1983
DOI: 10.1097/00000542-198311000-00012
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Influence of Mixed Venous Oxygen Tension (PVO2) on Blood Flow to Atelectatic Lung

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Cited by 104 publications
(43 citation statements)
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“…This finding challenges the concept that during unsupported SB the main mechanism of pulmonary blood flow redistribution is HPV; as in that case, the HPV should have been less effective at higher PvO 2 . 6 The PvO 2 -dependent HPV was either less important for the redistribution of pulmonary blood flow during SB (irrespective of the magnitude of the shunt) or a complementary, yet unidentified mechanism redistributing pulmonary blood flow independent of HPV was active during SB. The negative intrapleural pressure generated during SB might have a role in pulmonary blood flow redistribution, as negative-pressure ventilation has been recently shown to increase oxygenation and decrease pulmonary shunt compared with MV in surfactant-depleted rabbits 24 and in humans with acute respiratory distress syndrome.…”
Section: Discussionmentioning
confidence: 96%
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“…This finding challenges the concept that during unsupported SB the main mechanism of pulmonary blood flow redistribution is HPV; as in that case, the HPV should have been less effective at higher PvO 2 . 6 The PvO 2 -dependent HPV was either less important for the redistribution of pulmonary blood flow during SB (irrespective of the magnitude of the shunt) or a complementary, yet unidentified mechanism redistributing pulmonary blood flow independent of HPV was active during SB. The negative intrapleural pressure generated during SB might have a role in pulmonary blood flow redistribution, as negative-pressure ventilation has been recently shown to increase oxygenation and decrease pulmonary shunt compared with MV in surfactant-depleted rabbits 24 and in humans with acute respiratory distress syndrome.…”
Section: Discussionmentioning
confidence: 96%
“…Raising CO increases mixed-venous oxygen tension (PvO 2 ), and this results in higher oxygen tension at the HPV sensor site, attenuating the hypoxic vasoconstrictor response. [6][7][8] Moreover, a rising CO increases pulmonary artery pressures, which then distend/recruit pulmonary vessels perfusing nonaerated regions. 9 However, the effect of CO on shunt has not been examined during SB.…”
mentioning
confidence: 99%
“…An increased Q T decreases HPV due to a combination of increases in PvO 2 [29,30], pulmonary artery pressure [31], and pulmonary blood flow [32,33]. All these factors probably contributed to the transient decrease in HPV.…”
Section: Hypercapnic Acidosis and Hpvmentioning
confidence: 99%
“…In the setting of lung injury, however, breathing hypoxic gas does not reduce shunt suggesting either that vasoconstriction in response to alveolar hypoxia is attenuated in injured lung, or that the hypoxic gas may not reach the alveoli (39). In either instance, PvO 2 may become important such that, with decreases in cardiac output and an accompanying increase in oxygen extraction and reduction in PvO 2 , hypoxic vasoconstriction to shunt regions could increase, thereby decreasing perfusion to these unventilated regions (38)(39)(40)(41)(42). Others, however, have found that PEEP decreases shunt even when cardiac output is kept constant, indicating that at least a portion of the shunt reduction occurring with PEEP involves other mechanisms (29,43).…”
Section: Cardiac Output Reductionmentioning
confidence: 99%