scholarly journals Right to Left Intrapulmonary Shunt in a Case with COVID-19-aSociated Pneumonia

2021 ◽  
Vol 31 (01) ◽  
pp. S23-S25
Keyword(s):  
1986 ◽  
Vol 65 (Supplement) ◽  
pp. A496
Author(s):  
B. Burns ◽  
S. André ◽  
B. Sandage ◽  
M. McCauley ◽  
J. W. Choe ◽  
...  

1986 ◽  
Vol 14 (8) ◽  
pp. 689-692 ◽  
Author(s):  
JULIO SANDOVAL ◽  
ROGELIO LÓPEZ ◽  
ULISES BELTRÁN ◽  
ARTURO GOMEZ ◽  
WILFREDO MARTINEZ ◽  
...  
Keyword(s):  

1982 ◽  
Vol 10 (3) ◽  
pp. 236
Author(s):  
David H. Skinner ◽  
David M. Rose ◽  
David L. Farber ◽  
I. James Sarfeh

1995 ◽  
Vol 79 (6) ◽  
pp. 1951-1957 ◽  
Author(s):  
S. Deem ◽  
M. J. Bishop ◽  
M. K. Alberts

To elucidate the effects of anemia on intrapulmonary shunt, we studied a model of left lung atelectasis in anesthetized rabbits. In 10 rabbits, isovolemic anemia was produced by sequential hemodilution. Seven control rabbits were followed over time, without hemodilution. Intrapulmonary shunt (Qs/QT) was measured by using blood gas analysis and by quantitation of the percentage of blood flow to the collapsed left lung (QLl/QT) using fluorescent microspheres. In control rabbits, Qs/QT and QLl/QT decreased over time, whereas arterial PO2 increased. In hemodiluted rabbits, there was a trend toward increased Qs/QT and QLl/QT. There were significant differences in the behavior of Qs/QT, QLl/QT, and arterial PO2 between control and hemodiluted rabbits. Hemodynamic parameters, including cardiac output and pulmonary artery pressure, were not different between groups. In a third group of rabbits with pharmacologically induced acidosis but no hemodilution, Qs/QT and QLl/QT decreased over time, and arterial PO2 increased. We conclude that acute isovolemic anemia has a deleterious effect on pulmonary gas exchange, possibly through attenuation of hypoxic pulmonary vasoconstriction.


2010 ◽  
Vol 31 (1) ◽  
pp. 139-140
Author(s):  
Søren Møller ◽  
Aleksander Krag ◽  
Jan L. Madsen ◽  
Jens H. Henriksen ◽  
Flemming Bendtsen

Author(s):  
Roberta Sudy ◽  
Ferenc Petak ◽  
Liliana Kiss ◽  
Adam Laszlo Balogh ◽  
Gergely H. Fodor ◽  
...  

Diabetes mellitus increases smooth muscle tone and causes tissue remodelling affecting elastin and collagen. Since lung is dominated by these elements, diabetes is expected to modify the airway function and respiratory tissue mechanics. Therefore, we characterized the respiratory function in patients with diabetes with and without associated obesity. Mechanically ventilated patients with normal body shapes were divided into the control non-diabetic (n=73) and diabetic (n=31) groups. The other two groups included obese patients without diabetes (n=43) or with diabetes (n=30). The mechanical properties of the respiratory system were determined by forced oscillation technique. Airway resistance (Raw), tissue damping (G), and tissue elastance (H) were assessed by forced oscillation. Capnography was applied to determine phase 3 slopes and dead space indices. The intrapulmonary shunt fraction (Qs/Qt) and the lung oxygenation index (PaO2/FiO2) were estimated from arterial and central venous blood samples. Compared with the corresponding control groups, diabetes alone increased the Raw (7.6 ± 6 cmH2O.s/l vs. 3.1 ± 1.9 cmH2O.s/l), G (11.7 ± 5.5 cmH2O/l vs. 6.5 ± 2.8 cmH2O/l), and H (31.5 ± 11.8 cmH2O/l vs. 24.2 ± 7.2 cmH2O/l, (p < 0.001 for all). Diabetes increased the capnographic phase 3 slope, whereas PaO2/FiO2 or Qs/Qt were not affected. Obesity alone caused similar detrimental changes in respiratory mechanics and alveolar heterogeneity, but these alterations also compromised gas exchange. We conclude that diabetes-induced intrinsic mechanical abnormalities are counterbalanced by hypoxic pulmonary vasoconstriction, which maintained intrapulmonary shunt fraction and oxygenation ability of the lungs.


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