Output, pressure and shunt: misrepresentation of pulmonary haemodynamics

The role of intrapulmonary arteriovenous anastomoses (IPAVAs) and mechanisms regulating their behaviour are clearly of importance to physiologists and clinicians alike. By contributing to shunting, IPAVAs could worsen arterial oxygenation in a variety of settings; they might additionally serve as a conduit for paradoxical emboli. We were therefore disappointed not to be able to understand the topic better after reading a recent paper in The Journal of Physiology entitled: ‘Increased cardiac output, not pulmonary systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O₂’ (Elliott et al. 2014). It seems to us that the title and content of the manuscript raise two fundamental issues related to fluid mechanics.

First, it is self-evident that cardiac output cannot directly increase an intrapulmonary shunt, since the latter is simply a flow of blood down some tubes. The primary factors governing the flow of blood through IPAVAs are thus (i) their relative abundance and size, and (ii) the difference in pressure between the beginning and end of the tubes. If a flow increases in the presence of a constant drop in pressure across the tubes (as is claimed to occur for one drug administration protocol used by the researchers) this indicates a fall in the resistance of the tubes that has, in the first place, to be attributed to the drug infusion. It would seem desirable to avoid the use of vasoactive drugs, which might directly alter IPAVA tone independent of an effect on cardiac output. In a study that examined the behaviour of IPAVAs during a physiological state of elevated cardiac output (exercise), IPAVA flow under hypoxic conditions appeared to be greater at rest than during exercise (Bates et al. 2014), suggesting that there is not a straightforward relationship between increased cardiac output and IPAVA flow.

Second, implicit in the title is the notion that a ‘systolic pressure’ might be a candidate for driving flow through a pulmonary shunt over the whole cardiac cycle. This systolic pressure is an instantaneous maximum pressure in the pulmonary artery that can only drive a flow during, or briefly following, peak systole.

We are concerned that the complexity of this paper makes it difficult to draw any conclusions about mechanisms determining flow through IPAVAs, other than that atropine might have a slight dilatory effect. However, even this possible finding is weakened by the absence of a measurement of both the mean inflow pressure of the lung in the pulmonary artery and the mean outflow pressure in the left atrium. We agree with the authors that: ‘considering the unique experimental conditions used in the present study, it is difficult to extrapolate these findings to their potential physiological relevance’ (Elliott et al. 2014).

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Competing interests

The authors declare no conflict of interest in relation to this letter.