This chapter has no relevance to any specific Section of the 2017 CICM Primary Syllabus, and is probably irrelevant to most (all) ICU trainees, as it describes a fragment of medical trivia which had minimal relevance even during the heyday of the Swan-Ganz catheter. A modern ICU trainee may never meet anybody who has ever measured this variable, let alone see this variable being measured.  
In short, the pulmonary capillary hydrostatic pressure is the pressure inside pulmonary capillaries, which is slightly lower than PA diastolic pressure and which is slightly higher than the PAWP.  It can be measured by analysis of a transient pressure change which occurs after an acute PA occlusion. This capillary pressure supposedly has some clinical relevance, as it is thought to be the pressure which forces fluid out of the pulmonary capillaries into the interstitium, causing pulmonary oedema.
 
In summary:
  • Pulmonary capillary hydrostatic pressure (Pcap or Pcp):
    • This is the intravascular pressure in the pulmonary capillaries
    • It is usually about 8-10mmHg
    • It is usually a little higher in the arterial (pre-alveolar) capillaries
    • This pressure is one of the determinants of fluid flux through the capillary wall, and represents the vascular hydrostatic force behind the formation of pulmonary oedema 
  • Measurement of the pulmonary capillary hydrostatic pressure:
    • It can be estimated qualitatively from the shape of the curve seen following PA wedging
    • It can be calculated from the fast and slow decay components of that curve
    • It can be calculated from the Gaar equation: 
      PPC = LAP + 0.4 × (mPAP - LAP)
  • Interpretation of the value
    • One way of using this is to determine a threshold value (individual for each patient) at which pulmonary oedema develops, and then to titrate one's fluid management in a way which does not exceed this value.
    • Another is to use it as a diagnostic tool to exclude cardiac causes of pulmonary oedema (in cardiogenic pulmonary oedema, Pcap is elevated)
 
The pulmonary capillary circulation, and the pressures therein, is discussed in the chapter on the physiological characteristics of pulmonary blood vessels. Here, the focus will be on the practicalities of measuring this variable, and the possible ways of interpreting it. The best published material on this seems to be the review by Jukka Takala (2003), followed by the paywalled Levy (1996). For most people, more than a couple of paragraphs will already be excessive, which means that the Pulmonary capillary pressure section from Robin et al (2006) will suffice.

Estimation of pulmonary capillary hydrostatic pressure

Even though pulmonary artery occlusion pressure is not the same pressure as pulmonary capillary pressure, the capillary pressure can also be estimated from the shape of the pulmonary artery occlusion pressure trace.  In general some of the best images of this phenomenon and some of the most detailed discussion can be found in the freely available 2011 review by Juan Grignola, which was heavily strip-mined for its material. Without going into too much detail (that is covered in another chapter), it will suffice to say that the true pulmonary capillary pressure can be extrapolated from the fas and slow components of pressure decay, as the arterial pressure droops after a wedge occlusion.

Pulmonary capillary pressure estimation from wedge pressure decay curves

In slightly more detail,

  • As the pulmonary artery is occluded, the occluded artery discharges its blood volume:
    • First into the pulmonary arterial capillaries
    • Then the same blood travels into the postcapillary venules
  • This produces a biphasic pressure drop:
    • A fast pressure drop which occurs due to high pulmonary arterial capillary resistance (this accounts for about 2/3rds of the total pressure drop)
    • A slow pressure drop which occurs due to the low pulmonary venous capillary resistance
  • Thereafter, with all the excess blood discharged into the pulmonary venous circulation, the occluded artery's measured pressure equilibrates with the pressure in the pulmonary veins.

The pulmonary capillary pressure can, therefore, be determined from this graph by three main means:

  1. By eyeballing the curve and estimating where the inflection point is, or
  2. By extrapolating the slow and fast decay curves and plotting where they intersect, or
  3. By using the Gaar equation, described by Gaar et al (1967):

As you can see, the visual method and the extrapolated curve method tend to give slightly different values:

calculating the PCHP

That Gaar equation is:

PPC = LAP + 0.4 × (mPAP - LAP)

where

  • PPC = pulmonary capillary pressure
  • LAP = left atrial pressure
  • mPAP = mean pulmonary artery pressure

In other words, Gaar and co. determined that the capillary pressure was under most circumstances about 40% of the total fall from mean PA pressure down to left atrial pressure (which is your occlusion pressure):

pulmonary capillary pressure calculated by the Gaar equation

Is this empirically derived shortcut accurate? Of course not. In fact, of these methods, none are particularly reliable, and so one must conclude the discussion of pulmonary capillary pressure with the statement that truly, the only thing we can safely say about it is that it is somewhere between pulmonary arterial diastolic and pulmonary venous pressure. In fact, generally speaking, in ICU capillary leakiness is rarely a purely hydrostatic thing. What of sepsis, DIC etc?...
In short, what you are measuring might be pulmonary capillary hydrostatic pressure, but it is not always going to be relevant to your decisionmaking.

So, how do you use this thing?

Let's assume that you have overcome all the practical and intellectual barriers, and somehow managed to measure a pressure which is the 100% accurate pulmonary capillary hydrostatic pressure. You now have in your hands a value which describes a major determinant of  fluid flux across the pulmonary capillary wall. Put in a different way, this is the pressure wot you oedem with.  In more formal explanations of this concepts, it is integrated into the Starling equation, like so:

Fluid efflux = Kfc(Pcap -Pint) - Kdcap - πcap)

where

  • Kfc is the capillary filtration coefficient (product of capillary wall hydraulic conductivity and capillary surface area),
  • Pcap is the capillary hydrostatic pressure,
  • Pint is the pulmonary interstitial hydrostatic pressure,
  • Kd  is the reflection coefficient (where 0 = freely permeable to proteins, and 1 = completely impermeable), 
  • πcap is the capillary oncotic pressure, and
  • πcap is the pulmonary interstitial oncotic pressure.

So, basically, when one has a patient with pulmonary oedema, one may measure this variable, and - if it ends up being low - one should be able to say with some conviction that the oedema is clearly not the consequence of increased pulmonary capillary pressure, i.e. no cardiogenic cause, but some kind of capillary leakiness, as in ARDS. 

Alternatively, one can observe a threshold value (individual for each patient) at which pulmonary oedema develops, and then resolve to limit one's fluid management below that threshold, i.e. serially measuring this parameter and witholding further fluid boluses if it is met or exceeded.

References

Kumar, Anand, et al. "Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects." Critical care medicine 32.3 (2004): 691-699.

Levy, Mitchell M. "Pulmonary capillary pressure: clinical implications.Critical care clinics 12.4 (1996): 819-839.

Takala, Jukka. "Pulmonary capillary pressure." Intensive care medicine 29.6 (2003): 890-893.

Ganter, C. C., S. M. Jakob, and Jukka Takala. "Pulmonary capillary pressure. A review." Minerva anestesiologica 72.1-2 (2006): 21-36.

Robin, Emmanuel, et al. "Clinical relevance of data from the pulmonary artery catheter." Critical Care 10.3 (2006): 1-10.