This chapter has no relevance to any specific Section of the 2017 CICM Primary Syllabus, and is probably irrelevant to most ICU trainees. In fact its relevance will continue to diminish with every year, as the measurement of pulmonary capillary wedge pressure recedes further into the mists of history, becoming less and less attractive as an exam topic. The discussion which follows is offered here mainly to satisfy the authors' obsessive need for completeness.
For a more professional overview, one might instead want to read O'Quinn (1983). The idea of measuring LA pressure by means of a pulmonary capillary wedge is ancient (older than Swan and Ganz), but they specifically designed their catheter for this purpose, and so their original article is probably still worth reading.
Behold the Tube.
In it, a nameless fluid flows, with a flow rate of Q. It flows because there is a difference in pressure from one end of the tube to the other. This is the ΔP. The walls of the tube offer resistance to the flow, expressed as R.
Thus, this equation describes the rate of flow:
Q = ΔP / R
- Q = flow rate
- ΔP = pressure difference
- R = resistance
To rearrange it, so we describe the difference in pressure:
ΔP = Q × R
That is to say, the change in pressure from one end of the tube to the other is proportional to the product of the flow and the resistance. So, how does this relate to the PA catheter? In the pulmonary circulation, the ΔP we are interested in is the difference in pressure between the pulmonary capillaries and the left atrium. To rearrange this equation for these pressures of interest,
Pc - PLA = Q × R
- Pc = pulmonary capillary pressure
- PLA = left atrial pressure
Now, if you inflate the balloon and stop the pulmonary arterial flow, Q becomes zero. This is the key feature. Without flow, there can be no resistance. Thus:
Pc - PLA = 0 × R
Pc - PLA = 0
and so, finally,
Pc = PLA
If you had to explain this without multiple equations, you could certainly do so. Observe: when the catheter is wedged, flow distally top it ceases; i.e. it is connected to a part of the pulmonary venous circulation by a static column of fluid, and provided that fluid column remains unbroken, the catheter should measure the pressure at the nearest venous junction (i.e. wherever the flow resumes).
Why is this discussion of flow and "venous junctions" important? Observe:
That's right. Because there is no flow distal to the wedged catheter, a static column of fluid connects it to the rest of the pulmonary venous circulation. That basically means that the pressure you end up measuring is the pressure of the next point in the circulation where there is some flow, which would usually be a junction of pulmonary veins.
Which brings up the next question:
Well, scientifically speaking, no. It probably is not exactly LA pressure, because if there is any resistance to flow along the vessel from that venous junction to the atrium, the catheter pressure will overestimate the left atrial pressure. In reality, though some resistance must surely be present, this is somewhat unlikely to have a massive impact on the flow, as pulmonary veins are rather low resistance vessels. Borrowing the usual equations to calculate PVR and substituting some values for pulmonary capillary and venous pressures from Smiseth et al (1999), you'd get some preposterous value like 0.03 dynes-sec/cm–5/m2. So, realistically the next points of increased "resistance" will actually be the mitral valve, and so you can still have some confidence in the wedge pressure and the left atrial pressure being relatively close. Of course, by this stage, one might have gathered that this relationship musty be pretty tenuous, and dependent on a variety of factors. Those factors are the subject of the next couple of chapters, which deal with the relationship of the wedge pressure to left atrial pressure, and with the factors which influence the validity of the wedge pressure measurement. Ultimately, the very reasonable questions "why the hell does this matter" and "how could it possibly be useful" are answered in the chapter on PAC-guided haemodynamic management, which tries to examine the rationale behind this historically very popular strategy, as well as the reasons for its downfall.