Independent influence of blood flow rate and mixed venous PO2 on shunt fraction

Abstract

We have tested the independent and combined effects of changes in mixed venous PO2 (PvO2) and blood flow (QT) on shunt fraction (Qs/QT) in isolated blood-perfused canine left lower lobes with edema. The lobes were ventilated with pure O2. Inflow (Pi) and outflow (Po) pressures always exceeded lobar alveolar pressure. PvO2 was varied by means of a clinical bubble oxygenator with appropriate mixtures of O2 and N2. QT was varied by changes in Pi and Po with care not to produce changes in lobar weight. Changes in QT did not influence Qs/QT. Increasing PvO2 from 40 +/- 6 to 88.4 +/- 40 Torr at constant QT significantly increased Qs/QT from 5.5 +/- 2.0 to 15.6 +/- 7.0%. Combined increases in QT and PvO2 from 66.4 +/- 2.7 to 135.6 +/- 21.5 ml/min and from 38.8 +/- 1.3 to 61.8 +/- 2.2 Torr, respectively, also produced a significant increase in Qs/QT from 7.33 +/- 2.27 to 15.43 +/- 4.45%. However, this combined change was explained exclusively by changes in PvO2. We therefore concluded that, under the conditions of our experiment, changes in PvO2 influence Qs/QT, and this may account for apparent dependence of Qs/QT on cardiac output in pulmonary edema.

Pulmonary Shunt Is Independent of Decrease in Cardiac Output during Unsupported Spontaneous Breathing in the Pig

“…In all settings, and irrespective of the magnitude of the shunt, lower CO resulted in lower PvO 2 (as oxygen consumption was maintained), and, as expected, 22,23 lower PvO 2 was associated with lower Q va /Q t during MV and CPAP. However, despite an equally decreased PvO 2 , lower PvO 2 was not associated with altered Q va /Q t in unsupported SB settings, where Q va /Q t was already lower than during MV.…”

“…Increased blood flow, increased PvO 2 , 22,23 increased mean pulmonary pressure, and decreased pulmonary vascular resistance 17 are all associated with increased shunt. Sandoval et al propose that PvO 2 mediates the CO-dependent shunting, 22 and this raises the possibility that HPV would act as the link between CO and shunt, as HPV is attenuated not only by increased PvO 2 but also by increased pulmonary artery pressure. 9 In our data, PvO 2 seemed not to be able to explain all the effects of CO on Q va /Q t ; however, this study was not designed to answer such a question.…”

Hypercapnic acidosis transiently weakens hypoxic pulmonary vasoconstriction without affecting endogenous pulmonary nitric oxide production

“…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.…”

Laryngeal mask and bleeding diathesis

“…Many animal experiments, particularly in dogs after intravenous administration of oleic acid which produces an oedematous lung injury characterised by intrapulmonary shunting, suggest that the reverse is true, i.e. that Qs/Qt varies directly with cardiac output [I], and that this is a result of the associated change in mixed venous Po, modifying hypoxic pulmonary vasoconstriction [2]. It seems probable that, despite the different pathology, such a mechanism would also apply in anaesthetised man, in which case changes in Sao, resulting from changes in cardiac output would be minimised.…”

“…However, it has been proposed as an explanation for the increase in percentage shunt observed when pulmonary artery pressure is reduced by haemorrhage in dogs with a dependent collapsed lobe [I]. Since the compression collapse observed by Hedenstierna's group during anaesthesia [2] is invariably in the dependent zones, there is no reason why the same mechanism should not occur in man. As we stated in our paper, the object was to make anaesthetists aware of these two possible mechanisms in the hope that it would stimulate further study.…”