Global and regional ventilation and perfusion

This chapter is most relevant to Section F6(i) from the 2017 CICM Primary Syllabus, which expects the exam candidates to be able to "describe the concepts of global and regional ventilation and perfusion and the factors that affect these". No more detail is offered with regard to what exactly this means, and there are separate syllabus items which cover West's Zones, V/Q matching and various shunts and dead spaces, so one may be confident that "the concepts of global and regional ventilation and perfusion" don't cover any of that. The precise meaning is hard to tease out, because that specific phrase appears to be unique to the CICM syllabus and is not found anywhere else in the whole Interweb.  If one were unwilling to descend into unfairly critical antiestablishment polemic, one would prefer to believe that the syllabus-writers were earnestly intending this item to cover all the foundation concepts required to understand the more specific topics like Wests' Zones. It is with this assumption that this chapter is constructed. 

In summary:

There is no single resource which covers this topic, but if one had to pick a single best article, at least for factors affecting regional ventilation/perfusion relationships (which is usually where the marks are), one would probably go with Galvin et al (2007).

Global lung ventilation

In absence of any real scientific definition for this term, one could make something up; for example it would be relatively easy to say that global lung ventilation is the total volume of gas which passes through the lung per unit time. Though one could theoretically pick some random arbitrary volume units and time interval, the conventional way of expressing global lung ventilation is as the minute volume. Presumably for the purpose of making subsequent calculations neater, Nunn's gives  4L/min as the normal average minute volume, which corresponds to a tidal volume of 400ml with a respiratory rate of 10.

Regional variation in lung ventilation

There are substantial differences in the rate of air supply to different parts of the lung.  This unequal distribution of ventilation is the consequence of several factors:

• There is a gravity-related vertical gradient of pleural pressure which results in a difference in distending transpulmonary pressure during normal spontaneous ventilation. 
• Posture changes the direction of this gradient due to the effects of gravity , because of the weight of the lung, changes in chest wall excursion and the shifting of mediastinal and abdominal contents.
• Bases have more room to expand than apices. Transpulmonary pressure changes the most in the bases because the volume of the apical part of the chest cavity is anatomically rather fixed, wheres the base of it expands both down (by the diaphragm) and out (by the movements of the rib cage). 
• Compliance differences between lung regions are also responsible for uneven ventilation; the more compliant patch of lung is ventilated better at any given pressure, by definition. This accounts for some of the increased ventilation of the lung bases (that lung is relatively deflated and therefore more compliant, whereas the apical lung is almost fully inflated). Similarly, consolidated inflamed contused or atelectatic lungs will have poorer compliance and therefore regionally decreased ventilation.
• Pattern of breathing (eg. whether it is voluntary or not) can influence regional distribution of ventilation by preferentially expanding some regions of the thorax instead of others. For example Sampson et al (1984) were able to demonstrate that there is a difference in pleural pressure distribution and radioactive xenon washout between breathing which engaged intercostal muscles as compared to "routine" diaphragmatic breathing.

Global lung perfusion

Again, there is no credible scientific definition for "global lung perfusion" because it is probably completely unnecessary as a concept. If one had to invent a meaning for it, one could loosely define it as the total amount of blood circulating through the lung per unit time. Because the lungs receive a blood flow equal to the total volume of the blood pumped by the heart, it is convenient to express this as the cardiac output, in L/min. This global perfusion is split between the two lungs approximately equally, with some trivial variation. Cheng et al (2005) measured pulmonary blood flow in normal subjects using MRI and found the flow split 45%-55% at the most, with the right pulmonary artery getting a slightly larger amount of blood.

Regional variation in lung perfusion

The pulmonary circulation is (vaguely) regulated, in the sense that individual vessels have some degree of control over their diameter and therefore over their resistance. The changes in pulmonary vascular resistance is affected by a large number of factors, such as blood flow, lung volume, alveolar oxygenation, as well as various paracrine hormonal and metabolic factors. One can imagine that it would be extremely unlikely for these factors to be acting on the whole lung in a totally homogeneous fashion, and therefore different lung regions will have different factors affecting their vascular resistance, changing the regional distribution of blood flow.

In summary, regional blood flow is affected by the following factors:

• Variation in alveolar oxygenation: hypoxic pulmonary vasoconstriction creates increases in regional vascular resistance and redirects blood flow away from poorly ventilated regions. This is probably the most physiologically important aspect of regional perfusion inequality.
• Gravity-related hydrostatic pressure: because the lungs of an upright adult may be up to 30cm in apex-to-base height, the blood contained by these vessels creates a column of blood which exerts a hydrostatic pressure (i.e. at the bottom of it, the pressure would be 30 cm H2O, or 22 mmHg). This increase in hydrostatic pressure tends to recruit capillaries and increase blood flow to the basal regions of the lung.
• Basic architecture of pulmonary vessels:  the actual branching and forking pattern of the pulmonary vascular tree has an effect on directing blood flow.  Glenny et al (1997), by gradually filling the pulmonary vessels of dogs with coloured microspheres, were able to determine that blood flow was quite heterogeneous in even the same horizontal plane of the upright lung and remained stable over days. The authors reached the conclusion that at least some aspect of pulmonary blood flow heterogeneity was "baked in", structural in origin and unrelated to oxygenation and posture.

Relationship of ventilation and perfusion to lung regions

Having now discussed that the perfusion and ventilation differs across a lung, and that the differences are most pronounced between the bases and apices in an upright lung, we are now ready to represent this concept in the form of a graph:

Some version of this famous graph is repeated in virtually every physiology textbook and is usually attributed to West's textbook (1977). In actual fact, that is not where it is originally from. The ventilation slope probably dates back to Ball et al (1962) who measured the clearance of radioactive Xe¹³³ from pulmonary blood at different levels in the chest, and from West & Dollery (1960), who did something very similar with radioactive CO₂ (that's where that "3rd rib" thing seems to come from).

From the original graphs in these papers (shamelessly misappropriated here), one can see that the perfusion slope is much steeper than the ventilation slope. The graph known from modern textbooks seems to have been concocted from these data by West in his 1968 review for the Postgraduate Medical Journal. To represent the changing relationship of ventilation and perfusion along the span of the upright lung, West had graphed the ratio of these parameters on the same coordinate field.