even VA/Q on altitude exposure, since their shunt decreased 37%. At sea level, HAN increased their AaDO2 due partially to an increase of 110% in their shunt, and in part due to less even VA/Q as shown by augmented VD/VT ratios. Each group tended to have a more effective gas exchange in its own environment.


2002 ◽  
Vol 103 (s2002) ◽  
pp. 21S-24S ◽  
Author(s):  
Maria DEJA ◽  
Steffen WOLF ◽  
Thilo BUSCH ◽  
Bodil PETERSEN ◽  
Ursel JAGHZIES ◽  
...  

To investigate the hypothesis that the inhaled ETA receptor antagonist LU-135252 acts as selective pulmonary vasodilator, we compared inhaled LU-135252 and inhaled nitric oxide (iNO) in an experimental model of acute lung injury (ALI), in a prospective, randomized, controlled animal study. A total of 30 anaesthetized, tracheotomized and mechanically ventilated pigs underwent induction of ALI by repeated saline washout of surfactant. The animals were then randomly assigned to receive the nebulized ETA receptor antagonist LU-135252 (0.3mg·kg-1, inhaled over 20min; ETA-A group; n = 10), inhaled NO (30p.p.m. continuously; iNO group; n = 10) or nebulized saline buffer (5ml inhaled over 20min; control group; n = 10). Measurements of pulmonary gas exchange and haemodynamics were performed hourly over a 4h period after induction of ALI. In the ETA-A group, the arterial oxygen tension (Pao2) increased from 58±3 to 377±39mmHg at 4h after intervention, while the intrapulmonary shunt (QS/QT) decreased from 53±4% to 18±2% (P<0.01 compared with controls). In the iNO group, PaO2 increased from 62±4 to 224±48mmHg, and QS/QT decreased from 47±2% to 27±5%, at 4h after induction of ALI (P<0.05 compared with controls). In the ETA-A and iNO groups, the increase in mean pulmonary artery pressure was significantly attenuated compared with controls (ETA-A group, 14±4%; iNO group, 6±4%; values at 4h; P<0.01compared with controls). In contrast, there were no significant differences in changes of mean arterial pressure and cardiac output between groups. Thus, in this experimental model of ALI, both inhaled LU-135252 and iNO significantly improved gas exchange and prevented an increase in mean pulmonary artery pressure, without significant systemic effects, when compared with controls. Our results indicate the occurrence of selective pulmonary vasodilation in both treatment groups.


2009 ◽  
Vol 107 (3) ◽  
pp. 755-762 ◽  
Author(s):  
John Y. C. Tsang ◽  
Wayne J. E. Lamm ◽  
Erik R. Swenson

Previous studies reported that regional CO2 tension might affect regional ventilation (V̇) following acute pulmonary thromboembolism (APTE). We investigated the pathophysiology and magnitude of these changes. Eight anesthetized and ventilated piglets received autologous clots at time = 0 min until mean pulmonary artery pressure was 2.5 times baseline. The distribution of V̇ and perfusion (Q̇) at four different times (−5, 30, 60, 120 min) was mapped by fluorescent microspheres. Regional V̇ and Q̇ were examined postmortem by sectioning the air-dried lung into 900–1,000 samples of ∼2 cm3 each. After the redistribution of regional Q̇ by APTE, but in the scenario assuming that no V̇ shift had yet occurred, CO2 tension in different lung regions at 30 min post-APTE (PXCO2) was estimated from the V̇/Q̇ data and divided into four distinct clusters: i.e., PXCO2 < 10 Torr; 10 < PXCO2 < 25 Torr; 25 < PXCO2 < 50 Torr; PXCO2 > 50 Torr. Our data showed that the clusters in higher V̇/Q̇ regions (with a PXCO2 < 25 Torr) received ∼35% less V̇ when measured within 30 min of APTE, whereas, in contrast, the lower V̇/Q̇ regions showed no statistically significant increases in their V̇. However, after 30 min, there was minimal further redistribution of V̇. We conclude that there are significant compensatory V̇ shifts out of regions of low CO2 tension soon following APTE, and that these variations in regional CO2 tension, which initiate CO2-dependent changes in airway resistance and lung parenchymal compliance, can lead to improved gas exchange.


2015 ◽  
Vol 18 (1) ◽  
pp. 038 ◽  
Author(s):  
Mete Gursoy ◽  
Ece Salihoglu ◽  
Ali Can Hatemi ◽  
A. Faruk Hokenek ◽  
Suleyman Ozkan ◽  
...  

<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 />


2018 ◽  
Vol 57 (5) ◽  
pp. 647-654
Author(s):  
Masaomi Gohbara ◽  
Keigo Hayakawa ◽  
Azusa Hayakawa ◽  
Yusuke Akazawa ◽  
Yukihiro Yamaguchi ◽  
...  

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